Essentials of

Clinical Medicine
 Essentials of
Clinical Medicine

Samir Kathale
MBBS Intern. Std.
Mahatma Gandhi Memorial Medical College
and
Maharaja Yashwant Rao Holkar Hospital
Indore (MP)

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Essentials of Clinical Medicine

© 2006, Samir Kathale

All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or
transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or
otherwise, without the prior written permission of the author and the publisher.

This book has been published in good faith that the material provided by author is original. Every
effort is made to ensure accuracy of material, but the publisher, printer and author will not be held
responsible for any inadvertent error(s). In case of any dispute, all legal matters are to be settled
under Delhi jurisdiction only.

First Edition: 2006

ISBN 81-8061-615-0

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Printed at Gopsons Papers Ltd, A-14, Sector 60, Noida 201 301, India
 DEDICATED TO

MY GRANDPARENTS
PARENTS
Shri ANANT KATHALE
Smt. SAVITA KATHALE
BROTHER
SAGAR KATHALE
&
ALL MY WELL WISHERS
whose blessings have only made this venture possible...
 Preface

Medicine can be compared to an endless ocean. The farther we step into it, the more unboundable it seems to become. It
is an ever-growing science. The expanding clinical experiences, advancements in technologies, newer inventions and
better drugs in the field of pharmacology, all together have contributed to the enormous growth of literature in medicine.
While I was an undergraduate student, I felt dearth of a single comprehensive book in clinical medicine which could
provide most of the information that an undergraduate student should know to get a firm grip over clinical practices in
medicine, so as to become a full-fledged doctor. My friends also shared the same idea. Most textbooks of clinical
medicine originate from the West and many a times are difficult to be appreciated in the Indian setup. These authors
sometimes, unnecessarily, deal in great depth, with certain topics that does not suit to our setup, while leaving other
topics (though of similar importance) to the students. So, being constantly insisted and hard pressed by my beloved
friends and colleagues, I ultimately ventured to write a textbook on clinical medicine, which should be comprehensive as
well as oriented to improving the hands of our budding doctors in the field of clinical practices. This book also finds itself
to be examination oriented. My sole intention has been to write in a clear, concise and easily understandable way, in my
own style, keeping always a vigilant watch to the student’s interest.
An earnest attempt has been made to merge the clinical methods and principles of internal medicine and to present it
in a condensed form. To keep the size and volume compact, and small, only certain important clinical topics are included
in this manual, even references are not included since high-tech reference system is available in all good libraries.
This book is primarily intended for the undergraduate medical students and practicing physicians with special emphasis
on clinical methods and clinical features. The book does not provide much information about the investigations and
management part of various clinical disorders, because, the author is of the opinion that these can be read by the students
from any standard textbook of medicine.
The core skills of communications, clinical examination, objective assessment and planning are as important clinical
practices as ever. These skills can only be gained by learning and practice. Medicine is a noble profession, there is a
relationship of trust between patients and doctors, and the doctor is recognized to have acquired knowledge and skills
relevant to the practice of medicine. In addition, a code of ethics binds the doctors to certain modes of conduct in the
clinical relationship with a patient and in relation with colleagues. All these matters are a part of clinical method in the
modern world. Essentials of Clinical Medicine seems to teach an integrated approach to clinical practice, so that new
methods and techniques of examining a patient are merged into established patterns.
All of us find new things to learn everyday, and the more alert we are, more we find there is to learn. Knowledge and
understanding are the keys to good practice. With the advent of Internet, and easy availability of information, people are
generally better informed than in the past. The modern doctors need to be aware of this and to develop particular skills in
dealing with the informed patient and their family. A firm foundation in clinical methods is essential to this process.
This book is divided into six sections: The General History Taking, The Common Symptoms Presented by the Patients
and Questions to be Asked for Them, Symptomatology and its Causes; The General Examination; The Systemic Examination
and Common Cases Encountered in Clinical Medicine. It also includes X-rays, CT-scans, MRI, photographs, ECGs and
procedures routinely followed in medical wards. The whole text is organized into both body system-related and problem-
oriented chapters. The basic method of cardiology, neurology and other specialities are described in chapters devoted to
these topics. The special skills required in dealing with unconscious patients are also discussed. There are many illustrations
and diagrams to help the students to understand the topic well.
In preparing a textbook like this, I have freely utilized the knowledge and experience of the stalwarts in this profession
and I have consulted many books on clinical medicine and various established global journals.
I would sincerely like to acknowledge the supporting hands of MY TEACHERS; Dr (Mrs) SHWETA PAWAR; my
colleagues Dr KUMAR SAURABH GAUR, Dr (Ms) MEGHNA MAHESHWARI, and Dr SAURABH ARGAL and my
viii Essentials of Clinical Medicine

friends ABHISHEK SAXENA and ASHISH SAXENA (SOFTWARE ENGINEERS) for their full co-operation and
support. They all stayed besides me when I needed their help.
I sincerely thank my patients who allowed me to picture themselves in this textbook. I am deeply indebted to GOD
AND MY PARENTS for supporting and encouraging me during the complete period from writing to the printing of the
text.
Last but not the least, I wish to acknowledge the help and encouraging attitude of Editorial Board and the entire
staff of Jaypee Brothers Medical Publishers (P) Ltd. for their generous cooperation and coordination in bringing out
this first edition. I am definitely confident that this manual will help the students to look into the subject of clinical
medicine in much simpler, better and broader way.
Once again, my heartful thanks to Dr KUMAR SAURABH GAUR, Dr SAURABH ARGAL, Dr (Ms) MEGHNA
MAHESHWARI, ABHISHEK SAXENA and ASHISH SAXENA (Software Engineers) for encouraging me and providing
their invaluable help.

Samir Kathale
All that a man achieves and all that he fails to achieve is the direct result of his own thoughts.
James Allen
Love cures people, both, the ones who give it and the ones who receive it.
Dr Karl Menninger
Lack of will power has caused more failure than lack of intelligence or ability.
Flower A Newhouse
Some people see things and ask, why? Some people dream of things
that never were and ask, why not?
George Carlin
Nothing great was ever achieved without enthusiasm.
RW Emmerson

“Long Live Humanity

Long Live Medical Science...”
A great part, I believe, of the art of medicine is the ability to observe, leave nothing,
combine contradictory observations and allow yourself enough time.
Hippocrates
To study the phenomenon of disease without books is to sail an uncharted sea,
while to study books without patients is not to go to the sea at all...
Sir William Osler
There are no shortcuts for physical diagnosis. It is learnt only by practice, not a dull,
deary monotonous practice but practice with all the five senses alert.
Sir Robert Hutchison
 Contents

1. History Taking ....................................................................................................................................................... 1

2. Common Symptoms Presented by the Patients and Questions to be Asked for Them ................................ 9

3. Symptomatology and its Causes ........................................................................................................................ 24

4. The General Examination ................................................................................................................................... 61

5. Respiratory System ............................................................................................................................................. 79

6. Alimentary System ........................................................................................................................................... 103

7. Cardiovascular System ..................................................................................................................................... 133

8. Central Nervous System ................................................................................................................................... 172

9. Examination of the Spine ................................................................................................................................. 266

10. Common Cases Encountered in Clinical Medicine

• Hypothyroidism, Myxoedema and Thyrotoxicosis ..................................................................................... 284
• Diabetes Mellitus .......................................................................................................................................... 287
• Lymphadenopathy ......................................................................................................................................... 289
• Arthritis ......................................................................................................................................................... 290
• Renal System Presentation ......................................................................................................................... 293
• Skin Lesion .................................................................................................................................................... 295
• Case of Anemia ............................................................................................................................................. 296

11. Pelvic Pain .......................................................................................................................................................... 298

Appendix-I: Weights and Measurements of Normal Organs ................................................................................ 301

Appendix-II: Clinical Chemistry of Blood .......................................................................................................... 302

Index .................................................................................................................................................................... 307

 General

Through this book, the author has tried to make a sincere effort to look into the field of Clinical Medicine through the
eyes of a student. Keeping in mind the difficulties which the author used to face, as a student, in various elements of
clinical medicine, such as eliciting the relevant history in a correct manner, the perfect general as well as the local
examination, reaching to the provisional diagnosis and differentiating it from other similar illnesses and clinical disorders
(what is known as the differential diagnosis of the clinical problem), he has tried to simplify the work of a medical student
to get a tight grip over clinical aspects of internal medicine.
The author considers himself to be a part of the student community and hence, best understands the lacunae of the
students and the areas where they are likely to commit mistakes. The clinical medicine forms the foundation of the
internal medicine. Realising this, every possible effort has been made to make the clinical medicine easier, interesting and
easily absorbable.
The author sincerely suggests the students not to feel the subject of medicine a havoc but to grasp it in an easier and
interesting manner. Remember “It’s all Possible”. Just as the scientists have their research laboratories; the lawyers work
in the court room; so also the medical students have hospitals and clinics as their workshops. Therefore, it is expected
from them to attend the clinics regularly and sincerely so as to turn themselves into the undefeatable and ever-progressing
clinicians.
 Introduction

The word “patient” is derived from the Latin word patiens, meaning sufferance or forbearance. Although our health
experts have given a perfect definition of “health”, but they have not yet succeeded in defining the term “disease”. This is
because disease has many shades (called the spectrum of disease) ranging from inapparent (subclinical) cases to severe
manifestations of illness.The Oxford English Dictionary defines disease as “a condition of the body or some part or the
organ of the body in which its functions are disrupted”. The main aim of medical practice is to cure the patient or to
relieve the patient’s sufferings. In order to solve this purpose, it is of utmost importance to know how to approach to the
problems of the patient, to make a diagnosis and to design an appropriate scheme of management and treatment for each
patient.
To arrive at a correct diagnosis, a physician has to follow a certain path (or rules). This includes:
1. The interview or the history taking.
2. The physical examination which includes both the general as well as local examination.
3. Drawing a provisional diagnosis.
4. Performing the relevant investigations needed.
5. And at last, reaching to the final diagnosis of the illness.
The clinicians (and of course the students also) should always attempt to take a good history, as this practice will help
them to arrive at a correct diagnosis.
 1
History Taking
PROPER HISTORY TAKING
Proper history taking helps a clinician to come to 60-70
percent of the diagnosis of a clinical illness/problem.
History taking is an art, which forms an important part
in approaching the patient’s problems and arriving at a
correct diagnosis. History taking helps to form a healthy
doctor-patient relationship. It also helps a physician to win
the confidence of the patient.
Certain points are to be given attention to while eliciting
the history. The patient should be encouraged to tell about
his/her problems in his/her own words as far as possible.
Very few physicians are good interviewers and very few
patients are good narrators. Therefore, a careful elicitation
of the patient’s problems is needed. This needs an examiner
to have a thorough knowledge regarding the disease. For
example, the doctor may sometimes need to ask about past
history of fever, chronic cough and gradual weight loss if
he/she suspects tuberculosis in his/her patient.
Raising the Set-up (The General Scene)
Most of the medical introductions or consultations between
the patients and the clinicians occur in the out-patient setting.
The achievement of confidence and the assessment of
personality and social skills of each patient can be done
here. Either the doctor must himself go to fetch the patient
from the waiting room or the patient may be brought into
the consultation room by the nurse or receptionist (which
is usually seen). This creates a friendly atmosphere and the
patients too feel assured of being at the right place. Introduce
yourself and greet the patient gently. Try to observe his
response. Does the patient smile or look frightened or
anxious? Does he make good eye contact? Is he depressed
or normal? Do you find any signs of breathlessness? You
may try to feel his body temperature when you give him a
handshake. Always handshake by using both the hands of
yours. By this, the patient gets a feeling of being at your
concern and care (and your main purpose of feeling the
temperature is also solved). Pleasant surroundings are very
important. Both, the consultant and the patient, should feel
at ease with each other. Always try to make the patient to
sit to your left. This makes your observation more accurate
and even better.
Observing the Patient
The process of observing the patient must begin right from
the moment he walks into your chamber. While communi-
cating with him, try to make judgments about the patient’s
general demeanour. Does he present himself in a clean, well-
spoken, intelligent manner? Do you find any signs of
disability, whether mental or physical? What does the
gestural language of the patient says? Is the patient confident,
knowledgeable or perhaps depressed and miserable? Does
he or she describe his/her problem in a relevant manner? Is
there any embarrassment about something that is not spoken
of ? Is the patient talking about the things that really bothers
him? Have a look over the patient’s clothes and belong-
ings. This tells a lot about your patient’s language, interests
and educational level. Try to explore the patient’s knowledge
about his own illness or disease.
Persons Accompanying the Patient
A good clinician always likes to spend some time during the
initial exchange of greetings to know and identify who is
present and to get some idea of the persons accompanying
the patient. Identify the seniormost person present. Try to
know the expectations of this consultation. Inquire whether
the patient has taken medical care of any other physician.
Assure him that it is only to make his treatment better and
successful. Make sure why the accompanying persons wish
to be present, and, certainly, whether this is also the patient’s
wish. Sometimes the information obtained from a concerned
and observant relatives may be of great importance to you.
But avoid unnecessary interpretation by them.
In certain ethnic groups, including Asians and Muslims,
the patient is usually accompanied. A female patient may
2 Essentials of Clinical Medicine
come with several other family members. As far as possible,
always attend to and examine a female patient in the
presence of one of her family members (of course, an adult)
or a person with whom she is accompanied.
Communicating with the Patient
Never try to start the interview immediately. It is better to
engage in certain preliminary exchange of ideas. This way,
the patient will be at ease and this will also lend you the way
to go confidently. At times, you may try to create some humor
(of course, after judging the mood and condition of the
patient).
A word of caution—always check that you have the right
patient—there may be many patients of same name or same
surname (for example, there may be many Mr Sharma or
Mrs Shrivastava waiting for you). Check the address, date
of birth as well as name. Also, have a look at the patient’s
papers and hear what the patient has to say. Let communi-
cation be a two-way process.
Assuring the Patient
Always try to tell your patient that you expect him to talk
freely. Assure the patient that you will be able to reach to
the correct diagnosis only if he narrates to you the complete
and detailed facts. Assure him that his secrets will not be
disclosed to anybody and he/she is in the safe hands.
Explaining the Patient
From the patient’s perspective, the most important compo-
nent in the process of history taking and clinical examination
is “the explanation.” The clinicians who are gentle, patient,
interested and kind to the patient, those who encourage the
patient and relatives to ask questions and who spend the
time explaining the situation in a way it is understood are
regarded as “good doctors”. A clinician, who readily accepts
his mistakes instead of trying to hide it, is more respectable
in the eyes of the patients and his relatives. He should assure
them that still many “good things” can be done for the
patient. He should well explain the patient and his relatives
about the illness of the patient.
Role of the Medical Students
Every medical student should try to make his best efforts at
good history taking and thorough and complete clinical
examination. If the students are asked by a patient to give a
medical opinion, they should gently remind the patient of
their status and suggest them to undergo a more useful
consultation with the doctor. Always remember that an
undergraduate medical student is not there to give opinions
or medication to the patients. He is supposed to examine
the patients, to observe them,and then finally report to a
senior doctor about the findings in the patients and learning
more about the cases.
Taking the Notes
Try to keep eye contact with the patient while making notes.
Do not be in a hurry to make notes. First listen carefully to
the patient, make up your mind what is being said and record
enough (in the form of the points) to help you remember
the important points narrated by your patient. Later, you
can make a detail out of these points. Always use the words
narrated by the patient. Never try to use medical terminology
for the complaints described by the patient until and unless
you are very much sure about that. For example, never use
the words like vertigo for “chakkar” or dyspnea for
“difficulty in breathing.” The same is to be applied while
talking to the patient.
Requirement of Direct Questions
You will always find time and place for direct questions in
history taking. Direct questions are indeed an essential
component of relevant history taking. A good physician
always stores up the direct questions until the patient has
finished talking. If you are not sure of something, ask for
more details. If you have noticed an abnormality not
mentioned by the patient (for instance, a swelling, a rash,
an abnormal posture, a visible scar mark, etc.), ask about it
directly. Now if you think that you have a clear understanding
of the patient’s complaints, you should take each main
symptom in turn and have a detailed examination. Some
examples of direct questions are:
Have you ever coughed blood?
• Do you feel better after vomiting?
• Do you have fever with chills and rigors?
Non-Verbal Clues
A vigilant doctor will always try to look for non-verbal clues.
Look at the facial expressions of the patient. Whether it
shows any signs of grief, tiredness, stress or anxiety. Does
the patient catch his breath, appears confused, has abnormal
breathing pattern, looks pale or flushed, is restless or shows
any abnormal body posture or body movements? Does he
catch hold his head while speaking or takes along pause to
narrate the next point to you? Always behave peacefully
with such patients. Be sympathetic to them. Try to know
the causes of his worries; and if possible at your level, try to
solve his problem. You should put your pen down and listen
carefully to the patient and you should give an eye-contact
to the patient. Many a times, it may happen that the points
which the patient is narrating to you may not be useful for

you or for your process of history taking. In such a case,
you should be at your norm and should peacefully try to
explain him what you expect him to tell to you. Many
patients have the habit of telling about their complaints in
an exaggerated manner in order to gain your attention. They
may complain of “all the time” pain or headache or they
may complain of having anorexia or abdominal discomfort
for last few weeks. Indeed, in spite of his exaggeration, the
complaint is real (no doubt, it may be of mild degree), but
you should definitely pay your full attention to it.
Bearing the Insults
Many a times, the patient may be so frustrated and worried
about his problems, or he may be waiting for his turn since
long, that he may burst open on you. In such a situation,
you should handle the patient very gently. After the day’s
tiring work, it may seem difficult for you, but remember it is
not impossible. Always try to have a soothing attitude. After
all, you are there for the same. If at all the patient is so
angry that he tries to dominate you, it is good for both of
you “to end up the consultation”, to have the consultation
on some other occasion or some other day/date, or you may
even refer the patient to some other doctor also.
Five “W”s and One “H”
This stands for six utmost important questions to be asked
while taking the history. They are as follows:
• What are the chief presenting complaints? Or what has
made the patient to approach to you?
• When did the problem start?
• Where, i.e. the body part where the problem started first?
• Which steps the patient has taken to cure himself before
reaching to you? (This also includes the consultation
with some other physician.)
• Whether the patient has been taking medications for the
same illness earlier also and whether he has shown
himself to any other physician?
• How has the problem affected the daily activities of the
patient?
Summing Up
The summary is the main crux of the matter that you have
discussed with the patient. In this process the history narrated
by the patient is read in front of him within a very short
time (say, one or two minutes). For example, “Let’s have a
quick look at what we have discussed so far and please
correct me wherever I go wrong. You were absolutely alright
till last evening when you suddenly developed crushing pain
in the middle of your chest while you were watching the
History Taking 3
television. You turned sweaty and started vomiting and were
breathless also. Then you turned restless and could not sleep
the whole night. And this morning you are here. Am I right?”
Success of a Good Interview Depends Upon
Asking the relevant questions tactfully
↓
Yields accurate history Good basis for physical
examination, investigations and interventions
↓
Good doctor-patient relationship
↓
Patient is satisfied and trusts on you
↓
Good patient compliance
Qualities that Every Clinician must
Try to Develop
1. Technical skill, scientific knowledge and human
understanding.
2. Courage, humility and wisdom.
3. Edifice of character within himself.
4. A professional attitude, coupled with warmth and
openness.
5. Respect and sincere concern for the patient.
6. Alertness and consciousness.
7. Honesty and love for the job.
8. To be empathic.
9. To be an active listener and be vigilant.
10. To be articulate—knowing when to speak, what to
speak, how to speak.
11. To be best at his non-verbal communication.
12. To be caring, compassionate and friendly.
13. Show interest in other’s problems and be enthusiastic.
14. Never show impatience, even if you are short of time.
15. Never look tensed or worried. This is the worst
impression you can give to your patient. Keep aside
all your worries while attending the patient.
16. Be humble, modest and soft-spoken.
17. Be neat and tidy, well-dressed and up-to-date.
Elements in a Clinical History Taking
(The Proforma)
• Name
• Father’s name
• Husband’s name (for female patients)
• Age and sex of the patient
• Address
4 Essentials of Clinical Medicine

• Date and time of admission (if the patient is admitted) and dye industries; scrotal cancer—chimney sweeps; pneu-
• Marital status (single or married) moconiosis, silicosis and anthracosis—mining, sand blasting
• Socio-economic history and coal industries; lead poisoning—lead using industries
• Education (of both husband and wife) and plumbers; cirrhosis of liver—chemical industries;
• Religion, caste and race surgeons, traffic police and housewives—varicose veins.
• Occupation (of both husband and wife) Thus, the list goes on and on. Questions that you should
• Presenting complaints ask to the patient are:
• History of presenting complaints • Is your job dusty? What type of dust is it?
• History of any previous illness (past history) • Which tools make dust?
• Any medical history and treatment history (along with • How long have you been working there?
exposure to radiation) • Are the protective clothes provided ?
• Any surgical history • Are goggles and suits required and why ?
• History of any drug allergy or allergy due to some other • Any such illness affected any other fellow employee?
substances • Is the job sedentary type ?
• Personal history • Are the fumes, vapors and chemical substances invol-
• Family history. ved?
Occupational Diseases
DETAILS OF HISTORY TAKING
Occupational diseases are defined as the diseases arising
Name: Asking the name is an opening question in an
out of or in the course of employment. They are grouped
interview. It is good to use the patient’s name or the surname
as in Table 1.1.
(depending upon his age). This way the patient feels himself
to be at your concern; and no doubt, it helps to go on with Table 1.1: Occupational diseases
the discussion. For example, “Mr Paul, please come in,” Diseases due to physical agents:
Or, “Hello Ram, how are you?” 1. Heat Heat hyperpyrexia, heat exhaustion, heat
Age and sex: Certain diseases are more common at certain syncope, heat cramps, burns and local
effects such as prickly heat.
age groups. For example, atherosclerosis and certain degene- 2. Cold Trench foot, frost bite, chillblains
rative disorders occur at a later age, whereas certain 3. Light Occupational cataract, miner’s nystagmus
congenital anomalies manifest themselves at younger age 4. Pressure Cassion disease, air embolism, blast
except for a few disorders like valvular heart disease with a (explosion)
5. Noise Occupational deafness
mild degree of abnormality or syringomyelia that manifests 6. Radiation Cancer, leukemia, aplastic anemia, pancy-
at a later age. topenia
Certain diseases are more common in a particular sex. 7. Mechanical factors Injuries, accidents
For example, hemophilia manifests itself only in males, 8. Electricity Burns
whereas the carriers are the females. Atherosclerosis and Diseases due to chemical agents:
myocardial infarction are more common in males. But 1. Gases CO2, CO, HCN, CS2, NH3, N2 H2S, HCl,
SO2. These cause gas poisoning.
women too are not spared. Rheumatic mitral stenosis, breast 2. Dusts (pneumoconiosis)
cancer and thyrotoxicosis are commoner in females. i. Inorganic dusts:
Address: The place where the patient lives, i.e. the area, the a. Coal dust Anthracosis
b. Silica Silicosis
locality, the state or the country holds certain significance. c. Asbestos Asbestosis, cancer lung
For instance, endemic goiter is mostly seen in the foothills d. Iron Siderosis
of the Himalayas. Lathyrism caused by the long-term ii. Organic (vegetable)
consumption of khesri dal is commoner in the North Indian dusts:
a. Cane fiber Bagassosis
states. Skin diseases and respiratory disorders like b. Cotton dust Byssinosis
pulmonary tuberculosis is more common in people of lower c. Tobacco Tobacosis
socio-economic groups and those living in slums and d. Hay or grain dust Farmer’s lung
crowded, ill-ventilated environment. 3. Metals and their Toxic hazards from lead, mercury,
compounds: cadmium, manganese, beryllium, arsenic,
Occupation: The occupation and the working conditions of chromium, etc.
a patient can provide direct clues towards the etiological 4. Chemicals Acids, alkalies, pesticides
factors of the disease. For example, bladder cancer—paints Contd...
 History Taking 5

Contd... • Occupation:
5. Solvents Carbon disulphide, benzene, trichlo- – Current and previous
roethylene, chloroform, etc. – Exposure to hazards, e.g. chemicals, accidents
Diseases due to biological Brucellosis, leptospirosis, anthrax, – Unemployment—duration and reason
agents: actinomycosis, hydatidosis, psittacosis,
tetanus, encephalitis, fungal infections,
– Attitude to job or unemployment.
etc. • Economic condition:
Occupational cancer: Cancer of skin, lungs, bladder – Financial circumstances including loss of income
Occupational dermatosis: Dermatitis, eczema and debts.
Diseases of psychological Industrial neurosis, hypertension, • Relationships/domestic circumstances:
origin: peptic ulcer, etc.
– Marital status:
 Quality of relationship and any problems
Religion, caste and race: Although the patient may feel it
 Spouse’s occupation and attitude to patient’s
awkward and may also find it useless when you ask him
about his caste or religion; but you should try to explain illness
him that in some cases, it may provide important clues in  Sexual identity—any problems
 Other occupants of the house—any problems,
the diagnosis of the disease. Some of the diseases are more
common in particular groups or communities. For example, e.g. violence, health and bereavement.
the largest concentration of thalassemia patients is seen in – House:
 Type of home—size, owned or rented
South-East Asia, Sri Lanka, Bangladesh, North-West India,
Pakistan, Middle East countries, North Africa, Greece and  Problems with the house and neighbors
Italy. Its prevalence in India is high among Gujaratis,  Supporting friends or family.
Punjabis, Sindhis, Lohanas, etc. Over 30 million people are – Community support:
 Social and health services involvement
carriers of thalassemia gene in our country. Ten thousand
 Attitude to the help being provided.
thalassemic children are born every year in India. Sickle
– Leisure activities:
cell disease is common in Africa and in American Blacks
 Habits
and in aboriginal tribes in Central India (Mahars, Kunbi
 Tobacco
and Telis) inhabiting areas around Chhota Nagpur, in
 Alcohol
Maharashtra, in MP and extending to Orissa. Nearly 20
 Caffeine
million people are affected in India. Hemoglobin D disease  Illicit drugs
(also called hemoglobin Punjab) is seen in 10 percent of  Dietery restrictions/eating habits.
Punjabis and Gujaratis in India. Hemoglobin D thalassemia Presenting Complaints
is a very mild clinical syndrome like thalassemia minor. It • What are the complaints?
has been seen in Punjabis. Hemoglobin E thalassemia is • How long? (Duration)
common in West Bengal, Assam and in Bangladesh. • Note the complaints in non-medical terms (i.e. the way
Hemoglobin C thalassemia is seen in Italians (severe form) the patient describes them).
and in Blacks (relatively milder). • If there are more than one complaint, then they should
Social history: You should ask the patient about: be recorded in chronological order. For example:
• His upbringing (Whether it was at home or away from – Cough with expectoration = 1 month
his parents?) This question is especially important in – Breathlessness on exertion = 20 days
psychiatric cases. – Headache = 7 days
– Birth injury or complications – Vomiting = Since the previous night.
– Early parental attachments and disruptions • What is the mode of onset?
– Schooling, academic achievements and difficulties • Is there any progress in the symptoms? If yes, slow or
– Behavioral problems. fast?
• Insults: • Special time of occurrence?
– Emotional, physical or sexual abuse (this requires • Any kind of periodicity in the symptoms?
good training and skill) • Aggravating and relieving factors?
– Experiences of death and illness • Associated symptoms?
– Interest and attitude of parents. • Conclusion?
• Education/occupation: (When you have recorded the chief complaints, you should
– Higher education and training ask about each and every symptom in detail. This is because
6 Essentials of Clinical Medicine

a single (same) symptom may be due to the involvement of • Inquiry about sleep—duration and soundness of sleep
two or more systems. For example, dyspnea (breathlessness) • Sanitary habits
may be due to respiratory or cardiovascular system • Marital history, and if the patient is female, you should
involvement. As a medical person, you should be familiar take menstrual history and also inquire about the methods
with etiology of dyspnea. of contraception used by her.
Exertional dyspnea – cardiac origin • History of addiction is very important to be looked for.
Dyspnea occurring You should inquire about the substance for which the
paroxysmally, with – respiratory origin patient has addiction and also the form in which he
wheeze and associated consumes it. You should also ask about the duration of
with respiratory tract consumption. If the patient denies of any addiction
infection currently, then you should ask whether he had any such
• Any other special inquiry or questions? in the past and how long did he do it and how long had
History of any previous illness or past history: Try to make it been after giving up the consumption? Why did he
detailed inquiry about all the illnesses right from the patient’s gave up or whether there were any signs and symptoms
childhood, especially about those diseases/symptoms that of some illness fearing which he gave up the substance
are related to the presenting complaints and also their of abuse?
duration and severity. *Alchol intake:
• How long has the patient been taking it?
Medical history and treatment history: A detailed inquiry
• Quantity per day—Is there any change as compared to
should be made about significant illnesses which the patient
earlier?
had suffered in his life and whether he was ever admitted
• Type of alcohol consumed?
for that. What was the outcome of that illness? Is it still
• Money spent over it—Whether it is drunk alone or in
continuing? Did the patient took any medications to cure
group and place of drinking?
the disease? What were they? (If he still remembers the
• Whether consumed daily, weekly or on particular
names of those medicines?) How long did he do so? Was
occasions?
the complete treatment taken with proper dosages? And
• What is the the purpose of drinking?
few other questions which you find significant. Was there
• His attitudes towards drinking?
any recurrence of the illness? Were there any side effects
• Any withdrawal symptoms?
of the therapy and if yes, what were they?
(Similarly, the questions about tobacco chewing or smoking
Surgical history: Whether the patient was operated anytime can also be asked to the patient.)
for some illness? What was the case? What was the outcome
of the surgery? Was there any recurrence of the illness? Alcohol-Related Disorders
Were there any serious complications of the surgical 1. Alcohol dementia (cortical atrophy)
procedure? 2. Subdural hematoma
History of drug allergy (allergic reactions due to certain 3. Withdrawal symptoms
drugs): Has the patient ever shown allergic manifestations 4. Delirium tremens
due to any specific drug? What were they like? Also, inquire 5. Cardiomyopathy
about their severity and duration. What did the patient do to 6. Hypertension
get rid of these signs and symptoms? 7. Hepatic cirrhosis
Personal history 8. Portal hypertension
• Educational status of the patient? 9. Pancreatitis
– Any kind of addictions—smoking, alcohol or 10. Dupuytren’s contracture
tobacco? (see the details below)* 11. Proximal myopathy
• History of blood transfusion—the reason, the age, 12. Peripheral neuropathy.
number of times; and if the patient remembers, the Tobacco-related disorders: (You should inquire about the
amount of blood transfused. form in which the tobacco is consumed that is—smoking
• Immunization—received or not. If yes, complete or not? cigarettes or beedis, or chewing simply in betel leaf (paan)).
• Apetite, diet, thirst, frequency of micturition and bowel 1. Cardiovascular accidents
habits and constipation should be recorded. 2. Tobacco amblyopia
• History of weight change—gain, loss or the same? 3. Carcinoma mouth

4. Carcinoma lungs
5. Chronic obstructive pulmonary diseases (COPD)
6. Ischemic heart disease (IHD)
7. Peptic ulcer
8. Small babies and obstetric problems
9. PVDs.
Pack years (PYs): Duration of smoking in years × Number
of packets of cigarettes (or beedis) smoked per day. For
example, one pack of cigarettes smoked per day for thirty
years constitutes thirty PYs (Risk of bronchogenic
carcinoma increases when PYs exceed 40).
Smoking index (SI): Number of cigarettes or beedis smoked
per day and its duration. For example, a person smoking 20
cigarettes or beedis per day for the last 30 years has the SI
of 600. (Risk of bronchogenic carcinoma increases when
SI exceeds 300.)
SOME SPECIAL INQUIRIES IN CASE
OF FEMALE PATIENTS
Menstrual History
The following questions are to be asked:
• Age of menarche?
• Duration of each cycle?
• Type—Regular or irregular cycle?
• Approximate volume of blood loss in each menstrual
cycle?
• Age of attainment of menopause?
• Any postmenopausal bleeding?
Obstetric History
The following questions are to be asked:
• Number of times the patient conceived?
• Number of times the pregnancy was carried to term?
• Number of abortions?(spontaneous, therapeutic or
illegal)
• Number of living children, their ages, age of the last
child delivered? You should clearly understand the
difference between the age of the last child delivered
and the age of the youngest child of the patient. This is
a very common area of commiting mistake.
• The time interval between successive pregnancies/
abortions?
• Mode of delivery? (vaginal, forceps, assisted or cesa-
rean)
• Development of edema of legs, hypertension or seizures
in antenatal or postnatal period?
• Presence of impaired glucose tolerance test in the course
of pregnancy or
• H/o having given birth to a large baby may provide a
clue to the presence of diabetes mellitus in the patient.
• H/o contraception?
History Taking 7
Family history:
1. Whether any other member of the family had/has a
similar complaint?
2. Number of members living together.
3. Ages of the living members.
4. Their state of health.
5. If deceased, the cause of death and age at death.
6. Any history of (H/o) hypertension, ischemic heart disease,
diabetes mellitus, tuberculosis, gout, arthritis, asthma,
etc. in the family, if present, should be recorded.
In certain diseases, for example, hemophilia, you should
inquire the history of the male members of two or three
generations of the family. History of consanguinity, i.e.
marriage amongst blood relations should be given importance
in cases of heredofamilial diseases like epilepsy, mental
retardation, ataxia due to cerebellar lesions, Huntington’s
chorea, metabolic disorders like phenylketonuria, any
neurological disorders, muscular dystrophy, retinitis
pigmentosa, etc. (Table 1.2).
Table 1.2: Showing the general symptoms presented by
the patients and their inquiry
General Health
• General well-being.
• Sleep-whether sound sleep or not? Its duration? Any sleepy feeling
during the day?
• Inquire about the appetite
• Any significant weight change in recent few weeks or months—gain
or loss?
• Does he feel lethargic or energetic at the start of the day?
Cardiovascular System
• Any swelling over lower legs, especially ankle?
• Any palpitations?
• Orthopnea, dyspnea, paroxysmal nocturnal dyspnea (PND)
• Chest pain—at rest, on exertion or all the time?
• Pain in legs on exertion? (peripheral arterial disorders)
Respiratory System
• Dyspnea?
• Any H/o wheeze, recurrent cough and cold, upper respiratory tract
infections?
• Cough with sputum—color, amount, any unpleasant odor (if present)
of the sputum.
• Blood in sputum—hemoptysis (coughing of blood), its amount; does
the patient spit the blood with every bout of cough?
Gastrointestinal System
• Any disease of oral cavity—mouth, teeth, gums, tongue, palate, tonsils,
etc.?
• Difficulty in swallowing—dysphagia?
• Painful swallowing—odynophagia?
• Nausea and vomiting
• Any H/o or complaint of indigestion?
• Any complaints of heartburn?
Contd...
8 Essentials of Clinical Medicine
Contd...
• Any kind of pain or discomfort in the abdomen?
• Change in bowel habits?
• Stool color—dark, pale, black, fresh blood?
Urogenital System
• Pain on urination? (dysuria)
• Frequency of micturition, and any H/o nocturia?
• Abnormal (altered) urine color
• Number of sexual partners
• Males:
– In old age, prostatic symptoms like hesitancy in micturition,
poor stream, terminal dribbling, frequency, urgency, etc. are to
be noted.
– If appropriate, mental attitude to sex (libido), morning erections,
frequency of intercourse, ability to maintain erections, ejacu-
lation, urethral discharge, etc. are to be asked. A word of caution
—These questions are to be asked in a very tricky manner. You
should not irritate the patient.
• Females:
– The detailed menstrual history as mentioned earlier.
– If the patient is postmenopausal, ask her about any problem of
bleeding.
– Any problem like stress or urge incontinence?
– Ask about libido, dyspareunia (pain during intercourse).
Remember—Again, it is a tricky question and you need to be
tactful.
Contd...
Contd...
Central Nervous System
• H/o of recurrent headache, its duration, frequency, severity, does the
patient point out any particular area or part of the head for the pain
and any kind of medication taken for that?
• Fits (any H/o epileptic attacks, any H/o head injury or any central
nervous disorder in the past?)
• H/o of blackouts and faints, their severity, frequency, duration, any
kind of medication taken.
• Tingling sensations (paresthesia) and numbness in any part of the
body.
• Any complaint of muscle weakness?
• Any history or complaint of hearing problem, visual disturbances,
altered sense of smell or taste (any H/o of ear, nose or throat operation)?
Locomotor and Joint System
• H/o joint pain, stiffness, etc.?
• Muscle pain or weakness?
Endocrine System
• H/o heat or cold intolerance?
• Any alteration in sweating, weight loss or gain, etc?
• Prominence of eyes as seen in thyroid disorders.
• Any kind of swelling in the neck, its exact site, size (in centimeters),
number, color, temperature over the swelling, duration, mode of onset,
other symptoms associated with it, pain, progress of the swelling,
fever, presence of other swellings, secondary changes like ulceration,
softening, inflammatory changes, any impairment of function,
recurrence of the swelling, any family H/o such complaints
• Excessive thirst, hunger or frequency of micturition.
 2
Common Symptoms Presented
by the Patients and Questions
to be Asked for Them
ALIMENTARY SYSTEM
Pain (In General)
Latin: “Poena” means a fine, a penalty, or a punishment. As
defined by the International Association for the Study of
Pain (IASP), it is an unpleasant and emotional experience
arising from the actual or potential tissue damage. Pain
includes not only the perception of an uncomfortable
stimulus but also the response to that perception.
You should inquire about:
• Localization: What is the site of pain? Note whether the
patient points with a finger to one particular spot or uses
the whole palm to localize it. For example, if the pain is
in the chest, then you should ask whether it started all
over the chest or at a particular site, say the precordium?
(If possible, you should ask the patient to guess the depth
of that particular site from the surface. This will guide
you to know the most probable organ involved.)
• Mode of onset: What was the mode of onset of pain?
Does it start suddenly or increases gradually?
• Timing and duration: When did the pain start? How long
does the pain last? What is the interval between two
successive attacks of pain? Has it changed since it
began?
• Progress: What is the progress of the pain? Whether it
has increased or decreased after its first occurrence?
• Severity: How much severe is the pain?(Always keep
the fact in your mind that the patient may describe it in
an exaggerated manner to gain your attention). Does it
interfere with the daily activities of the patients or keep
the patient awake at night? If the patient complains of
having spent many sleepless days and nights, it is
definitely suggestive of anxiety or depressive symptoms.
• Character: What is the character of pain? Is it dull
aching, colicky, crushing, stabbing, burning, gnawing
or like a pin prick, etc.? Coliky pain makes the patient
to toss over the bed.
• Frequency: What is the frequency of pain? How many
times does it occur in a day, week or month?
• Movements of pain:
1. Radiation: In it, the pain moves from one site to
another, but the pain does not disappear from the
original site. For example, the gradual extension or
shooting of the pain along the distribution of a
peripheral nerve or nerve root (Fig. 2.1, Plate 1).
2. Shifting or migration: It is a type of movement of
the pain where the pain completely shifts from one
site to another that is the pain disappears from the
original site (starting point of pain).
3. Referred pain (Synonym—heterotropic pain,
sympathetic pain or synalgia): The pain seeming to
arise in an area other than its origin, as pain from
appendicitis, which often seems to occur in areas
other than that of appendix. It may be caused by
visceral pain or by proximal or deep musculoskeletal
injury and is usually referred to areas distant from
the source of problem, e.g. pain of appendicitis at
umbilical region.
• Special time of occurrence of the pain: Does the pain
appear at any particular time of the day? For example,
afternoon headache in sinusitis or headache of migraine
when exposed to sudden loud noise, strong flash of light
or after taking coffee drink, ice-creams, chocolates, etc.
• Periodicity of pain: Does the pain reccur after a particular
fixed period of time such as hours, days or weeks?
• Precipitating or aggravating factors: What initiates the
pain and what makes it worse? For example, the pain of
angina pectoris comes after certain amount of exercise.
Similar to the pain of angina is the pain of esophageal
origin which comes on a short time after eating.
• Relief from pain: What makes the condition better? Pain
of musculoskeletal origin may be relieved by position/
posture. Pain of duodenal ulcer is relieved after eating.
Pain of the lower gastrointestinal tract may be relieved
by passing stool or wind. Pain of angina may be relieved
by rest. The esophageal discomfort may get corrected
10 Essentials of Clinical Medicine
after belching. Whether the patient takes any kind of
medication for relieving pain should also be inquired.
• Associated symptoms: You should ask about:
– fever
– vomiting
– micturition
– weight and appetite
– swelling
– trauma
– abdominal distention
– menstrual history for ectopic pregnancy
– vaginal discharge
– rectal discharge
– type of discharge.
Appetite
• Has the appetite of the patient changed in the recent few
days or weeks or is it the same as before?
• Has it increased or decreased?
• It may be an indication of a serious disorder if the apetite
has become perverted.
• Any other associated symptoms?
Vomiting
Vomiting is a neurogenic response triggered by the
chemorecepters in the brainstem or reflexly through the
irritation of the stomach. Vomiting consists of a phase of
nausea, followed by hypersalivation, pallor, sweating and
hyperventilation. Retching, an involuntary effort to vomit,
then occurs followed by expulsion of gastric contents
through the mouth sometimes through the nose. A H/o
vomiting in itself is not very helpful because vomiting occurs
as a response to pain of any type. However, H/o vomiting
provides us certain important hints. In most of the cases,
nausea and vomiting are due to local pain in abdomen.
Painless vomiting suggests any neurological disorder.You
should ask about:
• What is the frequency of vomiting that is how many times
does the patient vomit in 24 hours?
• Try to inquire about the quantity, odor and taste of the
vomitus.
• Does the vomiting occur at any particular time of the
day that is after getting up in the morning, immediately
after any meals or drinks, after receiving any particular
kind of stimulus such as sudden loud noises, sudden
strong flashes of light, etc. or does it occur after any
attack of fever?
• What is the color of the vomitus? Does it indicate any
traces of fresh blood (bright red color), bile (greenish-
yellow color) or gastric contents (reddish-brown
color).
• Is the vomitus copious (copious means pure blood) and
sour-smelling?
• Whether it is associated with pain, colic, attacks of
myocardial infarctions or angina, after ingestion of
certain drugs or due to any metabolic disorder (if the
patient knows about it beforehand).
Flatulence
Excessive gas in the stomach and intestines.
• Whether the patient brings the wind up (i.e. belching) or
passes it down (i.e. flatus)?
• Does the patient want to get rid off flatulence but cannot
do so?
• Whether he gets relief on passing wind?
• Time of the day or the activities after which the
complaint/problem is maximum?
• How long (duration) is the patient suffering from such
a problem?
• Try to know about the severity of the problem
• Does the patient complain of excessive fullness in the
abdomen even after taking less amount of diet?
Water Brash
• Does the patient complain of his mouth getting filled
with tasteless saliva?
• When does he complain of it? (Time or any special event
related to it.)
• What is the duration and frequency of complaint?
• Are there any associated symptoms and what are they?
• Water-brash may be associated with heartburn.
Heartburn (Pyrosis)
• Does the patient complain of any bitter or sour fluid
coming in the mouth with burning?
• Whether this hot burning sensation is associated with
retrosternal discomfort?
• Does it occur after meals,on bending or lying down?
• Problem of heartburn is very common in pregnancy and
also in obese people.
Dysphagia
Dysphagia is defined as the difficulty in swallowing.
• Does the patient complain of something sticking in the
throat or the chest?
• Whether the problem is more with solids or liquids or
both equally?
• Whether the difficulty in swallowing was first with solids
or liquids ?
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 11
• Is it associated with pain, regurgitation, weight loss,
dysphonia, otalgia, mass in the neck, pooling of saliva
in pyriform fossa or at upper esophagus or due to any
emotional condition?
• What is the duration of the problem?
• What was the mode of onset—gradual or sudden onset?
• Is there any previous history of similar complaint?
• Is the patient able to localize the exact site of obstruction,
i.e. pharynx, mid-esophageal or lower esophageal?
• Is the problem persistent or intermittent or progressive
since it first appeared?
• Does it occur within one second of or little later on
swallowing?
• Whether associated with gurgling noise or bulge neck
or with cough ?
Diarrhea
A state in which an individual experiences a change in
normal bowel habits characterized by the frequent passage
of loose, fluid, unformed stools. It is a common symptom
of gastrointestinal disturbances. In case of diarrhea, you
should inquire about the following.
Questions to be asked in Case of Diarrhea
• What is onset, duration, and progress of symptoms?
• Is the diarrhea acute, chronic, or intermittent?
• Is it associated with tenesmus (anal irritation), urgency,
or incontinence?
• What is the consistency of stool—watery, unformed or
semisolid?
• What is the volume of stool—large or small?
(Large volume and not excessively frequent stools are
suggestive of small bowel disease; and small volume
and incisively frequent stools are suggestive of large
bowel disease).
• Are the stools associated with blood, mucus or pus?
• What is time of occurrence of diarrhea—early morning,
or late night? (diarrhea occurring at night suggests
organic disease).
• Is there any H/o contact with diarrhea or travel abroad?
• Inquire about sexual history (gay bowel syndrome, HIV)?
• Significant drug therapy—how long and for what
purpose?
• Past medical H/o gastrointestinal tract disorders, e.g.
gluten enteropathy, Crohn’s disease.
• Any other associated symptoms like vomiting, abdominal
pain, colic, etc.
• Any symptoms of systemic illness, for example, rigors
or arthralgia.
Constipation
Questions to be asked to Check Constipation
• What is the onset, duration and progress?
• Whether the constipation has been life long or is it of
recent onset?
• How much time does the patient spend straining at stool?
• How often do the bowel empty each week?
• Any associated symptom like pain in abdomen, pain on
defecation or rectal bleeding.
• What is the shape of stool/consistency of stool? Is there
any change than before? Is it pellet like?
• Any drug therapy taken/still continuing?
• Does the patient have a feeling of incomplete emptying
of the bowel?
• Inquire about passage of hard stool?
• What is the duration, mode of onset and progress?
• Is the patient restless, agitated and confused? (never itself
causes confusion and hence the problem may be serious.)
• Ask about the frequency of the problem.
• Is it associated with rectal bleeding or retention of urine?
• Does it alternate with diarrhea?
• Is there any associated abdominal distention or
vomiting?
• Is it habitual or of long duration?
• Take complete history of diet and sedentary habit/work.
• Any ongoing or recent drug therapy?
• How much time spent in straining at stool before actual
passage of the stool? This gives you an idea about the
severity of the problem.
• What is the color of the stool and whether it is associated
with passage of mucus in stools?
Jaundice
• What made the patient worried? Or, what made the
patient to come to you?
• What is the color of urine, stool and sclera and also the
general skin colour?
• How was the onset—sudden, subacute or insidious?
• Inquire about the duration and progress of the symptoms.
• Any association with fever, nausea or vomiting at onset?
• Whether the patient complains of pain in abdomen?
• Is there any waxing and waning of symptoms?
• Whether the patient is complaining of any itching of
skin?
• Is there any previous H/o jaundice?
• Progressive loss of weight or apetite?
• Is there any H/o previous blood transfusion(s)?
12 Essentials of Clinical Medicine
• Does the patient reveal a H/o any significant and
prolonged drug therapy? What was the reason, duration
and type of medication?
• Is there any family H/o jaundice?
• Any sexual contact history ?
• Travel history and immunization status
• H/o alcohol intake for long duration.
• Has the patient ever been indulged in the habit of skin
tattooing (Hepatitis B and C)?
• Any associated pruritis or rigor?
• Any alteration in bowel habit?
• Gastrointestinal bleeding?
Indigestion (Dyspepsia)
Indigestion is generally a vague term used by the patient to
describe some other symptoms such as:
1. nausea
2. heartburn
3. epigastric discomfort
4. abdominal pain
5. belching
6. postprandial bloating
7. angina
8. functional dyspepsia which may be—reflux like, ulcer
like or dysmolity like.
Hiccups (Hiccough)
(Probably of imitative origin) A spamodic periodic closure
of glottis following spasmodic lowering of diaphragm,
causing a short, sharp, inspiratory cough. It may be caused
by indigestion, irritation of diaphragm, alcoholism, new
growths of the pleura, certain cerebral lesions, hysteria or a
disturbance of phrenic nerve. If prolonged, it has serious
significance.
Treatment
Hiccups may be treated by antiemetic drugs, rebreathing in
a paperbag, briefly applying the ice-cubes to both sides of
the neck at the level of larynx, or inhalation of carbon dioxide.
Stimulation of nasopharynx with a soft rubber tube or
placement of a thin coating of dry granulated sugar in the
hypopharynx may also be tried. If these are not effective,
anesthetization of the phrenic nerve may be helpful.
Abdominal Distention
Can be examined in detail at the time of inspection only.
You should look for:
• Normal contour and fullness of the abdomen.
• The shape of the abdomen—scaphoid, oval, pot-like
belly, etc.
• General causes of abdominal distention are 6 “F”s—
fat, fluid, flatus, feces, fetus and full bladder.
• Is the distention localized or diffuse, symmetrical or
assymetrical?
• Any movements of the swelling?
• Is the abdominothoracic respiration visible or is it not
appreciable?
• Is the onset sudden or gradual?
• What is the duration and how is the progress?
• Any H/o vomiting, loose motions, chronic hepatic
disease, fever (especially low grade in the evening
hours), pulmonary tuberculosis?
• Any association with dyspnea or orthopnea?
• Edema over any body part or generalized edema
(anasarca)?
• Any significant change in bowel habits?
• Any loss of body weight—rapid or gradual?
• Is the swelling increasing in size or is stable?
• Does the swelling move from one area to another?
• Any association with fever or weakness?
Weight Loss
• Inquire whether there is excessive loss of fluid in the
recent few days or weeks?
• Take detailed notes on the nutritional habits of the
patient.
• Increased energy expenditure recently due to certain
reasons along with inadequate dietary intake?
• Any previous H/o significant weight loss?
• Associated symptoms/diseases?
• What is the rate and severity of weight loss?
• What is the duration and extent of weight loss?
• H/o anorexia or anorexia nervosa?
• H/o depression/tension?
• Any significant physical, psychological and social
factors associated with weight loss?
• Associated amenorrhea whether present?
• Changes in social well being and lifestyle?
Weight Gain
• Inquiries are similar to that of weight loss.
• In addition, inquire about hypertension, hyperlipidemia
and diabetes mellitus.
Rectal Bleeding (Hematochezia)
• In most of the cases, it is associated with hemorrhoids
(piles) or constipation.
• You should try to search for the causes of raised intra-
abdominal pressure—such as urethral stricture, enlarged
prostate, big pelvic tumor or pregnancy.
• Any past H/o or family H/o such complaints?
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 13

• Does the patient suffer from any bleeding disorders? 1. Oral hygiene
• H/o drug/alcohol abuse? 2. Oral infections
• Any H/o dyspeptic syndrome? 3. Atrophic rhinitis
• Complaint of recurrent vomiting or diarrhea? 4. Any tumor of nasal passage
• H/o anorexia or weight loss? 5. H/o of bronchiectasis
• Any complaint of dizziness or fainting? 6. H/o gastric outlet obstruction
7. Dietary/abuse habits
Blood in the Vomit (Hematemesis) and Blood
8. Drinking habits.
Loss in Stools (Melena)
• Onset: How many hours/days ago did the problem start? CARDIOVASCULAR SYSTEM
• Quantity: Roughly the quantity of blood lost (in terms
Dyspnea, Orthopnea, Paroxysmal Nocturnal
of cupfulls of blood).
Dyspnea (PND) and Dyspnea at Rest
• Color: Fresh or coffee colored.
• Any upper abdominal pain (relieved by food) a few • What is the onset, progress and duration of breath-
months or even years before the onset of hematemesis. lessness? Is the progress very rapid or it took a few days
• H/o chronic alcoholism or jaundice. or months to become severe?
• H/o of drug intake: Aspirin, other NSAIDs, corti- • Is it paroxysmal or is there any variability in the
costeroids or any anticoagulant drugs taken for a long symptoms?
time. • Does it trouble the patient continuously or worsens on
• Associated pain in abdomen. exertion only?
• If no H/o pain or drug intake, then ask for acute or • Is it precipitated by any allergen or change in weather?
chronic cough, respiratory tract infection or recent abdo- • Is it associated with chest pain or fever?
minal or thoracic surgery. • Any associated symptoms like cough (with or without
• H/o fever about a week preceding melena. sputum), hemoptysis, wheeze, etc.?
• H/o dyspepsia or upper gastrointestinal bleeding. • H/o cardiac or respiratory disorders?
• Is the bleeding preceded by intense retching? • Any H/o tobacco or alcohol addiction?
• H/o recent travel to abroad?
Xerostomia
• Aggravating and relieving factors, i.e. what makes the
(Stoma meaning mouth) Dryness of mouth caused by signs and symptoms more severe and what provides
abnormal reduction in the amount of salivary secretions. It relief to the patient?
may occur in diabetes, hysteria, paralysis of facial nerve • What is the severity of the disease—mild, moderate or
involving chorda tympani, acute infections, and some types severe?
of neuroses. It is induced by certain drugs such as nicotine
Chest Pain (Details in the Section of Pain)
and atropine.
Approach to the Patient
Dysgeusia
1. Could the chest discomfort be due to an acute, potentially
(Geusis—taste) Impairment or perversion of the gustatory
life-threatening condition that warrants immediate
sense so that normal tastes are interpreted as being unpleasant
hospitalization and aggressive evaluations?
or completely different from the characteristic taste of a
– Acute ischemic heart disease.
particular food or chemical compound. Other types of
– Aortic dissection.
abnormal taste sensations are—cacogeusia, heterogeusia,
– Pulmonary embolism.
hypogeusia, idiopathic and phantogeusia.
– Spontaneous pneumothorax.
Halitosis 2. If not, could the discomfort be due to a chronic condition
(Latin—Halitus meaning breath; Greek—osis meaning likely to lead to serious complications?
condition). Bad breath. – Stable angina.
You should inquire whether the patient is aware of his – Aortic stenosis.
bad breath, (i.e. either he himself might have realized it or – Pulmonary hypertension.
he might have been told by somebody else). You should 3. If not, could the discomfort be due to an acute condition
also inquire about his: that warrants specific treatment?
14 Essentials of Clinical Medicine
– Pericarditis.
– Pneumonia/Pleuritis.
– Herper zoster.
4. If not, the discomfort be due to another treatable chronic
condition.
– Esophageal reflux.
– Esophageal spasm.
– Peptic ulcer disease.
– Gallbladder disease.
– Other gastrointestinal conditions.
– Cervical disk disease.
– Arthritis of shoulder or spine.
– Costochondritis.
– Other musculoskeletal disorders.
– Anxiety state.
Palpitation
Palpitation is defined as the rapid, violent, or throbbing
pulsation, as an abnormally rapid throbbing or fluttering of
the heart. The palpitation is perceptible to the patient, i.e. a
condition in which the patient becomes aware of his own
heart beats. You should note the following:
• Whether it increases during exertion?(most probably the
answer will be “yes”)
• Are the palpitations regular or irregular?
• Pattern—Do they start suddenly, continue for some time,
and then disappear suddenly either spontaneously (or
after some physical exertion) or when external stimulus
ceases?(that is you have to inquire about the mode of
onset and termination)
• What is the frequency of occurrence?
• What is the duration of each attack?
• Any associated symptoms like coughing, vomiting,
fever, profuse sweating, breathlessness, epileptic attacks
(fits), etc. along with it?
Cough
• What is the mode of onset (sudden or gradual)?
• How long the patient has been suffering from such
problem (duration)? What is the duration of each attack
of cough?
• What are the aggravating and relieving factors?
• Does the coughing worsen at any time of the day or
night?
• What is the occupation of the patient (please see the
details of Occupational History—mentioned earlier in
the section of history taking).
• Did the patient have such attacks of cough earlier? Does
he suffer from recurrent attacks of cough and cold?
• Whether the symptoms are aggravated by anything like
dust, pollen, cold air, etc.?
• What is the nature of cough—dry or productive?
• What is the color, odor, viscosity, consistency, purulence
and appearance of the coughed out material?
• Ask about the amount (quantity) in cupfulls.
• Whether paroxysmal, spasmodic or with/without
wheezing?
• Any associated symptoms like pain in the chest,
vomiting, hematemesis, spontaneous passage of urine
or stool, etc.?
• Does it occur at a particular posture or position?And
whether the change in posture/position make any
difference?
• Any kind of medication sought?
Hemoptysis
• Does the patient cough out blood in sputum?
• Is the blood fresh (indicated by its bright red color), frothy
or altered?
• How often the patient complains of this?
• Ask about the duration of the complaint and its fre-
quency.
• You can also inquire about the type and degree of
hemoptysis.
• What is the mode of onset and progress of the symp-
toms?
• Is it associated with longstanding cough?
• What is the quantity of blood loss? Is it accompanied
with sputum or whether the patient simply passes fresh
blood?
• Any other associated symptoms like bluish discoloration
of nails or lips (if so, when), chest pain, etc.
• Whether the patient is suffering from known blood
disorders? Has he ever received blood transfusions? If
yes, when, how many times and why?
Edema
• Whether the patient is complaining of any swelling over
any part of his body (especially over the dependent
parts)?
• What is the mode of onset, duration and progress of the
swelling?
• Any H/o massive generalized edema (anasarca)? Take
details for that.
• Any kind of medication taken?
• Had he ever have the complaints of abdomal distention
which has followed the edema over the feet?
• What is the type of edema—pitting or non-pitting edema?
(This will be better understood on palpation—at the time
of examination.)
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 15
• Is the edema confined to a body part or is it of generalized
type?
• Additional important inquiries in case of edema:
– Fundal hemorrhage (a part of examination)
– Periorbital oedema
– Tonsils (a part of examination)
– JVP (jugular venous pressure) and blood pressure
(a part of examination)
– Cardiac size and pleural effusion (look at the X-ray
of the chest). Whether the patient describes about
any operation done for drawing water out of his
chest?
– Gynecomastia and sign of hepatic disease (a part of
examination)
– Any splenic or liver disorder? If the patient is aware
of that and you find him that intelligent
– Ascites and bowel sounds (a part of examination)
– Clubbing of nails, leuconychia, abdominal veins,
genital edema, hair distribution, petechial hemorr-
hage (all part of examination).
Fatigue
• Does the patient complain of getting tired too soon even
on mild/very mild exertion?
• What he does to relieve his fatigue?
• Any associated symptoms?
Dizziness and Syncope
• Ask about the mode of onset, duration, progress and
frequency of such attacks?
• What are the aggravating and relieving factors?
• Any associated symptoms like profuse sweating, black-
outs, etc.?
• Any special time of occurrence?
• Does the patient remember the events prior to such
attacks after recovery?
• Special inquiry about:
– Postural hypotension
– Vasovagal syncope
– Carotid sinus syncope
– Valvular obstruction.
– Stokes-Adams syndrome.
Cyanosis
Cyanosis is always associated with some other symptoms
and never alone.
• What is the mode of onset, duration and progress?
• Is it peripheral or central?
• Whether it is present since birth or developed recently?
Anemia
Reaching to the diagnosis of anemia requires combined
efforts of detailed history taking, careful and vigilant clinical
examination (i.e. inspection, palpation and auscultation) and
proper investigations. Therefore, a medical student should
look at the following points of history taking and
examination and should work accordingly.
Ask about → fatigue, syncope, dyspnea, orthopnea,
paroxysmal nocturnal dyspnea, tachypnea, tachycardia,
pallor, postural hypotension, pounding in ears, palpitation,
(See for—raised central venous pressure, displaced apex
beat, gallop rhythm, basal crackles while auscultating the
lungs, bilateral ankle edema, drenching night sweats
(lymphoma), bone pains, (myeloma or metastatic
carcinoma)), past H/o peptic ulcer, malignancy, autoimmune
diseases, prolonged drug therapy of aspirin, NSAIDs, etc.,
alcohol intake, gastritis, dietary history, family H/o blood
disorders, malaria, parasitic infection, H/o weight loss,
dysphagia, dyspepsia, chronic diarrhea, change in bowel
habits, rectal bleeding, gastrointestinal malignancies,
malabsorption syndrome, colitis, hemorrhoids, detailed
genitourinary history, childbearing age, menses, hematuria,
hematemesis, signs and symptoms of clubbing, cyanosis,
jaundice, coldness of the extremities, H/o admission in the
hospital due to severe heart failure and decrease in cardiac-
output, etc.
Pyrexia (Fever) (In General)
1. Continous fever: When the temperature is continuously
above the normal and the fluctuation in the temperature
is minimal (fluctuation less than 0.75 degree Celsius).
For example, fever in typhoid or typhus fever; pleurisy
with effusion.
2. Remittent fever: When the temperature is always above
normal but the fluctuation is fairly significant (fluc-
tuation more than 0.75 degree Celsius). This does not
signify any particular type of infection.
3. Intermittent fever: When the temperature is normal some
time during the course of the day. If the rise of
temperature is quite high and rapid and the fall is equally
rapid, then it is known as hectic fever. For example, fever
in pyogenic infections.
If the temperature rises on every third day, the fever is
called tertian fever; and if it rises on every fourth day, it
is called quartan fever. An example of this type of
temperature is fever in malarial infections.
4. Relapsing fever: When the temperature is up to 40 degree
Celsius for a few days and followed by afebrile period
16 Essentials of Clinical Medicine

of even up to one week. The pattern repeats itself. For • Daily caffeine and alcohol consumption
example, the Pel-Ebstein fever in case of Hodgkin’s • Drug therapy prescribed or self-medication.
disease in which the fever lasts for about 3 to 10 days • Nonspecific symptom of recent ill health (to consider
followed by afebrile period of the same duration. unusual causes such as infective endocarditis or Lyme’s
5. Low fever: When the temperature does not rise above disease.)
38 degree Celsius and occurs at any time of the day. For • If attacks are paroxysmal?
example, tuberculosis, chronic infection of any part of
– Precipitating factors ( exercise, stress or anxiety)
the body.
– Nature of onset of attack and associated symptoms
6. Hectic or septic fever:
• Accompaniments of fever (presyncope or chest discomfort)
– Chills – Relieving factors (breath-holding exercise).
– Tachycardia Table 2.3: Symptoms and clues
– Sweating
– Respiratory rate Cardiovascular Diseases Presenting with Non-Cardiac Symptoms Like:
– Herpes labialis • Stroke
• Abdominal pain
– Delirium
• Oliguria.
– Febrile convulsion. Facial Clues to Heart Diseases
• Corneal arcus
Table 2.1: History of diseases which can lead to the
• Xanthelasma
diagnosis of a cardiovascular disorder
• Cyanosis
1. Classical H/o rheumatic fever: • Malar flush
– Pain in the joints which fleets from one major joint to other. • Venous pulsations
(Remember that rheumatic fever may be present without joint Clues other than the Facial Clues
pains.) • Carotid bruit
– H/o sore throat, upper respiratory tract infections (URTI), fever • Palmar or tendon xanthomata.
and systemic infections.
– H/o “gnawing pains” may lead to the diagnosis of rheumatic Some Points about Infective Endocarditis
valvular disease in adulthood.
2. H/o syphilis: 1. Typical patient:
– Males: Exposure to infection followed by local sore.
– Females: H/o repeated abortions • Elderly with mitral or aortic valve disease.
– H/o of syphylitic aortitis, aortic regurgitation. • Younger with coronary HD (usually VSD or PDA)
3. H/o hypertension and diabetes mellitus: • Patient with prosthetic heart valves or intravenous
– Record of previous blood pressures.
drug abuse
– Symptoms like headache and dizzy spells.
– H/o polyuria, nocturia, polydipsia and polyphagia. 2. Major symptoms:
4. H/o tobacco consumption: • Nonspecific feverish (flu-like) illness.
– Required in cases of atherosclerotic cardiac disease. 3. Major signs:
• Fever, heart murmur (aortic or mitral regurgitation)
Table 2.2: History of complications produced by
cardiovascular disorders • Splinter hemorrhages and vasculitis
• Clubbing, Osler’s node, rash and Roth’s spot.
1. H/o embolization:
– Record of monoplegia or hemiplegia
Table 2.4: Jones criteria for rheumatic fever
– Hematuria with renal colic
– Sudden shooting pain in a limb with local swelling and cyanosis 1. Major criteria:
– Left hypochondrial tenderness, spleenic infarction – Carditis
– Sudden blindness. – Polyarthritis
2. H/o pressure symptoms due to enlargement of heart chambers: – Erythema marginatum
– LAH (left atrial hypertrophy)—hoarseness, dysphagia – Chorea
– Aneurysm of arch of aorta—pressure on sternum – Subcutaneous nodules
– Erosion of spine with local pain and even paraplegia in patients
2. Minor criteria:
with aneurysm of descending aorta.
– Fever
Arrhythmias – Arthralgia
– Previous rheumatic fever
• Family H/o premature heart disease or sudden death. – Elevated ESR (eosinophillic sedimentation rate) or C-reactive
• Past history of RF, previous heart attacks or other heart protein
diseases Contd...
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 17

Contd... [Polyphonic wheezes: Heard during expiration. It is

– Prolonged PR intervals. heard in cases of asthma and COPD (chronic
– Leukocytosis obstructive pulmonary disease)
– First-degree or second-degree AV block Monophonic wheezes: May be heard during inspi-
Plus: ration, expiration or both.]
• Supporting evidence of preceding streptococal infection: recent scarlet 6. Dyspnea: As mentioned earlier.
fever, raised antistreptolysin O or other streptococcal antibody titer, 7. Hemoptysis: As mentioned earlier.
positive throat culture. 8. Symptoms related to ENT (ear, nose and throat):
NB: Evidence of recent streptococcal infection is particularly important if – Recurrent sinusitis, rhinitis, asthma, bron-
there is only one major manifestation. chiectasis, carcinoma lung, hoarseness, weakness
Table 2.5: Venous and arterial ulceration of voice, carcinoma vocal cords.
9. Smoking history: As mentioned earlier.
Venous ulceration Arterial ulceration 10. Family H/o asthma, tuberculosis, eczema, hay fever
Features (allergy).
1. Age 40–60 yr, multiple > 60 yr 11. Occupational history: As mentioned earlier.
recurrences
2. Sex F>M M>F 12. Points to be stressed in general assessment:
3. Past medical H/o DVT, occult DVT Previous PAD and CVA – Physique
history is swelling after child – Voice
birth, hip-knee – Breathlessness
replacement or long – Clubbing
bone fracture.
4. Risk factors Thrombophilia, family Smoking, DM, hyper- – Cyanosis or pallor
H/o DVT, previous H/o cholesterolemia, hyper- – Intercostal recession
DVT tension – Use of accessory muscles of respiration.
5. Pain Not severe, improves Severe, except in DM – Venous pulsations
with elevation of limb neuropathy – Lymph node’s enlargement.
6. Site Pressure areas usually Pressure areas (maleoli, 5th
medial to long metatarsal base, metatarsal 13. Points to be assessed in the shape of the chest:
saphenous vein head) and toes (It is more likely a part of respiratory (systemic)
(20 percent lateral to examination)
short saph. vein) – Kyphosis—forward bending
7. Margin Irregular with neo- Regular, indolent, punched – Scoliosis—lateral bending
epithelium off
8. Base Pink and granulating Sloughy (green) or necrotic – Flattening
under green slough (black) with no granu- – Intercostal recession—drawing in of ICS with
lations inspiration
9. Surrounding Lipodermatosclerosis No venous skin changes – In COPD, laryngeal or tumors of trachea
skin always present – In COPD, the lower ribs often move inward on
10. Veins Full (usually varicose) Empty with guttering on
elevation inspiration instead of normal outward movement.
11. Swelling Present Absent/present 14. Measurement of the chest: (It is also a part of systemic
12. Temperature Warm Cold examination)
13. Pulses Present, difficult to feel Absent – Rate of respiration
– Rhythm
RESPIRATORY SYSTEM – Chest expansion
1. Cough: As mentioned earlier. – Symmetry.
15. Associated upper respiratory tract symptoms:
2. Sputum: As mentioned earlier.
– H/o recurrent cold, cough or sore throat?
3. Breathing: As mentioned earlier.
– Pain or pricking sensations in the throat?
4. Chest pain: Please refer to the section of pain.
– Any operation of URT?
5. Wheeze: – Intermittent nasal obstruction.
– Does the patient hear some noises while breathing – Sneezing
or other people are also able to hear it? – Rhinitis
– Does it occur all the time or at a particular time – Headache
or occasion of the day? – Epistaxis
– Any associated symptoms? – Hoarseness (dysphonia)
18 Essentials of Clinical Medicine

– Complete loss of voice (aphonia) GENITOURINARY SYSTEM

– Croaking (hypothyroidism)
In case of genitourinary symptoms you should inquire about:
– Laryngeal pain A. General:
– Laryngeal stridor 1. Pain while passing urine:
– Tracheal pain behind manubrium • Prior to, during, or following micturition?
– Tracheal stridor. • Occurs in urethra or suprapubic area?
16. Constitutional symptoms usually associated with • Along with increased frequency (i.e. passing
respiratory diseases: more than usual volume of urine) and urgency
– Fever (i.e. a sudden need to pass urine)?
– Sweating • With any change in volume of urine?
– Anorexia • Strangury: It means severe suprapubic pain
– Weakness associated with inability to pass urine. It may be
– Loss of weight due to pathologic involvement of associated or
– Edema. surrounding body parts.
17. Previous complaints of: 2. Polyuria: Passing larger volume of urine (as
– Pulmonary tuberculosis compared to normal of approximately 1.5 liters) in
– Pneumonia, pleuritis 24 hours. It is usually associated with increased
– Measles, whooping cough frequency of micturition.
– Wheezy bronchitis or recurrent bronchitis in 3. Ask about oliguria, nocturia and hematuria.
childhood 4. Hematuria:
– H/o chest injuries • With or without pain?
– Recent administration of general anesthesia or loss • Continuous or intermittent?
of consciousness. • Macroscopic or gross (visible to eyes)?
– H/o major illness in pregnancy • If continuous, painless and microscopic? paren-
– Recent travel to endemic places chymal renal disease
– H/o respiratory tract surgery • Intermittent, renal pain, macroscopic? renal
– H/o pulmonary embolism. tumors.
– Look for previous chest radiographs. 5. Take H/o urethral discharge—Amount, color,
18. Skin lesions which may yield information of diagnostic viscosity, odor, frequency, mixed with blood, etc.
importance. 6. Color of urine.
Alteration in urine color:
Table 2.6: Skin lesions and respiratory diseases or illness • Orange brown
Skin lesions Disease/Illness – Bilirubin (conjugated) concentrated normal
1. Erythema nodosum Tuberculosis and sarcoidosis urine (e.g. due to very low fluid intake).
2. Metastatic tumor nodules Bronchial carcinoma – Rhibarb, Senna.
3. Cutaneous sarcoidosis and Intrathoracic sarcoidosis • Red-brown
lupus pernio – Blood, myoglobin, hemoglobin porphyrins.
4. Lupus erythematosus Pulmonary or pleural manifestations
– Rifampicin (antitubercular drug), phenol-
5. Herpetic vesicles Unilateral chest pain
phthalein
19. Eye conditions in respiratory disorders: – Beetroot, black berries
• Brown-black
Table 2.7: Eye conditions and respiratory disorders – Bilirubin melanin, methemalbumin.
Eye conditions Respiratory disorders
– Levodopa, homogentisic acid (alkaptonuria).
B. Females:
1. Horner’s syndrome Carcinoma bronchus
2. Phlyctenular Primary tuberculosis 1. Stress or urge incontinence
keratoconjunctivitis 2. Menstrual irregularities:
3. Iridocyclitis Tuberculosis and sarcoidosis • Age of menarche
4. Choroidal tubercles Miliary tubercles • Menopausal age
5. Chemosis, conjunctival Superior vena cava obstruction
and retinal vein dilation
• Oral contraceptives or hormone replacement
therapy (HRT)
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 19
• LMP (last menstrual period)
• Frequency, regularity and duration of cycle.
• Amount of blood loss
• Associated pain.
3. Obstetric difficulties:
• Number of pregnancies, number of live births,
miscarriages and termination
• Any health problem during or after delivery:
– Anemia
– Hypertension
– Diabetes mellitus
– Thyroid diseases
– UTI
• Were the previous deliveries vaginal or cesarean?
• Whether the forceps or episiotomy were used?
4. Vaginal bleeding following intrauterine erosions,
polyps and malignancy.
5. Vaginal discharge—amount, color, viscosity, odor,
frequency, blood mixed.
6. Altered sexual functions—for example, dyspareunia
(painful coitus). You should inquire about:
• Number of sexual partners within last 12 months.
• Whether condoms were used—most of the time,
all the time or not at all?
• Whether the patient ever suffered from sexually
transmitted diseases (STDs)? Make detailed
inquiries.
7. Any problem in sexual drive, pain during coitus or
orgasm?
C. Males:
1. Delay in initiating urine flow (hesitancy), impaired
urinary flow, postmicturition dribbling, dribbling
incontinence. This will provide you the hints for
benign prostatic hypertrophy (BPH).
2. Urethral discharge—points similar to vaginal
discharge.
3. Altered sexual function (e.g. impotence).
4. Take detailed accounts of hernia, hydrocele,
varicocele, etc.
Common Causes of Urinary Incontinence
• Incoordination of bladder sphincter function in old age.
• Spinal cord trauma or compression.
• Multiple sclerosis.
Males—benign prostatic hypertrophy (BPH), prostatic
carcinoma.
Females—pelvic floor damage during childbirth.
NERVOUS SYSTEM
Headache
• Types of headaches described by the patient (may be
more than one)
• Temporal aspects of headache:
a. When does it begin?
b. Features of headache—periodic, daily, unremitting?
c. Duration, mode of onset and progress of each
headache.
• Character of headache:
a. Intensity of headache
b. Nature and quality
c. Site and spread
d. Associated symptoms
• Causative factors:
a. Precipitating or aggravating factor
b. Relieving factor.
• Responsiveness to environment:
a. Limitations imposed by headache
b. Medications and treatment received
c. What benefit did the patient get?
• Health beween the attacks:
a. Completely well or with persistent symptoms
b. Depression, anxiety or fear
c. Social and work-related consequences
d. What does the patient believe is the cause?
Guidelines for a Brief but Comprehensive
Neurological Assessment
A. Presenting complaints:
1. Time relationship:
a. When do the symptoms start/stop?
b. How long do they last?
c. Do they occur at certain time of the day/month/
week?
d. Evolve over seconds, hours, days, weeks or
months?
2. Localization:
a. Which part of the body is affected?
b. Is the patient able to localize it?
c. If widespread, is it symmetrical?
3. Precipitating factors:
Whether the symptoms are triggered by exercise,
sleep, posture, reading, eating, coughing, micturition,
sexual activity or by external stimuli, for instance,
light, sound, smell, heat or cold?
4. Associated symptoms:
Numbness, paresthesia, cold, warmth (sensory
defects)
a. Weakness, clumsiness, stiffness, unsteady gait
(motor defects)
b. Headache
c. Nausea, vomiting
d. Loss or alteration of consciousness
20 Essentials of Clinical Medicine

e. Visual disturbances • Are there any signs of cerebellar ataxia?

f. Psychological changes—depression, wheeping, • How are the tendon reflexes and plantar responses?
agitation, sleep, appetite, change in energy or • Does he show any involuntary movements
libido. (dyskinesia)?
B. Past medical history: • Does he have hypokinesia and bradykinesia?
• Pregnancy (length of term, intrauterine problems) • Is there a loss of any learned movement pattern
• Delivery (normal, assisted, operative) (dyspraxia)?
• Neonatal health (jaundice, respiration, infection, • Is there any change in the state of consciousness?
convulsion) (like sudden unconsciousness)
• Infancy (infection, convulsion, injuries) • Any change in behavior and mental state? frontal
• Childhood and adult life problem [health, head and lobe
spine injury, serious infections (meningitis, ence- • Mental deterioration along with speech defects,
phalitis, surgical operations, and drug therapy)]. sensory disability→parietal lobe
C. Family history of:
• Difficulty in dressing, disorientation, forgetfulness?
• Epilepsy
non-dominant parietal lobe.
• Migraine
G. Sensory system:
• Multiple sclerosis
• Stroke • Is the position sense in fingers, toes absent or present?
• Cerebral aneurysm (posterior column tract)
• Dementia • Is the vibration sense in the feet absent or present?
• Spinocerebellar degenerations (posterior column tract)
• Neuropathies. • Is the pin-prick sensation present in all the four limbs
D. Social history: and over the face? (lateral spinothalamic tract)
• Occupation • Is the light touch present?
• Marital status H. Gait:
• Smoking habits • Is it spastic, hemiparetic, ataxic or parkinsonian?
• Alcohol consumption • Does the patient have foot drop?
• Use of recreational drug I. Cranial nerves:
• Sexual orientation and habits. • Test ocular movements and nystagmus
E. Mental state: • Test facial movements
• Is history given accurately, concisely or vague? • Test tongue protrusion and palatal movement.
• Is memory normal? J. Visual fields:
• Neatly dressed and well-cared? Aphasia and abnormal visual field are proof of disease
• Is the behavior normal? above the tentorium cerebelli.
• Is he aphasic or dysarthric?
• Is there hemianopia?
• Is he confused most of the time?
• If so, homonymous, bitemporal, unilateral or some-
• Can he find way in and out of the room?
thing else?
• Can he dress and undress himself without help?
F. Motor system: • Central vision normal (by testing visual activity).
• Duration, onset and progress of the weakness. K. Higher functions:
• Which part of the body or group of muscles is • Altered consciousness?
affected? • How is the behavior and mental state?
• Is the weakness confined to a particular part of the • Testing the memory tells you about frontal lobe
body or is it generalized? • Is there any speech defect?
• What is the degree of weakness? • Is there any H/o convulsions?
• Is there any weakness of the outstretched upperlimb? L. Fundi:
• Is the muscle weakness distal or proximal? • H/o papilloedema or optic atrophy?
• Along with the weakness, is there any wasting of • H/o hypertension, uremic and diabetic changes?
the muscles? M. General:
• Is the muscle tone normal; or is the condition spastic • Examine the patient’s skull, spinal movements and
or extrapyramidal? posture?
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 21
• Look for cutaneous nevi.
• Listen for bruits in neck.
N. Checklist of epilepsy
• Childhood onset?
• Any association with headache?
• Any kind of focal symptoms?
• H/o alcohol or drug abuse?
• Inquire about sexual activity
• H/o epileptic attacks during pregnancy
• H/o hypertension, and cardiovascular diseases.
O. Checklist for history of falls: (syncope)
• Accidental:
– Does the patient recall the events prior to fall?
– How was the walking surface?
– What kind of footwares does the patient use?
– What kind of illuminations is generally used by
the patient?
– Take details of visual acquity.
• Spontaneous fall
– Inquire about the preceding symptoms
– Whether the onset is with head movements or on
standing upright?
– Associated with vertigo, deafness, or tinnitus?
– Associated with chest pain or palpitations?
– Whether the patient is aware of hitting the
ground—this will help you to know whether the
patient lost his consciousness before or after the
fall?
– Eyewitness account
– Inquire about the resulting injuries or inconti-
nence
– Is the patient able to regain the erect posture?
– Inquire about any previous confusion, dementia,
or parkinsonism, hypertension, blackouts, etc.
– Ask about any drug therapy taken by the
patient—antidepressants, sedative-hypnotics,
hypotensive agents, diuretics, etc.?
– Also ask about alcohol consumption by the
patient?
P. The nervous system—general observation
• Gait
• Rhomberg’s test
• Speech
• Handwriting
• Mental state
• Facial appearance
• Involuntary movements
• Movements of the neck and spine.
Q. Appearance behavior and communication
• What is the patient’s level of intelligence and
education?
• Whether the patient is disturbed, agitated or
confused or apathetic?
• Is the attention easily held or fleeting?
• Does the patient show interest in his surroundings?
• What is his reaction to your approach and greetings?
• Is the patient well-groomed or unkempt?
• Are there any unusual features, facial tics, or
inappropriate behavior?
• Whether the conversation flows easily or not?
• Is the patient silent, monosyllabic or overtalkative?
• Are the contents of speech and conversation
appropriate and consistent ?
• Is there any flight of ideas, or thought disorders?
• Whether the patient keeps on repeating your question
or their own remarks? (perseveration)
• Is there any disorder of language (aphasia), use of
strange words (neologisms), real words strung
together oddly (word salad)?
R. Emotional state:
• Does the patient look happy, joyful, distressed or
depressed?
• Does he says he enjoys life?
• Whether it appears from his talks that he has fed up
with his life? Do you find any risk of suicide?
• Whether the patient is perplexed at his own mental
state?
• Does the patient have an insight and understanding
of disorders and its implication?
• Is he irritable, recentful or whether your words are
received with suspicion?
• Does the patient sleep too long or too brief? If too
long, any action to precipitate this hypersomnia? If
little, waking frequently or early morning wake up
or unable to sleep again?
• Is there any physical cause of insomia like pain,
cough and asthma, etc.
• While taking history, you should observe whether
the patient has delusions and hallucinations,
orientation of time, place and person by asking
questions like where he is at present? On which floor
of the building is he standing? To whom is he talking?
Is it day or night now? What time of the day
(morning, noon or evening) or night is it? Does he
recognize the people surrounding him? You should
also try to search the clinical features of dementia in
him?
22 Essentials of Clinical Medicine

Table 2.8: Features of frontal, temporal and parietal lobe BLOOD

Frontal lobe features: You should ask about:
Impaired judgment 1. Anemia (as described earlier)
Altered blunted personality 2. Lassitude, dyspnea
Loss of emotional control 3. Infection
Loss of mental inhibition
4. Blood loss
Failure to plan ahead
Impairment of language production.
5. Skin problems
6. Dietary history
Temporal lobe features:
7. Past history
Loss of memory for recent events
Impaired immediate recall
8. Occupational history
Language disorder (Wernicke’s type of aphasia) 9. H/o glandular enlargement.
Formed visual or auditory hallucination
Parietal lobe features:
LOCOMOTOR SYSTEM
Disorientation in visual space Pain
Impaired visual recognition.
Receptive aphasia You should ask about:
Disturbed body image. i. Stiffness—early in the morning or after immobility
ii. Extra-articular features
S. Released reflexes in dementia and confusional state: iii. Variation with time
• Grasping and avoiding response iv. Effect of activity
• Palmomental reflex v. Site and distribution
• Glabellar tap reflex vi. Night pain
• Snout and sucking reflexes vii. Mood disturbance.
T. Speech and language: General Assessment
• Dysarthria
• Cerebellar dysarthria The SLAG (spine, limbs, arms, gait) screen or the locomotor
• Pseudobulbar (spastic) dysarthria screen.
• Bulbar dysarthria Screening history→
i. Any pain or stiffness in muscles, joint or the back?
• Cortical dysarthria
ii. Whether the patient has any difficulty in dressing
• Formal test for dysarthria
himself?
U. Aphasia: iii. Is he able to walk up and down the stairs without
You should look for: difficulty?
• The ability to use words in spoken speech. This Screening examination→
includes articulation, fluency, naming and accurate i. Gait: Watch the patient walking and turning
repetition of complex statements and concepts. ii. Spine: Inspect the patient standing
• The ability to comprehend spoken speech a. From behind—look for abnormal spine and
• The ability to read to oneself (not aloud) paraspinal anatomy and legs
• The ability to write b. From side—abnormal curves, ask to bend and
• The ablity to comprehend other symbols. For touch the toes.
example, mathematical, numerical symbols or c. From front—ask him to put his ears on shoulder
musical symbols d. Press the midpoint of supraspinatus (each) to
elecit tenderness.
• Gesture
iii. Arms:
V. Apraxia (Greek a,—not, + praxis—action) Inability to a. Ask him to put his hands behind the head and
perform purposive movements although there is no observe shoulder and elbow function.
sensory or motor impairment. In other words, it is the b. Ask for keeping arms straight in front of you.
inability to use objects properly. Different types of c. Make his hands and fingers straight out and turn
apraxia are: akinetic a., amnesic a., constructional a., them over. Observe pronation, supination, palmar
developmental a., dressing a., ideational a., limb a., motor surface and finger anatomy.
a., and sensory a, verbal a. d. Make a fist with both hands and observe his grip.
 Common Symptoms Presented by the Patients and Questions to be Asked for Them 23

e. Ask him to squeeze the hand across the meta- C. Ligaments:

tarsals. – Localized pain/tenderness at attachment or in
f. Ask him to touch each fingertip with thumb. ligament/tendon substance.
iv. Legs: – Pain on stretch
a. Observe the patient while he is standing. Observe – Instability if major tear.
the lower limbs for swelling, deformity or limb
D. Bursa:
shortening.
b. Then ask the patient to lie down. Flex each hip – Localized tenderness
and knee with a hand on knee to feel crepitus. – Pain on stretching adjacent structures.
c. Rotate each hip internally and look for pain and E. Muscular attachments:
limitations of movements. – Localized or diffuse pain and tenderness
d. Palpate each knee for warmth and swelling and – Pain on resisted action
press on the patella feeling for effusion. – Pain on stretch (e.g. hamstring).
e. Squeeze gently across metatarsals for tenderness.
f. Finally inspect soles for callosities and ulcers. SUMMARY
v. Look for any stiffness, swelling, and weakness.
Examination of Locomotor System
Physical Examination
General Observations
The Principles
• Gait
Anatomy: Bony, articular, ligamentous, tendinous, muscular • Posture
or neurological. • Movements
Inflammation: Tenderness, erythma, warmth, synovitis, • Deformity
effusion. • Muscle wasting
• Long bones.
Function: Range of movements, and specific functions
(walking, rising, power, grip). Fractures
Complications: Deformity, instability, muscle wasting, • Joint articulations
calluses, extra-articular features. • Tendon structures atached to joints
Localization of Site of Articular and • Skin appendages
Extra-Articular Features
Table 2.9: Joint articulations
A. Joint articular surfaces:
Assessment of joint tenderness:
– Diffuse pain and tenderness
• Grade – 1 The patient complains of joint tenderness
– Generalized joint swelling • Grade – 2 The patient winces due to pain
– Restriction of movements in all direction of • Grade – 3 Winces and withdraws part
movements • Grade – 4 Will not allow to touch
B. Tendon structures attached to joints: Extra-articular features of joint disease:
– Localized pain/tenderness at attachment (enthesis) • Cutaneous nodules
or in tendon substance • Cutaneous vasculitic lesion
• Lymphadenopathy (enlarged lymph nodes)
– Swelling, tendon sheath or paratendon • Edema swelling
– Pain or resisted action • Tendon sheath effusion
– Sometimes pain on stretch (Achilles). • Enlarged bursae.
 3
Symptomatology and
its Causes

WEIGHT LOSS – Presenting complaint may not relate to an organ

or a system most effected.
1. Caloric malnutrition:
a. Starvation/fasting
WEIGHT GAIN
b. Inappropriate diet (improper dietary habits).
2. Chronic infections: 1. Obesity:
a. Infective endocarditis i. Energy intake/expenditure imbalance
b. Tuberculosis (TB) ii. Leptin deficiency
c. Amebic liver abcess 2. Endocrine disorders:
d. Fungal infection i. Cushing’s syndrome
e. Chronic respiratory tract infection. ii. Hypothyroidism
3. Acute infections: iii. Acromegaly
a. Viral hepatitis 3. Hypothalamic disease:
b. Typhoid i. Craniopharyngioma
c. Septicemia. ii. Fröhlich’s syndrome (characterized by obesity and
4. Malignancy sexual infantilism, atrophy or hypoplasia of gonads,
5. Malabsorption syndromes and altered sexual characteristics caused by
6. Endocrine and metabolic disorders: disturbance of hypothalamus and hypophysis due to
– Hyperthyroidism (increased BMR) neoplasm. Syn: adipose genital dystrophy)
– Type – 1 DM (not type 2) iii. Hamartoma
– Panhypopituitarism 4. Drug induced:
– Adrenocortical failure (Addison’s disease) i. Steroids
– Anorexia nervosa (see below). ii. Psychotropic drugs
7. Anorexia nervosa 5. Increased water retention:
8. Diuretic therapy i. Cardiac failure
9. Increased energy expenditure ii. Cirrhosis of liver
10. Salt and water loss: iii. Nephrotic syndrome
– Vomiting iv. Hypoproteinemia
– Diarrhea v. Edema
11. Glycosuria (marked) 6. Systemic disorders:
12. Physical, psychological and social factor i. Hypertension
a. Grief depression ii. Diabetes mellitus (DM)
13. Weight loss with amenorrhea—anorexia nervosa iii. Hyperlipidemia
14. Chronic alcohol abuse • Waist/hip ratio (w/h ratio) provides a simple
15. Fever: assessment of visceral adipose fat
– Weight loss > 3 kg in 6 months is significant • Subjects with pear-shaped configuration and a
– Weight loss from any cause results in amenorrhea w/h ratio of 0.8 or less in females and < 0.09 in
– H/o family member is important males have a good prognosis
 Symptomatology and its Causes 25

• Apple-shaped conf. – with a greater w/h ratio 6. Renal faiture

have increased risk of CV disease. 7. DM
8. Drugs—metronidazole, phenformin
ANOREXIA 9. Ca. of stomach esophagus
10. Ca. of pharyngeal pouch
1. Viral hepatitis: Including anicteric hepatitis
11. Chr. gastritis
2. Tuberculosis
12. Sudden distaste of smoking in infective hepatitis.
3. Ca. of stomach and other malignancy
4. Endocrine disorder:
COATED TONGUE
i. Addison’s disease
ii. Panhypopituitarism 1. Early morning coating due to breathing by mouth at
5. Chronic wasting diseases: night
i. Uremia 2. Febrile illness with increased respiratory movements
ii. Cirrhosis of liver 3. Enteric infections.
iii. Chr. alcohol 4. Black-furred tongue—fungus infection following
iv. Chr. smoking antibiotic therapy
6. Drugs: 5. Unhygienic habits like improper washing after food
• Digitalis 6. Large papillae and fissures are normal anatomically.
• Quinine
• Metronidazole FEVER
7. Fever (also see in the section of “Common symptoms presented
8. Cardiac, renal failure or myxoedema and ….”)
9. Anxiety neurosis and depression
10. Megaloblastic anemia Common Causes
11. Gastric carcinoma.
12. Hepatocellular damage • Infections: bacterial, viral, rickettsial, fungal, parasitic.
13. Anorexia nervosa: • Autoimmune disease.
• Young females • Central nervous system disease including head trauma,
• Low BMR mass lesion.
• Subnormal temperature. • Malignant disease especially renal cell ca; primary or
Rest of the points are similar to wt. loss. metastatic liver cancer, leukemia and lymphoma.

EXCESSIVE APPETITE Less Common Causes

1. Parasitic infection • Cardiovascular diseases including myocardial infarction,

2. Malabsorption syndrome thrombophlebitis, and pulmonary embolism.
3. Psychological origin • Gastrointestinal diseases including inflammatory bowel
4. Hyperthyroidism disease, alcoholic hepatitis, granulomotous hepatitis.
5. DM. • Miscellaneous disease including drug fever, sarcoidosis
familial Mediterranean fever, tissue injury, hematoma,
PERVERTED APPETITE and factitious fever.

1. Pregnancy Special Types of Fever

2. Psychoneurosis
3. Anemia (pica). a. Fever with rigors:
– Malaria
LOSS OF TASTE – Kala azar
– Filaria
1. Lesion of facial n. – UTI
2. Lesion of glossopharyngeal n. – Cholangitis
3. Systemic disorders – Septicemia
4. GI disorders – Infective endocarditis
5. Chr. lung infection. – Abscesses at any site.
26 Essentials of Clinical Medicine

b. Fever with herpes labialis: – TB

– Pneumonia – Infective endocarditis.
– Malaria – Toxoplasmosis.
– Meningitis – Ebstein-Barr virus (EBV) infection
– Severe streptococcal infection. – Cytomegalovirus (CMV) infection.
c. Fever with rash: – Primary HIV infection.
– Chickenpox (1st day) – Brucellosis.
– Smallpox – Lyme disease.
– Measles (4th day) 2. Malignant disease (10–30 percent)
– Rubella – Lymphoma
– Typhus – Leukemia
– Allergy – Renal cell carcinoma
– Typhoid (7th day). – Hepatocellular carcinoma.
d. Fever with membrane in throat
3. Collagen vascular disease (15–20 percent)
– Diphtheria
– Adult Still’s disease
– Moniliasis
– Rheumatoid arthritis
– Vincent’s angina
– Systemic lupus erythematosus
– Inf. mononucleosis
– Wagener’s granulomatosis
– Agranulocytosis.
– Giant cell arteritis.
HYPERTHERMIA SYNDROME 4. Miscellaneous (10–25 percent)
– Drug fevers
1. Heat stroke: – Thyrotoxicosis
a. Exertional: Exercise in higher than normal head and/ – Inflammatory bowel disease
or humidity. – Sarcoidosis
b. Non-exertional: Anticholinergics, including antihista-
– Granulomatous hepatitis
mines, anti-parkinsonian drugs, diuretics, phenothiazines.
– Factitious fever.
2. Drug-induced hyperthermia:
– Familial Mediterranean fever.
a. Amphetamines, MAO inhibitors, cocaine, phency-
5. Undiagnosed (5–25 percent)
clidine, TCA, LSD.
3. Neuroleptic malignant syndromes:
a. Phenothiazines, butyrophinones, including haloperidol PHYSIOLOGICAL VARIATION OF TEMPERATURE
and bromoperidol, fluoxetine, loxapine, tricyclic 1. Menstruating women:
dibenzodiazepines, metaclopramide, domperidone, • Early morning subnormal temp 2 weeks preceding
thiothixene molindone. ovulation
4. Malignant hyperthermia • At ovulation, temperature increases by 0.6°C or 1°F
a. Inhalational anesthetics. • Chills: Sensation of cold in most fevers
b. Succinylcholine.
• Rigors: Profound chills with piloerection, teeth
5. Endocrinopathy
chattering, shivering
a. Thyrotoxicosis
• With every 1°F rise above 100°F
b. Pheochromocytoma.
– The pulse rate increases by 10
PYREXIA OF UNKNOWN ORIGIN (PUO) – Resp. rate increases by 4
– BMR increases by 7.
• Persistent temp of > 101.2°F (38.4°C) for > 3 wk and
defying. FEVER WITH RELATIVE BRADYCARDIA
• One week of evaluation is needed.
i. Typhoid fever
Causes ii. Meningitis
iii. Viral influenza
1. Infections (20–40 percent)
iv. Drug fever.
– Pyogenic abscess.
 Symptomatology and its Causes 27

Grading of temperature PAIN

• Normal – 37°C – 37.6°C (98.6°F – 99.6°F)
• Febrile – above 37.8°C (100°F) Abdominal Pain
• Hyperpyrexia - > 41°C ( > 106°F)
Peritonitis
• Hypothermia - < 35°C ( < 95°F)
• Febrile convulsions – > 40°C (Inflammatory condition)
Description of pain:
Drug Fever i. Very severe
Features ii. Begins suddenly
1. Prolonged duration iii. Located directly over the inflamed area.
2. With relative bradycardia and hypotension iv. Aggravated by change in position. Therefore, the patient
3. With pruritis rash and arthralgia lies still in bed.
4. Begins 1 to 3 weeks after start of drug and persists 2 to Silent abdomen: Felt as board-like rigidity. Later
3 days after withdrawal becomes generalized.
5. Eosinophilia present. v. If due to perforation of hollow viscera, then liver
dullness is absent.
Drugs that Induce Fever vi. Rebound tenderness present.
1. Sulfonamides Conditions Causing Peritonitis
2. Aminosalicylic acid a. Acute appendicitis
3. Penicillins Description of pain:
4. Iodides and propylthiouracil 1. Initially poorly localized in periumbilical or epigastric
5. Anti-TB drugs region
6. Antipsychotics 2. Later becomes somatic, more severe and to right
7. Amphotericin lower quadrant.
8. Antihistamines.
3. Accompanied by anorexia, vomiting, fever,
constipation (Murphy’s syndrome—Pain + Vomiting
Benefits of Fever
+ Temperature )
Release of endogenous pyrogen which activate the T-cells 4. Tenderness at Mc.Burney pt.
and enhance host defense mechanism. 5. Pain is dull in non-obstructive appendicitis.
6. If nausea and vomiting precede abdominal pain, the
Harmful Effect of Fever disease is more likely an infection like gastroenteritis.
1. Hypercatabolism–N2 wastage and wt. loss 7. The reason of pain at umbilicus is that the sensory
2. Fluid and electrolyte imbalance (sweating) innervation of appendix corresponds to 10th spinal
3. Convulsions segment
4. Brain damage 8. Accompanied by local tenderness, guarding and
5. Circulatory overload, arrythmia, etc. rebound tenderness, (peritoneocutaneous reflex,
Morley’s reflex), fever of moderate degree and
HYPOTHERMIA leukocytosis, constipation but some time diarrhea,
especially with pelvic appendicitis with local peri-
1. Endocrine
• Hypothyroidism/myxoedema appendicular abscess formation.
• Hypopituitarism (Simmonds’ cachexia) 9. A coated tongue with fetor oris (foul breath) is
• Hypoglycemia commonly seen in acute appendicitis.
2. Toxic b. Catarrhal appendicitis
• Alcohol intoxication Description of pain:
• Barbiturate poisoning 1. Gradual onset pain
• Ketoacidosis 2. Dull and aching
3. Exposure to cold 3. The patient carries his duty with discomfort
4. Autonomic dysfunction or dysautonomias. 4. With anorexia, nausea, vomiting.
28 Essentials of Clinical Medicine

c. Obstructive appendicitis: 2. It is most severe of all abdominal pains.

Description of pain: 3. Tends to pierce to back or left loin.
1. Pain sudden in onset 4. Becomes severe when the patient lies down or sits
2. The patient goes back to bed with severe colicky with leaning forward.
pain with fever and vomiting. 5. Constant pain and not colicky in nature.
d. Non-obstructive appendicitis: k. Acute colonic diverticulitis:
Description of pain Description of pain:
1. Dull and aching pain 1. Pain in left illiac fossa
e. Retrocecal appendicitis: l. Acute regional ilietis:
Description of pain: Description of pain:
1. Hardly any tenderness and rigidity 1. Pain in right illiac fossa like acute appendicitis but
2. Some tenderness and rigidity in right flank or more has long H/o intestinal colic (due to intestinal
posteriorly obstruction not present in appendicitis) and diarrhea.
3. If appendix is in close relation to right ureter, there 2. Tenderness in right iliac fossa.
may be 3. When the complaint is of pain in right illiac fossa
– Hematuria along with anal fissure, fistula or edematous skin
– Radiation from loin to groin, this confuses with tag, the diagnosis is certain.
ureteric stone m. Acute salpingitis:
4. H/o initial pain around umbilicus, Rovsing’s sign and Description of pain:
Psoas test positive. 1. Pain mainly felt in sides of hypogastrium or even in
f. Pelvic appendicitis: illiac fossa.
Description of pain: 2. Pain of appendix starts at umbilicus and shifts to
1. Hardly any tenderness and rigidity on anterior right illiac fossa where the pain is static at Rt. iliac
abdominal wall. fossa.
2. Confusing features are: 3. Temp rises to 102°F or more
• Diarrhea 4. Scalding pain during micturition
• Rise of temperature 5. Vaginal discharge is characteristic
• Strangury 6. Cervix is softened but causes tremendous pain when
• Irritation of rectum moved.
• Rovsing’s test and obturator test positive. n. Acute non-specific mesenteric lymphadenitis:
g. Acute appendicitis in infancy and childhood: Description of pain: (Differential diagnosis—D/D from
Description of pain: acute appendicitis)
1. At point of maximum tenderness, the child will put 1. Pain starts around umbilicus
its hands away. 2. May be of colicky nature
h. Acute appendicitis in pregnancy: 3. Over a diffuse area above and medial to position of
Description of pain: appendix
1. Hardly any tenderness and rigidity due to laxed 4. No shifting of pain
abdomen 5. Too much rigidity is never present
i. Acute cholecystitis: 6. Shifting tenderness (Klein’s sign) is patho-gnomonic.
Description of pain: After locating the area of tenderness in supine
1. Pain severe in Rt hypochondrium radiating to inf. position, the patient is rolled to left side and kept
angle of Rt. scapula or top of Rt. shoulder. such for a few minutes. Tenderness moves to left
2. Charcot’s triad (but Meckel’s diverticulitis may also show such
• Pain shifting type of tenderness.)
• Jaundice o. Acute ulcerative colitis:
• Rigor Description of pain:
3. Pain and rigidity over gallbladder 1. Pain of toxic colitis
j. Acute pancreatitis: p. Subdiaphragmatic (subphrenic) abscess:
Description of pain Description of pain:
1. Pain over epigastrium is excruciating and agonising 1. Pain occurs usually over abscess in hypo. region

2. Referred to corresponding shoulder due to irritation
of diaphragm.
3. An area of tenderness over affected area.
q. Amebic liver abscess:
Description of pain:
1. Acute pain in Rt. hypochondriac or epigastric area.
2. Increased by alcohol, walking, riding or jarring.
3. The patient usually supports the upper right side of
abdomen with his hands when he expects jarring or
vibration.
4. Pain associated with pyrexia, rigors, profuse
sweating at night.
r. Perforation:
1st stage (Peritonism)
1. Adult male with H/o peptic ulcer complains of acute
burning pain over epigastrium.
2. May be reffered to tip of shoulder due to diaphrag-
matic irritation.
3. Pain may gradually radiate down along paracolic
gutter to right illiac fossa (confused with acute
appendicitis).
4. Muscle guard over upper half of Rt return muscle.
5. Late stage—pain may be felt on right iliac fossa
which gives confusion.
2nd stage (Stage of reaction)
1. The intensity of symptom seen in 1st stage dwindles
although fire is still under burning ashes.
2. Rectal examination may reveal tenderness in recto-
vescicle or rectouterine pouch.
3rd stage (Stage of diffuse peritonitis) (A step further
towards grave)
1. Facies Hippocratica: pinched, anxious, sunken eyes,
and hollow cheeks
2. Rising pulse, low in vol. and tension.
3. Persistent board-like rigidity and increasing dis-
tention.
s. Perforation of typhoid ulcer:
Description of pain:
1. Sudden pain, definite tenderness and rigidity, very
severe
t. Perforation of ulcerative colitis:
Description of pain:
1. Sudden pain with distention and shock arouses
immediate suspicions.
u. Perforation of diverticular disease of colon:
Description of pain:
1. Generalized peritonitis is rare
2. More often localized abscess
3. If generalized, mortatity is high and not less than 50
percent
Symptomatology and its Causes 29
General Character of Pain in Perforation
(Perforative Peritonitis)
Description of pain:
1. Sudden
2. Very severe
3. Initially located directly over the inflamed area.
4. Intensity depends on type and amount of irritating
substance and rate at with this substance is poured into
peritoneal cavity due to perforation .
5. Aggravated by changes in tension of peritoneum
6. The patient lies still (board-like rigidity)
7. Later on, rigidity is generalized and pain also becomes
generalized.
Mechanical Obstruction to Hollow Viscera
a. Small bowel obstruction:
Description of pain:
1. Pain is colicky in mid. abdomen that is peri-and supra-
umbilical region.
2. Occurs in paroxysm and the patient is well between
pains
3. Borborgymi sound is heard during pain.
4. Later pain becomes less severe as motility is
decreased in edematous intestine.
5. In strangulation—pain is steady, severe, localized,
without colicky nature.
6. Pain is accompanied by feculent vomiting, singultus
and obstipation (no passage of feces or gases)
7. When obstruction is in jejunum and high in ileum,
the colics appear in waves at intervals of 3 to 5
minutes.
8. Lasts for 30 seconds.
9. The interval becomes longer in obstruction of
terminal ileum where it is about 8 to 10 minutes.
10. The site of pain will give an indication of site of
obstruction. For example, small intestinal cramps
are referred in epigastric or umbilical region, whereas
colonic cramps to lower abdomen (hypogastrium).
11. In lower obstruction, pain is situated over umbilical
region.
b. Colonic obstruction:
Description of pain:
1. Colicky abdominal pain is of much less intensity.
2. Felt at any site over abdomen depending on part of
colon involved, e.g. hypogastric pain in sigmoid colon
involvement.
3. Feculent vomiting is rare.
4. Constipation progresses to obstipation.
Nature of Obstruction
A. Simple obstruction
1. Presence of intestinal colic
30 Essentials of Clinical Medicine

B. Strangulation Volvulus of Cecum

1. No complete remission of pain between colics. So Description of pain:
colicky pain of simple obstruction is replaced by 1. Features are very much similar to low small bowel
continuous pain. obstruction
2. Presence of muscle rigidity and rebound tenderness
immediately makes the diagnosis. Meconium Ileus
3. Two hours of gastric suction if fail to relieve pain Description of pain:
indicates internal strangulation. 1. Feature of small bowel obstruction.

Paralyticus Ileus Volvulus of Midgut

Description of pain:
1. Absence of colicky pain.
1. Features of small bowel obstruction.
2. Silent abdomen in auscultation.
2. Appearance of dehydration—very fast.
Causes of Obstruction Gallstone Ileus
1. Congenital malformations: Description of pain:
• Cong. atresia of esophagus 1. Often the previous history of chololithiasis is present
• Cong. pyloric stenosis 2. Recurrent mild colics accompanied by vomiting.
• Meconium ileus
Mesenteric Valvular Obstruction
• Cong. atresia of duodenum or ileum.
• Hirschsprung’s disease, etc. Description of pain:
1. Occurs in those who are suffering from cardiac valvular
2. In infancy:
disease or atherosclerosis.
• Intussusception and obstruction due to worms.
2. Pronounced shock, colicky pain (quite severe),
3. In adolescence: distention and frequent vomiting.
• Intussusception band or adhesion resulting from 3. Localized rigidity and tenderness over the infarcted area
Meckel’s diverticulum. can be elicited.
• Local peritonitis due to appendicitis
• Tubercular peritonitis. Intestinal Obstruction Due to Worms
• Tabes mesenterica, etc. Description of pain:
4. In adults: 1. A swelling may be palpable in right iliac fossa which
i. Obstruction by band, volvulus or growth pits on pressure.
5. In old age: 2. The only complication of significance is perforation
i. Previous history of cholelithiasis if present with peritonitis in which worms penetrate the intestinal wall.
intestinal obstruction, possibility is of gallstone. Bolus Obstruction
ii. Strangulated hernia may be at any age. Description of pain:
Acute Intussusception 1. Due to insufficiently masticated food.
Description of pain: Vascular Disturbances
1. Child screams in abdominal pain and draws his legs when Superior mesenteric artery occlusion:
touched Description of pain:
2. Attacks usually last for a few minutes and come back 1. Mild continuous diffuse pain present 2 to 3 days before
within 15 minutes vascular collapse or peritonitis sets in.
3. In between the attacks, the patient looks somewhat 2. No tenderness or rigidity.
drawn 3. Bloody diarrhea.
4. Absence of distention with severe colic in abdomen and 4. In chr. mesenteric artery insufficiency, abd. pain occurs
pallor should clinch the diagnosis. after intake of food (abd. angina)
5. Thromboembolism, sickle cell crises, rupture of
Volvulus of Sigmoid Colon aneurysm, etc.
Description of pain: Abdominal Wall Causes
1. The sudden onset with acute pain on left side. (Trauma or infections of muscles)
 Symptomatology and its Causes 31

Description of pain: Intestinal Colics

1. Constant, aching pain. Description of pain:
2. Aggravated by movements, prolonged standing and 1. Occurs in small intestinal obstuction and toxic (catarrhal)
pressure enteritis.
3. May be a part of generalized myositis 2. Occurs due to food poisoning.
4. Fatty hernia through linea alba.
Appendicular Colic
5. Trauma or infection of muscle, etc.
Description of pain:
Colics 1. Colicky pain in right iliac fossa.
2. Vomiting and rise of temp. present.
• Intestinal colics
• Ureteric colics Renal Colic
• Renal colics Description of pain:
• Biliary colics 1. Fixed dull ache in angle between the lower border of
• Appendicular colics. last rib and lateral border of sacrospinalis.
2. Also felt anteriorly in hypochondriac region.
Common Features of Colics 3. Gets worse on movement like running, jolting and
1. Sudden appearance of griping pain which stays for a climbling up stairs and gets better with rest.
period during which the patient tosses over bed and
Referred Pain
then it passes off as suddenly as it came.
2. Nausea, vomiting, belching, retching. (in case of abdomen)
3. Varying degree of collapse. Description of pain:
4. Absence of muscle guard. 1. Usually by inflammatory or neoplastic disease
2. Sharp, cutting in nature well localized and superficial.
Biliary Colics or Gallbladder (Gallstone) Colic 3. Usually felt more laterally than visceral pain which is
Description of pain: felt more in midline.
1. Severe colicky pain over the Rt. hypochondrium radiating 4. Usually radiates over a fixed pathway.
to inf. angle of Rt. scapula and Rt. shoulder. – In lesion of stomach, duodenum and jejunum (T5–
2. Tenderness over gallbladder region may or may not be T8)—epigastrium.
present. – In affection of ileum and appendix (T9–T10)—
3. Jaundice may or may not be present, depending on around umbilicus.
whether the stone is in common bile duct or cystic duct. – In case of colon (T11, T12, L1, L2)—in hypo-
4. Called colic as it is intermittent. But the patient describes gastrium
it as griping pain. – Any irritation of undersurface of diaphragm (C3,
C4, C5) – Corresponding shoulders mainly C4.
Ureteric Colic – Renal colic—from loin to groin, testis and inner thigh
Description of pain: (genitofemoral ) (L1, L2).
1. The patient is seized with sudden pain in loin and radiating – Bilcary colic—from Rt. hypochondrium to inf. angle
to testis, groin or inner side of thigh (genitofemoral n. of right scapula (T7–T9).
L1 and L2). – Irritation of parietal pleura in pleurisy, hemothorax
2. Testis of affected side may be drawn up. or pneumothorax—abdominal wall.
3. Often with vomiting and profuse sweating. • It must be emphasized that segmental n. supply
4. Tenderness over renal angle. as has been referred to in this section is sympathe-
5. Previous H/o similar colic, passage of stone in urine and tic never supply of viscus. Of course, the same
skiagraphy reveals stone. viscus also receives the parasympathetic supply
6. Frequency in micturition and strangury present if stone mostly from vagus (with the exception of hindgut
is in lower end. and bladder which receive sacral sympathetic
supply).
7. Hematuria present.
8. This colic occurs when a stone in the renal pelvic Refferred Pain is Seen in Cases of:
temporarily blocks the pelvi-ureteric junction or enters 1. Pneumonia—pleuritic pain
the ureter to block it. 2. Pleurisy—pleuritic pain
9. The patient tosses over bed. 3. IHD
32 Essentials of Clinical Medicine

a. Angina—substernal or heavy pain. Acid Peptic Disease: (Ulcer Pain)

b. MI—Pain similar to angina or pain due to long-
standing diabetes. Duodenal Ulcer
c. Ischemic cardiomyopathy Description of pain:
d. Cardiac arrest i. Often episodic, recurrent, epigastric, periodic
e. Sudden cardiac death ii. Sharp, burning or ill defined
f. Asymptomatic CAD (silent ischemia) iii. Characteristically occurs from 90 min to 3 hr after
4. Panniculitis (Inflammation of fatty subcutaneous tissue eating and awakens the patient from sleep
layer over abdomen) iv. Pain is relieved by food, antacid or H2 blocker.
5. Torsion of testis or ovary Therefore, the patient calls it “hunger pain”.
6. Spine v. Steady, gnawing, burning or hunger-like discomfort
7. Genitalia. vi. In epigastric region, slightly right of midline
Metabolic Causes vii. Does not radiate. Only when ulcer penetrates and
1. DM adheres to pancreas, it is dull boring at back
2. Uremia viii. Awaken the patient early morning.Thereafter, a biscuit
3. Porphyria or a glass of milk should be taken immediately after
4. Pb (lead) poisoning getting up.
5. HS purpura ix. Periodicity: The symptoms appear and last for a few
6. DKA (diabetic ketoacidosis) days and then disappear for an interval of a few weeks
7. Hyperlipidemia or even months without any reason. Exacerbation of
8. C-1 estarase deficiency. the symptoms tend to last longer and pain-free
Neurogenic Causes intervals become shorter; and after a few years, pain
1. Herpes zoster is fairly constant.
2. Tabes dorsalis. Changes in character of pain suggest development of
a. Causalgic pain complication:
– Burning pain i. Pain radiating to back—penetration of ulcer
– Limited to distribution of peripheral n.. ii. Pain aggravated by food and accompanied by
– Touch or any normal stimulation. vomiting—gastric outlet obstruction.
– No muscle spasm or change with respiration or iii. Abrupt, severe abdominal pain—perfortion of ulcer.
food intake iv. When accompanied by coffee ground vomitus and
b. Lancinating type:
malena—ulcer bleed.
– Pain from spinal nerve or roots
– Caused by H. zoster, arthritis, tumors, herniated Gastric Ulcer
nucleus pulposus. Description of pain:
– Diabetes, syphilis i. Epigastric pain which is worsened by taking food.
– Aggravated by movement of spine and is usually ii. Relieved by vomiting.
confined to a few dermatomes.
iii. Relief with antacid is less consistent than that of
– Hyperesthesia is common.
duodenal ulcer pain.
Psychogenic Abdominal Pain iv. Felt more to left of midline.
v. Burning or aching, atypical and a sensation of bloating
Description of pain: or discomfort.
• No relation to meals vi. Precipitated after ½ hr of food.
• Onset usually at night vii. Therefore, loss of wt occurs, the patient is afraid of
• No nausea or vomiting eating.
• No abdominal muscle spasm.
viii. Relieved by alkalies
• No change with respiration but restricton of depth.
ix. No nocturnal pain
Distention of Visceral Surfaces x. Nonperiodicity of pain
Pain occurs due to the stretching of the hepatic or renal xi. Often caused by anti-inflammatory drugs, psycho-
capsules (See details below). logical tension and irregular food habits.
 Symptomatology and its Causes 33

Hepatic Pain Hemorrhage

Description of pain: 1. Rupture of ectopic gestation
i. Occurs in the right hypochondrium. 2. Ruptured lutein cyst
ii. Due to stretchting of capsule by inflammation or 3. Spontaneous rupture of malarial spleen
congestion. 4. Rupture of leaking aortic aneurysm
iii. Severe, constant, aggravated by deep breathing and 5. Aortic dissecting aneurysm.
coughing as they cause movement of diaphragm which
irritate the hepatic capsule. Torsion of Pedicle

Abdominal Distention: (May Cause Pain) 1. Twisted ovarian cyst

2. Spleen, etc.
1. Fat
2. Flatus Extra-Abdominal Causes of Pain in Abdomen
3. Faeces
4. Fluid – Ascites 1. Parietal conditions:
i. Cirrhosis i. Superficial cellulitis of abd. wall
ii. Malignancy ii. Gas gangrene of abd. wall
iii. Nephrotic syndrome iii. Abscess of abd. wall
iv. Tuberculous peritonitis iv. Rupture of rectus abdominis muscle
v. Cardiac or pericardial disease v. Tearing of inf. epigastric a.
vi. Hepatic or portal vein obstruction 2. Thoracic conditions:
5. Fetus i. Diaphragmatic pleurisy
6. Intestinal obstruction ii. Lobar pneumonia
7. Intestinal colic iii. Spontaneous pneumothorax
8. Chronic simple constipation with irritable bowel syn- iv. Pericarditis
drome. v. Angina pectoris
vi. Coronary thrombosis, etc.
Painless Abdominal Distention in Women 3. Retroperitoneal conditions:
1. Presenting symptoms of ovarian cyst i. Uremia
2. Undisclosed pregnancy ii. Pyelitis
3. Psuedo-obstruction: iii. Dietl’s crisis
a. Nonmechanical obstruction. iv. Retroperitoneal lymphangitis and lymphadenitis
b. Neuropathy v. Leaking aneurysm of aorta
c. Elderly patient. vi. Dissecting aneurysm of aorta.
d. Drugs like anticholinergic, tricyclic antidepressant 4. Diseases of spine: spinal cord and intercostal nerves:
e. Abdomen distention with constipation early childhood i. Pott’s disease
in absence of fecal soiling suggest ii. Acute osteomyelitis of lower, dorsal or lumbar
f. Hirschsprung’s disease vertebrae
g. Irritable bowel syndrome iii. Gastric crisis in tabes dursalic
Acute Intestinal Obstruction iv. H. zoster of lower intercostal nerves
v. Intercostal neuralgia.
a. Mechanical
5. General diseases:
i. In lumen—gallstone, round worms, fecolith, etc.
i. Malaria
ii. In wall—tubercular stricture, intussusception,
ii. Typhoid fever
growth
iii. Porphyria
iii. Outside the wall—additional bands, volvulus, internal
hernia, etc. iv. Diabetic crisis
b. Toxic—paralytic ileus v. Sickle cell anemia
c. Neurogenic—Hirschsprung’s disease vi. Hemophilia
d. Vascular—occlusion of mesenteric vessels by embolism vii. Purpura
or thrombosis. viii. Smallpox, etc.
34 Essentials of Clinical Medicine

In Children Description of pain:

A. Acute appendicitis 1. Midline, restrosternal, constrictive, compressive or
B. Intussusception squeezing, diffuse.
C. Intestinal obstruction by round worm, congenial 2. Lasting more than 2 and less than 10 min.
bands, or by bands including Meckel’s diverticulum 3. Heaviness or tightness in the chest
D. Acute nonspecific mesenteric lymphadenitis 4. Stabbing, sharp, excruciating and likewise.
E. Meckel’s diverticula 5. Severe pain
F. Primary peritonitis. 6. Retrosternal burning
In Females 7. Unstable angina—10 to 20 min similar to stable angina
A. Ruptured ectopic gestation but occurs with low level of exertion or even at rest.
B. Ruptured lutein cyst. 8. Postprandial angina have also been noted.
C. Twisted ovarian cyst Radiation:
D. Acute salpingitis 1. Left shoulder
E. Tubo-ovarian abscess 2. Medial border of left arm.
F. Torsion or degeneration of a uterine fibroid. 3. Left side at angle of jaw
6. Myocardial infarction 4. Rt. shoulder and arm
7. Dissecting aortic aneurysm 5. Both arms simultaneously
8. Acute vertebral collapse: 6. Epigastrium
Lateralized pain restricting movement. Marked tenderness 7. To back in interscapular region.
overlying the involved vertebrae.
Duration:
9. Cord compression:
1. Does not last for more than 2 to 3 min.
i. Pain on percussion of thoracic spine.
2. Any pain lasting for more this is either noncardiac or
ii. Hyperesthesia in dermatomal distribution.
due to ischemia or infarction.
10. Pleurisy:
i. Lateralized pain on coughing Aggravating factors:
ii. Chest signs, e.g. pleural rub. 1. Exertion.
11. H. zoster: 2. Uphill or upstairs
i. Hyperesthesia in dermatomal distribution. 3. Emotional upsets:
ii. Vescicular eruption. a. Anxiety
12. DKA (Diabetic ketoacidosis): b. Anger
Cramp-like pain. c. Excitement
13. Salpingitis or tubal pregnancy: 4. After a heavy meal due to blood diversion.
i. Suprapubic and iliac 5. Cold weather due to peripheral vasoconstriction.
ii. Fossa pain and tenderness 6. Psychological stress.
iii. Nausea, vomiting, fever. 7. Pain at rest is due to spasm of coronary a. (Prinzmetal
14. Torsion of testis/ovary syndrome)
i. Lower abdominal pain Relieving factors:
ii. Nausea, vomiting 1. Rest
iii. Localized tenderness. 2. Nitrates
3. Warm up before exercise.
CHEST PAIN
Associated factors:
Cardiac Causes 1. Pallor
a. Ischemic heart disease: 2. Palpitation and chocking
• There is usually no correlation between severity and 3. Sinking sensation in epigastrium
duration of pain and seriousness of condition. 4. S4 gallop or mitral regurgitation murmur during pain.
Angina Pectoris Myocardial Infarction
Site: Description of pain:
1. Usually substernal 1. Site, radiation remain same
2. Rarely precordial 2. Pain may come at rest
3. Rarely absent in chest and felt at site of radiation. 3. Usually for > 30 min to a few hours
 Symptomatology and its Causes 35

4. In severe cases, pain is accompanied by all signs and Infective Endocarditis

symptoms of shock. Description of pain:
5. Not rapidly relieved by drugs or rest. 1. Osler’s nodes (painful violaceous) raised lesion of
6. Accompanied with: fingers, toes and feet.
– sinking feeling 2. The initial symptoms or signs of endocarditis may be
– sweating caused by arterial thrombi or cardiac damage.
– nausea, vomiting, giddiness, hypotension
– profound restlessness Cardiomyopathy
– sudden unconsciousness Description of pain:
– unexplained low BP. 1. Angina on effort
– elderly and diabetics may have silent painless attack 2. Dyspnea on effort
– feeling to defecate. 3. Syncope on effort
Clinical findings: 4. Sudden death.
1. Shock
Valvular Heart Disease
2. Cyanosis
3. Severe pallor A. In MS—chest pain (which occurs in 10 percent) occurs
4. Hypotension due to pulmonary hypertension or myocardial ischemia
5. Atrial gallop rhythm secondary to accompanying coronary atherosclerosis.
6. Apical systolic mitral murmur B. In MR—Rt. heart failure with painful hepatic failure.
7. Pericardial rub. C. In MVP—substernal, prolonged, poorly related to
exertion and rarely resembles typical angina.
Pericarditis D. In AS—similar to angina pectoris with late peaking
Description of pain: systolic murmur radiating.
1. Steady, substernal discomfort which mimics MI
– Worsened by lying down Dissecting Aneurysm of Aorta
– Relieved by sitting and leaning forwards. Description of pain:
– Inflammation of diaphragmatic pleura causes pain 1. Excruciating pain usually beginning in ant. chest (center)
in shoulder and neck. 1. Radiating to back and downwards as dissection
– Catching sensation. progresses and between shoulder blades.
– Irritation transmitted to lateral parts of diaphragm 2. Confused with MI
(by T6–T9) is referred to chest and upper part of 3. Lasts for many hours
abd 4. Not aggravated by changes in position or respiration.
– Pericardial friction rub. 5. Associated with unequal or absent pulses
– Relieved by NSAIDs 6. Tearing or ripping sensation knife like
– Worsened by respiration and change of position 7. Associated with hypertension, Marfan’s syndrome,
– Pain lasts for hours to days together like murmur of aortic insufficiency. Pericardial rub,
– Pain is retrosternal or towards cardiac apex pericardial tempanode, loss of peripheral pulses
– May radiate to left shoulder. bradycardia. Early diastolic murmur, syncope, focal
Pericardial pain has 3 types of presentation: neurologial symptoms and signs.
1. Pleural type: 2. Respiratory causes:
– Sharp cutting pain felt in neck or shoulder or lateral a. Pleurisy (or pleuritis):
side of chest wall. Description of pain:
– Aggravated by coughing, deep breathing and 1. Sudden in onset.
swallowing. – Sharp, cutting stitch-like pain, knife like.
2. Pain similar to MI: – Localized superficial pain.
i. Steady, continuous, boring type – Aggravated by coughing, deep breathing and
ii. Severe sneezing.
iii. Due to inflammation, irritation of efferent cardiac n. – Relieved by lying down on affected side due
fibres in adventitial layers of coronary arteries. to restriction of movements
3. Rarely pain at left shoulder or left lat. side of precordium – Referred along intercostal nerve, radiation of
is felt with every beat. pain felt over sites away from thorax.
36 Essentials of Clinical Medicine

– Pleural inflammation which involves the area 1. Pain on deep inspiration

supplied by T8–T12 will cause pain which is 2. Presence of slight bruising over chest
referred to abdomen . 3. On palpation, local bony irregularity, tenderness
– Involvement of diaphragmatic pleura causes and crepitus.
pain in sup. ridge of trapezius muscle on same 4. Compression test is positive.
side (5th and 6th intercostals n.) 5. The clinician should run this finger along each
– Apical pleurisy presents as a dull pain in apical rib to reveal tenderness.
areas of lungs not affected by respiratory 6. Signs of concomitant injury such as lung, liver
movement, as there is minial expansion of (on Rt. side) spleen (Lt. side)
these area during respiration. 7. Surgical emphysema denotes lung injury.
– Pain of diaphragmatic pleura is referred to b. Vertebral collapse
tip of shoulder, neck, trapezius, radiates down c. Costochondritis
to upper abdomen when peripheral part of d. Myositis of pectoral muscles.
diaphragmatic pleura is involved simulating
acute abdomen (6th–12th ICN) 4. GIT causes:
b. Pulmonary embolism: a. Esophageal reflux or reflux esophagitis
Description of pain: Description of pain:
1. Abrupt onset 1. Lasts for 10 to 60 min.
2. Several minutes to a few hours 2. Burning type
3. Pleuritic type of pain 3. Substernal, epigastric region
4. Often lateralized on side of embolism. 4. Worsened by postprandial recumbency
5. Accompanied with dyspnea, tachypnea, 5. Relieved by antacids.
tachycardia and hypotension. b. Esophageal spasm:
c. Pulmonary hypertension: Description of pain:
Description of pain: 1. Lasts for 2 to 30 min.
1. Variable duration 2. Pressure, tightness, burning type
2. Pressure type 3. Retrosternal
3. Substernal 4. Closely mimic angina.
4. Dyspnea, sign of increased venous pressure c. Peptic ulcer:
including edema and jugular venous distention. Description of pain:
d. Pneumonia or pleuritis: 1. Prolonged
Description of pain: 2. Burning
1. Variable duration 3. Epigastric, substernal
2. Pleuritic type 4. Relieved with food or antacids.
3. Unilateral, often localized d. Gallbladder disease:
4. Dyspnea, cough, fever, rales, occasional rub. Description of pain:
e. Spontaneous pneumothorax: 1. Prolonged
Description of pain: 2. Burning, pressure type
1. Sudden onset 3. Epigastric, right upper quadrant, substernal.
2. Lasts for several hours 4. May follow meal.
3. Pleuritic type
e. Hiatus hernia
4. Lateralized to the side of pneumothorax
f. Pancreatitis
5. Dyspnea, decreased breath sounds on the side
of pneumothorax. g. Cholecystitis
6. Worsens on breathing. h. Splenic flexure syndrome.
f. Malignancy: Constant pain, unrelated to breathing 5. Others:
g. Traumatic hemo-and pneumothorax. a. Herpes zoster:
3. Musculoskeletal causes: Description of pain:
a. Rib fracture 1. Variable duration
Description of pain: 2. Sharp or burning
 Symptomatology and its Causes 37

3. Dermatomal distribution Table 3.1: In general - nature of various types of pain

4. Vescicular rash in area of discomfort. 1. Vague aching pain:
b. Neuropathic pain: – Mild continuous pain.
Description of pain: – No other specific features.
2. Burning pain:
1. Unusual burning, tingling or electric shock-like
– Burning sensation
quality – e.g. -
2. Triggered by very light touch • Peptic ulcer
3. Sensory deficit is definitely increased in the • Reflux esophagitis.
corresponding dermatome, e.g. 3. Throbbing pain:
e.g. Pyogenic abscess.
• Diabetic polyneuropathy 4. Scalding pain:
• Peripheral afferent damage in H. zoster. – Type of burning sensation
c. Tietze’s syndrome: – During micturition, in presence of:
Description of pain: - • Cystitis
• Acute pyelonephritis
1. Painful swelling of one or more costochondral
• Urethritis.
articulation. 5. Pins and needle sensation:
2. Usually 2nd or 3rd ribs. – Injury to peripheral sensory n.
6. Emotional and pshychiatric conditions 6. Shooting pain:
Description of pain: – In sciatica, along its course.
7. Stabbing pain:
– Variable duration – Sudden, severe, sharp, short lived
– May be fleeting in nature – Perforation of peptic ulcer.
– Variable quality 8. Constricting pain:
– Variable location, may be retrosternal – As iron band tightening around the chest
– Typical of angina.
– Situational factors may precipitate the symptoms 9. Distention:
– Anxiety or depression often detectable with careful – Diseases of any structures encircled or restricted
history. 10. Colic:
7. Functional – When muscular wall of a hollow tube is attempting to force
certain content out of it.
8. Chronic cough
– Appears suddenly and goes suddenly
9. General causes of chest pain: – Pain is of gripping nature.
a. Non-central—pleural: – Often associated with vomiting and sweating.
• Pneumonia 11. Twisting pain:
• Pulmonary infarction i. Volvulus of intestine
ii. Torsion of testis
• TB iii. Ovarian cyst
• Malignant disease 12. Just a pain:
b. Non-central—chest wall: – No explanation of pain by the patient.
• Rib fractures 13. Movement of pain:
– Radiation
• Direct invasion of chest wall by tumor or rib
– Referred
metastatic lesion. – Shifting or migration.
• Spinal nerve root involvement by vertebral
disease (usually vertebral body collapse) and HEADACHE
herpes zoster
Intracranial Causes
• Coxsackie B-infection (Bornholm disease).
c. Retrosternal: Migraine
• Tracheitis Description of pain:
• Mediastinal tumors 1. Most common cause of vascular headache 15 percent
• Acute mediastinitis women and 6 percent men, all ages.
• Mediastinal emphysema 2. Severe headache attacks, regardless of cause, described
• Lesion of heart and great vessels as:
• Esophageal disorders. – Throbbing
38 Essentials of Clinical Medicine

– Associated with vomiting ii. Moderate-to-severe head pain, pulsating quality,

– Tenderness of scalp unilateral location.
3. Milder headache attacks: iii. Aggravated by walking stairs or similar routine
– Light, band-like discomfort often entire head. activities
4. Associated signs and symptoms according to prevalence: iv. With nausea, vomiting, photophobia, phonophobia,
• Nausea - 89 percent v. Multiple attacks (each of 4–72 hr).
• Photophobia - 80 percent Migraine with Aura
• Lightheadedness - 70 percent
i. Headache associated with characteristic premonitory,
• Scalp tenderness - 60 percent
sensory, motor or visual symptoms.
• Vomiting - 55 percent
ii. Focal neurological disturbances are more common
• Visual disturbance - 35 percent
during headache.
• Photopsia - 25 percent
iii. Focal neurological disturbances without headache or
• Fortification spectra - 10 percent
vomiting are known as migraine equivalent or
• Paresthesia - 30 percent
migraine accompaniments and more common in 40
• Vertigo - 30 percent and 70 years.
• Alteration of consciousness - 18 percent iv. Complicated migraine—transient focal neurological
• Syncope - 10 percent disturbance or a migraine attack that leaves a persistent
• Seizure - 4 percent residual neurological deficit.
• Confusional headache - 4 percent v. Visual—dysfunction of occipital lobe neurons.
• Diarrhea - 16 percent • Scotoma and hallucination in central portion of
Recognized by “activators”: visual fields and expand into “C” shape.
• Red wine • Luminous angles at enlarging outer edge, becoming
• Menses colored and moves to periphery of involved 1/2
• Hunger of field, and disappearing over the horizon of
• Lack of sleep peripheral vision
• Glare • Entire process lasts for 20 to 25 min vision.
• Estrogen This phenomenon is pathognomonic for migraine and has
• Worry never been described in association with cerebral structural
• Perfumes anomaly (fortification syndrome—zigzag line on visual
• Let-down periods acquity testing) because serrated edges of hallucinated
• OC pills. “C”seemed a fortified town with bastions all around it
Recognized by “deactivators”: “spectrum” is used in sense of an apparition or specter.
• Sleep Basilar Migraine
• Pregnancy
1. Symptoms of disturbance in brainstem
• Exhilaration – vertigo
• Sumatriptan. – dysarthria
Types of Migraine – diplopia
a. Migraine without aura (common migraine) 2. A form of basilar migraine (Bickerstaff ’s migraine)
b. Migraine with aura (classic migraine) occurs primarily in adolescent females
– total blindness
c. Ophthalmoplegic migraine
– vertigo
d. Retinal migraine
– ataxia
e. Childhood periodic syndrome that can be precursors to
– dysarthria
or associated with migraine
– tinnitus
f. Migraine disorder without fulfilling the above criteria.
– distal and perioral paresthesia
Migraine without Aura – confusional state
i. No focal neurological disturbance precedes the – 20–30 min
recurrent headache. – throbbing occipital headache

– now also occur in children and adults >50 years.
– Altered sensorium for 5 days and may have con-
fusion like psychotic reactions.
– Full recovery is rule.
Carotidynia: lower half headache or facial migraine
Description of pain:
1. Most common among older 4th–6th decades
2. Pain is usually located at jaw or neck although periorbital
or maxillary pain may occur.
3. May be continuous, deep, dull and aching, becomes
pounding and throbbing episodically
4. Superimposed sharp, ice-pick like jaws
5. One to several times a week, each lasting for several
min. to hours.
6. Tenderness and prominent pulsations of cervical carotid
a. and soft tissue swelling overlying carotid ipsilaterally.
7. Many patients complain throbbing, ipsilateral headache
with carotidynia as well as between attacks.
8. Dental trauma is a common precipitating factor for this
syndrome
9. Carotid tenderness more common in hemicranial migraine
attacks.
Non-pharmacological approach to migraine:
1. Identify and avoid:
– Alcohol (red wine)
– Foods (chocolate, certain cheese, monosodium-
glutamate, nitrate containing food)
– Hunger
– Irregular sleep pattern (both lack and excess)
– Odors (organic)
– Sustained exertions
– Acute changes in stress level
– Miscellaneous (glare, flash)
2. Attempt to manage environmental shifts:
– Time zone shifts
– High attitude
– Barometric pressure
– Weather changes
3. Assessment of menstrual cycle relationship.
Migraine attacks build up usually over hours and
maintained for several hours to days and
characteristically relieved by sleep.
Few Other Features of Migrainous Headache
1. Sickening, dull ache or throbbing ache
2. Marked severity
3. Unilateral—different sides on different occasions
4. Attack usually lasts for 24 to 72 hours but occasionally
less than 6 hours.
Symptomatology and its Causes 39
5. Attacks with sudden or subacute in repeated short
bursts with pain free intervals lasting weeks or months.
6. Attacks are usually cyclical, weekly or monthly,
premenstrual
7. Condition is well between attacks
8. Headache at times of stress relief (e.g. weekend and
holidays)
9. Relieved by analgesic or 5-HT agoinsts like sum-
patriptan
10. In 15 to 20 percent of patient visual disturbances (tie-
chopsia and fortification spectra) and/or peripheral
and circumoral paresthesiae occur before headache
phase (migraine aura)
11. Cessation of headache during pregnancy, especially
in 2nd or 3rd trimester is pathognomonic of migraine.
Cluster Headache or Raeder’s Syndrome or
Histamine Cephalalgia or Sphenopalatine Neuralgia
Description of pain:
Severe pain, waking the patient from sleep in early hours of
morning.
All ages, above 10 years, mainly in men.
1. Distinctive and treatable vascular headache.
2. Episodic type is most common.
3. One to three short-lived attacks of periorbital pain per
day over 4 to 8 weeks followed by pain-free interval
that averages 1 year.
4. Chr. pain has sustained periods of remission.
5. Each form may transform into other.
6. Men >8 times of female.
7. Usually 20 to 50 years, may be in 1st decade.
8. Propanolol and amitryptyline—ineffective.
9. Lithium unlike migraine is effective here.
10. The cluster headache is clinically, genetically and
therapeutically different from migraine.
11. Periorbital or temporal pain without warning and
reaches a crescendo within 5 minute.
12. It is excruciating and deep, nonfluctuating and
explosive, rarely pulsatile.
13. Strictly unilateral and affects same sides in subsequent
months.
14. Lasts for 30 minutes to 2 hours.
15. With homolateral lacrimation, reddening of eye, nasal
stiffness, lid ptosis, nausea.
16. Alcohol provokes it
17. On-off vulnerability to alcohol is pathognomonic to
cluster headache.
18. Unlike migraine, only rarely do foods or emotional
factors precipitate pain
19. Stricking periodicity of attacks in 85 percent.
40 Essentials of Clinical Medicine

20. At least one bout of daily attacks recurs at about same Petechiae are found on trunk and lower extremity, in
hour each day for duration of cluster bout. mucous memb. and conjunctiva and on palms and sole.
21. Reaches peak over 3 to 5 minutes, remain maximum • Increased ICP (intracranial pressure)
for about 45 minutes and taper off. – > 180 mm H2O in 90 percent cases.
– > 400 mm H2O in 20 percent cases.
Chronic Paroxysmal Hemicrania
• Signs of ICP include:
Similar to cluster headache – Decreased consciousness.
Tension-Type Headache – Papilloedema.
• Episodic tension type – Dilated poorly reactive pupil.
• Chronic tension type. – 6th n. palsy.
Description of pain: – Decerebrate posturing.
a. Used to describe chronic headache. – Cushing’s reflex—bradycardia.
b. Characterized by bilateral tight band-like discomfort.  Hypertension
c. In cycles which repeat after several years.  Irregular
d. Feels as if the patient is in vise and posterior neck muscles  Respiration
are taut. – Cerebral herniation.
e. Pain typically builds slowly, fluctuates in severity and • Causes of neck stiffness:
may persist more or less continuously for many days. – Meningitis.
f. Exertion does not increase pain. – SAH (subarachnoid hemorrhage)
g. Episodic or chronic (> 15 days/ months). – Tetanus.
h. Common in all age groups and females tend to – Strychnine poisoning.
predominate. – Hysteria.
i. In some, anxiety or depression coexist with tension – Cervical spondylosis.
headache. – Meningism.
j. Relaxation always relieves headache; for example, – In meningitis, neck stiffness is absent in severe and
bedrest, massage, or formal biofeedback training. terminal cases or in very young infants.
k. For chronic type tension headache, prophylactic therapy
is recommended. Viral Meningitis
1. Syndrome includes:
Meningitis – Fever.
Bacterial Meningitis – Headache.
– Meningeal irritation coupled with inflammatory CSF
Description of pain:
profile.
• Acute severe headache.
2. Fever may be accompanied by:
• Stiffness of neck and fever.
• Striking accentuation of pain with eye movement – Malaise.
• May be confused with migraine because both have – Myalgia.
pounding headache, photophobia, nausea, vomiting. – Anorexia.
• Acute fulminant illness that progresses rapidly in a few – Nausea/vomiting.
hours or as a subacute infection that progressively – Abdominal pain .
worsens over several days. – Diarrhea.
• Classic triad is: – Lethargy/drowsiness.
– Fever. 3. Profound alteration in consciousness, such as stupor,
– Headache. coma and confusion.
– Nuchal rigidity (stiff neck). 4. Seizures, cranial nerve palsy, suggest parenchymal
• Alteration in mental state—lethargy to coma. involvement but are not typical of uncomplicated viral
• Kernick’s sign and Brudzinski’s sign are classical of meningitis.
meningeal irritation. 5. Headache is usually frontal or retro-orbital and often
• Seizures occur initially in 40 percent. associated with photophobia and pain on moving eyes.
• Rash of meningococcemia—diffuse erythematous 6. Nuchal rigidity is present in most cases but may be mild
maculopapular rash, skin lesion becomes petechial. and present only near limit of neck anteflexion.

7. Evidence of severe meningeal irritation such as Kernick’s
and Brudzinski’s sign usually absent.
Chronic and Recurrent Meningitis
1. Persistent headache with or without stiff neck and
hydrocephalus, cranial neuropathies, radiculopathies and
cognitive or personality changes.
2. CSF flow provides a pathway for rapid spread of
infection and malignant processes over the brain, spinal
cord, cranial and spinal n. roots.
Intracranial Meningitis
1. Hydrocephalus and increase ICT.
2. Headache, vomiting, apathy or drowsiness, gait,
instability, papilloedema, visual loss, impaired gaze, or
palsy of VII nerve.
3. Cognitive and behavioral changes.
4. Basal meningitis:
– Inflammatory deposits around brainstem, cranial n.
and undersurface of frontal and temporal to lobes.
– Multiple cranial neuropathies
• Visual loss - II n.
• Facial weakness - VII n.
• Hearing loss - VIII n.
• Diplopia - III, IV and VI n.
Sensory or motor
abnormality of pharynx - IX, X, XII n.
• Decreased olfaction - I n.
• Facial sensory loss
and masseter
weakness - v n.
Spinal Meningitis:
1. Injury to motor and sensory system root.
2. Multiple radiculopathies with combination of radicular
pain, sensory loss, motor weakness, sphincter dysfunc-
tion.
3. Myelopathy.
4. Patients with multiple cranial and/or spiral n. root are
likely to have chronic meningitis.
Systemic manifestation:
1. A complete H/o travel, sexual practice, exposure to
infective agents taken.
2. Infective causes are associated with fever, malaise,
anorexia, and signs of localized or disseminated infection
outside the CNS.
3. In immunosuppressed patients such as AIDS, chronic
meningitis is present without headache, fever.
4. Noninflammatory disorders often produce systemic
manifestation but meningitis may be, initial manifestation.
Symptomatology and its Causes 41
Idiopathic Intracranial Hypertension
(Pseudotumor Cerebri)
1. Present that like of brain tumor.
2. It is due to decreased absorption of CSF by arachnoid
villi.
3. Transient visual obscurations and papilloedema with
enlarged blind spot and loss of peripheral visual fields.
4. Most patients are young, females, and obese.
5. H/o exposure to provoking agents such as vitamin A
and glucocorticoids.
Brain Tumor
Description of pain:
All ages, both sexes.
1. About 30 percent with brain tumor present with pain in
head.
2. Intermittent deep, dull aching of moderate intensity which
may worsen with exertion or change in position and
may be associated with nausea and vomiting.
3. Disturbs sleep in about 10 percent.
4. Vomiting that precedes the appearance of headache by
weeks is highly characteristic of posterior fossa brain
tumor.
5. History of amenorrhea or galactorrhea indicates
prolactin-secreting pitutary adenoma (or polycystic ovary
syndrome).
6. Headache arising de novo in patient with known
malignancy suggests either cerebral metastasis or
carcinomatous meningitis.
7. Head pain appearing abruptly after bending, lifting or
coughing can be due to a posterior fossa mass (or a
Chiari malformation)
Intracranial Hemorrhage
Intraparenchymal Hemorrhage
Description of pain:
Most common types of intracranial hemorrhage:
1. Hypertension, trauma and cerebral angiopathy cause
the majority of these hemorrhage.
2. Advanced age, heavy alcohol and cocaine use in young
are important risk factors.
3. Hemorrhage may be small or a large clot may form
and compress adjacent tissue causing herniation and
death.
4. Blood may dissect into IV space and may cause
morbidity and hydrocephalus.
5. Most hypertensive intraparenchymal hemorrhages
develop over 30 to 90 minutes, whereas those
associated with anticoagulant therapy may evolve for
as long as 24 to 48 hours.
42 Essentials of Clinical Medicine
6. Hemorrhage occurs always when the patient is awake
and slightly stressed.
7. Presents as abrupt onset of focal neurological deficit.
8. Seizures are uncommon.
9. Focal deficit typically worsens steadily over 30 to 90
minutes and is associated with decreased conscious-
ness and sign of increased ICP such as headache and
vomiting.
10. Putamen is the most common site for hemorrhage
and adjacent internal capsule is invariably damaged.
11. Contralateral hemiparesis is sentinel sign.
12. When mild—face sags on one side over 5 to 30 minutes
speech becomes slurred, the arms and leg weaken
and eyes deviate away from side of hemiparesis.
14. When severe—drowsiness appears, and also stupor
and sign of upper brainstem compression.
15. Coma with deep, irregular or intermittent respiration,
a dilated and fixed ipsilateral pupil, bilateral Babinski’s
signs and decerebrate rigidity.
16. In milder cases—edema in adjacent brain may cause
progressive deterioration over 12 to 72 hours.
17. Thalamic hemorrhage produces a contralateral
hemiplegia or hemiparesis from pressure into int.
capsule.
– Prominent sensory deficit in all modalities
– Aphasia with preserved verbal repetition
apractagnosia or mutism in nondominant hemorr-
hage
– Homonymous visual field defect
– Deviation of eyes downwards and inwards,
unequal pupils with absence of light reflex, skew
deviation with the eye opposite to the hemorrhage,
displaced downwards and medially, ipsilateral
Horner’s syndrome, absence of convergence,
paralysis of vertical gaze and retraction nystag-
mus. Patients may later develop a chronic,
contralateral pain syndrome.(Dejerine-Roussy
syndrome)
In pontine hemorrhage, deep coma with quadriplegia
usually occurs over a few minutes.
– Prominent decerebrate rigidity and pinpoint (1 mm)
pupil that reacts to light.
– Impairment of reflex, horizontal eye movement
evoked by head turning (doll’s head, oculocephalic
maneuver) or by irrigation of ears with ice cold water.
– Hyperpnea, severe hypertension and hyperhidrosis
are common.
– Death usually occurs within a few hours, but there
are occasional survivors.
Cerebellar hemorrhage—(may develop over several
hours)
– Characterized by occipital headache, repeated
vomiting and ataxia of gait.
– Dizziness or vertigo may be prominent.
– Paresis of conjugate lateral gaze towards side of
hemorrhage, forced deviation of eyes to opposite
sides or ipsilateral 6th n. palsy
– Ocular sign may include blepharospasm, involuntary
closure of one eye, ocular bobbing and skew devia-
tion.
– Dysarthria and dysphagia
– No Babinski’s sign until late.
– Later the patient becomes stuporous and comatose.
Other Causes of Intraparenchymal Hemorrhage
1. Cerebral amyloid angiopathy.
2. Cocaine-induced stroke.
3. Head injury.
4. Anticoagulant therapy.
5. Hematological disorders.
6. Hemorrhage into brain tumor.
7. Hypertensive encephalopathy.
8. Primary intraventricular hemorrhage.
Subarachnoid Hemorrhage
• Sudden transient loss of consciousness in 1/2 of the
cases
• It may be preceded by brief moment of excruciating
headache.
• The patient often calls the headache “as the worst
headache of my life”.
• Usually generalized and vomiting is common.
• Although sudden headache in the absence of focal
neurological symptoms is hallmark of aneurysmal
rupture, focal neurological deficits may occur.
• Hemiparesis, aphasia and abulia develops
• Third n. palsy associated with papillary dilatation, loss
of light reflex and focal pain above or behind eye may
occur with an expanding aneurysm at the junction of
posterior communicating artery and internal carotid
artery.
• Sixth n. palsy may indicate an aneurysm in cavernous
sinus and visual field defect may occur with expanding
supraclinoid carotid or anterior inf. cerebellar artery
aneurysm.
• Pain in or behind the eye and in low temple can occur
with an expanding MCA (middle cerebral artery)
aneurysm.
• Growing aneurysm rarely cause headache in the absence
of neurological symptoms and signs.

• Aneurysm can undergo small rupture and leak of blood
into subarachnoid space. Therefore called “sentinel
bleeds.”
DELAYED NEUROLOGICAL DEFICIT
Re-Rupture
a. In first month following SAH is about 30 percent with
peak at 7 days
b. Sixty percent mortality, poor outcome
Hydrocephalus
a. Can cause stupor and coma.
b. Develops over a few days or weeks.
c. Progressive drowsiness or slowed mentation (abulia)
with incontinence.
d. Chronic hydrocephalus may develop weeks to month
after SAH and manifest as gait, difficulty, incontinence
or impaired mentation.
e. Lack of initiative in conversation or failure to recover
independence.
Vasospasm
a. Signs of ischemia appear 4 to 14 days after hemorrhage,
Mostly 7 days.
b. Spasm of MCA causes contralateral hemiparesis and
dysphagia.
c. Proximal Ant. cerebral artery vasospasm causes abulia
and incontinence.
d. Severe vasospasm of postcerebral artery causes
hemianopia.
Hyponatremia
a. Develops within first 2 weeks after SAH.
b. Cerebral salt - wasting syndrome clears over the course
of 1 to 2 weeks.
Vascular Anomalies
Congenital
True arteriovenous malformations (AVM):
Description of pain:
1. Headache, focal seizures and IC hemorrhage.
2. AVM occurs in all parts of cerebral Hemisphere, brain-
stem and spinal cord, the largest one, are most
frequent. In posterior half of hemisphere—commonly
a wedge-shaped lesion extending from cortex to
ventricle.
3. Although lesion is present from birth, bleeding or other
symptoms are most common between ages 10 and
30 years and sometimes late 50.
Symptomatology and its Causes 43
4. Mostly in men and rarely familial.
5. Headache (without bleeding) may be hemicranial and
throbbing like migraine or diffuse.
6. Focal seizures with or without generalization in 30
percent.
7. 1/2 of AVM cases present as IC hemorrhage.
8. Hemorrhage may be massive leading to death, or may
be small as 1 cm leading to minor focal symptoms or
no deficit.
9. Large AVM of ant. circulation may be associated with
a systolic and diastolic bruit (sometimes self-audible)
over eye, forehead, or neck and bounding carotid
pulse.
10. Headache at onset of AVM rupture is not generally as
explosive as with aneurysmal rupture.
Venous Anomalies
1. Development of anomalous cerebral, cerebellar or
brainstem drainage.
Capillary Telangiectasia
1. Are true capillary malformations that often form extensive
vascular networks through an otherwise normal brain
structure.
2. Pons and deep white matter are typical location and these
capillary malformations can be seen in patients with
hereditary hemorrhagic telangiectasia (Osler-Rendu-
Weber syndrome)
3. If bleeding does occur, it rarely produces mass effect
or significant symptoms.
4. No treatment option exist.
Acquired Vascular Lesions
a. Cavernous angiomas
1. Familial cavernous angiomas have been mapped to
several different chromosomal loci, the gene
responsible for 7q linked form encodes a protein
that interacts with a member of RAS family of
GTPases.
2. Seizures may occur if malformation is located near
the cerebral cortex.
b. Dural AV fistula
1. Patients may complain of a pulse-synchronous
cephalic bruit (pulsatile tinnitus) and headache.
2. Increased ICP.
• So vascular etiology of headache may be due to:
– IC aneurysms
– Malignant hypertension
– SAH, etc.
44 Essentials of Clinical Medicine

Table 3.2: The clinical features of arterial, neurogenic and venous claudication
Arterial Neurogenic Venous
Pathology Stenosis or occlusion of major Lumbar nerve root or cauda Obstruction to the venous outflow of the
lower limb arteries equina compression (spinal stenosis) to iliofemoral venous occlusion
Site of pain Muscles, usually the calf but may III-defined. Whole leg. May be
involve thigh and buttock associated with numbness and tingling Whole leg. ‘Bursting’ in nature
Laterality Unilateral if femoropopliteal, and Often bilateral Nearly always unilateral
bilateral if aortoiliac disease
Onset Gradual after walking the Often immediate upon walking or Gradual, often from the moment walking
claudication distance even standing up commences
Relieving features On cessation of walking,
pain disappears completely Eased by bending forwards and Usually necessary to elevate leg to relieve
in 1–2 minutes stopping walking. May have to sit discomfort
down to obtain relief.
Color Normal or pale Normal Cyanosed. Often visible varicose veins.
Temperature Normal or cool Normal Normal or diseased
Edema Absent Absent Always present
Pulses Reduced or absent Normal Present but may be difficult to bellowing to
edema
Straight leg raising Normal May be limited Normal

Skeletal Anomalies
a. Metastasis
b. Paget’s disease:
Description of pain:
1. Enlargement of skull is often unnoticed by patients except
by awareness of increasing hat size.
2. Facial pain and headache are initial complaints in some.
3. Backache is dull or shooting or knife like in lumbar region
and may radiate into buttocks or lower extremities.
4. More serious neurological complications can result from
overgrowth of bone at base of skull (platybasia) and
compression of brainstem.
5. Compression of spinal cord may cause paraplegia.
6. Pathological fracture of vertebrae may also produce
spinal cord lesions.
Tumors, Granulomas and Abscess
Headache is dull aching, either hemicranial or generalized,
progressively becomes severe and refractory to therapy.
Fever occurs in 50 percent cases and is of low grade.
Post Lumbar Puncture
Description of pain:
1. Usually begins with 48 hours, may be delayed up to 12
days.
2. Incidence 10 to 30 percent.
3. Positional (usually)—begins when the patient sits or
stands upright; relief upon reclining or with abdominal
compression.
– Worsened by head shaking and jugular vein com-
pression.
4. Pain is usually dull ache but may be throbbing, its location
is occipitofrontal.
5. Nausea and stiffness often accompany headache.
6. Some report blurred vision, photophobia, tinnitus and
vertigo.
7. May resolve over a few days but may persist for months
or weeks.
8. Often seen in patients over 10 years of age.
9. Both sex.
Extracranial Causes
Temporal (Giant-Cell) Arteritis
Description of pain:
1. An inflammatory disorder of arteries that frequently
involves the extracranial carotid circulation.
2. Usually over 55 years, either sex.
3. Average age of onset is 70 years and women account
for 65 percent of cases.
4. About 1/2 patients with untreated temporal arteritis
develop blindness due to involving of ophthalmic artery
and its branches, indeed the ischemic optic neuropathy
induced by giant cell arteritis is a major cause of rapidly
developing bilateral blindness in patients over 60 years.
5. Typical presenting complaints are headache,
polymyalgia, rheumatica, jaw claudication, fever,
weight loss.
6. Headache is a dominant symptom and often appears
in association with malaise and muscle aches.
7. Headache may be unilateral or bilateral and is located
temporally in 50 percent but may involve any and all
aspect of cranium.
 Symptomatology and its Causes 45

8. Pain reaches peak over a few hours. Postconcussion

9. Quality of pain is only seldom throbbing, it is almost Description of pain:
invariably described as dull and boring with superim- • Trivial head injury and particularly after rear-end motor
posed episodic ice pack lancinating pain similar to sharp vehicle collisions.
pains that appear on migraine. • Headache, dizziness, vertigo, impaired memory, anxiety,
10. Scalp tenderness is present, to a marked degree. irritability, difficulty with concentration.
Brushing the hair, resting the head over pillow may be • May remit after several weeks or persists for months
impossible because of pain.
and even years after injury.
11. Headache is usually worse at night and is often
• Typically, the neurological exam. is normal with the
aggravated by exposure to cold.
exception of behavioral abnormality and CT or MRI are
12. Reddened tender nodules or red streaking of the skin
normal. Chronic subdural hematoma may mimic this
overlying the temporal artery may be found in patients
condition.
with headache, as in tenderness of temporal or less
commonly the occipital artery. The cause of this headache is not known, and treatment
is symptomatic support.
Skeletal Causes
Coital Headache
i. Paget’s disease
ii. Torticollis Description of pain:
1. Spasmodic torticollis is characterized by tendency • Male-dominated (4 : 1) synd.
for head to turn to one side. • Attacks occur periorgasmically, very abrupt in onset
2. The designation anterocollis indicates head is and subside in a few minutes if coitus is interrupted.
flexed forwards. • Nearly always benign and usually occurs sporadically.
3. Retrocollis—pulled backwards. • If persists for hours or is accompanied by vomiting,
4. Spontaneously remission occurs occasionally, SAH must be excluded.
especially in first few months but later becomes Psychogenic
permanent and may worsen with time.
• Alcohol
Referred Pain • Nitrates and monosodium glutamate ingestion.
i. Glaucoma
Temporomandibular Joint
a. Prostrating headache associated with nausea and
vomiting. In osteoarthritis.
b. H/o of headache started with eye pain. Cervical Spine
c. Eye is often red with a fixed moderately dilated
In cervical spondylosis.
pupil.
ii. Sinusitis Teeth
In frontal sinusitis, headache occurs after 2 to 3 hours In dental sepsis.
after awakening and subsides as day progresses.
iii. Myopia and eye strain. Arteries
iv. Aural headache. In cranial arthritis.
Cough Insomnia
Description of pain:
1. Male-dominated (4 : 1) syndrome. Drug-Induced Headache
2. Transient, severe headache upon cough, bending, lifting • Bromides.
sneezing or stooping. • Ergotamine (withdrawal)
3. Persists for seconds to a few minutes. • Glyceryl trinitrate.
4. Usually diffuse, but in 1/3 cases it is lateralized. • Hydralazine.
5. MRI is indicated in patients with cough, headache. • Indomethacin.
6. Term “effort migraine” has been used for this syndrome • TNF-alpha
to avoid the ambiguous term, exertional headache. • Intravenous immunoglobulin
46 Essentials of Clinical Medicine

• Sibutramine 6. Occipital neuralgia.

• Sildenafil 7. Central causes of head and facial pain other than tic
douloureaux.
Fibromyalgia
Table 3.4: Headache symptoms that suggest a serious
Table 3.3: Headache associated with vascular disorder
underlying disorder
1. Acute ischemic cerebrovascular disorder.
“Worst” headache ever had.
2. Intracranial hematoma.
Such severe headache for the first time
3. SAH.
Sub-acute, worsening over days or weeks.
4. Unruptured vascular malformation.
Fever or unexplained systemic sign.
5. Arteritis.
Vomiting precedes headache.
6. Carotid or vertebral a. pain.
Induced by bending, lifting, cough.
7. Venous thrombosis.
Disturbs sleep or presents immediately upon awakening.
8. Arterial hypertension.
Known systemic illness.
9. Other vascular disorder.

Headache Associated with Nonvascular Table 3.5: Headache caused by systemic illness
Intracranial Disorder • Inf. mononucleosis.
1. Increased pressure of CSF • SLE.
• Chronic resp. failure (hypercapnia).
2. Decreased pressure of CSF • Hashimoto’s thyroiditis.
3. IC infection. • Drugs (glucocorticoids withdrawal, OCPs, ovulation promoting drugs).
4. Sarcoidosis and other noninflammatory diseases. • Inflammatory bowel disease.
5. Related to intrathecal drug administration. • HIV.
• Malignant hypertension, pheochromocytoma (diastolic pressure of
6. IC neoplasm. at least 120 mm Hg are required for headache).
7. Other IC disorders. • Orthostatic headache suggests subdural hematoma or benign IC
hemorrhage or a lumbar puncture done a few hours back.
Headache Associated with Substances • Headache due to ICT is more in early morning, causes sleep
or Their Withdrawal disturbances associated with projectile vomiting with or without focal
1. By acute substance use or exposures. neurological deficit.
2. By chronic substance use or exposures. Table 3.6: Pain sensitive and insensitive structures
3. By withdrawal (acute use).
Pain sensitive structures of CNS:
4. By withdrawal (chronic use). Scalp.
Headache with Noncephalic Infection Aponeurosis.
Middle meningeal a.
1. Viral postherpetic pain. Dural sinuses.
2. Bacterial. Flax cerebri.
3. Others. Proximal segments of large plial artery
Pain insensitive structures of CNS:
Headache with Metabolic Disorders Most of brain parenchyma.
1. Hypoxia (decreased O2 supply). Ventricular ependyma.
Choroid plexus.
2. Hypercapnia (increased CO2 accumulation). Plial veins.
3. Mixed hypoxia and hypercapnia.
4. Hypoglycemia. There is a midbrain locus for generation of headache.
5. Dialysis.
6. Others. JOINT PAIN

Cranial Neuralgias, Nerve Trunks Pain and Refer to textbook of orthopaedics.

Deafferentation Pain
DYSPNEA
Description of pain:
1. Persistent (in contrast to tic like) pain of c.r. origin. Definition
2. Trigeminal neuralgia (V n.). 1. Breathlessness inappropriate to the level of physical
3. Glossopharyngeal neuralgia. exertion or even occurring at rest is called dyspnea.
4. Nerves intermedius neuralgia. – Abnormal awareness of breathing occurring either
5. Sup. laryngeal neuralgia. at rest or due to unexpectedly low level of exertion.
 Symptomatology and its Causes 47

Grades of Dyspnea Classification of Pulmonary Edema

Based on Initiating Mechanism
• Grade I – Dyspnea on severe (unaccustomed)
exertion. Imbalance of Starling Forces
• Grade II – Dyspnea on accustomed exertion. 1. Increased pulmonary venous pressure without left
• Grade III – Dyspnea on mild exertion. ventricular failure (e.g. mitral stenosis).
• Grade IV – Dyspnea at rest. 2. Increased pulmonary venous pressure secondary to left
Newer NYHA (New York Heart Association) gradation ventricular failure.
of dyspnea is as follows: 3. Increased pulmonary capillary pressure secondary to
• Class I – Asymptomatic increased pulmonary arterial pressure (so-called
• Class II – Symptoms on unaccustomed exertion. overperfusion pulmonary edema).
• Class III – Symptoms on accustomed exertion
• Class IV – Symptoms at rest. Decreased Plasma Oncotic Pressure
1. Hypoalbuminemia.
Mechanism
• Mainly seen in LHSF Increased Negativity of Interstitial Pressure
• In acute pul. edema and orthopnea, it is mainly due to 1. Rapid removal of pneumothorax with large applied
elevated left atrial pressure that shows negative pressures (unilateral).
↓ 2. Large negative pleural pressures due to acute airway
↑ pul. capillary pressure obstruction alone with increased end-expiratory volumes
↓ (asthma).
↑ transudation into lungs Altered alveolar—capillary membrane permeability (acute
↓ respiratory distress syndrome).
edematous and stiff – Infectious pneumonia; bacterial, viral, parasitic.
– Inhaled toxins (e.g. phosgene, ozone, chlorine,
Mechanism of Exertional Dyspnea Teflon fumes, nitrogen dioxide, smoke).
• Factor 1. Exercise – Circulating foreign substances (e.g. snake venom,
↓ bacterial endotoxins).
sharp ↑ in left atrial pressure – Aspiration of acidic gastric contents.
↓ – Acute radiation pneumonitis.
dyspnea by pulmonary congestion – Endogenous vasoactive substances (e.g. histamine,
• Factor 2. Respiratory muscle fatigue kinins).
• Factor 3. Effects of exertional acidosis on peripheral – Disseminated intravascular coagulation.
chemoreceptors. – Immunologic—hypersensitivity pneumonitis, drugs
(nitrofurantion), jeukoagglutinins.
Mechanism of Orthopnea – Shock lung in association with nonthoracic trauma.
Lying flat – Acute hemorrhagic pancreatitis.
↓ Lymphatic insufficiency:
steep rise in LA pressure in patients with heart failure – After lung transplant.
↓ – Lymphangitic carcinomatosis.
pulmonary congestion – Fibrosing lymphangitis (e.g. silicosis)
↓ Unknown or incompletely understood:
severe dyspnea. – High altitude pulmonary edema.
– Neurogenic pulmonary edema.
Mechanism of PND (Paroxysmal Nocturnal – Narcotic overdose.
Dyspnea) – Pulmonary embolism.
Frank pul. edema on lying flat – Eclampsia.
↓ – After cardioversion
in standing- gravitational pooling of blood to – After anesthesia.
lower the left atrial pressure – After cardiopulmonary bypass.
48 Essentials of Clinical Medicine

Causes of Cardiogenic Pulmonary Edema

• LV failure—AS, AR, MR, systemic hypertension and
cardiology.
• LA failure—MR, MS.
Causes of Non-Cardiogenic Pulmonary Edema
• Installation of toxins and irritants, phosgene gas.
• Aspiration of gastric contents or acid/alkali poisoning.
• Drowning
• Gram-negative septicemia.
• Insecticide poisoning.
• Hemorrhagic pancreatitis.
• High altitude.
• Narcotic overdose (Heroin, methadone).
• Snake bite. Fig. 3.1C: Radiological features of heart failure: Enlargement of
• Fulminant hepatic failure. lung base showing septal or ‘Kerley B’ lines (arrow)
Rapid evacuation of large pneumothorax or pleural effusion.
SYMPTOMS IN CHRONIC HYPER-
Table 3.6: Possible mechanisms of dyspnea in selected conditions
VENTILATION SYNDROME
Condition Mechanism
• Light headedness, faintness, dizziness.
1. Asthma Increased sense of effort.
Stimulation of irritant receptors in airways
• Dullness of hearing and tinnitus.
2. Neuromuscular disease Increased sense of effort. • Peripheral and circum oral paresthesia.
3. COPD Increased sense of effort • Cold hands and feet and cold sweats.
Hypoxia. • Muscle cramps, muscle aches, trembling shivering.
Hypercapnia
Dynamic airway compression
• Constant tiredness and generalized weakness.
4. Mechanical ventilation Afferent mismatch • Breathlessness at rest with sighing and yawning.
Factors associated with underlying • Chest tightness, heaviness, and palpitation.
condition. • Abdominal “butterflies”, cramps and bloating.
5. Pulmonary embolism Stimulation of pressure receptors in pul-
monary vasculature or right atrium
• Urgency and frequency of defecation and micturition.
(possible) [Figs 3.1A, (3.1B, Plate 1), • Restlessness, anxiety and panic attacks.
3.1C]
Causes
1. Physiological
– Mountaineers
– Exercise
– Hyperpyrexia
– Anemia.
2. Respiratory
– Airway obstruction
– Bronchial asthma
– COPD
– Pulmonary infections
– Pulmonary edema
– Pulmonary embolism
– Bronchogenic Ca
– Pleural effusion
– Pneumothorax
– Emphysema
– Fibrosis
– Miliary TB
Fig. 3.1A: Radiological features of heart failure: Chest radiograph
of a patient with pulmonary edema – Bronchiolitis in children.
 Symptomatology and its Causes 49

3. Cardiac – Hand-foot-mouth
– Acute infections – Vincent’s angina (ulcerative gingivitis)
– Valvular heart disease – Glandular fever
– LVF 3. Miscellaneous:
– Congenital acyanotic heart disease – Trauma from teeth/dentures
– Left vent systolic dysfunction – Leukoplakia
– Hypertension – Carcinoma
– Cardiomyopathies 4. Associated with systemic disorders
– Arrhythmias—AF – Drug allergies—sulfonamides, gold, cytotoxics
– Orthopnea indicates severe heart failure. – Iron, folate, vit-B12 def.
4. Metabolic – Leukoplakia
– Hypokalemia – Acute leukemia
– Uremia – Reiter’s syndrome
– Diabetes – Beçhet’s disease
5. Neurological – Crohn’s disease
Respiratory center depression as in – Ulcerative colitis
– Syringobulbia
– Coeliac disease
– Motor neuron disease
5. Associated with skin disorders
– Guillain-Barré syndrome
– Lichen planus
– Bulbar polio
– Erythema multiforme
– Myasthenia gravis
– Pemphigoid
6. Psychogenic
– Pemphigius vulgaris.
7. Pharmacological:
– Drug-induced respiratory disorders
– Drug-induced cardiac disorders. SORE TONGUE
(Small multiple ulcers centrally located)
SORE MOUTH • Vit-B complex (vit-B12) deficiency
i. Aphthous ulceration. • Iron deficiency
ii. Sharp edges of caries teeth (traumatic ulcers). (ulcers which are laterally located)
iii. Vincent’s angina. • Malignant ulcers
iv. Thrush (Candida albicans). • Leukoplakia
v. Spirochetal in origin.
vi. Ill-fitting dentures (traumatic ulcers). BAD BREATH
vii. Angular stomatitis (riboflavin). (Halitosis)
viii. Scurvy—recurrent gingivitis. • Chronic infection of upper respiratory tract
– Blood dyscrasia—recurrent gingivitis. • Caries tooth
– Persistent ulceration due to agranulocytosis. • Pyorrhea
– Local malignancy. • Stasis in pharyngeal pouch, esophagus or stomach
(pyloric stenosis or ca.)
Causes of Painful Mouth • Achalasia cardia
1. Idiopathic—recurrent aphthous mouth ulcers. • Bronchiectasis or lung abcess by E. coli and B.
2. Infections: pyocyaneus
– Candidiasis • Musty breath in hepatic coma (dead mouse)
– Dental sepsis • Uriniferous in uremia
– Herpes simplex virus (HSV-1) • Sweet—diabetic acidosis
– Coxsackie virus • Alcohol, paraldehyde and organophosphates give peculiar
– Herpangina smell.
50 Essentials of Clinical Medicine

DISORDERS OF SALIVATION 4. Large amounts brought about 12 to 48 hours after

food
Increased salivation: – Pyloric obstruction.
• Irritating painful lesion of mouth or oral cavity 5. Periodic episodes of vomiting preceded by unilateral
• Persistent in esophageal ca. headache.
• Any condition which causes nausea – Migraine.
• Parkinsonism 6. Self-induced
• Trigeminal neuralgia – In patients with gastric or duod ulcers.
• Water brash
• Pregnancy Character of Vomitus
• Heavy metal poisoning
a. Quantity
Decreased salivation: • Large—pyloric obstruction
• Mouth breathers • Small—esophagitis or gastritis
• Any condition causing dehydration b. Odor
• DM • Sour odor—pyloric obstruction
• Fluid loss due to diarrhea • No sour odor—achalasia cardia
• Febrile illness – Pharyngeal pouch
• Disease of salivary glands – Achylia gastrica
• Anticholinergic drugs. c. Color
• Bright red—hematemesis
ACID REGURGITATION • Coffee ground—cerebral hemorrhage terminal even
in unconscious patients
• Peptic ulcers • Yellow or green (bile)
• Hiatus hernia – Intestinal obstruction distal to 2nd part of duod.
• Esophagitis – It is absent in vomiting due to pyloric obst.
• Gastritis d. Constituents
• Heartburn—retrosternal irritation of esophageal mucosa. • Mucus
– Gastric statis
NAUSEA AND VOMITING (Table 3.7) – Malignancy
• Foods
a. NAUSEA (feeling of imminent desire to vomit)
– 8-12 hours—pyloric obstruction
• Vasomotor – Achalasia cardia
• Automatic disturbances will cause fainting, weak- – Hour glass stomach
ness, pallor and increased perspiration. • Pus
b. VOMITING—a forcible expulsion of GIT contents – Rupture of extrinsic abscess in stomach
through mouth – Suppurative gastritis
(Retching—a term applied to labored respiratory • Foreign bodies
movement which precede or accompany vomiting). – Round worm—heavy infestation
1. Early morning vomiting. – Gallstones—cholecystogastric or cholecysto-
– Pregnancy duodenal.
– Uremia
– Chr. gastritis due to alcohol HICCUPS (HICOUGH)
– Increased ICT (but characteristically not asso- Sound produced by spasmodic contraction of diaphragm
ciated with nausea) with adduction of vocal cords
2. Vomiting immediately after food Usually produced by structures supplied by the phrenic
– Functional causes or vagus nerves.
– Reflex vomiting
– Local gastric irritation Causes
3. Recurrent bouts 2 to 4 hours after food 1. Reflex origin
– Pylorospasm due to gastric or duodenal ulcer or – In hypersensitive subjects (temp. change hot or cold
duodenitis. food, etc.)
 Symptomatology and its Causes 51

Table 3.7: Causes of nausea and vomiting – Brain tumor, etc.

Obstructing disorders Cardiopulmonary disease
– Apoplexy
9. Psychological
• Pyloric obstruction • Cardiomyopathy
• Small bowel obstruction • Myocardial infarction – Hysterical
• Colonic obstruction Labyrinthine disease – Neurosis
• Superior mesenteric artery • Motion sickness 10. Epidemic hiccups.
syndrome Hiccups are due to related sudden diaphragmatic
Enteric infections • Labyrinthitis contraction, often triggered by upper gastrointestinal
• Viral • Malignancy
• Bacterial Intracerebral disorders
irritation, but occasionally due to brainstem disease.
Inflammatory disease • Malignancy Hiccups are spasmodic periodic closure of glottis
• Cholecystitis • Hemorrhage following spasmodic lowering of diaphragm, causing a
• Pancreatitis. • Abscess sharp, short, inspiratory cough. They are also called
• Appendicitis • Hydrocephalus singultus.
• Hepatitis Psychiatric illness
Impaired motor function • Anorexia and bulimia nervosa
Hiccups may be caused by indigestion, irritation of
• Gastroparesis • Depression diaphragm, alcoholism, new growths of pleura, certain
• Instestinal pseudo-obstruction • Psychogenic vomiting cerebral lesons, hysteria or a disturbance of phrenic nerve.
• Functional dyspepsia • Postoperative vomiting If prolonged, it has a serious significance.
• Gastroesophageal reflux • Cyclic vomiting syndrome
• Biliary colic
COUGH
• Abdominal irradiation
Respiratory Causes
2. Irritation of phrenic nerve Table 3.8: Organs involved, causes and characteristics of cough
– Phrenic nerve neuritis.
– Pressure due to eosophageal tumors, diaphragmatic Organ Causes Characteristics
involved
hernia, pericarditis.
1. Pharynx Postnasal drip Usually persistent
– Irritation due to influenza, bronchitis, asthma.
2. Larynx Laryngitis, tumors Harsh, barking, painful, persis-
3. Dilatation of stomach whooping cough tent, associated with stridor.
4. Abdominal 3. Trachea Tracheitis Painful
– Liver abscess. 4. Bronchi Bronchitis (acute and Dry or productive, worse in
chronic is COPD) morning hours.
– Peritonitis
Asthma Dry or productive worse at night
– Subphrenic abscess, etc. Bronchial carcinoma Persistent often with
– Dilation of stomach. hemoptysis.
– Carcinoma of stomach. Pneumonia Dry initially, later productive.
– Hepatic and splenic disease irritating the diaphragm Bronchiectasis Productive, change in posture
induces sputum production.
– Following abd. surgery. Pulmonary edema Often at night (may be pro-
5. Toxic cond. ductive of pink frothy sputum)
– Anemia End-stage interstitial Dry, irritant and distressing.
– Febrile illness. fibrosis
Pressure over trachea
– Septicemia.
and brachia from outside
6. Metabolic
– Uremia Lungs: Pneumonia, tuberculosis, and lung abscess, tropical
– Diabetes eosinophilia, pulmonary edema, infarction, interstitial fibrosis.
7. Thoracic
Pleural: Pleural effusion pneumothorax.
– Aortic aneurysm
– Mediastinal glands
Cardiac: Left ventricular failure, mitral stenosis, aneurysm
of aorta.
– Substernal goiter, etc.
8. Neurological Mediastinum: Enlarged lymph node, mediastinal tumors.
– Encephalitis Reflex: Wax or foreign body in the ear, subphrenic abscess
– Meningitis or liver abscess, etc.
52 Essentials of Clinical Medicine

Sputum • Blood-stained sputum—tuberculosis

Table 3.9: Types, appearances and causes/conditions of sputum
• Anchovy sauce sputum—ruptured amebic liver abscess.

Type Appearance Cause / Condition HEMOPTYSIS (See Table 3.10)

1. Serous Clear, watery, frothy Acute pulmonary edema
may be pink Bronchioalveolar cell Differential Diagnosis of Hemoptysis
carcinoma (rare)
2. Mucoid Clean grey-white Chronic bronchitis, COPD Sources other than the lower respiratory tract upper airway
may be frothy or chronic asthma. (nasopharyngeal) bleeding, gastrointestinal bleeding.
black (soot)
3. Mucopurulent Yellow, green, brown All types of bronchopulmo- Tracheobronchial Source
or purulent nary bacterial infection
(eosinophils cause sputum Neoplasm (bronchogenic carcinoma, endobronchial)
to appear purulent).
metastatic tumor, Kaposi’s sarcoma, bronchial carcinoid)
4. Rusty Rusty, golden yellow Pneumococcal pneumonia
• Bronchitis (acute or chronic).
• Bronchiectasis.
Nocturnal Cough
• Airway trauma.
It may be seen in conditions like: • Foreign body.
• Bronchial asthma.
• Left-sided heart failure. Pulmonary Parenchymal Source
• Chronic bronchitis.
• Aspiration. • Lung abscess.
• Postnasal drip. • Pneumonia.
• Tropical eosinophillia. • Tuberculosis.
Drug-induced cough is seen in drug therapy with ACE • Mycetoma (Fungus ball).
inhibitors. • Goodpasture’s syndrome.
• Idiopathic pulmonary hemosiderosis.
Causes of Postural Cough
• Wegener’s granulomatosis.
• Bronchiectasis • Lupus pneumonitis.
• Lung abscess
• Lung contusion.
• Bronchopleural fistula (BPF)
• LVF/pulmonary edema
Primary Vascular Source
• Mitral stenosis.
(ARDS is a non-cardiac cause of pulmonary edema) • Arteriovenous malformation.
• Pulmonary thromboembolism.
Copius Sputum Production • Elevated pulmonary venous pressure (esp. mitral
It occurs in: stenosis).
• Bronchiectasis. • Pulmonary artery rupture secondary to balloon tip
• Lung abscess. pulmonary artery, catheter manipulation. Miscellaneous/
• Empyema rupturing into bronchus. rare causes pulmonary endometrosis, systemic
• Necrotizing pneumonia. coagulopathy, use of anticoagulants, thrombolytic
• Alveolar cell carcinoma. therapy.
Large amounts of colorless sputum are seen in alveolar cell
carcinoma HEMATEMESIS

Color of Sputum and Associated Conditions Local Causes: According to the

Site of Hemorrhage
• Green or yellow thick—bacterial infections (the green
color is due to enzyme myeloperoxidase). Esophagus
• Black colored sputum—coal worker’s pneumoconiosis. i. Gastroesophageal varices.
• Rusty sputum—pneumococcal pneumonia. ii. Reflex esophagitis.
• Red currant jelly-like—Klebsiella pneumoniae. iii. Hiatis hernia.
• Pink frothy sputum—pulmonary edema iv. Mallory-Weiss syndrome.
 Symptomatology and its Causes 53

Table 3.10: Hemoptysis

Pulmonary causes Cardiac Miscellaneous
Inflammatory Neoplastic Other
• Bronchiectasis Pulmonary and • Pul thromboembolism Mitral stenosis aortic • Collagen vascular disease
metastatic lung cancer aneurysm, arteriovenous
malformation. Rarely
systemic hypertension
• Bronchitis Bronchial adenoma • Primary pul • Bleeding disorder
hypertension
• Tuberculosis Secondaries from • Acute pul edema • Vit.C deficiency.
other site ·
• Lung abscess • Deficiency of coagulation
factors
• Pneumonia • Accidents/trauma
• Whooping cough · • Drugs like NSAIDs, antico-
agulants in higher doses
• Hemorrhagic fever, especially
septicemia
· · • After tonsillectomy
· · • Investigations like broncho-
scopy
· · • Infection
· · • Like pulmonary mycosis

v. Barrett’s ulcer. Of the various causes mentioned above, the common causes
vi. Polyps and carcinoma. are:
vii. Achalasia and foreign bodies. i. Chronic peptic ulcer.
ii. Acute ulcers and multiple erosions.
Stomach and Duodenum iii. Esophageal varices.
i. Chronic duodenal ulcer. iv. Mallory-Weiss syndrome.
ii. Chronic gastric ulcer.
Dealing with the Patient of Hematemesis
iii. Multiple erosions and acute peptic ulcer.
iv. Tumors, polyps and carcinoma. 1. If in shock:
– Measure BP, (i.e. manage shock), blood / plasma
Small Intestine expanders, then —
i. Very rarely, Meckel’s diverticulum may present with – Upper GI endoscopy, then —
hematemesis. – Seal that particular site of bleeding (varices are
ii. Peutz-Jeghers syndrome. present, as cherry red spots.)
• Inject at that site, sclerosing agent to obliterate
iii. Polyps.
the varices (e.g. absolute ethyl alcohol but now-
iv. Vascular malformation.
a-days 3 percent polido canal is used).
v. Various tumors. • If gastric varices – polido canal is not affectve.
We use Nectacryl (glue), when comes in contact
General Causes with tissue, it solidifies. But if this gets released
i. Hemorrhagic disorders—thrombocytopenia, purpura anywhere during the process, it will solidify and
may damage this endoscope, if fall in eyes,
hemophilia, pernicious, and other anemias, Ehlers-
corneal damage.
Danlos syndrome, DIC, liver disease, periarteritis
– Variced banding—tie the varices.
nodosa, amyloidosis, Turner’s syndrome, Kaposi’s – Thermal probe—we can seal that varices.
sarcoma, neurofibromatosis, etc. • In case of MW tear and Boerhaeves—we have to do
ii. Ingestion of drugs—steroids, NSAIDs, etc. surgical procedure.
iii. Salicylates and alcohol. – Upper GI bleeding, treatment is totally symptomatic.
54 Essentials of Clinical Medicine

Table 3.11: Differences between hemoptysis and hematemesis PRECIPITANCY AND HESITANCY OF URINE
Hematemesis Hemoptysis Definitions
1. With vomiting • With cough
Hesitancy: The patient notices that he must wait for urination
2. Not frothy • Frothy due to admixture of air.
3. Altered or coffee color • Frank red color
to start. If he strains, he has to wait more as the median
4. pH acidic • pH alkaline lobe bends down on straining to obstruct the internal urethral
5. Clots may be passed • Fresh frothy. orifice.
with frank blood Dysuria: The stream is often weak and tends to dribble
6. Mixed with food particles • Mixed with macrophage and towards the end of micturition because of increasd urethral
neutrophil resistance and derangement of internal urethral opening,
7. With food • Without food
more force is required for urination.
8. Gastrointestinal symptoms • Respiratory symptoms present.
present Frequency: This seems to be the earliest symptom in majority
9. Malena present • Malena absent of cases. In the beginning, frequency is mostly nocturnal.
10. Vomitus not stained for • Sputum is tinged pink for The patient gets up twice or more during night. Such
following days following 2–3 days frequency is mainly due to vesical introversion of the
11. Previous H/o peptic ulcer • Previous H/o. respiratory disease sensitive prostatic mucous membrane due to its enlargement
disease
upwards. Gradually, the frequency is experienced in both
12. Diagnosis made by • Diagnosis made by gastroscopy
by day and night. This is due to irritability of bladder and
bronchoscopy
amount of residual urine
Urgency: Intense desire to urination due to obstruction.
PALPITATIONS
Renal causes—bladder neck obstruction.
1. Physiological—exercise, emotional or sexual • Prostate—enlarge prostate (benign prostatic
excitements, etc. hypertrophy).
2. Excessive—tea, coffee, tobacco, alcohol consump- • Cerebral causes—cerebrovascular accidents (CVA)
tion. cerebral tumors, head injuries/trauma.
3. Anxiety state.
4. Extrasystoles—atrial, ventricular. FREQUENCY OF MICTURITION AND NOCTURIA
5. Tachyarrythmias—atrial and ventricular. 1. Renal causes—pyelitis, stone, TB, movable kidney.
6. Endocrinal causes—pheochromocytoma, thyro- 2. Urinary bladder—congenitally contracted bladder (small-
toxicosis, hypoglycemia. sized bladder), tumors, cystitis, vescicular calculus,
7. High output states—anemia, pyrexia, aortic regurgi- cystocele, benign prostatic hypertrophy causing incom-
tation, PDA, beri-beri, A-V fistula, Paget’s disease. plete evacuation.
8. Drugs—atapine, adrenaline, aminophylline, thyroxine. 3. Ureter—ectopic ureter partial stricture of ureters, stone.
9. Psychogenic – prolonged anxiety states (soldier’s heart, 4. Urethra—stricture of urethra, incompetent internal
neurocirculatory asthenia, Da Costa’s syndrome). urethral sphincter, urethritis, neoplasm, balanitis,
10. Non-cardiac conditions: Thyrotoxicosis, hypogly- phimosis.
cemia, pheochromocytoma fever. 5. Prostatic causes—prostatitis, senile enlargement and
malignant prostate.
POLYURIA 6. Other causes—all the causes of polyuria (as described
earlier)
• Excessive water drinking. — PSU psychogenic, pregnancy pressure due to
• Diuretic therapy. enlargement of surrounding structures.
• Cold weather.
• Stress/anxiety. RETENTION OF URINE
• Diabetes mellitus.
Causes
• Diabetes insipidus (pituitary and nephrogenic).
• Renal-chronic renal failure, recovery phase of acute Mechanical
tubular necrosis. i. Urinary bladder—stones, tumors, blood clots, and
• Psychogenic—psychogenic polydipsia. contracture of bladder neck.
 Symptomatology and its Causes 55

ii. Prostate—prostatic abscess, benign and malignant Disease of Adjacent Viscera

prostatic enlargements.
Acute appendicitis, salpingitis, pelvic abscess. The carci-
iii. Urethra—urethral strictures, rupture, congenital
noma of rectum, cervix uteri may infilterate the bladder to
valves, foreign body, acute urethritis, stone, growth,
cause hematuria.
pin-hole meatus, meatal ulcer with scarring.
iv. Prepuce—phimosis.
General Causes
From Outside a. Blood disorders—purpura, sickle cell anemia, hemophilia
Pregnancy (retroverted gravid uterus), fibroid, ovarian cyst, scurvy, malaria.
Ca cervix, Ca rectum, any pelvic growth. b. Infarction—arterial emboli from myocardial infarct
Neurogenic SABE.
c. Congestion—right heart failure, renal vein thrombosis.
i. Spinal cord disease, e.g. disseminated sclerosis, tabes d. Collagen—disease.
dorsalis, transverse myelitis.
ii. Injuries and disease of spine, e.g. fracture, dislocation, Drugs
Pott’s disease, etc.
iii. Miscellaneous, e.g. postoperative retention, hysteria, Anticoagulant drugs, hexosamine, sulfonamides, and
tetanus drugs such as anticholinergics, smooth muscle salicylates—in large doses.
relaxants, tranquilizers, etc. Painful Hematuria
• Renal calculus
HEMATURIA (Fig. 3.2, Plate 1) • Urinary tract infection
Lesion of Urinary Tract • Reflux nephropathy
• Renal papillary necrosis.
Kidney • Acute renal vascular disease, e.g. embolism.
Congenital — Polycystic kidney
Traumatic — Ruptured kidney. Painless Hematuria
Inflammatory — Tuberculosis, acute nephritis • Tuberculosis
(rare) • Schistosomiasis
Neoplastic — Angioma, carcinoma of kidney, • Urogenital tumors.
nephroblastoma of kidney, • Glomerulonephritis.
papilloma or carcinoma of renal • Renal cystic disease.
pelvis. • Hypertension.
Others — Stone, infarction, essential hema- • Chronic renal vascular disease.
turia hemorrhage. • Urinary tract infection.
Ureter ANURIA
Stone, papilloma or carcinoma of urothelium.
A. Prerenal — Shock
Bladder B. Renal — Pyelonephritis glomerulonephritis, in-
Traumatic — Ruptures compatible blood transfusion, crush
Inflammatory — Cystitis, tuberculosis, bilharziasis syndrome, renal tuberculosis.
Neoplastic — Papilloma and carcinoma C. Postrenal — Calculus anoxia.
Others — Stone. — Accidental ligature of both ureter
during operation of hysterectomy.
Prostate
Benign and malignant enlargement. DYSPHAGIA
Urethra Pre-esophageal Causes
Traumatic — Rupture a. Oral phase
Inflammatory — Acute urethritis b. Disturbances in mastication—trismus, fracture of
Neoplastic — Transitional cell carcinoma mandible, tumors of upper or lower jaw, disorders of
Others — Stone. temporomandibular joints.
56 Essentials of Clinical Medicine

i. Disturbances in lubrication—xerostomia following • Malignancy of lymph nodes.

radiotherapy, Mickulicz’s disease. • Pharyngeal pouch.
ii. Disturbane in mobility of tongue—paralysis of • Cervical spondylosis.
tongue, painful ulcers, tumors of tongue, lingual
Thoracic
abscess, total glossectomy.
iii. Defects of palate – cleft palate, oronasal fistula. • Aneurysm of aorta.
iv. Lesions of buccal cavity and floor of mouth stoma- • Mediastinal tumor.
titis, Ludwig’s angina, ulcerative lesions. • Lymphadenopathy in Hodgkin’s disease.
c. Pharyngeal phase: • Malignancy and TB.
i. Obstructive lesions of pharynx—tumor of tonsils, • Cardiac enlargement.
soft palate, pharynx, base of tongue, supraglotic • Pericardial effusion.
larynx or even obstructive hypertrophic tonsils. • Retrosternal goiter.
ii. Inflammatory conditions—acute tonsillitis, peri- • Dysphagia lusoria due to an aberrant blood vessel.
tonsillar abscesses retro-or parapharyngeal abscess, Abdominal
acute epiglottitis, edema larynx.
• Hepatic enlargement.
iii. Spasmodic—condition—tetanus, rabies.
iv. Paralytic condition— Functional Causes
— Paralysis of soft palate—due to diphtheria bulbar Globus hystericus
palsy, cerebrovascular accidents Quantification of Dysphagia:
— Paralysis of larynx—lesions of vagus, and • Grade I
bilateral superior laryngeal nerves. Dysphagia to solid and liquid intermittently
Esophageal Causes • Grade II
a. In the lumen— To solids.
— Foreign body. • Grade III
— Large bolus. Absolute dysphagia
b. In the walls:
1. Congenital — Tracheo-esophageal fistula. Factors Aggravating Dysphagia
— Stricture. Dysphagia is aggravated by:
2. Traumatic — Corrosive poisoning. • Anxiety
3. Inflammation — Hiatus hernia with lower • Depression
esophagitis. • Life stress
— After exanthemata Dysphagia is relieved by:
4. Neoplasms — Leiomyoma • Anxiolytics
— Carcinoma of esophagus • Nitrates
5. Neurological — Paralytic • Ca blockers
— Spasm cricopharynx and eso- Precipitated in—food taking in groups no H/o wt. loss
phagus usually obese in these people.
— Tetanus. Wherever in obstructive case—wt. loss is seen.
— Myasthenia gravis.
6. Miscellaneous — Paterson-Brown-Kelly syn- Inquiry about Dysphagia Relief
drome. I and II usually relieve by glass of water/soda
(Plummer-Vinson syndrome) III no relief—even by surgery
— Achalasia.
Investigate a Case of Dysphagia
— Diverticulum.
1. Barium X-ray of esophagus
Pressure on the Esophagus Triphasic study done in 3 phases:
• 1st Phase:
Cervical – Single constrast study
• Malignancy of thyroid gland. – Only a column of opacity is seen

– Diagnosis of obstr. lesions (seen luminal or extra-
luminal)
• 2nd Phase:
– Double constrast study
– To diagnose ulcers and muscle lesion.
• 3rd Phase:
– Follow through study of esophagus
– Image intensifier study
– Done for motility disorders
2. 24 hrs. pH monitoring
A narrow lumen fire catheter is used and end is kept 5
cm above LES and kept for 24 hr. These patients will
perform all normal activities. And pH is recorded with
the help of small recorders.
To diagnose severity of reflex esophagitis.
3. Pressure monitoring
To study pressure changes in esophagus
– Balloon catheter
– Pull the catheter gradually out
– As soon as we reach LES, we keep the catheter
here for 10-30 sec and pressure changes are studied.
(normal is 10-30 mm Hg during act of swallowing)
– If pressure > 30, then hypertensive LES
– If pressure < 10, then GERD (Gastroeosphageal
Reflex Disease)
Then 10-30 sec at midesophagus (normal pr. = 30-70
mm Hg)
– If pressure > 70, motility disorder
– If pressure > 100, nutcracker esophagus
– If pressure < 30, achalasia cardia
Then catheter toward UES (Cricopharyngeus) (normal
60-80 mm Hg)
– If pressure > 80, then hypertensive UES
– If pressure < 60, then hypotensive UES
4. Upper GI endoscopy
– Esophageal direct endoscopy
– Exclude other pathological disorders
– Motility disorder is not pathology but a functional
disorder.
– (Sensitivity of barium X-ray only 65 percent)
– In endoscopy, one can mark out any signs of
inflammation and site of inflammation and distance
from incisors.
– Severity of lesions/obstruction.
• Grade I—Streak of blood vessels esophagitis
• Grade II—Streak + patchy esophagitis
• Grade III—Streak + patches + ulcers
– By endoscope, we can make out varices (portal
hypertension)
– To differentiate between malignant and benign
carcinoma, we use chromoendoscopy.
Symptomatology and its Causes 57
We spray Lugol’s iodine on area:
• Yellow color—normal
• No stain—malignant
Endoscopy: Then methylene blue is used—Blue color, i.e.
malignant will become blue.
• Then water—to remove extra strain
• Then biopsy and then lab.
Endosonography: (sensitivity = 60-70 percent)
Small US (ultrasound) wave is sent through endoscope.
• To diagnose the carcinoma of submucosal region, i.e.
very early stage-very sensitive
• To diagnose—mediastinal carcinoma
(up to duodenum upper endosonography)
Gamma Scintigraphy: (Sensitivity = 90 percent)
• To diagnose reflex esophagitis.
Amount of regurgitation is studied with the help of gamma
camera.
To Differentiate Between Angina and
Due to Esophagus
1. ECG – typical changes but not so effective in esophageal
disorder (also similar changes may be seen).
2. Tread Meal Test (TMT)
3. Thallium scan—film of heart is taken with gamma or
(exercise thallium scan) scan.
4. Endoscopy.
CONSTIPATION
Table 3.12: Types of constipation and causes
Example
• Recent onset
• Colonic obstruction Neoplasma: Structure: Ischemic,
diverticular, inflammatory.
• Anal sphincter spasm Anal fissure, painful haemorhoids
• Medications
• Chronic irritable bowel
syndrome Constipation–predocument, alter-
nating.
• Medications Ca blockers, antidepressant.
• Colonic pseudo-obstruction Slow transit constipation
Megacolon (rare, Hirschsprung’s,
Chagas)
• Disorders of rectal evacuation Pelvic floor dysfunction, anismus,
descending perineum syndrome, rectal
mucosal prolapse, rectocele.
• Endocrinopathies Hypothyroidism, hypercalcemia,
pregnancy
• Psychiatric disorders Depression, eating disorders, drugs.
• Neurologic disease Parkinsonism, multiple sclerosis,
spinal cord injury
• Generalized muscle disease Progressive systemic sclerosis.
58 Essentials of Clinical Medicine

DIARRHEA • Addison’s disease.

• Congenital electrolyte absorption defects.
Acute Diarrhea
Osmotic Causes
Diarrhea of abrupt onset of < 2 weeks duration.
• Osmotic laxatives (Mg++, PO43–, SO43–).
Causes • Lactose and other disaccharide deficiencies.
1. Bacterial infection • Nonabsorbable carbohydrates (sorbitol, lactulose,
– Vibrio cholera polyethylene glycol.)
– Toxigenic E. coli
Steatorrheal Causes
– Salmonella
– Shigella • Intraluminal maldigestion, pancreatic exocrine
– Campylobacter insufficiency, bacterial overgrowth, liver disease.
– Yersinia enterocolitica • Mucosal malabsorption (celiac sprue, Whipple’s disease,
– Invasive E. coli infections, abetalipoproteinemia).
2. Viral infection • Postmucosal obstruction (1o or 2o lymphatic obstruc-
– Rotavirus tion).
– Adenovirus Inflammatory Causes
– Norwalk virus. • Idiopathic inflammatory bowel disease (Crohn’s disease,
3. Parasitic infection ulcerative colitis) microscopic and collagenous colitis.
– Giardia lamblia Immune-related mucosal disease (primary immuno-
– Cryptosporidium deficiencies, food allergy, eosinophilic gastroenteritis,
– Entamoeba histolytica graft vs host disease).
4. Drugs
– Laxatives Infections
– Sorbitol • Invasive bacteria, viruses and parasites.
– Digitalis • Radiation injury.
– Propranolol • Gastrointestinal malignancies.
– Theophylline Dysmotile Causes
– Heavy metals
– Antacids • Visceral neuromyopathies.
– Lactulose • Hyperthyroidism.
– Colchicine • Drugs (prokinetic agents).
– Quinidine Factitial Causes
– Diuretics • Munchausen.
– Alcohol, etc. • Bulimia.
5. Food poisoning.
EPISTAXIS
Chronic Diarrhea
General Causes
Secretory Causes 1. Cardiovascular system—hypertension, arteriosclerosis,
• Exogenous stimulant laxatives. mitral stenosis, pregnancy (hypertension and normal).
• Chronic ethanol ingestion. 2. Disorders of blood and blood vessels:
• Other drugs and toxins. Aplastic anemia, leukemia, thrombocytopenia, purpura,
• Endogenous laxatives (dihydroxy bile acids) hemophilia, Christmas disease, scurvy, vit K. deficiency,
• Idiopathic secretory diarrhea. hereditary hemorrhage, telangiectasia, Hodgkin’s
• Certain bacterial infections. disease.
• Bowel resection, disease or fistula (decreased absorp- 3. Liver disease—hepatic cirrhosis (prothrombin defi-
tion). ciency).
• Partial bowel obstruction or fecal impaction. 4. Kidney disease—chronic nephritis, chronic renal failure,
• Hormone producing tumors (carcinoid, medullary toxemia.
cancer of thyroid, mastocytosis, gastrinoma, colorectal 5. Drugs—excessive use of salicylates and other analgesics,
villous adenoma). quinine, anticoagulant therapy.
 Symptomatology and its Causes 59

6. Mediastinal compression—tumors of mediastinum, it is neurological signs like unconsciousness or convulsions,

also caused by whooping cough and pneumonia. nausea and vomiting.
7. Acute general infections—influenza, measles, chicken-
Table 3.13: Differences between peripheral and central vertigo
pox, whooping cough, rheumatic fever, infection,
typhoid, pneumonia, malaria, dengue fever. Signs and symptoms Peripheral (Labyrinth) Central (Brainstem
8. Vicarious menstruation (epistaxis occurring at the time or cerebellum)
of menstruation). 1. Direction of asso- Unidirectional fast Bidirectional or
9. Environmental causes. ciated nystagmus. phase opposite lesion unidirectional
2. Purely horizontal Uncommon Common
nystagmus without
HOARSENESS torsional
component
Refer to ENT Textbook.
3. Vertical or purely Never May be present
torsional nystagmus
VERTIGO OR GIDDINESS 4. Visual fixation Inhibits nystagmus No inhibitation
and vertigo
1. Ear pathologies (please refer textbooks of ENT) 5. Severity of vertigo Marked Often mild.
2. Cardiovascular causes: 6. Direction of spin Towards fast phase Variable
i. Hypertension with other sclerotic changes in the 7. Direction of fall Towards slow phase Variable
blood vessels supplying labyrinth cerebrum and cere- 8. Duration of Finite (minutes days May be chronic
bellum. symptoms weeks) but recurrent
9. Tinnitus and/or Often present Usually absent
ii. Hypotension. deafness
iii. Cardiac diseases like bundle branch block, aortic 10. Associated central None Extremely common
stenosis, mitral regurgitation or arrhythmias. abnormalities
3. Neurological diseases: 11. Common causes Infection (laby- Vascular, demyelin-
i. Vertebrobasilar artery syndrome. rinthitis) Ménière’s ating neoplasm.
neuronitis, ischemia,
ii. Disseminated sclerosis. trauma, toxins
iii. Tumor or abscess in cerebellum and brainstem.
iv. Aura preceding migraine, epilepsy.
v. Increased intracranial tension. SYNCOPE
vi. Head injury. 1. Disorder of vascular tone or blood volume.
4. Metabolic disorders: – Vasovagal (vasodepressor, neurocardiogenic).
i. Diabetes mellitus causing neuritis of eighth nerve. – Postural (orthostatic) hypotension:
ii. Hypoglycemia. i. Drug induced (especially antihypertensive and
iii. Hypothyroidism. vasodilator drugs).
5. Anemia—causing diminished oxygen supply to labyrinth ii. Peripheral neuropathy (diabetic, alcoholic nutri-
and brain. tional, amyloid).
6. Ophthalmic causes iii. Idiopathic postural hypotension.
– Diplopia. iv. Multisystem atrophies physical de-conditioning.
– Refractory errors.
v. Sympathectomy.
– Glaucoma.
vi. Acute dysautonomia (Guillain-Barré syndrome
7. Cervical spondylolysis as the osteophytes reduce the
variant).
blood supply to the labyrinth by compressing the
vii. Decreased blood volume (adrenal insufficiency,
vertebral arteries.
acute blood loss, etc.)
Non-Pathological Vertigo – Carotid sinus hypersensitivity.
– Situational
i. High altitude. i. Cough.
ii. Spinning movements. ii. Micturition.
iii. Sudden change of floor texture. iii. Defecation.
iv. Valsalva’s.
Functional Vertigo v. Deglutition.
Vertigo of labyrinthine origin is never accompanied by – Glossopharyngeal neuralgia.
60 Essentials of Clinical Medicine

2. Cardiovascular disorders: 2. Functional—faulty dietary habits, addictions, etc.

• Cardiac arrhythmias 3. Psychogenic—neurosis, repressed emotions, etc.
i. Bradyarrhythmias.
a. Sinus bradycardia, sinoatrial block, sinus Table 3.14: Functional dyspepsia
arrest, sick sinus syndrome. Type Symptom
b. Atrioventicular block. 1. Reflex type Acid reflex and heartburn relieved by antacids
ii. Tachyarrythmias. 2. Ulcer like Localized epiagastric pain and nocturnal pain,
a. Supraventricular tachycardia with structural relief with vomiting food, or antacids,
cardiac disease. 3. Dysmotility like Nausea, belching, premature, satiety, bloating
abdominal distention (Fig. 3.3, Plate 1).
b. Atrial fibrillation associated with Wolff-
Parkinson-White syndrome
c. Atrial flutter with 1:1 atrioventricular conduc- Approach to a Case of Acid Peptic Disease
tion. (APD) with Weight Loss
d. Ventricular tachycardia. Benign gastric peptic ulcer, carcinomatous gastric peptic
• Other cardiopulmonary etiologies: ulcer, chronic gastritis, chronic gastric outlet obstruction.
i. Pulmonary embolism.
Ruling Out One by One
ii. Pulmonary hypertension.
iii. Atrial myxoma. 1. Benign gastric peptic ulcer:
iv. Myocardial disease (massive myocardial • Postmeal pain in abdomen (left hypochondirism)
infarction). • The patient is reluctant to eat.
v. Left ventricular myocardial restriction or (Pain is because of stretching of inflamed gastric mucosa
constriction. as well as by acid secretion).
vi. Pericardial constriction or tamponade. 2. Carcinomatous gastric peptic ulcer:
vii. Aortic outflow tract obstruction. • Family H/o carcinoma of stomach
viii. Aortic valve stenosis. • H/o of chronic smoking/alcoholism.
ix. Hypertrophic obstructive cardiomyopathy. 3. Chronic gastritis:
3. Cerebrovascular disease • Abdominal pain after eating
– Vertebrobasilar insufficiency. • Features of type A—autoimmune gastritis
– Basilar artery migraine. • Features of malabsorption syndrome
4. Other disorders that may resemble syncope • Clinical features of pernicious anemia.
– Metabolic 4. Chronic gastric outlet obstruction:
i. Hypoxia. Postmeal vomiting is the most important clinical
ii. Anemia. presentation of this disorder.
iii. Dimensional carbon dioxide due to hyperventilation
iv. Hypoglycemia. HEMATOCHEZIA
– Psychogenic Defined as escape of bright, red (fresh) blood per rectum.
i. Anxiety attacks.
ii. Hysterical fainting. Causes of Bright Red Rectal Bleeding
– Seizures.
• Hemorrhoids anal fissure.
HEARTBURN (OR PYROSIS) • Colorectal malignancy.
• Inflammatory bowel disease.
1. Organic causes—reflex esophagitis, GERD (gastro- • Complicated diverticular disease.
esophageal reflux disorders), hiatus hernia, peptic ulcer. • Ischemic colitis.
 4
The General Examination
INTRODUCTION
The general examination (or the physical examination) forms
an important part in the process of examining a patient. The
general examination is also called “Tip to Toe” examination.
Examination of a case is said to be incomplete without the
performance of the patient’s general examination. The serious
mistakes which most students commit is that after taking
the history of the case, they directly switch over to the
system which appears to be affected or over to the
complaints which the patient narrates about.
The general examination should always precede the
systemic examination. No words to say that the examination
should be carried out as gently as possible without much
disturbing the patient. His comforts should always be in the
minds of a good clinician. In severely ill patients, it may be
necessary to postpone a routine examination and to perform
only the examination required for provisional diagnosis and
treatment. Very ill patients must obviously be treated with
special care and attention.
The examination should be carried out in a stepwise
manner. The best approach is –“The system affected is the
last to be attended”. It appears to be so surprising but the
arguments for this comes in the manner that attending the
affected system first may cause the clinician to miss some
of the important signs of the disease process, (either related
to the same pathology or related to some other clinical
illness), which could be the diagnostic clues for the
management of the clinical problem.
A fairly complete examination can be carried out with a
patient sitting in a chair, but this is difficult and sometimes
impossible (when the patient is completely bedridden). Every
attempt should be made to relax and reassure the patient.
A good clinician starts the examination of his patient as
soon as he meets him and only carries it on as the history
taking proceeds further. It has been rightly said: “The
experienced and talented doctor begins the examination on
meeting the patient and continues taking the history until
the consultation ends.”
The general examination is performed in the following
manner:
First of all, the general examination includes the recording
of certain vitals. The assessment of the general condition
of the patient starts as soon as the doctor meets the patient.
There are many conditions which can be diagnosed at the
first sight. It is called “Spot Diagnosis”. Conditions like
gross obesity, increased arterial pulsations in the neck as in
aortic incompetence, blue sclera in osteogenesis imperfecta
can be very easily diagnosed by just looking the patient.
SHAKING HANDS WITH THE PATIENT
A good clinician offers a warm and friendly handshake to
his patients. It helps in the proper on going of the examination
procedure by winning the confidence of the patients. The
handshake may provide many important clues to the doctor.
It may be an index of patient’s personality. Handshake may
be abnormal in certain conditions like neurologic and
locomotor disorders like spastic hemiparesis, a severe
Dupuytren’s contracture (thickening and shortening of
palmar fascia resulting in flexion deformities).
Table 4.1: Diagnositic clues provided by handshakes
Features of handshake Diagnostic clues
• Large hands with excessive sweating Acromegaly
• Hot and sweaty hands Thyrotoxicosis
• Cold and sweaty hands Anxiety
• Dry and course skin Hypothyroidism
• Delayed relaxation of grip Dystrophica myotonia
POSTURE AND GAIT
Useful information can be obtained by observing the gait of
the patient. Any abnormality in gait may indicate a
neurological or locomotor disturbance.
a. Hints provided by gait about the neurological abnor-
malities:
62 Essentials of Clinical Medicine
This has been described in great detail in the section of
“Neurological Examination”.
b. Hints provided by gait about the locomotor abnorma-
lities.
i. Any trauma to the lower limb—indicated by cast
(plaster) or wound dressing.
ii. Painful gait: If the gait is moderately painful, the
patient spends as short a time as possible with the
affected foot on the ground. This gives rise to a dot
darn pattern of rhythm, the dot represents the time
spent on the painful limb. If the pain is very severe,
the whole limb is held flexed and foot is placed
delicately on the ground for a very very short period.
The painful gait usually requires a support for
walking.
iii. Painless gait: In a painless gait, the normal smooth
rhythm is disturbed either because of short limb, a
deformed or because of stiff joint or weak muscles.
The effect of muscle weakness will depend on the
site and degree of muscle pathology. For example,
unilateral abductor muscle weakness at the hip
produces Trendelenburg’s gait.
Bilateral weakness of gluteal muscles causes a
waddling gait. If the gait is bizarre or seems greatly
exaggerated in comparison with other objectives,
finding psychological causes should be considered.
However, in adolescents, disk problem may also
present with bizarre gait.
Clothing
The clothing of a person may provide important clues like:
• The place to where the patient belongs? Its culture,
tradition, etc.
• The socioeconomic status may also be judged.
• Sometimes the clothings may provide hint about the
occupation of the patients.
• The clothing may give as the idea about the patient’s
personality, state of mind, social circumstance.
• It may provide hints about the neurological disorders
like fecal soiling of clothes indicate towards learning
difficulties or dementia. Improper/inappropriately juvenile
dress may suggest anorexia nervosa.
COMPLEXION
The color of the face depends upon the variations in
oxyhemoglobins, reduced hemoglobin, melanin and to a
lesser extent carotene. Unusual skin colors may help us to
make a clear-cut diagnosis of the disease process; for
example, shallow brownish tinge. The bluish tinge of
“enterogenous” cyanosis, produced by abnormal hemo-
globins such as sulphemaglobin and methemoglobin may
also be caused by drugs such as dapsone and some
sulfonamide.
The pink color characteristic of carbon monoxide
poisoning from coal gas is due to excessive carboxy
hemoglobin in the blood. Metabolites of same drugs cause
striking abnormal coloration of skin; for example, mepacrine
(yellow), clofazamine (red) and phenothiazines (slate gray
on exposed areas), the artificial lightening may influence
the appearance of the normal skin color. Therefore, it is
always suggested that the physical examination of the patient
should be carried out in the normal daylight as far as possible.
PALLOR
Pallor is defined as lack of color or paleness.
Seen in conditions like:
• Anemia or progressive anemia (if the pallor increases
continuously in magnitude).
• Vasoconstriction.
• When the person is faint or frightened.
(Examination of the mucous membranes may help to
distinguish the pallor of anemia from that of other causes)
Causes of Pallor without Anemia
• Peripheral circulatory failure.
• MS/AS severe.
• Myxoedema.
• Nephrotic syndrome
• Sheehan’s syndrome
• Vasovagal attack.
PLETHORIC COMPLEXION
• Vasodilation causes deep pink complexion even in the
absence of anemia.
• Polycythemia, some alcohol abuser’s with a pseudo-
Cushing’s syndrome and Cushing’s syndrome.
CYANOSIS
The word cyanosis has been derived from a Greek word
“Kyanos” meaning dark blue and “osis” meaning condition.
It is defined as the bluish, grayish, slate like or dark purple
discoloration of the skin and mucous membrane caused by
the presence of abnormal amounts of reduced hemoglobin
in the blood. At least a level of 5 gm percent of reduced
hemoglobin should be present in the blood for cyanosis to
appear.
 The General Examination 63

Central Cyanosis cyanosis may be brought about either by an increase in the

Central cyanosis results from imperfect oxygen of the blood quantity of venous blood as the result of dilatation of the
as in heart failure and some lung disease or due to admixure venular and venous ends of the capillaries or by a reduction
of desaturated venous blood with arterial oxygenated blood in the SaO2 in the capillary blood.
due to right to left (venous-arterial) shunts in the heart. In In general, cyanosis becomes apparent when the mean
this case, the cyanosis is general and cyanosed extremities capillary concentration of reduced hemoglobin contraction
are warm, but the bluish discoloration of the tongue is a of O2 from normally saturated arterial blood. It results from
more reliable indicator of the central cyanosis. Central vasoconstriction and diminished peripheral blood flow, such
cyanosis is seen in conditions like (besides the above- as occurs in cold exposure, shock, congestive failure and
mentioned conditions): peripheral vascular disease. Often, in these conditions, the
• Pneumoninsa. mucous membranes of the oral cavity or those beneath the
• Bronchial asthma. tongue may be spared.
• Pulmonary infarction.
• Allergic alveolitis. Table 4.2: Differences between central and
• Any disease causing pulmonary fibrosis. peripheral cyanosis
(All these conditions should be severe for cyanosis to occur). Features Central Peripheral
Site: Clinically central cyanosis is manifested both in the 1. Mechanism Decreased arterial Decreased flow of blood to
extremities and lips, conjunctivae and tongue, but the tongue oxygen saturation local part
is the reliable indicator of central cyanosis. 2. Sites On skin and mucous On skin only
membranes, e.g.
tongue, lips, cheeks,
Peripheral Cyanosis etc.
Peripheral cyanosis affecting the face and neck and 3. Temperature Warm Cold
of the limb
sometimes the upper limbs is one of the features of superior 4. Clubbing and Usually associated Not associated
vena cava obstruction (SVC obstruction). It is due to polycythema
excessive reduction of any hemoglobin in the capillaries 5. Local heat Cyanosis persists Abolished
when the blood flow is slowed. This may happen on 6. Effect of pure Cyanosis decreases Persists as such.
exposure to cold, when there is venous obstruction and in (100%) oxygen
heart failure. The cyanosed extremity or extremities are cold
and the tongue is unaffected. The cyanosis of heart failure Causes of Cyanosis (Differential Diagnosis)
is often due to both central and peripheral causes severe a. Decreased arterial oxygen saturation:
chronic hypoxia of either pulmonary or cardiac origin is • Decreased atmospheric pressure—high altitude.
often associated with polycythemia and extreme degrees of • Impaired pulmonary function like
cyanosis, partly central and partly peripheral.
– Alveolar hypoventilation.
A similar bluish discoloration may be produced by
– Uneven relationship between pulmonary venti-
methemoglobinemia or sulphemoglobinemia usually due to
intake of drugs like phenacetin. lation and perfusion.
• Anatomic shunts seen in
Pathology – Certain types of congenital heart disease.
– Pulmonary arteriovenous fistula.
It refers to a bluish discoloration of skin and mucous – Multiple small intrapulmonary shunts.
membranes resulting from an increased quantity of reduced • Hemoglobin with low affinity for oxygen.
hemoglobin, or of hemoglobin derivatives, in the small blood
b. Hemoglobin abnormalities:
vessels of those areas. It is usually most marked in lips,
• Methemoglobinemia — Hereditary, acquired.
nailbeds, ears, and malar eminence. The florid skin
• Sulphemoglobinemia — Acquired
characteristics of polycythemia vera must be distinguished
from true cyanosis discussed here. A cherry red flush, rather • Carboxyhemoglobinemia — (not true cyanosis)
than cyanosis is caused by COHb. The degree of cyanosis Peripheral Cyanosis
is modified by the color of the cutaneous pigment and
thickness of the skin, as well as by the state of cutaneous • Reduced cardiac potassium.
capillaries. The increase in the quantity of the reduced • Cold exposure.
hemoglobin in the mucocutaneous vessels that produces • Redistribution of blood flow from extremities.
64 Essentials of Clinical Medicine

• Arterial obstruction. a. Melanin underproduction: Seen in vitiligo (patchy

• Venous obstruction. depigmentation of skin), albinism (total absence of
melanin synthesis in the body) and hypopituitarism
Table 4.3: Differentiation between respiratory (partial absence of melanin synthesis).
cyanosis and cardiac cyanosis
b. Overproduction of melanin: Addison’s disease (due to
Respiratory cyanosis Cardiac cyanosis adrenal insufficiency), pregnancy (due to estrogen,
Associated respiratory condition No associated respiratory condition progesterone and pituitary melanotrophica peptides),
present intake of large quantity of heavy metals like iron (as in
Appears later on in life May appear at immediately after
birth
hemochromotosis), freckles and pigmented nevi (in
Dsypnea present Tachypnea present conditions of local overproduction). In Addison’s disease
On crying- cyanosis decreases On crying – cyanosis increases the melanin deposition (brown pigmentation) of skin
On administration of 100% O2 PO2 does not rise substantially on occurs over the bony prominences, in creases, scars,
(hypoxia test) – PO2 > 150 giving 100% O2
or in areas exposed to pressures such as braces, belts,
PCO2 may be increased PCO2 usually normal or low.
etc. Pregnancy is characterized by increased pigmen-
Approach to the Patient tation over the face (called melasma or chloasma) and
of the areolae, lonea alba and around external genitalia.
1. History taking—onset (cyanosis present since birth is
usually due to congenital heart disease) and possible Hypercarotenemia
exposure to drugs or chemicals that may produce
abnormal types of Hb. Hypercarotenemia is seen in cases where a person eats a lot
2. Clinical differentiation between central and peripheral of raw carrots and tomatoes. It is a rare condition. The
cyanosis. condition is characterized the orange-yellow discoloration
3. Objective evidence by physical or radiographic exami- in subcutaneous fat and epidermis, over face, palms, soles
nation of disorders of respiratory and cardiovascular but not in the sclera (this is the distinguishing feature
system. between jaundice and hypercarotenemia). A yellow
4. Massage or gentle warming of a cyanotic extremity will discoloration of face may also be seen in condition of
increase peripheral blood flow and abolish peripheral hypothyroidism due to impaired hepatic metabolism of
but not central cyanosis. carotene.
5. Presence or absence of clubbing of digits clubbing
without cyanosis is frequent in patients with infective JAUNDICE (Hyperbilirubinemia)
endocarditis and ulcerative colitis. It may occasionally In this condition, the sclera, mucous membrane and skin
occur in healthy persons; and in some instances, it may appear lemon yellow in color. But sublingual mucosa is the
be occupational, e.g. in jack hammer operators. The
most reliable site for diagnosing the condition.
combination of cyanosis and clubbing is frequent in
a. Hemolytic jaundice: The features are:
patients with congenital heart disease and right to left
• Increase in circulating unconjugated bilirubin.
shunting and is seen occasionally in persons with
• Bilirubin being unconjugated is not excrete in urine –
pulmonary disease such as lung abscess or pulmonary
urine color normal.
arteriovenous fistulae. In contrast, peripheral cyanosis
• Stools are dark and urine though normal, contains
or acutely developing central cyanosis is not associated
an excess of urobilinogen.
with clubbed digits.
b. Hepatocellular and obstructive jaundice: The features
6. Determination of PaO2 tension and SaO2 and spectro-
are:
scopic and other examinations of blood for abnormal
• Conjugated bilirubin excreted in urine (as it is water
types of hemoglobin (critical in differential diagnosis of
soluble and easily passes through renal glomeruli).
cyanosis).
• Urine is dark yellow/brown like beer and stools tend
MELANIN to be pale in color like putty because of reduction in
the amount of bile in feces.
Melanin (melanocytes) is responsible for the skin color of • Scratch marks may be prominent in this type of
an individual. Conditions causing the underproduction and jaundice because of pruritis due to retention of bile
overproduction of melanin are as follows: acids.

In case of deep and longstanding jaundice, a distinct
greenish color develops in the sclerae and in the skin owing
to the oxidation of bilirubin to biliverdin which is greenish
in color.
INVOLUNTARY MOVEMENTS
They have been described in detail in the section of section
of “Neurological Examination”.
VOICE AND SPEECH
Each individual has his/her own characteristic (typical) voice
and speech. Any disturbances in the functioning and
structure of tongue, palate, nose, integrity of mucosa, and
nerve supply of larynx and capacity of lung causes
abnormality in the normal speech. Many of the causes of
abnormality may be recognized by inspection; for example,
a cleft palate, nasal obstruction, loose dentures or a dry
mouth. Voice in myxoedema may be so characteristic that
diagnosis can be made over the telephone without seeing
the patient. The normal infections or tone disappear, speech
is low pitched, slow and deliberate and seems to require
more effort than normal and also it sounds thick. These
changes are due to myxoedema infiltration of the tissues
concerned in voice production.
The following points are to be considered in the
examination of speech and language:
• Spontaneous speech.
• Articulation.
• Fluency.
• Paraphasios (it is a form of aphasia, the misuse of spoken
words or word combinations).
• Grammar.
• Syntax (a way that words and phrases are put together
to form a sentence in a language).
• Naming objects concepts.
• Comprehension of spoken comments.
• Repetition of spoken phrases.
• Reading aloud.
• Handwriting.
ODORS
Sometimes “odors” can help the clinician to come to the
diagnosis of certain disease processes.
• Fetor hepaticus—liver failure.
• Sweetness of breath—in diabetes and severe starvation,
ketoacidosis.
• Smell of certain wounds—Pseudomonas aeruginosa or
ulcers.
The General Examination 65
• Wet ginger, chronic suppuration, necrotic tumors and
certain skin disorders give out characteristic odors.
• Halitosis (Latin-Lalitus, breath + Greek Osis condition).
Bad breath or malodorous breath is often unrecognized
by the patient. Halitosis is often caused by the remains
of food particles in the mouth, any pathologic conditions
like gingivitis, stomatitis, atrophic rhinitis, tumors of
nasal passages, as well as pulmonary suppusation.
• Offensive breath is also seen in conditions like bron-
chiectasis (with foul-smelling expectoration). Gastric
outlet obstruction (like scarring, pyloric stenosis, gastric
carcinoma) may cause foul-smelling erructations.
• Addictive substances like alcohol, tobacco and marijuana
can be identified by their smell.
HEIGHT AND WEIGHT
Obesity
Obesity is defined as a condition when energy intake (in the
form of diet) exceeds the energy expenditure. It is a
multifactorial condition. It is often associated with
hypertension, hyperlipidemia, and diabetes mellitus. Obesity
also has a familial (hereditary inheritance).
Types of Obesity
1. Generalized obesity: It is deposition of excess amount
of fat uniformly all over the body. The most important
cause seems to be overeating. It is characterized by the
presents of double chin.
2. Android obesity: Excessive deposition of fat over the
region of waist.
3. Gynoid obesity: Excessive fat deposition over hips and
thighs.
4. Superior (central) type of obesity: Excessive fat deposi-
tion over face, neck and upper part of trunk. The arms
are thin, e.g. Cushing’s syndrome. Regional distribution
of fat holds greater prognostic significance than absolute
degree of obesity. Simple and best assessment of this is
done by calculating waist-hip ratio.
• Hip measurement: Done at a level of maximum
measuring portion, i.e. over the buttocks.
• Waist measurement: Done at a level of minimum
(narrowest) measuring portion, i.e. between the bony
cage of rib and iliac crest.
If the waist-hip ratio is 0.8 or less and the con-
figuration (type of obesity) is pear shaped, then the
subjects have better prognosis over those who have
their waist-hip ratio of 0.9 or more and configuration
of apple-shaped type because these people have a
greater chance of developing cardiovascular disease.
66 Essentials of Clinical Medicine
(Causes of “weight gain” and weight loss have
been described in the section of symptomatology).
Complication of Obesity
• Benign intracranial hypertension.
• Sleep apnea.
• Exertional breathlessness.
• Reflux symptoms.
• Increased blood pressure.
• Gallstones.
• Abdominal striae.
• Impaired fertility.
• Stress/urge incontinence.
• Gynecological malignancy.
• Osteoarthritis.
• Varicose veins.
• Dependent edema.
• Pes planus (flat foot).
Hydration
About sixty to seventy percent of our total body weight is
comprised by water. Two-thirds of it is intracellular, another
two-thirds is interstitial fluid and rest is in the form of
circulation blood.
Assessment of Hydration
• Skin elasticity test: Skin over different body parts,
especially the extremities and the trunk, is pinched for 5
seconds and then left to regain its normal position. If
the skin is well hydrated, it will immediately return to its
normal condition; whereas it will take comparatively
longer time to do to if it is dehydrated.
• Other tests for assessing hydration are:
– Recording of intraocular pressure (IOP). It falls as
the dehydration continues. Normal IOP varies
between 10 and 25 mm Hg (with a mean of 16 ±
2.5).
– Recording the blood pressure.
– Looking for a postural drop in blood pressure.
• Presence of edema: It is checked by applying firm
pressure (for at least 3-10 seconds) over the angle behind
the medial malleolus. And, if it is present, then its extent
elsewhere is assessed by pressing over the shin of tibia,
in medial thigh region and in sacral area also. It may
also be assessed by pressing over the dorsum of the
foot with the thumb.
• Recording of JVP: It is another way to assess the state
of hydration.
• Dehydration: It occurs in conditions like vomiting,
diarrhea, sweating, polyuria. A detailed history about the
nature and quantity of fluid loss should be taken. Loss
of skin elasticity should be assessed carefully because it
may be due to other causes like collagen damage also.
Elevation of hemoglobin concentration, packed cell
volume (PVC) and plasma osmolality provide of evidence
of severity of dehydration.
EDEMA
The term edema has been derived from the Greek word
oedema meaning swelling. It is defined as a local or
generalized condition in which the body tissue contains an
excessive amount of tissue fluid. A generalized edema was
previously called dropsy; now it is called anasarca. Various
terminologies have been given depending upon the site of
accumulation of tissue fluid as follows:
• Ascites – Abnormal collection of fluid in
peritoneal cavity.
• Hydrothorax – Abnormal accumulation of fluid
in pleural cavity.
• Anasarca – Generalized edema.
• Pericardial effusion – Abnormal collection of fluid in
the pericardial cavity.
• Pleural effusion – Pathological collection of fluid in
the pleural cavity.
Conditions Causing Anasarca
Anasarca is generalized swelling all over the body.
Causes are:
• Severe anemia with hypoproteinemia.
• Nephrotic syndrome.
• CCF (Rt.) pericardial effusion.
• Chronic malabsorption with hypoprotein.
• Hepatic cirrhosis, protein losing enteropathy.
• Allergic—angioneurotic edema.
Causes of Pedal Edema
• CCF.
• Cirrhosis of liver.
• Anemia with hypoproteinemia.
(Pitting on pressure is noticed when the circumference of
the limb increases by 10% of the original).
 The General Examination 67

Table 4.4: Differences between renal, cardiac and hepatic edema

Features Renal Cardiac Hepatic

• Site Face Leg Abdomen
• Neck vein signs of CCF No Yes No
• Signs of portal hypertension No No Yes – Epigastric vein, splenomegaly
• Urinary albumin Massive Trace to nil Nil

Table 4.5: Differences between venous edema and lymphatic edema Blood Pressure
Venous edema Lymphatic edema • Record the BP in all the four limbs.
1. Pitting Non-pitting Jugular Venous Pressure (JVP)
2. Venous collaterals present No venous collaterals present
3. Homan’s sign present Not present • Raised or normal?
4. Peu de orange skin not present May be present
5. Reversible after treatment Usually not reversible
HAIR
Areas of Special Attention in You should look for:
Case of Edema • Presence (normal or sparse) and color of sparse hair.
Assessment • Presence (normal, sparse or excessive) and distribution
• Fundal hemorrhage. hair over the body parts.
• Periorbital edema. According to the age, 3 different types of hair are seen
• Tonsils. over the body:
• JVP (Jugular venous pressure). – Lanugo/fine long hair covering the body of fetus but
• Cardiac size. normally shed about a month before birth.
• Gynecomostia and other signs of hepatic disease. – Lanugo hair are replaced by vellous hair (which cover
• Blood pressure. much of the body surface).
• Pleural effusion signs. – They are replaced by terminal hair on the scalp.
• Signs of liver and spleen disorders. • Inspection of scalp hair for its lusture, calibre, structure,
• Ascites, bowel sounds. tensile strength and density.
• Clubbing leukonychia. • If defect is alopecia, then determine whether the
• Abdominal veins. pathology is of hair or scalp itself.
• Edema of genital parts.
• Fungal infection, lice, or nits.
• Petechial hemorrhage.
• Pedal edema. • Examine secondary sexual hair for its nature and
distribution.
PHYSICAL EXAMINATION • Presence of dandruff over the scalp.
Vitals The amount and distribution of hair varies in normal
individuals and is characterized by their familial and racial
Pulse factors; for example, Asians—long, straight hair; Mongoloids
• Pulse rate. —sparse facial and body hairs, Negroes—curly hair,
• Regular or irregular (rhythmic or non-rhythmic). Europeans—wavy hair.
• Normovolemic, hypervolemic, or hypovolemic.
• What is the tension in the pulse? Related to Scalp Hair
• Conditions of vessel wall. • Alopecia—loss of hair
• Any special characteristic. – Alopecia areato—hair fall in patches.
• Radiofemoral delay. – Alopecia universalism—loss of all body hair.
• Peripheral pulsations present or absent. Fungal infection (affected areas contain hair broken off
Temperature close to the skin).
• Whether the patient is febrile or afebrile? You should look for posterior cervical lymphadenopathy
• If febrile, how much is the temperature in oF? (infection by nits and lice).
68 Essentials of Clinical Medicine
Facial and Body Hair
Terms related to them:
Hirsutism: Excessive growth of coarse hair in females on
the face, trunk and limbs in the pattern that is normally see
in males. Pubic hair also may show a change in the pattern
from normal flat topped distribution up towards the
umbilicus (called male escutcheon). Mild hirsutism is a
common condition and a little increase in facial hair is
common after menopause.
In case of androgen-secreting tumor or pituitary tumor,
hirsutism may be associated with other signs of virilization
like development of male physical features in a female,
including enlargement of clitoris and menstrual irregularity
(or cessation).
Hypertrichosis: Excessive growth of coarse hair that do
not follow the androgen-induced pattern. The causes are:
minoxidil and cyclosporin therapy, trauma, and cutaneous
porphyria, familial, sexual precosity, hypothyroidism, adrenal
hyper- plasia/tumor, virilizing ovarian tumors.
Secondary Sexual Hair
Failure in their development may occur in condition of
hypogonadism; decrease in their quantity occurs in old age
and total loss is seen in hypopituitarism or hepatic cirrhosis.
SKIN LESIONS
Inquiries to be made are:
• What is the color, shape size of lesions?
• How is their margins and surfaces?
• On which part is it located—localized, all over the body
or symmetrical?
• Onset, duration and progress of leision.
• Does it appear only on the specific sites like bony
prominences, etc.?
• Any area spared by lesion?
• Occupational/environmental conditions of the patient?
• Any other associated features?
Certain Specific Conditions of Skin
• Generalized depigmentation of skin—albinism (seen in
Chediak-Higashi syndrome, phenylketonuria, etc.).
Patch depigmentation—vitiligo (autoimmune conditions
and DM).
• Hypopigmentation—leprosy (Hansen’s disease), tenia
versicolor.
• Generalized hyperpigmentation—Addison’s disease,
Cushing’s syndrome, hemochromatosis.
• Hyperpigmentation in the form of patches—porphyria,
pellagra, chloasma (in pregnancy), café au lait spots,
malar rash (butterfly rashes) in SLE, drug reaction and
allergies.
• Purple striae—Cushing’s syndrome.
• Purpuras, ecchymosis—low platelet count.
• Hemangiomas.
• Spider nevi—liver pathology, superior vena cava
obstruction.
• Palmar erythema—chronic liver disease, polycythemia,
thyrotoxicosis, pregnancy.
• Xanthoma—Hyperlipidemia states.
• Malignant conditions—migratory thrombophlebitis in
carcinoma of pancreas, acanthosis nigricans—adeno-
carcinoma of gastrointestinal tract.
Extremities
Point to be looked for are:
• Strength of the grip (for upper limb).
• General shape—acanthosis, burn contractures (bony
deformity).
• State of joints (pathology of joints, mobility stiffness,
pain swelling, inflammations, range of movements).
• Clubbing (grade-4) (for upper limb).
• Nailbed infarcts.
• Movements (tremor, tetony clonus).
• Posture (hemiplegia, paraplegia, quadriplegia, etc.)
• Size span (described earlier in this book).
• Color—burn, scar, marks, injuries, operative scars,
occupations like dye industries, miners, etc.
• Temperature.
• Fingertips
– Osler’s nodes in SABE.
– Grade 4 clubbing.
• Webs in scabies, trophic ulcers in leprosy, syringomylia,
etc., gangrene.
• Nerves – neuropathies, sensations, motor activities.
• The feet have to be examined for pitting edema (ankle
and dorsum of foot), peripheral vascular disease (skin
shiny with no hair), signs of ischemic foot, trophic ulcers
in diabetic peripheral neuropathy (diabetic food).
NAILS
Nails provide important diagnostic clues.
Table 4.6: Important signs in the nails
Features Condition
Bitten nails Anxiety
Finger clubbing (see details below)
Splinter hemorrhage Minor trauma, systemic vasculitis.
Koilonychia Chronic iron deficiency anemia.
Contd...
 The General Examination 69

Contd... 3. Hypoxic:
Features Condition – Persistent hypoxia causes opening of deep A-V
Pitting Psoriasis.
fistulae of the terminal phalanx.
Onycholysis. Trauma, psoriasis 4. Ferritin:
Straie leukonychia Minor trauma, may be a normal finding – Decreased ferritin in systemic circulation – dilatation
Severe leukonychia (white Hypoalbuminemia, chronic liver disease of AV anastomosis and hypertrophy of terminal
nails or Terry’s nails) and other wasting disease. phalanx.
Transverse ridging (Bean’s Recent acute illness. 5. Platelet-derived growth factor (PDGF):
lines) due to temporary
– Released secondary to infection anywhere in the body
arrest of nail growth
Fungal infection Thickening, crumbling and discolor- also causes vasodilation and this is latest and “most
ation. acceptable” theory of clubbing.
Red half moons Congestive cardiac failure.
Causes of Clubbing
Blue half moons Hepatolenticular degeneration, Wilson’s
disease. • Respiratory causes
Half and half nails Chronic renal failure. – Bronchial carcinoma.
Black nails Silver poisoning, Addison’s disease (rarely) – Intrathoracic suppuration.
Nailbed infarcts Vasculitis, especially in SLE
– Bronchiectasis.
(systemic lupus erythematosus) and in
polyarteritis. – Empyema.
– Lung abscess.
Clubbing – Fibrosing alveolitis.
– Pulmonary tuberculosis.
Clubbing is a condition that affects the fingers and toes in • Cardiovascular causes
many diseases of varying etiologies. The most outstanding – Cyanotic congenital heart disease.
feature of clubbing is the lateral and longitudinal curvatures – Bacterial endocarditis and subacute bacterial endo-
of the nails accompanied by soft tissue enlargement, carditis.
presenting a bulbous shiny appearance (Fig. 4.1) • Chronic abdominal disorders:
Theories of Clubbing – Hepatic cirrhosis.
– Ulcerative colitis.
1. Related to nervous system: – Crohn’s disease.
– Vagal stimulation causes vasodilation and clubbing. – Coeliac disease.
2. Endocrinal: d. Congenital:
– GH, PTH, estrogen, PG, and bradykinin cause vaso- – Familial clubbing.
dilation and clubbing. – Cervical rib is a common cause of unilateral clubbing.
Grades of Clubbing
• Grade I — Slight hollowing between the finger pulp
and nail.
This angle becomes full (obliterated) in
early stages of clubbing.
• Grade II — Abnormal motility of nails in the nailbeds
due to spongy thickness of the hyper-
trophied nailbeds (parrot beak appea-
rance).
• Grade III — Thickening of nailbed, producing bulbous
enlargements of ends of fingers (drum-
stick appearance).
• Grade IV — Fingers are markedly enlarged and the
nails and bones are also hypertrophied.
These changes may be associated with
thickening of ends of long bones
(hypertrophied osteoarthropathy).
Fig. 4.1: Clubbing of nails
70 Essentials of Clinical Medicine
The normal angle between the nail and nailbed is 160°
and is known as lovibond angle. The minimum duration
required for clubbing to manifest is 2 to 3 weeks. And index
finger is the first to be involved.
Schammroth’s Maneuver or Schammroth’s Sign
As shown in Figure 4.2, when the dorsum of the distal
phalanges of the fingers of both hands (especially the index
fingers) are brought in close contact with each other, a gap
is visible through it and this gap is of diamond shaped (due
to the presence of lovibond angle). The clubbing is diagnosed
by the disappearance of this gap (due to the obliteration of
angle of lovibond) (Fig. 4.3, Plate 2).
If the normally visible space formed between the nails
of two approximating index fingers is obliterated, then
Schammroth’s sign is said to be positive and clubbing is
said to be confirmed (Fig. 4.4, Plate 2 and Fig. 4.2).
EXAMINATION IN THE HOSPITAL WARDS
If the patient is examined in the hospital wards (patient lying
on the bed), then the examination pattern should be as
follows.
Decubitus
Decubitus means the position of the patient in the bed. This
term is generally used for the lying down position:
• Whether the patient is lying supine, prone or in lateral
position?
• Whether the patient is sitting over the bed and in what
position?
Fig. 4.2: Testing for fluctuation of the nailbed
For example
– Sitting with back straight?
– Leaning forwards?
• Hands over the abdomen chest, head or any other body
parts?
Appearance
• Whether the patient looks restless, anxious, agitated,
angry, emotional, depressed, or in agony of severe pain?
• Whether the bedside has certain items like oxygen
cylinder, drip bottle, container for collecting urine, stool
or vomitus, etc? Sometimes the appearance may provide
clues for spot diagnosis of cases. For example, blue
sclera in case of osteogenic imperfecta, scleroderma
facies with beaking of nose and taut skin around mouth,
acromegaly facies or leg of elderly male with scurvy
showing large ecchymosis in thigh (woody leg) with
perifollicular hemorrhages in calf muscles.
Posture (or Attitude)
• Posture/attitude of the patient should be observed both
in lying down (decubitus) as well as sitting and standing
position, if possible.
• Posture of the patient sometimes provides a very strong
clue about the system involved and nature of the disease
process. This has been explained as follows.
Posture Related to Nervous System Involvement
Photophobic attitude
• The patient turning away from the source of light?
• Keeping clothes or hands over the face?
• Lying curled up with legs flexed over the trunk and
bending interiorly?
It signifies inflammation or irritation of meninger.
Pleurosthotonus: Body arched to one side or lateral curling
of the body.
Opisthotonus: Arching of the back (extreme spasm of the
back muscles) and body weight supported by head and feet
only, rest of the body being above the bed.
It signifies tetanus, strychnine poisoning, meningitis
preparalytic poliomyelitis. It is also seen in a case of major
burn. In severest cases of meningitis, the neck may be bent
backwards so that the head appears to bore into the pillow.
This is called neck retraction.
Hemiplegic
Acute Stage: In early stage, the patient lies supine with his
eyes, head and neck turned to one side. The direction of
eyes and head is in the direction (side) of the brain, head or
eyes affected limbs of the affected side are flaccid without
any movement and lower limbs are externally rotated with
a foot drop.

In Late Stage: No rotation (movements) of eyes, head and
neck. Assymetry of face with loss of nasolabial furrow on
the affected side. The upper limbs show flexion at elbow
joint and slight pronation with flexion of fingers at
metacarpophalangeal joints. The shoulder joint shows
adduction and internal rotation. The lower limbs show
extension at hip joint and knee joints along with plantar
flexion of the foot.
Posture Related to Cardiovascular and
Respiratory System Involvement
Orthopnea/Dyspnea: The patient with heart failure or with
any respiratory system disorder is usually found sitting
upright over the bed. He becomes uncomfortable as he lies
down (orthopnea). Two or more pillows, kept over the bed,
on one another, may provide an important clue about the
dyspnea. It is also seen in cases of gastroesophageal reflux
disorders (GERD) where the patient is advised to sleep with
his head held above the level of abdomen (to prevent reflux
from the stomach). Orthopneic posture is seen in cardiac
causes like left ventricular failure, pericardial effusion, cor
pulmonale; respiratory causes like emphysema, bronchial
asthma, massive pleural effusion, pneumothora, etc.
Forward bending position (with kneeling or without
kneeling): It is seen in cases of severe dyspnea. The patient
sits up in the bed, bends forwards with a support on his lap
on which he kneels. The hands usually support the sides so
as to make better and efficient use of normal and accessory
muscles of respiration by providing a fixed point at their
point of insertion.
It signifies massive pleural effusion, severe degree of
congestive cardiac failure, aortic aneurysm. It is also
sometimes (but rarely) seen in cases of pancreatic carcino-
mas and abdominal aortic aneurysms so as to relieve pain
caused by the pressure over the spine.
Build
• Normosthenic: Persons with normal body built.
• Asthenic: Slender, thin, long body with flat chest. They
are prone to neurasthesia and visceroptosis.
• Sthenic: Short-heighted persons with muscular body,
muscular chest, short neck and extremities and stumpy
and short fingers.
• Height: Height mostly depends upon the hereditary and
racial factors.
[Normally, the height of a person is equal to his arm
span that is distance between the fingertips when hands are
stretched parallel to the ground and normal upper segment
—to lower segment ratio of the body (e.g. the ratio of
The General Examination 71
distance between the top of the head and symphysis pubis
to that between symphysis pubis and sole of the feet) is
1 : 1].
Conditions in which the height is greater than arm span:
• Hyperpituitarism.
• Adrenal cortex tumor.
• Precocious puberty.
• This occurs before puberty when epiphysis of bones
are not united.
Conditions in which arm span is greater than height:
• Marfan’s syndrome.
• Klinefelter’s syndrome.
• Eunuchoidism.
• Hypogonadism.
• Homocystinuria.
Conditions in which the upper segment is greater than the
lower segment of the body.
• Adrenal cortex tumor.
• Precocious puberty.
Conditions in which lower segment is greater than the
upper segment of the body
• Klinefelter’s syndrome.
• Marfan’s syndrome.
• Homocystinuria.
• Eunuchs.
• Hypogonadism.
DWARFISM: (SHORT STATURE)
The causes are:
• Familial trait (hereditary)—constitutionally small.
• Racial—certain tribes of African continent.
• Constitutional growth delay.
• Causes before the birth like intrauterine growth
retardation; infections like TORCH, AIDS, syphilis, etc.;
excessive consumption of tobacco, alcohol by the
pregnant mother; certain genetic disorders like Down’s
syndrome, Turner’s syndrome; metabolic disorders like
glycogen storage disease; skeletal abnormalities like
achondroplasia; osteogenic imperfecta, chondro-
dystrophies:
• Causes after birth like malnutrition (protein energy
malnutrition, anorexia nervosa); endocrinal disorders
such as pituitary-hypothalamic axis defects, (Frohlisch’s
syndrome), pituitary defects (pituitary dwarfs), thyroid
hypofunction since birth (cretinism) and gonadal
abnormalities; chronic diseases like tuberculosis;
cardiovascular disorders like cyanotic and acyanotic
heart disease, early onset rheumatic heart disease;
respiratory disorders like Kartagener’s syndrome, cystic
72 Essentials of Clinical Medicine
lung disease, childhood asthma; renal disorders like renal
tubular necrosis, renal rickets, nephrotic syndrome,
chronic anemia, like thalassemia, sickle cell anemia,
leukemia; psychosocial disorders like maternal
deprivation syndrome, paternal deprivation syndrome;
gastrointestinal disorders such as coeliac disease,
malabsorption syndrome, gluten enteropathy, Crohn’s
disease, cystic fibrosis, etc.
STATE OF NUTRITION
The state of nutrition indicates a correlation between height
and weight. It nutrition depends upon the distribution of
adipose tissue in the body. The condition of the skin, muscle
mass and distribution of subcutaneous fat should be looked
for when assessing the state of nutrition of the patient.
• Body mass index (BMI) = weight in kg/height in m2
• Normal BMI = 19-25 males = 20–25
females = 18–23
• If BMI < 18—underweight.
• If BMI 25-30—overweight.
• If BMI 30-40—obese.
• If BMI > 40—very obese.
Note: Causes of weight loss and weight have been
enumerated in the section of symptomatology.
In case of obesity, you should inquire about:
• Family history.
• Obstetric history.
• Psychological stress.
• Anxiety and depression.
• Binge eating.
• Alcohol and other fluid intake.
• Symptoms of diabetes.
HEAD
The examination of head includes the examination of hair,
cranium, face, forehead, eyes, ears, nose and mouth. The
examination of mouth further includes—inspection of
(outside in) lips, teeth, gums, tongue floor of the mouth,
mucosa of cheeks, palate tonsils, oropharynx:
Hair
Discussed earlier.
Skull
Shape and Size of the Skull
Macrocephaly: Abnormal enlargement of head along with
proportionately larger size of brain. The ventricles are
normal in size.
Hydrocephalus: (Kephale = head). The condition is associated
with increased accumulation of cerebrospinal fluid (CSF)
within the ventricles of the brain, resulting from the
interferences with normal circulation and with absorption
of the fluid and especially from destruction or blockage of
foramina of Magendie and Luschka. It may be caused by
developemental anomalies, infection, injury or brain tumors.
In severe cases in children, the head is usually globular or
pyramidal in shape. The condition is seen in children before
the sutures have united. The face is disproportionately small
and eyeballs are pushed downwards with the sclera being
visible above the corners (sunset sign). There occurs bulging
of fontanelles and poor hair growth. After the skull has
formed in older individuals, there are headache, vomiting,
choked disks, atrophy of optic nerve, mental disturbances.
Hydrocephalus is also called hydrencephalus.
Abnormal enlargements of head due to hypertrophy of
bones as seen in Paget’s disease.
Microcephaly: The head is abnormally small in size and
brain growth is poor. The condition is usually associated
with mental retardation.
Craniostenosis: Skull shape is abnormal and is usually due
to early closure of the sutures.
Tower skull (oxycephaly, or turricephaly): The condition of
having a malformed cranial vault with a high or peaked
appearance (a vertical index above 77). It is caused by
premature closure of the coronal, sagittal and lambdoid
suture. It is also called acrocephaly.
Dolichocephaly: The term has been derived from the Greek
word Dolichos meaning long and kephale meaning head. It
is defined as a condition having a skull with a long
anteroposterior diameter with prominent eyebrows and
occiput.
Brachycephaly: It is a condition caused by early closure of
coronal sutures, the head is wider. The skull may show
unilateral flattening on occipital side with a corresponding
flattening of opposite forehead which results in plagio-
cephaly (appearance of twisted or lopsided head). The
cephalic index is 81.0 to 85.4. This is considered a short
head but not necessarily abnormal, as this index falls within
the standard range of variation among humans.
It is usually due to disease in infancy which forces the
patient to lie down with his head turned to one side for a
long time.
Platybasia (Basillar invagination): Head is extended, and
rests over a short neck with the hair line at a low land
usually seen in condition of craniovertebral anomalies.

Appearance of Skull in Certain Special Conditions
Rickets: Elongated skull with prominent frontal and parietal
eminences.
Congenital syphilis: (hot cross bun skull) prominence of
frontal eminence, forehead is more vertical and nasal bridge
is depressed.
Rickets: Another abnormal condition of skull seen in early
rickets is craniotabes. It is a condition where skull bones
become soft and they immediately return to normal position
if the pressure is applied over them by the index finger and
released.
Irregular nodules over skull in metastatic malignancies.
Cracked pot sound (on percussion) in children in
condition of hydrocephalus or raised ICT (intracranial
tension).
Examination of Sutures and Fontanelles
In addition to what has been described above, there are
certain conditions which cause separation of sutures and
bulging of fontanelles. Some of the conditions are hydro-
cephalus, meningitis. In contrast, there are certain conditions
which cause “sunken fontanelle”, e.g. dehydration.
The condition associated with early closure of sutures
has been described above. The conditions causing delayed
closure of sutures is seen in rickets, cretinism, malnutrition
and congenital syphilis.
Forehead
Conditions where Forehead is Prominent
• Rickets.
• Frontal bossing in haemolytic anemia (thalassemia).
• Acromegaly.
• Chronic hydrocephalus.
• Frontal balding in myotonic dystrophy.
Presence of Wrinkling
Bilateral wrinkling: Various states of moods like anxiety
surprise; etc.
Conditions of bilateral ptosis (the patient tries to pull his
eyelids in the upward direction by performing the act of
wrinkle seen in bilateral third n palsy, bilateral Horner’s
syndrome, myasthenia gravis).
Unilateral wrinkling:
• Unilateral ptosis.
• Unilateral 3rd n palsy.
• Unilateral Horner’s syndrome
Absence of Wrinkling
Bilateral absence:
• Hyperthyroidism (Joffroy’s sign).
• Myotonic dystrophy.
The General Examination 73
Unilateral absence: Bell’s palsy.
Facies
Face is examined as follows:
Facial Appearance
Facial appearance is altered in certain disorders like:
endocrinal disorders such as cretinism, myxoedema (puffy
face), acromegaly (broad jaw), Cushing’s syndrome (moon-
like face); congenital disorders such as congenital hemolytic
anemia, thalassemia (hemolytic facies), mongolism,
hypertelorism; renal diseases such as nephrotic syndrome
(characteristic puffy face). Infective disease such as leprosy
(Leonine facies), congenital syphilis, measles (measly face)
hippocratic facies; central nervous system disorders such
as parkinsonism (mark-like face), facial palsy (plegic face,
myasthenia gravis) (tired and dull-looking face), myopathies,
tabes dorsalis; cardiovascular disorders, aortic stenosis
(Elfin’s facies) such as mitral stenosis, (malar flush)
congenital heart disease; respiratory diseases like chronic
obstructive lung disease and many other such important
causes.
• Puffy face—edema over the face, swelling around the
eyes (periorbital edema).
• Moon-like face—round face, with fish-like mouth (slit-
like mouth)
• Hemolytic faces—increased intercanthal distance
(hypertelorism), flat nasal bridge, mouth mostly open,
tongue may be protruded.
• Leonine facies—modular lesions, lion-like face.
• Hippocratic face—cheeks and temples are hollow, eyes
sunken, complexion leader and lips relaxed.
• Mask-like face—expressionless face with little or no
animation.
• Elfin’s facies—wide mouth with large lips, widely
spaced teeth, broad forehead, pointed chin, protruding
ears and eyes set wide apart.
Eyes
Eyebrows
Loss of outer 1/3 of eyebrows in seen in:
– Myxoedema.
– Neurosyphilis.
In leprosy, the hair over the eyebrows may be totally
lost. Rarely, the loss of hair over the eyebrows may be a
part of generalized absence of hair in rare cases of
ectodermal dysplasia.
Loss of Lateral Part of Eyebrows
• TB
• Amyloidosis
74 Essentials of Clinical Medicine
• Myxoedema
• Leprosy
• Malnutrition/Malabsorption.
Eyelids
Retraction of eyelids, widening of palpebral fissure and sclera
is visible both above and below the iris. due to sympathetic
overactivity as in parkinsonism and local irritative disease
of eyes like trachoma.
Drooping (Ptosis) of Upper Eyelids
It occurs due to:
• Paralysis of third nerve.
• Paralysis of ocular sympathetic nerves.
• Local diseases like myopathies.
a. Congenital causes of ptosis are:
– Congenital maldevelopment (weakness) of levator
palpebrae superioris mus (LPS muscle).
– Weakness of superior rectus muscle.
– As a part of blepharophimosis syndrome.
– Congenital synkinetic ptosis (Marcus-Gunn jaws-
winking ptosis, i.e. on winkling jaw, ptosis occurs/
increase)
b. Acquired ptosis occurs due to:
– Myogenic causes like disorders of LPS muscle or
of myoneural junction, myasthenia gravis, dystrophia
myocular myopathy, oculopharyngo muscular
dystrophy, trauma to the LPS muscle.
– Aponeurotic causes like defect in levator aponeurosis
function, involutional ptosis, postoperative ptosis,
traumatic dehiscence, disinsertion of aponeurosis.
– Neurogenic causes like third nerve palsy, Horner’s
syndrome, ophthalmoplegic migraine, multiple
sclerosis.
– Mechanical ptosis due to lid tumors, multiple
chalazion, bid edema, trachoma, etc.
c. Pseudoptosis
There is no ptosis of eyelid and no defect in the eyelid
functioning. The ptosis occurs due to abnormality of other
structures and their functions like lack of support of upper
eyelid in cases of microphthalmos, shrunken eyeball (phthisis
bulbi), enophthalmos, empty socket.
Palpabral Fissure
• Oblique fissure - Mongolian facies
• Wide fissure - Parkinsonism, hyperthyroidism,
and rarely in cervical sympathe-
tic stimulation.
• Narrow fissure - In Horner’s syndrome and
paralysis of third nerve blepharo-
spasm, photophobia—photo-
phobia also occurs in migraine
and is associated with meningeal
irritation.
• Eyeballs - The eyeballs may be either
protruded, retracted or absent (in
case of evisceration or enuclea-
tion).
Enophthalmos—Thyrotoxicosis.
• May be congenital.
• Rarely in chronic cor pulmonale or in patients with tower
skull (oxycephaly).
• Sometimes the condition which causes local deposits
behind the eyeballs; for example, in cases of thrombosis
of superior sagginess, leukemia, tumors may cause
exophthalmos.
• Exophthalmos in only one eye (unilateral exophthalmos)
is seen in case of intraortibal local tumor and in vit C
deficiency state (scurvy).
Enophthalmos—Condition of loss of excessive fluid from
the body (severe dehydration)
• State of severe shock.
• Hippocratic facies.
• It can be an important diagnostic clue in certain
conditions like diabetes acidosis.
• Enophthalmos is also seen in Horner’s syndrome.
Sclera
[A common mistake which students usually commit is that
they say—
The sclera showing yellow “color”, or blue “color”. But
the correct terminology is yellow “discoloration” or blue
“discoloration”. Students should remember that normal color
of sclera is white and any other color of the sclera, besides
white, is an abnormality (i.e. discoloration)].
• Yellow discoloration or icterus is diagnostic of jaundice.
• Blue discoloration is seen in osteogenesis imperfecta,
Marfan’s syndrome, Ehlers-Danlos syndrome, pseudo-
anthoma ilasticum, buphthalmos, high myopia, and healed
scleritis.
Muddy sclera is usually seen in elderly people, or in
people whose occupational environment is very dusty or
smoky. But it may sometimes be seen in young people also
without any specific association to any cause.
Inflammatory condition like scleritis both episcleritis.
Conjunctiva
You should examine bulbar and palpabral conjunctiva.
You should look for:
• Pallor: Over the palpabral conjunctiva. You should
examine both the lower and lower palpabral conjunctiva.
• Subconjunctival hemorrhages: It causes an alarming
bright red splash of blood. It is seen in conditions like
whooping cough, labor, local trauma, bleeding disorders,

sometimes convulsions, severe vomiting or severe
hypertension may also cause subconjunctival hemorr-
hage.
• Conjunctival inflammation (Conjunctivitis):
It gives rise to a condition of red eye with the injection
maximal toward fornix.
Conditions causing red eyes are:
1. Trauma
2. Keratitis
3. Conjunctivitis Remember:
4. Uveitis Tom Kruise Called to USA
5. Subconjunctival hemorrhage
6. Acute glaucoma
The other conditions to be looked for in conjunctiva are
—pingeculae, pterygium, foreign bodies, etc.
Cornea
The conditions to be looked for in the cornea are:
• Loss of transparency and lusture—corneal edema (acute
glaucoma).
• Extensive damage to corneal epithelium in advanced
exophthalmos, chemical corneal injuries, vit. A def., or
severe dry eye syndrome, which may be associated with
connective tissue disorders (Sjögren’s syndrome) or may
occur as a part of sicca syndrome.
• Localized corneal haze—trauma with foreign bodies,
ulcers due to infections, the herpes simplex virus being
a common cause.
• Corneal congestion due to various causes.
• Corneal arcus (arcus senis) – normal if seen in old age.
But if it occurs in young individuals, it may indicate
hypercholesterolemia.
• Kayser-Fleischer ring, a yellow or brown deposit of
copper at periphery of cornea, found in Wilson’s disease
(hepatolenticular degeneration). It occurs due to
deficiency of enzyme “Ceruploplasmin” that plays an
important role in the metabolism of copper in the body.
• Corneal calcification: It occurs at medial and lateral
aspects of corneoscleral junction and suggests
longstanding hypercalcemia.
• Loss of corneal sensations.
Nerve Damage to Iris
Normal color of iris is black, or brown. In some individuals,
it is bluish, light greenish or slighty grayish-black.
Heterochromia (different colors of iris) may indicate
intraocular disease. Iritis causes muddy iris with a small
pupil and ciliary congestion. Iritis may be a manifestation
of systemic illness.
The General Examination 75
Lens
Normally, the lens is not visible on inspection (due to its
transparency). Any condition causing loss of or decrease
of transparency of lens is pathological. For example, cataract,
intraocular pressure:
• Raised in glaucoma.
• Decreased in dehydration.
Pupils
Normal conditions of pupils are described as:
a. CCRTL—Central circular reacting to light.
b. PERLA—Pupils equal and reactive to light and
accommodation.
Ocular Movements
The ocular movements should be tested in all the directions
of gaze as shown below. Normally, the visual axes of two
eyes are parallel to each other in the “primary position of
gaze” and this alignment is maintained in all positions.
A misalignment of the visual axes of the two eyes is
called squint or strabismus. Strabismus can be broadly
classified as:
1. Apparent squint (or pseudostrabismus).
2. Latent squint (or heterophoria).
3. Manifest squint (or heterotropia).
• Concomitant squint.
• Inconcomitant squint.
1. Pseudostrabismus: The visual axes are in fact parallel,
but the eyes seem to have a squint.
Pseudoesotropia or apparent convergent squint may
be associated with a prominent epicanthal fold. This
epicanthal fold covers the visible nasal aspect of the
globe and gives false impression of esotropia.
Pseudoexotropia or apparent divergent squint may
be associated with hypertelorism, a condition of wide
separation of two eyes.
2. Heterophoria: It is a condition in which the tendency of
the eyes to deviate is kept latent by fusion. Therefore,
when the influence of fusion is removed, the visual axis
of one eye deviate away.
3. Concomitant squint: It is a type of heterotropia (manifest
squint) in which the amount of deviation in the squinting
eye remains constant in all the directions of gaze, and
there is no associated limitation of ocular movements.
4. Inconcomitant squint: It is a type of heterotropia
(manifest squint) in which the amount of deviation varies
in different directions of gaze.
5. Paralytic squint: It is defined as the ocular deviation
resulting from complete or incomplete paralysis of one
or more extraocular muscles.
76 Essentials of Clinical Medicine
Nose
Examine the nose for:
• Deformity—injury, fracture, congenital deformity.
Saddle nose: Depression of bridge of nose seen in
congenital syphilis and leprosy, trauma, nasal sniffing
of cocaine, Wegener’s granulomatosis.
Rhinophyma: Bulbous, enlarged and red nose due to
hypertrophy.
• Narrowing (or pinched appearance) of nose in children
suffering from adenoids (adenoid facies) and rarely in
spinal muscular atrophy.
• Widening of nose—early feature of acromegaly.
• Nasal polyps.
• Epistaxis.
• Nasal discharge.
• Deviated nasal septum and its complications.
• Movements of accessory muscles—movements like alae
nasi—in respiratory distress.
Ears
Examine the ears for:
• Genetic deformities: Down’s syndrome in which the
auricles are usually small and lobule may be rudimentary
or absent.
• Helix of the ear is a recognized site of gouty tophi –
white chalky nodules of sodium biurate crystals
deposited in the cartilage.
• Trauma – hemorrhage.
• Low set ears in Mongols and mentally retarded children.
• Malformed ears are associated with congential urinary
anomalies in children.
• Thickening of skin over the ears and ear lobe is the
earliest sign of leprosy.
• Acute otitis media usually causes earache, which may
be severe, but in infants, it may present as an acute
febrile illness without local pain and auroscopy is
indicated in all such children and any patient with
headache or a hearing difficulty.
• Common abnormalities as inspection of drum are acute
inflammation.
• Wax and foreign bodies are to be given special attention.
Lips
Lips should be examined for pallor cyanosis.
• Dryness followed by desquamation, wrinkling and
dehydration. Crackling of lips is seen when lips are
imposed to cold or heat. Therefore, hydration should be
specially looked for.
• Cheilosis occurs due to riboflavin, (vit. B6) deficiency
and the line of closure become red with denuded
epithelium, peeling towards the mucocutaneous junction.
• Angular stomatitis with painful and inflamed cracks is
usually caused by ill-fitting dentures allowing saliva to
dribble out of mouth, followed by infection with Candida
albicans. Iron and vit B deficiency can also cause angular
stomatitis.
• Drug reactions like exfoliative dermatitis, Stevens-
Johnson syndrome causes severe cheilitis (may be even
with ulcers).
• Congenital syphilis causes “Rhagades”—ulcerate fissures
at the angles of the mouth along with white linear
radiating scars.
• Marked swelling of lips—angioneurotic edema or
hemangioma or due to insect bite, trauma, etc.
• Ulcers pyogenic, syphilitic, or rarely tuberculous.
• Fissure of lip in adult which fails to heal in spite of
treatment, should be regarded as a possible epithelioma
and biopsy must be adviced.
• Vesicular eruptions over lips and perioral areas are seen
in patients with herpes simplex infections and in
pneumonia.
• In anemic conditions, the lips are pale and they appear
blue in central cyanosis.
• Hare lip is a congenital deformity of upper lip and appears
to be an indentation lateral to midline. It may be unilateral
or bilateral and may be associated with cleft palate.
Teeth
Points to be looked for in teeth are:
• Number.
• Appearance.
• Any disease process.
• Caries of teeth is related to each of fluorides and requires
regular dental care. Excessive caries may indicate self-
neglect. Caries cause discoloration with cavity formation.
Irregularity and malformation of teeth may cause
ulcerations due to constant trauma.
• Discoloration is usually due to staining of teeth from
tobacco or poor hygiene. Devitalized teeth are usually
gray in appearance. The teeth may be pitted and mottled
yellow in fluorosis. Milk teeth may be discolored and
deformed in children due to long-term antibiotics
(especially aminoglycosides) treatment during infancy
or pregnancy.
• Missing teeth (usually the molars) are important in
connection with alimentary symptoms.
• In congenital syphilis (Hutchinson’s teeth), the upper
incisors are notched, separated and peg-shaped.
• Juvenile hypoparathyroidism gives rise characteristically
to poorly developed teeth.

• Delay in eruption indicates delayed development or seen
in rickets.
Gums
• Pallor—anemia.
• Excessive red color—gingivitis (inflammation of gums).
It causes bleeding to occur and a narrow line of
inflammation is seen at free border of gums and swelling
appears over the interdental papillae.
• Cyanosis—bluish-colored appearance.
• Pyorrhea alveolaris—accumulation of food debris,
bacteria and pus between the teeth and gum margin.
• Spongy red hypertrophy and bleeding on touch vit. C
deficiency (scurvy).
• Plain gingival hypertrophy is seen in epileptics who are
on prolonged therapy of phenytoin.
• Pale bleeding gums without hypertrophy is seen in blood
dyscrasias like leukemia, aplastic, anemia and pancy-
topenia.
• Halitosis (bad breath)—seen in conditions of tooth decay,
and in pyorrhea and teeth may even become loose. Pus
or even a loose tooth may be aspirated into bronchial
free and it may lead to pneumonia.
• Infected gums (especially Streptococcus) may cause
infective endocarditis, especially in patients with valvular
heart disease.
• Ulceration:
– Marked ulceration and sloughing in agranulocytosis.
– A linear or pigmented patchy line in chronic lead
poisoning or other heavy metal intoxication.
– Painful ulcero-membrane gingivitis in Vincent’s
angina.
Gum in Relation to Systemic Condition
1. Chronic lead poisoning: A stippled blue line called
burtonian line, is seen on the gums in fifty to seventy
percent of cases. It appears due to subepithelial deposits
of granules at the junction with teeth, only near dirty or
carious teeth, within a week of exposure, especially on
upper jaw. It is due to formation of lead sulfide by the
action of hydrogen sulfide formed by decomposed food
in the mouth. A similar blue line may be seen in cases of
poisoning by mercury, copper, bismuth, iron, and silver.
2. Scurvy—soft and hemorrhagic gums.
3. Acute leukemia—hypertrophical and hemorrhagic.
4. Cyanotic congenital heart disease—spongy and hemorr-
hagic.
5. Phenytoin treatment—firm and hypertrophied.
The General Examination 77
Buccal Mucosa
Stomatitis: (inflammation of buccal mucosa). The causes
are—deficiency of vit. B6 and B12 (most common cause);
trauma due to irregular and pointed teeth, ill-fitting dentures;
infections like thrush (oral candidiasis), Vincent’s angina,
aphthous stomatitis, tuberculosis, syphilis, measles like viral
infections, following antibiotic therapy. Cancrum oris is a
severe form of stomatitis seen in debilitating disease,
especially in children.
Pigmentation: Addison’s disease, and pulmonary tuber-
culosis or chronic debilitating diseases.
Koplik’s spots: Bluish white spot with a red base. They are
diagnostic of measles.
Leukoplakia: White plain plaques on buccal mucosa.
Submucous fibrosis: Painful situation which is often caused
by excessive consumption of tobacco, betel nut, betel leaf.
In this condition, fibrous tissue of mouth buccal mucosa is
replaced by submucous tissues. It predisposes to malignancy.
Chronic ulceration: It may be due to malignancy and hence,
needs biopsy for diagnosis.
Tongue
The tongue is to be examined for color and hydration. Change
in color may be due to food articles, or they may be due to
quantitative and qualitative changes in hemoglobin. Hence,
detailed enquiry has to be made into the cause of color
change.
• Color change in the tongue is easily noted :
– Pallor—anemia.
– Red tongue—Vit. B6, B12 def.
– Central cyanosis—hypoxic condition.
– Clean tongue, often red with prominent papillae—
antibiotic F/F.
– Clean tongue with diffuse atrophy of papillae—iron
or vit. B12 deficiency.
• Fiery red tongue—in scarlet fever due to hypertrophy
of fungi form papillae.
• Furring of tongue—collection of epithelial cells, micro-
organisms and food debris. Seen in those with digestive
disturbances and those who breath through mouth due
to upper respiratory tract infections or in chronic
smokers. A special condition called “tongue caking” is
seen in fever and dehydration which also leads to severe
furring congenital fissuring has no pathological
significance.
• Transient denuded islands (geographical tongue), in
conditions related to tongue papillae, is a symptomless
change and is of no known significance. It is actually
an asymptomatic inflammatory condition of the tongue
with rapid growth and loss of filiform papillae which
78 Essentials of Clinical Medicine

causes wondering red patches across the surface of the chronic smokers. A bulge on the surface of PPW is seen in
tongue. retropharyngeal abscess. Ulceration of PPW is seen in
• Bald tongue—absence of papillae, seen in pernicious agranulocytosis.
anemia, iron deficiency anemia, pellagra, syphilis.
• Leukoplakia—a precancerous condition characterized Salivary Glands
by gray opaque areas interspersed with a few red
While carrying out the examination of mouth, the opening
inflamed patches.
of parotid duct may be seen on the buccal mucosa as small
• Fasciculation of the tongue at rest—motor neuron
papillae opposite the second upper molar tooth. Purulent
disease.
infections of the salivary glands may be investigated by
• Wasting of tongue muscles—lesion of hypoglossal n.
which causes the tongue to deviate to affected pide. culturing the pus expressed through the opening of ducts
• Enlarged tongue—Down’s syndrome, acromegaly, of these glands.
myxoedema, in somes cases of amyloidosis. Causes of Enlargement of Parotid Glands
• Mumps.
Palate
• Sarcoidosis.
• Look for cleft palate. • Tumor.
• High-arched palate is congenital. It may not have clinical • Suppurative parotitis.
significance but may be present in condition of Marfan’s • Obstruction of the duct causes intermittent swelling with
syndrome or mongolism (Down’s syndrome). High pain while eating.
arching of palate may also be seen in those with mouth • Obstruction due to salivary calculi is very commonly
breather’s such as in patients with recurrent attacks of seen in submandibular ducts.
cold, cough, URIC and adenoids.
• Perforation of palate may be seen in syphylitic gumma- Lymph Glands
tous involvement.
• Uvula varies greatly in shape and size. It seldom presents Causes of Lymphadenopathy
clinical problem except to some patients, with obsessional Inflammation
anxiety. • Acute—acute lymphadenitis
• Chronic—chronic lymphadenitis due to TB
Tonsils
• Syphilis
Tonsils are massive of subepithelial lymphoid tissues • Septic causes.
scattered in the pharynx. • Filariases
• Streptococcal tonsillitis causes the tonsils to be swollen • Lymphogranuloma inguinal (Fig. 4.5, Plate 2).
and inflamed, often with pus exudating from the tonsillar
crypts. Follicular tonsillitis may cause yellowish spots Neoplasm
on the surface of the tonsils. Diphtheria causes grayish • Primary—lymphosarcoma
white membrane on the surface of tonsils and, therefore, • Secondary—carcinoma, sarcoma, malignant melanoma.
has to be very carefully differentiated from follicular
tonsillitis. Quinsy (peritonsillar abscess) causes bulging Blood Related
of ant pillar of fauces and palate on the affected side. • Chronic lymphatic leukemia (CLL)
Enlargement of the tonsils may occur in systemic • Hodgkin’s lymphoma
condition like lymphoma. Tumors of the tonsils may • Non-Hodgkin’s lymphoma.
occur either in isolation or as a part of lymphatic leukemia • HIV and AIDS.
or lymphomas.
Immunity Related
Posterior Pharyngeal Wall (PPW) • SLE
The posterior pharyngeal wall becomes red and inflamed in • Drug reaction
pharyngitis, chronic granular pharyngitis, causes multiple • Rheumatoid arthritis (RA)
granular enlargements in the PPW and is mostly seen in • Serum sickness.
 5

Respiratory System

Like all the other “System Examinations” (except the • Severe grade dyspnea for prolonged duration
“Nervous System”), the “Respiratory System” examination (chronic)
is also carried out in four steps (Fig. 5.1, Plate 2): • Type-1 respiratory failure.
1. Inspection. 3. Bronchitis obliterans with organizing pneumonia
2. Palpation. (BOOP):
3. Percussion. • Clinical features of pneumonia
4. Auscultation. • Associated features of connective tissue disorders
But before moving to systemic examination, we must • Occupational history, constant exposure to pollution.
have an approach to patients of respiratory system. 4. Lung abscess:
• H/o of pneumonia.
APPROACH TO PATIENTS OF • H/o of hospital-acquired infection / pneumonia within
RESPIRATORY SYSTEM 72 hours of admission.
• Immunocompromised state.
Approach to a Case of Respiratory Tract • Recurrent infection by Staph aureus, Klebsiella.
Infection with Weight Loss • H/o recurrent aspiration pneumonia.
• Chronic bronchitis • H/o of chronic smoking/alcoholism (chronic alco-
• Bronchitis obliterans (BO) holism causes recurrent aspiration).
• Bronchitis obiliterans with organizing pneumonia (BOOP) • H/o of dyspepsia (similar to gastroesophageal reflex
disorder).
• Chronic pyogenic infection
• H/o of diabetes mellitus.
• Lung abscess
• H/o of pyorrhea (gum infection).
• HIV/AIDS
• Pediatric age group.
• Malignancy
5. Malignancy:
• CHSP (Chronic hypersensitivity pneumonitis)
• H/o of hemoptysis.
• CHSP with eosinophilic pneumonia.
• History of paraneoplastic syndromes (ADH,
Ruling Out the Causes One by One Erythropoietin – hyperviscosity syndrome, Eaton-
1. Chronic bronchitis: Lambert syndrome, Cushing’s-like features, etc.).
• H/o of chronic smoking. 6. Tuberculosis
• H/o of constant exposure to pollution—for this you • Evening rise of temperature.
need to take occupational history. • H/o of contact.
• H/o of chronic respiratory illness. • H/o of weight loss.
• Investigation for alpha antitrypsin—for emphysema. 7. HIV/AIDS:
2. Bronchitis obliterans (BO): • H/o of chronic respiratory illness
(Inflammation of distal airways and surrounding areas) • H/o of sexual contact (sexual history) with an infected
• H/o chronic smoking person.
• H/o of recurrent viral infections • H/o of blood transfusion, drug abuse, etc.
• Clinical features of autoimmune disorders 8. Chronic hypersensitivity pneumonitis (CHP):
• H/o of hospital-acquired infections. (Farmer’s lung actinomycetes, Chlamydia, moldy hair)
80 Essentials of Clinical Medicine
• H/o chronic exposure to allergens
• H/o progressive dyspnea.
9. CHSP with eosinophillic pneumonia:
• It is an allergic phenomenon.
• Seen in tropical eosinophilic syndrome, ascariasis,
Loeffler’s pneumonia.
• H/o of chronic mild/moderate grade fever.
• Progressive weight loss.
Progressive Dyspnea
Before carrying out the inspection, it should be well known
and understood that the chest (thoracic portion of the body)
is divided into certain quadrants by some imaginary lines. It
helps us to perform the examination process in a more
accurate manner. It also gives an idea about the boundaries
of the thoracic contents. This is explained as follows:
Significance of Angle of Louis (Sternal Angle)
It is felt as a transverse ridge about 5 cm below the supra-
sternal notch. It marks the manubriosternal joint, and lies at
the level of second costal cartilage interiorly and the disk
between the fourth and fifth thoracic vertebrae posteriorly.
This is an important landmark for the following reasons:
1. The ribs are counted from this level downwards. There
is no other reliable point (anteriorly) from which the
ribs may be counted. The second costal cartilage and
rib lie at the level of sternal angle. The ribs are counted
from here by tracing the finger downwards and laterally
(because the lower costal cartilages are crowded and
the anterior parts of intercostal spaces are very narrow).
2. It marks the plane which separates the superior media
stinum from the interior mediastinum.
3. The ascending aorta ends at this level. The arch of aorta
begins and ends at this level. The descending aorta begins
at this level only.
Fig. 5.2: A. Ant wall of chest; B. Areas of thoracic region
4. The trachea bifurcates into 2 principal bronchi at this
level.
5. It marks the upper unit of the base of the heart.
6. The pulmonary trunk divides into two pulmonary arteries
just below this level.
7. The cardiac plexuses are situated at this level.
Before starting the inspection of respiratory system
proper, the examiner should make some important
assessments about the upper and lower respiratory tracts.
The examination of upper respiratory tract includes
(a) the inspection of oral cavity—oral hygiene, dental status/
hygiene, signs and symptoms of any oral pathology,
condition of tonsils, etc., (b) inspection of nose/nasal cavity
for—deviated nasal septum, nasal polyps (as seen in allergic
asthma, cystic fibrosis, Wegener’s granulomatosis, etc.),
epistaxis, recurrent attacks of cold and cough, and (c)
inspection of pharynx for—granulation, postnasal drip,
lymphoma deposits, etc.
INSPECTION (Figs 5.2 and 5.3)
Inspection is a very significant part of examination of
respiratory system because it may provide important clues
about the nature and site of the disease process.
For inspection to be accurate, the chest should be
inspected from (a) the front (it is best to examine the patient
from the foot end of the patient as it may highlight any
bulging present on any side of the chest as well as the position
of apex beat if they are visible properly), (b) the back with
the patient in the sitting position, (c) from the sides—it
solves the purpose of examination more meaningfully, and
(d) from above downwards over the shoulders of the patients,
examine the apical areas.

Fig. 5.3: Post wall of thoracic cavity (Back)
SIZE AND SHAPE OF THE CHEST
The size and shape of the chest vary with the individual.
• Chest in sthenic individual—broad, short and deep set
chest.
• Chest in asthenic individuals—long, narrow, and flat.
Normally, the chest is bilaterally symmetrical and
ellipsoidal in cross section (Figs 5.4 and 5.5). The transverse
diameter of the chest is more than the anteroposterior
diameter (the ratio being 7.5). The intercostal spaces are
broader in the front than posteriorly. There is a depression
(normal) in the sternum which is most prominent at its
lower end. The subcostal angle is acute and varies from
70°-11° (average 90°). It is more in females as compared
to males.
ABNORMALITIES IN THE SHAPE OF CHEST
This is a very important of the examination process because
there are certain disease which produce significant changes
in the shape (contour) of the chest. Missing these changes
may lead the examination on the path of incorrect diagnosis.
Fig. 5.4: The normal rib cage
Respiratory System 81
Deformities which are Symmetrical in Nature
1. Rachitic chest (also called keel breast, or pigeon chest
or pectus carnitum).
There occurs protrusion of the anterior chest wall,
with sternum and costal cartilages protruding anteriorly.
Along with anterior protrusion of the sternum and costal
cartilages, there may be a sort of depression on either
side of sternum in association with bead-like enlargement
at costochondral junction (defined as rickety rosary)
and a transverse sulcus (groove) passing outwards from
the lower end of sternum (xiphisternum) to mid-axillary
line (known as Harrison’s sulcus). Rickety rosary (seen
especially in the lower ribs) is due to enlargement of
metaphyseal end of the ribs. A similar cases of scurvy,
in which case, it is known as scorbutic rosary or
scorbutic beads. The Harrison’s sulcus are horizontal
depression on the chest wall corresponding to the
attachment of diaphragm. Their extent is from 6th and
7th costal cartilage downwards from the xiphoid process
producing transverse construction of the thoracic wall
Fig. 5.5: Cross sectional view showing shape of the chest
82 Essentials of Clinical Medicine
(sometimes instead of horizontal grooves, longitudinal
grooves may be seen on the outer chest wall. They are
produced by the softened ribs being pulled inwards due
to negative pressure in the thoracic cavity. Harrison’s
sulcus are also seen in children with chronic respiratory
disease, childhood asthma, rickets, adenoids causing
blocked nasopharynx, pigeon chest is also seen in
Marfan’s syndrome).
2. Funnel chest (also called cobbler’s chest or pectus
excavatum). In this type, the body of sternum is curved
backwards producing a deep depression in the lower
part of outer chest wall. The center of this depression
being the xiphisternal junction. The etiology may be
congenital, due to rickets in childhood or as an
occupational deformity seen in cobblers. The thoracic
cage appears to be narrow and longer. Mild deformity is
usually symptomless. Severe degrees of deformity may
produce symptoms like breathlessness (dyspnea),
palpitation (indicating shift in the position of heart or
lungs), dysphagia (due to pressure over esophagus)
chest radiography shows enlarged cardiac shadow of
the term pomfrets heart has been given to this type of
cardiac shadow. Funnel-shaped chest is also seen in
Marfan’s syndrome.
3. Barrel chest: The shape of the chest is like a barrel is the
anteroposterior diameter of the chest is equal to
transverse diameter (1:1), widening of subcostal angle
occurs, there is prominence of sternal angle, sternum
shows arching, concavity of spine is in the forward
direction (kyphotic changes) and obliquity of ribs is
decreased and they become more horizontal and appear
fixed in position of deep or mid-inspiration. The
respiratory movements of the chest are decreased and
are mainly of abdominal type. There also occurs the
hypertrophy of accessory muscles of respiration.
This condition is most commonly seen in emphy-
sema (COPD) which is an overinflation of the lungs
and their fixation in a position of overinflation.
4. Flat chest: (AP diameter : Transverse diameter = 1:2)
It is also called phthinoid chest. In this type of deformity
of chest wall, the AP diameter of chest is reduced and
the thoracic cage becomes narrow and long. In severe
cases, the sternum may reach near to the vertebral
column and scapula shows winging (alar chest). The
condition usually results from chronic nasal obstruction,
due to various reasons like adenoid hypertrophy, or from
tuberculosis or rickets in childhood.
Deformities which are Asymmetrical in Nature
These are usually associated with the deformities of the
vertebral column.
1. Scoliosis: It denotes the lateral curvature of the spine
and is the most common thoracic of the spine deformity.
The condition may be associated with some degree of
rotation of vertebral column. Due to convexity on one
side, the ribs are separated widely on that side and show
angulation at their posterior side indicating the rotation
of vertebral column. There occurs crowding of the ribs
on the concave side. The crowding of ribs causes
compression of the lungs on that side.
2. Kyphosis: In this condition, there occurs angular
curvature of thoracic spine. The convexity appears on
the posterior side. The condition is characterized by the
appearance of a lump at the back. The outer chest wall
and sternum show forward bulging resembling the
pigeon chest.
(A condition called kyphoscoliosis is also sometimes
seen which is a combination of kyhosis and scoliosis. It
may result in severe displacement of thoracic viscera.)
Bulging of Chest Wall
a. Unilateral bulging is seen in pleural effusion, pneumo-
thorax, tumors, aneurysm, empyema, cardiomegaly,
scoliosis may also give rise to unilateral bulging.
b. Localized bulging is seen in aortic aneurysm, pericardial
effusion liver abscess, tumor of chest walls.
Retraction
a. Unilateral retraction of chest wall may occur in conditions
like fibrosis, collapse, pleural adhesion, unilateral muscle
wasting seen in poliomyelitis, the condition may also
arise as a congenital abnormality like absence of pectoralis
muscles.
b. Localized retraction is seen in pulmonary tuberculosis
and pleural fibrosis (retraction especially in the lower
part of chest).
Respiratory Rate
• Normal rate – 16-20 / min (in adults)
– 40 / min (in children)
• Resp. Rate : Pulse rate = 1.4 (normal).
Causes of Increased Respiratory Rate (Tachypnea)
• Exertion and excitement exercise.
• Fever (pyrexia) due to any reason.
• Anoxemia and acidosis.
• Anemia.
• Poisoning.
• Pain while breathing (e.g. pleurisy).
 Respiratory System 83

Causes of Decreased Respiratory Rate Excessive use of accessory muscles of respiration (alae
(Bradypnea) nasi, trepezius sternocleidomastoid) by the patient indicate
• Narcotic poisoning—morphine, codeine, etc. respiratory distress:
• Brain tumor or other space-occupying lesions of brain
Table 5.2: Causes of tracheal/mediastinal shifts
(SOLS) like hemorrhages.
Causes of hyperpnea—increase in the depth of Central position Deviation towards Deviation towards
respiration are 1. Acidosis, 2. Hysteria, and 3. Brainstem same side opposite side
lesion. • Bronchial asthma
• Bronchitis Fibrosis Pneumothorax
Movements of Respiration • Bronchiectasis Collapse Hydropneumothorax
• Emphysema Thickening of pleura Pleural effusion
Usually, the chest walls shows bilateral and uniform • Lung abscesses
movements with no bulge or depression over it. Some • Interstitial fibrosis
pathological conditions cause diminution of chest wall • Pneumonia
[Remember- 3
movements.
Beautiful and Exquisite
a. Diminution of movements or one side of the chest: (pair of) LIPS].
• Pleural effusion.
• Hydropneumothorax. Rhythm of Respiration
• Massive collapse.
• Consolidation. Normal individuals have regular respiration in which the
• Fibrosis of lungs. duration of inspiration is greater than that of expiration.
• Pleural adhesion. Sometimes the respiratory process becomes irregular. Some
• Obstruction in the main bronchus. of the conditions causing irregular breathing are discussed
b. Diminution on both sides: below.
• Emphysema. The skin over the chest wall should be examined
• Bronchial asthma. for:
• Fibrosis affecting both lungs. 1. Engorged veins and collateral veins – over the out chest
• Bilateral collapse, consolidation or hydropneumo- wall indicates superior vena cava (SVC) obstruction.
thorax. The cause is generally a mass in mediastinum (may be
Table 5.1: Types of breathing
Type of breathing Description Causes
1. Cheyne-Stokes respiration (Fig. 5.6A) Period of apnea is followed by gradual Central respiration failure.
increase in the rate and amplitude of resp. Left ventricular failure.
movements which reach a peak and again Increased intracranial pressure with damage
gradually subside to apneic phase to both cerebral hemisphere and diencephalons.
Narcotic poisoning–opium, etc.
Uremia.
2. Bitot’s breathing (chaotic breathing) Respiration is of irregularly-irregular type Advanced central respiratory failure meningitis.
(Fig. 5.6B) Two or three inspiratory movements are Meningitis
superimposed upon are another before the Raised intracranial pressure.
expiratory movement. There are periods
of apnea in between several periods of
shallow or deep inspiration
3. Kussumaul’s breathing (Fig. 5.6C) Characterized by deep and rapid respiration Diabetes ketoacidosis.
(air hunger). The resp. has a sighing Alcoholics.
character Starvation ketoacidosis.
Uremia.
4. Stridor Prolonged inspiration through an obstructed Growth in mediastinum.
upper airway Laryngeal diphtheria.
Trached or laryngeal obstruction.
5. Wheeze Prolonged expiration through an obstructed Bronchial asthma.
lower airway Cardiac asthma.
Renal asthma.
6. Stertorous breathing Rattling sound in the throat Coma Deep sleep
Dying patient (Death rattle)
84 Essentials of Clinical Medicine
Fig. 5.6
neoplastic in nature). Sometimes small veins are seen
along the lateral chest wall in emphysema.
2. Subcutaneous nodular (sarcoidosis and malignancy).
3. Intercostal scar (drained pleural effusion, empyema or
pneumothorax).
4. Discharging sinuses (as in TB).
5. Empyema necessitans causes intercostal swelling close
to sternum.
Trails Sign (or Sternocleidomastoid Sign)
This is a very important sign for the diagnosis of tracheal
shift (i.e. shift of trachea from its normal midline position).
Trails sign is defined as the undue prominence of the
clavicular head of sternocleidomastoid muscle on the side
to which the trachea is deviated/shifted. This occurs because
the pretracheal fascia covering the clavicular head of
sternomastoid on that side is relaxed resulting in the
prominence of the clavicular head of the muscle on the side
of tracheal deviation (shifting).
Apex Beat
The examiner should look for the position of the apex beat.
Shifting of apex beat from its normal position (Lt. 4th
intercostal space medial to midclavicular line) indicates a
pathology in the mediastinum. The apex beat is shifted to
the side of mediastinal shift.
PALPATION
Aims of Palpation
• To confirm the findings of inspections (especially those
regarding the movements of chest wall).
• To confirm the position of the apex beat and trachea—
tactile vocal fremitus (TVF).
• To note the presence of any other findings.
Confirming the Respiratory Movements
Diminished movements overlying portion of the chest wall
is due to reduced distensibility of a portion of lung.
Therefore, any change in the movement of chest walls
should be carefully noted.
Assessing the Movements of
Outer Thoracic Wall
This can be studied under the following headings:
a. Movements of upper lobe of lung.
b. Movements of middle lobe.
c. Movements of diaphragm.
Movements of upper lobe:
Procedure: The patient is made to face the examine and
then the examiner keeps the palms of his both hands
symmetrically over the outer thoracic wall and fingers overlie
the trapezius muscles of both sides. The tips of both the
thumbs approximate each other in the midline without
touching the chest wall. After deep inspiration, the degree
of expansion is compared on both sides by involvements of
thumb away from midline.
Inference: Healthier upper lobes will cause equidistant
movements of the thumb from the midline and if any of the
lobe in affected, then the thumb will move only a little
distance from the midline.
Middle lobe movements:
Procedure: Middle lobe expands both in anteroposterior and
transverse lateral direction. However, the method described
here is more to confirm the lateral movements of middle
lobes. In this procedure, the fingers of both the hands are
kept in the corresponding axillae and palms lie flat against
chest wall.
Inference: Deep, inspiration will cause the thumbs to move
away from the midline and for normal healthy middle lobes
the movements of the thumb will be symmetrical. If any
lobe is pathologically involved, then the movements will be
diminished on the affected side.
Movements of diaphragms:
Procedure: The patient is made to lie supine. The examiner
places his hands over the lower ribs with thumbs laid along
the costal margin and their tips meeting near the xiphoid
process.
Inference: If movements of diaphragm is normal, then the
thumbs will show symmetrical movements.
 Respiratory System 85

Assessing the Movements of Posterior Mediastinal shift

Thoracic Wall To opposite side To same side
Assessing the Movements of Lower Lobe Pleural effusion Fibrosis
Pneumothorax Collapse
Lower lobe movements: Hydropneumothorax
Procedure: The procedure is very much like that done for Large tumor
assessment of upper lobe movements. The palms are placed Pleural rub: Felt as harsh grating sensations below the
over the posterior chest wall and fingers pass below the palpating hand. Rhonchial fremitus or palpable rales can be
margins of the scapula. Again, the movements of thumbs easily palpated if they are prominent.
are noted. Surgical emphysema gives a characteristic spongy feeling
Inference: Same as that for upper lobe examination in the subcutaneous tissues.
Note: Ankylosing spondylitis is the non-respiratory cause
leading to poor chest expansion. TRACHEAL SIGNS: TUG (OLLIVER’S)
The examiner stands behind the patient to raise his chin. By
Tactile Vocal Fremitus (TVF) using both his hands, the examiner holds the cricoid
On speaking, vibrations are generated by the larynx and cartilages now, if a downward tug is felt by the fingers
these vibrations are then carried out to the periphery of the during each systole of the heart, the sign is said to be positive.
lungs. These can be easily felt by the palpating hand. They The sign is positive in case of aortic arch aneurysm (AAA)
can be more clearly felt if the examiner uses the ulnae border post. The sign is said to be false positive in conditions of
of his hand because it is the most sensitive part of the palm. mediastinal tumor attached to aortic arch. The sign is false
The patient is asked to repeat certain words like “nine- negative in case of non-pulsatile aortic aneurysm (in condition
nine-nine” or “one-one-one” or one-two-three” and the of thrombosis).
vibrations are felt by ulnae border of the hand by the
examiner. It is a wrong procedure if the examiner first TENDERNESS
palpates the different areas of same side of the chest and Table 5.4: Tenderness over chest wall
shifts his hands to the other. Besides, the correct procedure
May be due to
is to compare the corresponding parts of both the sides • Local injury • Local inflammation of
simultaneously because in this way the examiner will be parental pleura, soft tissues.
able to appreciate the difference in the quality of sounds • Myositis • Osteomyelitis
coming from the two sides of the outer chest wall. • Empyema • Pyogenic abscess of liver
The conditions in which TVF is decreased are: • Amebic liver abscess
• Pyogenic abscess of liver
a. Pleural causes:
• Pleural effusion. PERCUSSION
• Pneumothorax.
• Hydropneumothorax. For percussion to be fruitful in the term of correct diagnosis,
b. Bronchial causes: the position of patient, while percussing should be given
• Bronchial asthma. utmost importance (Fig. 5.7).
• Bronchial obstruction.
c. Lung disease:
• Emphysema.
• Pulmonary fibrosis (?)
• Total pulmonary collapse (?)
• Tactile vocal fremitus/vocal resonance.
Table 5.3

Increase in TVF Decrease in TVF

Consolidation Pleural effusion
Superficial cavity Pneumothorax
Emphysema
Collapse/fibrosis
Bronchial obstruction
Fig. 5.7: Surface marking of the pleura
86 Essentials of Clinical Medicine

Positions of the Patient
In percussion of outer chest walls, the hands of patient
hang by the side of his body and he sits with his back in the
erect posture. In percussion of post-thoracic wall, the patient
is made to cross his arm over the outer chest wall and he
keeps his hands on the opposite shoulders. The patient also
bends his head forwards while percussing the lateral thoracic
wall, the patient sits with his hands held over his head.
Aims of Percussion
Percussion is carried out to assess the amount (degree) of
resonance over the various areas of chest and to find out
those areas which have abnormal note.
Basic Mechanism
In a normal individual, the percussion note is due to the
normal amount of air present in the air vesicles, air sacs
and passages. Normally, the percussion note has a low pitch.
The percussion note on the outer chest wall is usually more
resonant than that on the posterior thoracic wall because
the front of the chest has less musculature as compound to
the back.
Basic Principles of Percussion
2. The middle finger (or sometimes the index finger) of
the examiner’s right hand that is used with the middle
phalanx of pleximeter is called the plexor.
3. The movement of the percussing hand (the hand that is
used to strike) should be allowed only at the wrist joint.
The elbow joint should remain fixed while percussing.
4. The percussum should proceed from the area of normal
resonance to the area of abnormal note. This helps clear
appreciation of the difference in notes produced.
5. The pleximeter should be kept parallel (in the direction
of) to the border of the organ which is being percussed.
Sites over the Outer Chest Wall (Figs 5.8 and 5.9)
1. Medial 1/3rd of clavicle.
2. Kronig’s isthmus (supraclavicular region).
It is a band of resonance of 5 to 7 cm. In width it is
used to assess the resonance of lung apices. The
boundaries of this area are:
Medially: Scalenus muscle of neck, laterally the
acromion process of scapula, anteriorly the clavicle and
posteriorly – trapezius. Emphysema leads to hyper-
resonance and pul TB or malignancy of lung often causes
impaired resonance over this area.
3. Region just below the clavicle.
4. Intercostal spaces—especially second to sixth.

1. The middle finger of the examiner’s left hand that is
placed tightly over the chest wall (over the intercostal
spaces) is called the pleximeter. The term pleximeter is
derived from a Greek words—plexis = stroke and metron
= measure. The other finger should be kept free (away
from) from touching the chest wall.
Sites over the Lateral Wall of Chest
Intercostal space, especially fourth to seventh.
Sites over the Back
Usually involves the complete back, i.e. in the suprascapular,
interscapular and infrascapular regions.

Fig. 5.8: A. Sites for percussion—anterior and lateral chest wall, B. Sites for percussion—posterior chest wall
 Respiratory System 87

Features of Percussion over Normal Lung

• Percussion note over the normal lung tissue is low pitched
and is also called normal lung resonance.
• Percussion note is more resonant over the front wall as
compared to back because of heavy musculature over
the back.
• Relative cardiac dullness: It is the area of improved note
over the surface of the heart.
• Absolute cardiac dullness: When the percussion is
continued more medially towards the sternum, the dull
note becomes still more dull and flatter, over the area,
which is not produced by the lung tissues. The area is
of no clinical significance.

Fig. 5.9: Technique of percussion Tidal Percussion

Table 5.5: Abnormal percussion notes The lower border of the lung can be percussed up to the
6th intercostal space in midclavicular line, up to the 8th
Percussion note Description Condition intercostal space in the midaxillary line and up to 10th
1. Hyper resonant The percussion note Emphysema (generalized intercostal space in the midscapular line. The tidal percussion
note is greater in inten- or compensatory)
sity than the normal Pneumothorax
helps to differentiate upward enlargement of liver or
one [resonare (Latin) Large cavity subdiaphragmatic abscess from the right-sided parenchymal
means to resound] Congenital lung cyst or pleural disorders.
Emphysemotous bullae
Eventration of diameter Interpretation
2. Skodiac (sub- It is a peculiar quality Above the level of pleural After full range of inspiration (deep inspiration), if the
tympanic) note and is produced due effusion
to relaxation of lung previous dull note in the fifth right intercostal space on the
tissues (above the midclavicular line becomes resonant, it is an indication that
level of perfusion). dullness was due to liver (which has now been pushed down
3. Tympanic note Drum like resonance Over the hallow viscous, by the downward movement of diaphragm on deep
or tympanitic over the tension pneumo-
note thorax or over the large inspiration). In contrast, if the dullness persists even after
cavity or emphysematous deep inspiration, then it is an indication of underlying right-
bullae of lung sided prolonged or pleural pathological involvement.
4. Impaired note Due to decrease in Consolidation
the amount of air in Fibrosis
the alveoli, the lung Infiltration Traube’s Semilunar Space
fails to vibrate enough Collapse of lung
on percussion
It is present in the midclavicular line around the left 7th
5. Dull note More decrease in Consolidation space. Its relations are—on its right left lobe of liver; on its
resonance as com- Fibrosis left spleen; superiorly—heart, inferiorly—left costal margin.
pared to impaired Infiltration The presence of air in the fundus gives rise to tympanic
note. Collapse of lung
Thickening of pleura. note.
6. Amphoric Note is low pitch and Pneumothorax
resonance is characteristic in Large cavity
Interpretation
nature. It is a type of The lateral extension of Traube’s space to outer axillary line
tympanic resonance. indicates massive collapse of left lung (or left lower lobes).
Has a peculiar hollow
quality. Obliteration of Traube’s space indicates pleural effusion on
7. Cracked pot The note produced Large cavity communi- the left side. Obliteration also occurs in cases of enlarged
resonance resembles to that cating with the bronchus. left lobes of liver, fully filled stomach, fundal growth and
produced while
massive pericardial effusion.
percussing over a
broken earthenware Upward shifting of Traube’s space is seen in:
vessels. • Fibrosis of left lung.
88 Essentials of Clinical Medicine
• Collapse of left lower lobe.
• Left diaphragmatic paralysis.
Percussion in Pleural Effusion
1. Ellis “S” shaped curve:
It denotes the upper level of fluid in a patient suffering
from pleurisy with effusion. In moderate degree of pleural
effusion, the uppermost level of dullness due to fluid is
highest in the axilla (as compared to anterior or posterior
surfaces) – giving an “S” shape to the upper level of
fluid in this presentation is thought to be due to capillary
suction mechanism. As the two layers of pleura are very
close to each other in the axillae, and we know that fluid
rises to the highest level in the capillary, which is the
thinnest, therefore the fluid level reaches the highest
level in axillae. However, some believers are of the opinion
that it may be only a false radiological appearance.
2. Grocco’s triangle:
It is a triangular shaped area of dullness elicited in some
patients with pleural effusion. It can be appreciated on
opposite side of pleural effusion close to the vertebrae.
The thoracic spine forms the medial border of the
triangle. At the base of the triangle, lies the 10th intercostal
space for about 5 to 7 cm. And by joining these two
sides with each other, we get a complete triangle. The
posterior mediasternum is thought to be the reason for
this dullness.
Percussion in Hydropneumothorax
(Shifting Dullness)
Just as we elicit the shifting dullness in case of ascites, so
we do in case of pleural effusion also. Firstly, the patient is
made to sit with his back straight, and the upper level of
fluid is marked by percussing. Now the patient is made to
lie down and the same area is percussed again. Resonant
note this time indicates shifting of pleural fluid.
Percussion in Pneumothorax (Coin Test)
The examiner keeps a metallic coin over the anterior chest
wall of the patient and strikes it with another similar coin.
On simultaneous auscultation over the back of the patient,
a clear metallic sound can be heard. This is because the
sound travels through the air easily without getting
deteriorated indicating a cavity in side.
Percussion in Case of Cavity in the Lungs
When there is a communication pathway between the cavity
and the air passages (especially the main bronchi), there
occurs an alteration in the percussion on deep inspiration
and expiration. This can be better elicited when the patient
is made to breath through open mouth (Wintrich’s sign). A
change in the note appears when the patient breaths while
the mouth is closed. Another situation is seen when the
cavity has both air and fluid (partially filled cavity) this time
the percussion note over the affected area changes with
change in posture of the patient (Gerhardt’s sign).
Table 5.6: Stony dullness and impaired note
Stony dullness Impaired note
Pleural effusion Pneumonia
Massive collapse-consolidation Collapse
Solid tumors Thickened pleura
Fibrosis
Sequestration of lung
Abscess
Infarct
AUSCULTATION
Aims
1. To find out the type and amplitude of breath sounds.
2. To know the quality and amplitude of conducted voice
sounds.
3. Additional sounds—their number, position; and type.
General Principles
1. Most of the sounds coming to the chest wall from the
underlying lung tissues and air passages lie in the low-
frequency range (low pitch). Therefore, the bell (bell of
the stethoscope) with a rubber rim over it should be
preferred over diaphragm (the diaphragm of the
stethoscope). There is another significant reason why
the bell is preferred. The skin and hair under the
diaphragm during deep breathing produces some sounds,
which may be confused with pleural rub or crepitations.
The third important reason for selecting the bell is the
difficulty in making full contact between the diaphragm
and chest wall in case of debilitated and thin individuals.
2. Sounds produced by the partial closure of nose (due to
discharges present in the nasal cavity) can be avoided
by making the patient to breath through his mouth (fully
open) while performing auscultation.
3. Avoid auscultation within 2 to 3 cm. From the midline,
it generally has bronchial character.
The auscultation should be carried out in a very
systematic manner. The sequence of auscultation should
be—the outer wall of chest, the axillae and the back.
 Respiratory System 89

Area of Auscultation • Generalized (emphysema)

• Localized (obstruction by tumor)
You should auscultate interiorly from above the clavicle
• Bronchial asthma.
down to the 6th rib, laterally from axilla to 8th rib and
• Lung collapse.
posteriorly down to the level of 11th rib.
b. Due to reduced conduction to chest wall:
• Thick chest wall (obese, thick musculature).
BREATH SOUNDS
• Pleural effusion.
As the air passes in and out of the lungs during inspiration • Pleural thickening.
and expiration, the breath sounds are produced. On • Small pneumothorax.
inspiration, a strong force of air rushes into the lungs after
passing the larynx, trachea ultimately reaching the alveoli. Bronchial Breath Sounds
Due to this strong gush of air, a kind of turbulence is produced
• Characterized by active inspiration due to the passage
when the inspired air strikes the bronchi at the bifurcations.
of air into the bronchus.
Similarly, during expiration also, a kind of turbulence is
• Alveolar phase is absent invoking inspiration also to be
produced by the outgoing air. The sound produced by the
active and hence the duration of expiratory and
turbulence of air is transmitted to the chest wall through
inspiratory sound is same. The ratio is 1:1.
underlying parenchymal tissues. The vibration of the alveoli
• Sound has a hollow bronchial character and rustling is
(by the air) also contributes to the production of normal
absent, it has blowing quality too.
rushing sound of breathing
• Bronchial breath sound is high pitched, with guttural
quality.
Type of Breath Sounds (Fig. 5.10)
• There is a pause between inspiration and expiration.
Vesicular Breath Sounds • They are either heard over areas of lobar pneumonia
The important features are: due to consolidation or over collapse of the lung when
• Low pitch, rushing in nature. the overlying bronchus or main bronchus remains patent.
• Heard all over the lung parenchyma (except in inter- Also heard over areas affected by pulmonary infarction
scapular area and near right apex. Here the sounds are of lungs.
bronchovesicular due to its closeness to main bronchi). Table 5.7: Types of bronchial breathing
• Inspiratory sound has rushing character. It is more
prolonged than expiration and is also better audible. Types Character Condition
• Expiratory sound is fainter and shorter in duration than Tubular • High pitched • Consolidation
inspiratory sound (about 1/3rd of it) ratio of inspiratory • Appear shrill • Above the level of pleural
effusion
sound : expiratory sound = 3:1. There is no pause • Over a cavity
between inspiratory and expiratory sound (passive Cavernous • Low pitch • Over cavities
expiration occurs because of the elastic recoil of alveoli, • Hallow tone • Communicating pneumo-
which occurs maximally in the early phase of expiration thorax
giving an apparent impression of short expiration). • Resemble sound
produced by blowing
Causes of diminished vesicular breath sound are: into an empty vessel
a. Due to reduced air flow: Amphoric • Low-pitched bronchial • Over cavities/especially
sounds with high- over thin-walled tuber-
pitched over tones culosis cavities.
• Metallic quality. • Over cavities/especially
• Resembles sound pro- over thin-walled tuber-
duced by blowing culosis cavities.
through a hallow pipe • Over pneumothorax com-
municating with the lung

Bronchovesicular Breath Sound

Fig. 5.10: Breath sounds
The features are:
• Expiratory phase is equal to or even more than inspiratory
phase (due to increased resistance in the airway due to
spasm).
• No pause between inspiration and expiration.
90 Essentials of Clinical Medicine
• When the alveoli contain a mixture of air and fluid,
bronchovesicular sounds are produced.
• Inspiratory phase is similar to that of vesicular breathing.
• The expiratory phase is prolonged and harsher.
• Duration of inspiration is equal to expiration (1:1).
• No pause between expiration and inspiration.
• They are heard in pneumonitis, tuberculosis, congestive
cardiac failure, bronchial asthma, chronic bronchitis,
and emphysema.
Conditions in which the breath sounds are absent:
• Pneumothorax.
• Pleural effusion (severe).
• Thickening of pleura.
• Collapse of lung.
• Severe attack of asthma.
• Congenital conditions like agenesis of lung tissues.
• Surgical procedures like pneumonectomy.
Adventitious Sounds
The adventitious sounds are those vibrations which are
produced by pathological process in the respiratory tract in
lungs, tracheobronchial tree or pleura. Whenever an
adventitious sound is heard, it always indicates underlying
pathology.
RHONCHI (also called Wheeze)
Rhonchi is a continuous musical sound caused by narrowing
of the lumen of a respiratory passage. They may be low
pitched (sonorous), arising from large airways or high
pitched (sibilant) arising from small airways.
Rhonchi are produced whenever a portion of tracheo-
bronchial tree is narrowed, either by the spasm or
sometimes due to presence obstructing neoplasm or due to
inflammatory swelling (such as bronchitis or allergy).
Narrowing of bronchi during expiration makes the rhonchi
better audible during expiration.
Causes of Rhonchi
i. Bronchial asthma.
ii. Chronic obstructive pulmonary diseases (COPD)
iii. Bronchitis.
iv. Tumors.
v. Cardiac failure (congestive heart failure).
vi. Allergic conditions like tropical eosinophilia.
Classification of Rhonchi
a. Sonorous rhonchi: The features are:
• Produced due to spasm of larger bronchi.
• Low pitched.
• Hollow character.
• Best heard in the early phase of inspiration.
b. Sibiliant rhonchi: The features are:
• Produced due to spasm of smaller bronchi.
• High pitched.
• Shrill in quality.
• Best heard at the end of expiratory phase.
c. Intermediate rhonchi: The features are:
• Produced due to spasm of intermediate sized bronchi.
• Medium pitched (between sonorous and sibilant).
d. Polyphonic rhonchi: The features are:
• They are complex musical sounds produced during
expiration.
• The sound contains various notes of different pitch.
• Usually, all the components of musical notes start at
the same time, continue and also end together in
expiration.
• They are usually produced by the osillation of various
large bronchi simultaneously, e.g. emphysema.
e. Monophonic rhonchi: The features are:
• They are single musical sounds resulting from
localized narrowing of airway.
• Monophonic rhonchis can be further divided into
(i) Fixed monophonic and (ii) Random monophonic
rhonchis.
RALES/CRACKLES/CREPITATIONS
Rales are a type of adventitious lung sounds heard on
auscultation of the chest produced by air passing out retained
airway secretion or the sudden opening of collapsed airways.
It may be heard on inspiration or expiration. A crackle is a
discontinuous, non-musical adventitious lung sound as
opposed to a wheeze which is continuous. Crackles are
described as fine or coarse or medium rales. The classi-
fication is made on the basis of their pitch and also on the
predominant phase of inspiration in which they occur.
a. Coarse rales: Louder, rather long, low pitched, lung
sounds, arise from bronchus and bronchioles. The coarse
inspiratory and expiratory crackles indicate excessive
airway secretions.
b. Fine crackles: Soft, very short, high pitched lung
sounds. Fine late inspiratory crackles are often heard in
pulmonary fibrosis and acute pulmonary edema. Fine
rales are also called crepitations. They arise from alveoli
and are due to the presence of fluid in the alveoli and
hence heard only at the end of deep inspiration. The
sound of crepitation is usually compared to that produced
by rubbing a lock of hair between the fingers.
Crepitations are present in conditions which produce
 Respiratory System 91

fluid in the alveoli. For example, tuberculosis, pneumonia, a. Laryngeal stridor:

left ventricular failure (LVF) or pulmonary edema. • High-pitched sound.
c. Medium rales: Produced by small sized bronchi. They • Auscultated over larynx.
are best audible in mid inspiratory phase. They have • Heard in laryngeal obstruction due to various causes
high pitch (as compared to coarse rales). Commonly such as foreign body, diphtheria, etc.
seen in conditons like bronchiectasis. b. Tracheal stridor:
• Low-pitched sound.
Common Causes of Rales • Auscultated over trachea.
• Heard in tracheal obstruction due to various causes.
1. Inflammatory causes like bronchitis, broncho-
pneumonea and pneumonia. Table 5.9: Differences between stridor and wheeze
2. Lung abscess, cavitation of lungs and bronchiectasis. Features Stridor Wheeze
– Left heart failure – rales increase by exercise.
1. Phase of respiration Inspiratory Expiratory
– Pulmonary edema, congestion. 2. Portion of respiratory tract Upper airway Lower airway
– Pulmonary fibrosis. 3. Etiology Foreign body Asthma
– Airway obstruction (severe).
According to the phase of respiratory cycle in which Pleural Rub: (or Pleural Friction Rub)
they are produced, the rales have been classified as:
1. Inspiratory rales which include: The features are:
a. Early inspiratory rales. • In a normal individual, the 2 layers of pleura: parietal
b. Midinspiratory rales. and visceral slide smoothly against each other. But in
c. Late inspiratory rales. certain pathological conditions like inflammation, a harsh,
grating friction sound is produced by two inflamed
2. Expiratory rales.
layers sliding (rubbing) against each other.
Table 5.8: Types of rales • They are produced during later part of inspiration and
Type Description Conditions associates
early part of expiration.
• Usually heard over the bases of the lungs.
1. Inspiratory Due to opening of Chronic bronchitis
a. Early larger airways which • It increases on pressing the chest wall with the chest
were closed by air piece of the stethoscope.
capturing mechanism • Disappears on holding the breath.
during previous • Audible over a localized area.
expirations, scanty, • No change of intensity coughing (whereas rales change
low pitched and
posture independent on coughing).
b. Mid Audible in the middle Bronchiectasis cavity in • Always associated with local pain and tenderness.
part of inspiratory lung abscess • Occasionally, the rub may be palpable as local fremitus.
cycle.
c. Late Delayed opening of both Fibrosis, pulmonary edema Table 5.10: Differences between rales and pleural rub
the lungs (as seen in
Rales Pleural rub
restrictive defects)
e. Expiratory Due to reopening of Seen in cases of severe air- • Not necessarily heard at Always auscultated at the base of
temporarily closed way obstruction. the base of lungs lungs
airways • Noncontinuous Continuous sound.
• At the beginning of inspi- They are heard at the end of inspi-
ration and expiration ration and beginning of expiration
Stridor • Coughing changes its intensity No such change noticeable.
• No change as applying Louder on applying pressure
Stridor is a Latin word meaning a harsh sound. It is a high pressure by stethoscope
pitched, harsh sound heard during respiration. It resembles • Usually audible over a Localized
large area.
the blowing of the wind due to obstruction of upper airways.
• No local pain or tenderness Local pain and tenderness present
They are usually produced during inspiration and are also • They are neither superficial They are both superficial and loud.
called inspiratory stridors. nor loud

Classification Succussion Splash

The stridors have been classified according to the structure Succussion splash is a type of splashing sound heard over
from which they are produced. They are: the chest area (either by stethoscope or by applying ear
92 Essentials of Clinical Medicine
close to the chest wall of the patient suddenly shaking the
patient. to and fro.
It is heard in conditions like hydropneumothorax and
diaphragmatic hernia.
Gurgling sound: Heard in case of bronchopleural fistula.
Mechanism of production may be the air entering the pleural
fluid through the fistula.
Auscultatory Vocal Resonance (AVF)
Vibration of vocal cords in the larynx gives rise to certain
audible sound (audible through stephoscope). This sound
is called vocal resonance (VR).
Procedure
The patient is made to repeat certain words like “nine-nine-
nine or “one-one-one” or “one-two-three” and the different
corresponding areas of chest wall on both sides are
auscultated one by one. The common mistakes which
students do is to completely auscultate one side of the chest
first and then shifting to other side. This is wrong. You
should alternately auscultate the corresponding areas of chest
wall.
Interpretation
Normally, the sound is not heard clearly with the
stethoscope. In fact, it is heard as a weak, rumbling sound
where words appear to mix with each other. The sound
appears as if coming from the area near to chest piece of
the stethoscope. In normal conditions, the AVF is heard
maximum at the right apex and interscapular area and louder
in men than women.
Causes of Decreased AVF
• Pleural effusion.
• Pneumothorax.
• Thickened pleura
• Emphysema.
• Bronchial obstruction (partial or complete).
• Collapse of lung.
• Fibrosis of lung (?)
Conditions in which TVF is Increased
or Altered
The TVF is altered in conditions where the lungs become
more dense.
Bronchophony:
• Sounds are louder and clear.
• The sound appears to be coming from the ear piece of
the stethoscope (rather than the chest piece).
• Syllable are not clearly distinguishable.
• Spoken pectoriloque – When lung parenchyma becomes
completely dense, the sound is heard more clearly and
hence called spoken pectoriloque.
Conditions: Consolidation, collapse of lung with the patient
(normal), bronchi, a large tumor, massive pleural effusion.
Whispering pectoriloque: The patient is asked to whisper
“one-two-three” or “nine-nine-nine” and the sound is
auscultated.
Interpretation: In normal lungs only rustling sound can be
heard. But if the sound is clear and audible, it is called
whispering pectoriloque.
Conditions:
• Massive consolidation of lung near to the bronchis.
• Cavity communicating with the bronchus.
Egophony: When AVR is auscultated as a nasal sound over
the chest wall, usually heard above the level of pleural
effusion.
Mechanism: Mechanism of production has been thought to
be the relaxation of alveolar membranes just above the level
of pleural effusion. Therefore, there occurs an alteration in
normal transmission of sound to the chest wall.
Conditions:
• Above the level of pleural effusion.
• Pneumothorax.
• Sometimes over the area of consolidation and lung
cavities partially filled with exudates (Fig. 5.11).
CASE TAKING
Respiratory System
1. A patient with low-grade fever and weight loss has poor
excursion on the right side of the chest, with decreased
fremitus, flatness to percussion, and clear cased breath
sounds on all the right. The trachea is deviated to the
left. The likely diagnosis is:
Pleural effusion
2. A 30-year-old male is admitted to the hospital after a
motorcycle accident that resulted in the fracture of right
femur. The fracture is managed with traction; three days
later, he becomes confused and tachypnoic. A petechial
rash is noted over the chest. Lungs are clear to auscul-
tation. Arterial blood gas shown PO2 of 50, PCO2 of 28,
pH of 7.49. The most likely diagnosis is:
Fat embolism
3. A patient is found to have an unperfectly high volume
for diffusing capacity. This finding is consistent with:
Intrapulmonary hemorrhage
 Respiratory System 93

Fig. 5.11: Clinical findings in: A. Right-sided effusion, B. Right-sided consolidation, C. Collapse, with bronchial obstruction
on the right-side and with patent bronchi on the left side, and D. Right pneumothorax

4. A 65-year-old man presents with progressive shortness
of breath. Other than a history of heavy tobacco use,
the patient has a benign past medical history, breath
sounds are absent, two-thirds of the way on the left
side of the chest. Percussion of the left chest reveals
less resonance than normal while you place your hand
on the left side of chest and have the patient say “ninety-
nine”, no tingling is appreciated in the hand. The trachea
appears to be deviated towards left. Which is the most
likely diagnosis?
Bronchial obstruction
5. A 65-year-old man presents for an evaluation because
he is “feeling poorly”. Symptoms include morning
headache, and poor sleep quality. He is quite tired during
the day and frequently falls asleep while he reads or
watches television. Physical examination reveals a ruddy
complexion but is otherwise normal except for elevation
in hematocrit and plasma HCO3 concentration. Poly-
sonography demonstrates a decreased ventilatory
response to hypercapnia and many episodes of central
apnea (no diaphragmatic activity) is noted. The maximum
respiratory pressure that he generates against an occluded
airway is general. Which is the most likely cause of the
patient’s problem?
Carotid body dysfunction
94 Essentials of Clinical Medicine

BRIEF ILLUSTRATION OF SOME If any of these is present, then it is an exudative type of

IMPORTANT CASES pleural effusion otherwise transulative.
Pleural Effusion Transulative
History taking in Pleural Effusion • ECF
• Embolus
• Chest pain—usually localized, increases with respiration,
• Nephrotic syndrome
plural pain disappears means that information subsided
a pleural effect has developed after dry pleurisy. Exulative—TB
• Non-production cough—dry. Pleural biopsy (closed biopsy): It is sometimes the last
• Pain referred to epigastrium if medial part of diaphragm option to test/confirm pleural effusion.
involved, pain is referred to shoulder—if used lateral
part involved. Table 5.11: Characteristics of pleural fluid
• History of fever with evening rise. Tests Transudate Exudate
Findings in a Case of Pleural Effusion Color Clear Yellow
Protein Less than 3 gm% More than 3 gm%
1. Indrawing of ICS (massive) LDH Low-less than High-greater than 1000
2. More resp. movement on normal side 1000 IU/L IU/L
3. Collapsed lung on affected side Pleural fluid/serum Less than 0.6 More than 0.6
4. Organization of fluid, fibrosis and thickening - size is LDH ratio
decreased Glucose Same as blood Less than 30 mgm %. In
empyema, rheumatoid
5. Percussion—stony dull note arthritis, malignancy
6. Shift of mediasternum to normal side effusion
7. Trachea and heart also shift More than 500 I.U in
8. Auscultation. Amylase pancreatitis
Specific protein C3 C4 complement. Low is
Massive SLE and rheumatoid
arthritis
• Almost absent breath pH More than 7.3 Less than 7.3
• No added sound Specific gravity 1010 More than 1010
Cytology Under Over 100,000/cumm suggest
Moderate a. RBC 10,000/cu mm infarct, traces neoplasm
• Dull note in affective area, shifting dullness. b. WBC Over 1,000, 50% lympho-
cytes, 50% polymorphs, TB,
Resting neoplasm, empyema, 10%
• Plueral rub harsh, grating feeling at peak of inspiration eosinophilic
c. Mesothelial cells Collagen disorders 10-20%
• To differentiate it from pericardial rub is that we ask to neoplasm
hold breath pericardial rub continues. d. Malignant cells Malignant effusion
9. If bronchopleural fistula is present—then we can get
bronchial sound. Etiology of Pleural Effusion
Investigations Table 5.12: Causes of transudative and exudative pleural effusion
• X-ray chest—costophrenic angle is obliterated. Transudative Exudative
• USG (50 ml can also be detected)
• CCF • Acute practerial pneumoniles
• Thoracocentesis (diagnostic and therapeutic) PTB
(Pleural effusion can be transulate and exudate). • Cirrhosis • Pancreatitis
– Routine examination • Nephrotic syndrome • Esophageal perforation
– Protein and LDH • Myxoedema • Liver spleen
– Glucose and amylase • Constructive pericarditis • Hemothorax
• Meige’s syndrome • Drugs—Methysergide,
– T and B cell count Dantrolene
– Specific gravity. • Peritoneal dialysis • Chylothorax
• Malignancy
Light’s Classification • Collagen disorders
1. Pleural fluid protein / SP (serum protein) > 0.5 • Pulmonary embolism
2. Pleural fluid LDH/Serum LDH > 0.6 • Miscellaneous—asbestos,
uremia, Dressler’s synd.
3. Pleural fluid LDH > 2/3 normal serum LDH.
 Respiratory System 95

1. Tuberculosis 3. Causes below diaphragm:

– About 80 to 90 percent causes exudative pleural – Subdiaphragmatic abscess
effusion – Amebic liver spleen
– Due to hypersenstivity in lungs 4. Clinical differentiation between a case of pleural
– Fever low grade effusion and hydropneumothorax:
C/F – Same – Shifting dullness present.
Diagnosis – The upper level of pleural effusion is not horizontal
– Thoracocentesis but is so in hydropneumothorax.
– WBC count—lymphocyte Causes of Chylous Pleural Effusion
– Straw colored
– ADP estimaition Fluid is milky, with low cholesterol concentration
– PCR (Polymerase Chain Reaction) • Lymphoma.
– Routine microscopy • Lymphatic obstruction.
– AFB (but result – after 4 weeks) • Trauma.
– Culture • Carcinoma lung with mediastinal spread.
T/t– SCC (short course chemotherapy). • Idiopathic.
2. Effusion with pneumonia • Obstructions to thoracic duct.
– Along with parenchymatous involved, it can also • Trauma to thoracic duct.
affect pleura (parapneumonial effusion) • Thrombosis of left subclavian vein.
– USG, CT chest, X-ray. • Retroperitoneal fibrosis.
C/F – High-grade fever, consolidation, cough and
pneumonia on one side – may Causes of Hemorrhagic Pleural Effusion
T/t – Streptokinase (2.5 lacs of streptokinase or • Trauma
1 lac of urokinase) • Malignancy in pleura
3. Malignant pleural effusion: • Primary mesothelioma
– Lung cancer—70 to 80 percent • Secondary to bronchogenic Ca
– Breast Ca—70 to 80 percent • TB occasionally
– Lymphoma—70 to 80 percent • Bleeding diasthesis—purpura, hemophilia
– But there may be other causes also. • Acute hemorrhagic pancreatitis
Signs and symptoms • Coxsackie viral infection.
– Rapid development of pleural effusion • Patients on anticoagulant therapy.
– Sudden onset dyspnea.
– Not fever Causes of Recurrent Pleural Effusion
Diagnosis / T/L: • Mesothioloma.
Pleurodysis ? (Putting sclerosing agent slowly between • Lymphoma.
2 pleura) • Secondary bronchogenic carcinoma.
(Putting doxycycline soln slowly bet 2 pleura)
4. CCF associated Pl. effusion: Causes of Acute Pleural Effusion
– Mostly bilateral • Trauma.
– Use diuretic therapy and a few days after it resolves. • Pancreatitis.
– Thoracocentesis. • Pulmonary infarction.
• Rupture of esophagus.
Differential Diagnosis of Pleural Effusion • Dissecting aneurysm of aorta with leak into pleural cavity.
1. Causes in lung
– Collapse. Drugs Causing Pleural Effusion
– Fibrosis. Practolol, Methylsergide, procainamide, hydralazine,
– Hydatid cyst. nitrofurantion, sulfa drugs, PAS, salicylate.
– Consolidation. Causes of Both Emulative and
2. Causes in pleura Transudative Pleural Effusion
– Pleural effusion.
– Emphyema. • Amebic liver abscess—reactive effusion—transudation
– Mesothelioma. after rupture—exudating pericardial.
96 Essentials of Clinical Medicine

• Myxoedema usually exudate, with pericurchial effusion • Pleural adhesions

transudate. • Bronchiectasis.
• SLE exudate, with pericordial effusion transudate.
Table 5.13: Causes of dullness and hyper-resonance over base of chest
• CCF transudate, with diuretic therapy cell count may
increase and appear as exudate. Dullness over base of chest Hyper-resonance over base
of chest
Causes of Bilateral Effusion
Pleural causes Pneumothorax
• Transudate – CCF, nephrotic syndrome myxoedema. Pleural effusion Eventration diaphragm
• Exudate – TB, septicemia, multiple. Empyema Phrenic nerve palsy
Pleuropulmonary metastasis and drugs. Hemothorax Large empty cavity
Lung causes Emphysema
Yellow Nail Syndrome Consolidation Compensatory emphysema
Collapse Empty cyst
• Hypoplasia of lymph nodes.
Fibrosis
• Edema of limbs. Hydatid cyst
• Dystrophic changes in nails. Causes below the level of diaphragms
• Intractable pleural effusion. Subdiaphragmatic abscess
Liver abscess
Viral Causes of Pleural Effusion
• Adenovirus. EMPHYSEMA, CHRONIC BRONCHITIS,
• Influenza. BRONCHIAL ASTHMA
• Cytomegalovirus.
• Infective hepatitis. Clinical Features of Emphysema
• Epstein-Barr virus. A. Symptoms:
• Breathlessness.
Diagnosis of a Case of Pleural Effusion • Cough with expectoration.
In massive effusion, patients would have orthopnea and • Wheezing
will like to lie down on the affected side. Absent or diminished • Weakness
movement of chest on effected side. Bulging on the affected • Headache, drowsiness.
side. Trachea shifted to opposite side. Vocal fremitus (VF) • Coma due to ventilatory insufficiency—CO2 narcosis.
diminished on the affected side with stony dullness on B. Signs:
percussion on the affected side. Ellis S-shaped curve, • Middle or old age male mostly affected.
skodise resonance or bony resonance above pleural effusion. • Central cyanosis.
If the effusion is on the left side, obliteration of Traube’s • Fast respiration
space is present. A triangle area of dullness against the • Decubitus propped up.
vertebral column at the back of opposite lung (grocco
triangle). On auscultation, there is diminished absent breath Essentials of Diagnosis
sounds with bronchial breathing at the upper level of pleural
• Barrel-shaped chest.
effusion (Aegophony). Diminished vocal resonance.
• Inspiratory-expiratory difference is reduced, normal is
Quantity of Fluid more than 5 cm that is 2 inch chest is fixed.
• Accessory muscles working.
• Clinical signs are produced by 300 ml fluid in pleural • Ribs more horizontal.
cavity. • Subcostal angle wide.
• Radiological signs with 150 cc of fluid. • Sternum arched, upper dorsal spine kyphotic, supra-
clavicular fossa full, apex not visible.
Complications of Pleural Effusion
• Spread to pericordium and peritoneum. Findings on Palpation and Percussion
• Acute miliary TB • Hyper-resonant.
• Pulmonary edema • Liver dullness and cardiac dullness obliterated. Apex beat
• Pulmonary embolism not localized.
• Venous thrombosis • VF, VR decreased, breath sounds decreased. Vesicular
• Permanent collapse breathing. Liver and spleen palpable.
 Respiratory System 97

Complications of Emphysema • Congenital cyst.

• Klebsiella.
• CCF
• Bronchogenic cyst.
• Acute respiratory failure, chronic respiratory failure
• Bronchogenic carcinoma.
• Spontaneous pneumothorax • Malignancy.
• Secondary infection—pulmonary tuberculosis • Actinomycosis.
• Polycythemia. • Pseudocavities—emphysematous bullae.
• Papilloedema. • Hydatid cyst rupture.
• Sleep apnea.
• Nocturnal hypoxis. Causes of Clubbing in a Case of PTB
• Respiratory muscle dysfunction. • Massive fibrosis.
• Carbon dioxide narcosis. • Bronchopleural fistula.
• Pulmonary emboli and thrombosis. • Associated secondary bronchiectasis.
• Amyloidosis.
Cheyne-Stokes Breathing Causes of Hemoptysis
It is seen in: • PTB
• Healthy infants. • Mitral stenosis.
• Adults during sleep. • Bronchiectasis.
• High altitude. • Lung abscess.
• Severe CCF. • Carcinoma bronchus.
• Uremia. • Anticoagulant therapy.
• Narcotic poisoning. • Goodpasture’s syndrome.
• Raised intracranial tension.
• Severe pneumonia. Causes of Hypotension
Acute: Shock, dehydration, hemorrhage, aluminum phos-
Table 5.14: Differences between broncial asthma and cardiac asthma
phide poisoning, Waterhouse-Friedrichson syndrome, acute
Feature Bronchial asthma Cardiac asthma MI with LVF.
• Past history Allergy and atopy No H/o. allergy
positive
Chronic: Addison’s disease, Sheehan’s syndrome,
• Family H/o Late night Negative Shydragger syndrome, postural hypotension in autonomic
• Onset Scanty and tenacious Early morning neuropathy due to DM.
• Expectoration +++ Profuse, pink and
frothy Cough (> 2 months) in TB
• Wheeze (wheeze) + +
• Cyanosis Yes + It is due to:
• Pulsus paradoxus No No • Post-tubercular bronchiectasis
• Pulsus alternans Yes • Drug failure
• Liver dullness and
cardiac dullness • Residual cavity
• Chamber hyper- May be obliterated Cardiomegaly • Fibrosis.
trophy
• Heart sounds RVN LVH Signs of Cavity
• Rhonchi Muffled Gallop rhythm
• Crepitation + + a. In empty cavity, the following signs are seen:
• May have Silent chest +++ Increased VF, increased VR, presence of bronchial
Breath sound not breathing, resonance on percussion, whispering
altered pectorlique.
b. In cavity filled with secretion:
PULMONARY TUBERCULOSIS
VF decreased, VR decreased, no breath sound, per-
Differential Diagnosis of cussion is dull, VP is absent.
Cavity in the Lungs Common Complications of Pulmonary Tuberculosis
• TB • Hemoptysis
• Lung abscess. • Miliary TB
98 Essentials of Clinical Medicine

• Spontaneous pneumothorax resistance like AIDS, chronic, alcoholism, DM, etc.

• TB empyema Pneumonia due to connective tissue disorders.
• Bronchiectasis
• Disseminated TB-TB meningitis Factors Predisposing to Pneumonia
• TB abdomen • Unconsciousness—alcoholism, seizures, general
• Secondary amyloid anesthesia
• Cor pulmonale • Coma—in all these states there is suppressed cough
• Scar carcinoma. reflex.
• Old age.
Different Types of TB According to Parts Affected
• Thoracic and upper abdominal surgery.
• Pulmonary • Neuromuscular disease.
• Serosal
• Smoky impaired ciliary movements.
• CNS
• COPD, CCF, right to left cardiac shunts pulmonary
• Tonsillor
congestion.
• Bones and joints
• Mesenteric • AIDS.
• Intestine • Altered immunity—hypogammaglobulinemia, IgA
• Genitourinary efficiency, patients on steroid and anticancer therapy.
• Cutaneous
• Rarely thyroid, larynx, adrenal gland. Differential Diagnosis of Pneumonia
• Pleural – Not confined to lobe or segment. No
Pneumonia effusion expectoration, stony dullness present.
Clinical Signs of Lobar Pneumonia X-ray chest shows no air broncho-
gram. Both cardiophrenic and costo-
• Inspection – Movements diminished on affected phrenic angles are obliterated.
side, ale nase working
• Pulmonary – No fever. Hemoptysis present.
• Palpation – Vocal fremitus increased, trachea is
infarction Predisposing factors like heart disease,
central.
venous thrombosis and prolonged
• Percussion – Dullness.
immobilization.
• Auscultation – Vocal resonance increased.
• Bronchogenic– Patch of pneumonia adjacent to man.
– Bronchial breathing present.
carcinoma Hilar lymph node enlarged
– Crepitations appear during resolution.
• Atelectosis – Mediastinal shift to the side of lesion.
Complications of Pneumonia Postoperative trauma and foreign body
• Pulmonary – Delayed resolution, bronchiectasis, are the predisposing factors.
lung abscess. • Extrinsic – Exposure to allergen, fine crepts all
• Pleural – Pleural effusion, empyema, pyopneu- allergic over the lungs. Ground glass or nodu-
mothorax. alveolitis lar shadow in X-ray chest, raised IgA
• Cardio- – Endocarditis, pericarditis, cardiac and IgG.
vascular arrhythmia, peripheral circulatory • Subphrenic – H. amebic liver abscess, right dome
failure, CCF. raised and immobile.
• Neurological – Meningitis, cerebral abscess.
• Non-specific – Herpes labialex, septicemia shock, Causes of Recurrent Pneumonia
deep vein thrombosis. • Underlying bronchiectasis.
• Immunocompromised host.
Causes of Delayed Resolution in Pneumonia • Esophageal disease leading to frequent aspiration of
Pleural effusion, TB, malignancy, fungal pneumonia, esophageal contents, e.g. achelasia cardia, carcinoma
inappropriate therapy or inadequate therapy, decreased host of esophagus, stricture of esophagus.
 Respiratory System 99

Table 5.15: Clinical features of penumonia caused by various organs

Pneumococcal Staphylococcal N. meningitidis Klebsiella Pneumoniae H influenzae pneumoniae

pneumonia pneumonia pneumoniae
Abrupt onset Infants and younger Miliary Chronic debilitated patients In patients over 50 yr with

children COPD, alcohol.

Labor distribution Common in chronic Recruits Elderly Bilateral, diffused
lung disease
Homogeneous and debilitated patient Patchy Alcoholic and diabetics Bronchopneumonia
opacity
Air-filled Productive cough Lower lobe involved Signs of consolidation in upper Signs of effusion
bronchogram lobes are accompanied by effusion
Fever comes down Pleuritis, lung abscess Cavitation and lung abscess occur
by lysin
Inappropriate ADH X-ray shows unilateral Suptum shows gram-negative bacilli Gram-negative organism in sputic
bronchopneumonia with Bulging of interlobar fissure in chest X-ray chest shows bilateral diffuse
pleural effusion or X-ray along with consolidation, bronchopneumonia
bilateral countating lesion effusion and abscess are seen
Gram-positive cocci in Patients bring out red currant Consolidation
sputum. jelly sputum Pleural effusion
Complications like
emphyema and pneumo-
thorax.
Atypical Presentation of Pneumonia • Amphoric breathing in bronchopleural fistula (open
• Altered sensorium, in old age pneumothorax).
• Jaundice • Coin test positive.
• Cyanosis Auscultatory Signs of Consolidation
• Pain in epigastrium due to involvement of diaphragma
pleura in basal pneumonia • VR increased.
• Pleuritic pain radiating to shoulder due to involvement • Bronchial breathing present.
of lateral part of diaphragm • Whispering pectoriloque present, bronchophony present.
• Shock due to Addison’s crisis. Auscultatory Signs of Collapse
Causes of Non-bacterial Pneumonia • Breath sounds decreased, no adventitious sound present.
• Lipid pneumonia • VR decreased.
• Loeffler’s pneumonia • Bronchial breathing if the patient’s bronchus present
• Irradiation pneumonia above the collapsed lung.
• Hamman-Rich syndrome Table 5.16: Differences between phneumothorax
• Pulmonary alveolar proteinosis and hydropneumothorax
• Wegener’s granulomatosis Pneumothorax Hydropneumothorax
• Cholesterol pneumonia Hyper-resonance Lower part dull with upper part hyper-resonant
• Uremic pneumonia. No dullness Dullness up to a horizontal level
No splash Succussion splash present
Hydropneumothorax/Pneumothorax No shifting dullness Shifting dullness present

Diagnostic Signs of Hydropneumothorax Coin Test

• Straight line on percussion dullness in axilla is not at a
higher level compared to anterior and posterior parts of
chest. In pleural effusion, one sees higher level in axilla.
• Succussion splash.
• Shifting dullness.
• Auscultatory signs of pneumothorax
• Air entry poor, breath sounds decreased
• VR decreased.
Coin test is done to diagnosis pneumothorax. A stethoscope
is applied in front of chest and the examiner puts a coin flat
on the back and strikes on it with another coin. A peculiar
metallic sound is heard tips ringing of a distant bell.
Causes of Pneumothorax
• Rupture of subpleural emphysematous bullae.
• Subpleural trabecular focus.
100 Essentials of Clinical Medicine

• Penetrating injury to chest. ECG Changes in Pneumothorax

• Rupture of honeycomb lung. • Right side shift of QRS axis.
• Bronchiectasis. • Decreased T in precardial leads.
• Rupture of esophageal carcinoma. • Phasic voltage alternans.
• Gas forming organism in pleura. • Changes are more with left pneumothorax
• Rupture of staphylococcal abscess.
• Congenital cyst rupture. Complications of Pneumothorax
• Bronchial asthma, whooping cough.
• Failure to re-expand.
• Cystic fibrosis.
• Recurrence.
• Endometrial pneumothorax—seen in females, due to
• Respiratory failure.
endometrosis.
• Hemopneumothorax.
• Bronchogenic carcinoma.
• Pyopneumothorax.
Table 5.17: Differences between large pulmonary • Re-expansion pulmonary edema.
cavity and pneumothorax • Acute cor pulmonale.
Pnemothorax Pulmonary cavity • Pneumomediasternum.
Shift of trachea present No shift of trachea • Subcutaneous emphysema (also called surgical emphy-
Breathlessness No breathlessness sema).
Signs are generalized anterior, posterior Localized • Thickened pleura.
Amphoric breath sounds present Cavernous bronchial breathing
Abrupt onset Gradual onset
Chest pain present No chest pain Points to Remember
Movements decreased generalized Locally restricted
Coin test positive Negative Tympanic Note on Percussion
• Pneumothorax.
Traumatic Causes of Pneumothorax • Superficial empty big cavity.
• Pleural biopsy. • Over emphysematous bulla.
• Lung biopsy. • Subpleural lung cyst.
• Transbronchial aspiration. • Sliding hiatus hernia—left side.
• Thoraconcentesis.
• Subclavian vein occlusion. Causes of Tracheal Shift without any
• Patients on ventilator and with positive expiratory Lung Pathology
pressure. • Severe scoliosis.
• Non-iatrogenic chest trauma. • Enlarged lymph nodes in one side of neck huge
Causes of Bilateral Pneumothorax enlargement of one lobe of thyroid gland.
• Aneurysm of arch of aorta.
• Emphysema.
• Any superior mediastinal growth.
• Cystic disease of lung.
• Rupture of bilateral apical bleb. Traube’s Space
• Bilateral primary spontaneous pneumothorax.
It becomes dull in:
Radiological Signs of Tension Pneumothorax • Left-sided pleural effusion.
• Displacement of trachea. • Enlarged left lobe of liver.
• Collapsed lung. • Enlarged or ruptured spleen.
• Depressed diaphragm. • Situs invertus totalis.
• Sulcus sign—X-ray shows deep lateral costophrenic • Achalasia cardia.
angle on the involved side. • Massive pericardial effusion
 Respiratory System 101

CHEST RADIOGRAPHS (Figs 5.12 to 5.17)

Fig. 5.12: Chest radiograph of carcinoma of lung. Fig. 5.14: Chest radiograph of carcinoma of lung. This
This patient has left hilar mass patient has a large mass in the right upper lobe

Fig. 5.13: Chest radiograph showing rising fluid level in left Fig. 5.15: Chest radiograph post-pneumonectomy
hemothorax rising fluid level in left hemothorax
102 Essentials of Clinical Medicine

Fig. 5.16: Pneumothorax showing mediastinal shift and Fig. 5.17: Retrosternal goiter causing deviation
compression of contralateral lung of trachea (arrows)
 6

Alimentary System

The human alimentary system is the most complex system 28. Proteinuria, anuria, oliguria, polyuria, nocturia, dysuria
of the body next only to the nervous system. The gastro- 29. Urinary frequency, urgency, urinary incontinence
intestinal tract consists of various interconnected organs enuresis
and perhaps, the alimentary system is the only system in 30. Pyuria, hematuria, isolated hematuria without
our body that has such a variety of organs, each performing significant proteinuria, hemoglobinuria
different functions (control of passage, digestion, absorption 31. Pneumaturia—rare symptoms consist of passing air
and removal of ingested food materials). bubbles in urine, most often caused by a fistula bet-
The history taking plays a highly crucial role in the process ween bladder and color usually as a diverticular
of diagnosing a gastrointestinal tract (GIT) disorders. The abscess or a malignant tumor.
various important symptoms of GIT disorders are:
1. Pain in abdomen Examination of Alimentary System
2. Dysphagia/odynophagia (painful swelling) The examination of alimentary system includes:
3. Heart burn (Pyrosis) a. The general examination; b. The systemic examination.
4. Indigestion (dyspepsia)
5. Flatulence and belching The points to be noted in the general examination of alimen-
6. Hiccups tary system are as follows.
7. Vomiting General Appearance
8. Constipation and diarrhea Whether the patient appears to be in severe pain, agony, or
9. Abdominal distension (bloating) restlessness or anxiety? (as in case of colicky pain—renal,
10. Weight loss and anorexia intestinal or biliary colic)
11. Bleeding
12. Hematemesis Assessing the Nutritional Status of the Patient
13. Rectal bleeding (hematochezia) It forms a very important part of examination of the patient.
14. Malena Severe degree of malnutrition can be judged very easily, but
15. Dry mouth (xerostomia) it becomes too difficult for a clinician to recognize mild
16. Excess salivation (water brash) degrees of undernourishment (or malnutrition), especially
17. Painful lips, tongue, mouth in the presence of other associated illnesses and symptoms
18. Altered taste sensations (dysgeusia) like edema, hypoalbuminemia, etc. or if the malnourishment
19. Foul taste in mouth (cacageusia) is due to any underlying pathology like malabsorption
20. Bad breath (halitosis) syndrome, improper digestion, etc. Another most common
21. Feeling of lump in throat (globus) cause of malnutrition in the developing countries (including
22. Retrosternal chest pain India) is starvation.
23. Nausea and vomiting Thus, it becomes an important necessity for the physician
24. Jaundice, itching (pruritus) to recognize and understand the nutritional status of the
25. Aerophagia patient in order that he may take prompt actions to cure his
26. Fecal incontinence patient. The clinical history taking, the dietary history,
27. Maroon-colored stool the physical examination including anthropometrics
104 Essentials of Clinical Medicine
measurements are some of the important ways to assess
the nutritional status of the patient. Other methods include
muscle function test, daily (24 hours) creatinine output,
serum albumin level assessment of anemia, hypoalbumi-
nemia, ferritin and iron-binding capacity and prothrombin
time also hold crucial position.
Assessment
• Hydration
• Weight and height
• Obesity
• Edema
• Various GIT symptoms (mentioned in the beginning of
this chapter).
• Anemia.
• Nails for cyanosis, clubbing, pallor.
• Conjunctiva for pallor, icterus.
• Lymphadenopathy.
• Blood pressure, jugular venous pressure.
• Fever.
• Addition to alcohol, smoking.
• Past history of TB, malaria, kala azar, leukemia and drugs,
etc.
• Oral cavity for teeth, tongue, tonsils, oropharynx, lips
skin, face, eye, parotid, etc.
• Cyanosis.
• Jaundice, etc.
All form an unseparable part of clinical assessment of
the gastrointestinal tract (all these points have been discussed
in detail in the section of “The General Examination”).
Signs of Liver Cell Failure
1. Scanty hair (alopecia).
2. Palmar erythema—erythema is a Greek word which
means redness. It is a form of macula showing
diffused redness of skin. It is due to capillary congestion
which occurs as a result of dilation of superficial
arterioles.
3. Spider nevi (or nevus araneus). It is a branched growth
of dilated capillaries on the skin, resembling a spider.
It may be associated with cirrhosis of liver.
Spider nevi—spider nevi has central arteriole with
radiating vessels resembling legs of spider, is seen in
SVC (superior vena cava) territory, due to increased
circulating estrogen. Besides being an important sign
of liver cell failure, it is also seen in 2 percent of healthy
individuals and in pregnancy.
4. Parotid swelling.
5. Gynecomastia, testicular atrophy, loss of secondary
sexual characters.
6. Dupuytren’s contracture.
7. Flaps (asterixis).
8. Paper money skin.
9. Foetor hepaticus—a mousy odor in the breath of a
person with severe liver impairment. It is due to methyl
mercaptan derived from methionine, occurring in
hepatocellular failure.
10. Jaundice.
11. Xanthelasma (Greek—xanthos = yellow + elasma =
plate).
12. Sometimes, signs of chronic cholestasis such as
scratch marks of pruritus may also be seen.
Nine Regions of the Abdomen
For the purpose of describing the location of viscera, the
abdomen is divided into nine regions by four imaginary
planes, two horizontal and two vertical (Fig. 6.1). The
horizontal planes are the transpyloric and transtubercular
planes. The vertical planes are right lateral and left lateral
planes.
Sometimes, another horizontal plane, the subcostal, is
used instead of transpyloric plane.
The transpyloric plane (of Addison) passes midway
between the suprasternal notch and pubic symphysis. It
lies anteriorly, it passes through the tips of ninth costal
cartilages; and posteriorly through the body of vertebra L,
(near its lower border).
The subcostal plane is sometimes used instead of
transpyloric plane. It passes through the lower borders of
10th costal cartilages and the body of vertebra L3 (near its
upper border).
The right and left lateral planes correspond to the mid-
clavicular or mammary lines. Each of these vertical planes
passes through the midinguinal point and crosses the tip of
the ninth costal cartilage.
The nine regions marked out in this way are arranged in
three vertical zones, median, right and left. From above
downwards, the median regions are epigastric, umbilical
and hypogastric (pubic). The right and left regions, in the
same order, are hypochondriac, lumbar (lateral) and iliac
(inguinal).
INSPECTION
Inspection forms a very important part of examination of
the “alimentary system”. The patient should be made to lie
supine with arms loosely by his/her sides, on a firm surface
and head and neck supported by enough pillows.
Examination should be done in proper illumination and in a
well-ventilated room. The examiner is expected to stand by
the side of the patient (usually right side of the patient) and
his/her abdomen. If possible and if the patient allows, the

Fig. 6.1: Showing the various regions of the abdomen
examiner should also inspect the groin and genitalia because
a patient presenting with intestinal obstruction may have a
strangulated femoral or inguinal hernia as the underlying
pathology. (Remember: You cannot force the patient to
expose his private parts against his/her will. This is absolutely
against the rules of conduct of medical profession.)
In inspection, the following points should be given attention.
Shape or Contour of the Abdomen
The shape or contour of the abdomen varies in different
individuals; but for the sake of convenience of examination,
the abdomen has been roughly categorized into the following
shapes:
a. Generalized fullness or distention
fat, fluid, flatus, feces fetus or full urinary bladder
(“6 Fs”)
b. Localized distention—may be symmetrical or
assymetrical.
i. Symmetrical and centered around the umbili-cus,
small bowel obstruction.
ii. Asymmetrical—gross enlargement of spleen or liver
or ovary.
c. Scaphoid abdomen (boat-shaped abdomen)—advanced
stages of starvation and malignant disease, particularly
carcinoma of esophagus and stomach, and also in
muscle wasting disorders.
Alimentary System 105
Special Points
• Note if there is any movement of swelling, either with
or without independent respiration.
• Chronic urinary retention may cause palpable enlarge-
ment in the lower abdomen.
• It is very important to note whether the bulging is more
laterally, i.e. in the flanks (as seen in accumulation of
fluid in the abdomen, and sometimes also due to obesity,
pregnancy or large ovarian cyst) or bulging is in antero-
posterior diameter which is produced by intestinal
obstruction or gaseous distention. Visible bulges may
also be due to gross enlargement of liver, spleen, or
kidney or due to large tumors. Pyloric obstruction causes
bulging in the upper part of abdomen.
• Diverticulation of rectus is seen in—congenital defects,
after pregnancy, in obesity, ascites.
• Generalized distention is seen in ascites, obesity,
excessive flatus. Localized distention is seen in
neoplasms, hepatomegaly (in right hypochondrium), full
bladder (in hypogastrium).
• Differentiating the “6 Fs” as the cause of distention—
(i) Fat—the abdomen is pendulous and cutaneous folds
are symmetrical, and enlarged, (ii) Fluid in the abdomen
may be noted by fluid thrill, shifting dullness and horse-
shoe-shaped dullness (this is a part of percussion),
(iii) Flatus (on percussion, tympanic note is obtained
106 Essentials of Clinical Medicine
more towards periphery), (iv) Faeces—distention is seen
more in the flanks and on palpation you can feel the
fecal mass, (v) Detection of fullness of bladder is again
part of palpation, the abdomen is tender, rounded, and a
cystic mass may be felt just above pubic symphysis.
The disappearance of the swelling/mass after urinary
catheterization (in case of chronic retention) or after
micturition makes sure short diagnosis that the distention
was due to fullness of the bladder, and (vi) The distention
which is due to fetus is usually central in position with
tympanic note in the flanks. There will be a history of
amenorrhea and palpation of fetal parts may be possible
The Umbilicus
Normally, the umbilicus is slightly retracted, inverted and
situated centrally in mid-abdomen. The position of normally
situated umbilicus is such that it lies exactly at the center of
the line joining the xiphisternum and pubic symphysis. The
distance between the xiphisternum and umbilicus is equal
to that between the umbilicus and pubic symphysis. And
any change in position indicates a pathology. The various
conditions of umbilicus and its causes are:
i. Umbilicus in ascites:
• Transversely stretched (smiling umbilicus).
• May be flattened or everted (in severe ascites).
• In massive ascites, fluid may be seen oozing out
of umbilicus (cyring umbilicus).
• There is downward shift of umbilicus along the
same vertical line. The distance between the
xiphisternum and umbilicus is greater than that
between umbilicus and pubic symphysis.
• Smiling umbilicus is also seen in cirrhosis of liver
with ascites. Oozing of clear fluid from umbilicus
may be seen in patent urachus.
ii. Umbilicus is ovarian tumor
• Everted or flat.
• Distance between xiphisternum and umbilicus is
less than that between umbilicus and symphisis
pubis. There is greater bulge in the lower part of
abdomen (as the ovaries are located there, the
appearance is of a vertical slit).
iii. Umbilicus in hernia
• Everted
• Herniation of bowel or fat present.
• Herniation can be confirmed by feeling an expan-
sile impulse on palpation of the swelling when
the patient coughs.
• The hernial sac may contain omentum, bowel or
fluid.
iv. Umbilicus in omphalolith
• It is usually seen in elderly obese women where
there is a concentration of inspissated desqua-
mated epithelium and other debris.
v. Umbilicus in obesity
• Umbilical cleft is deeper than normal.
vi. Abnormal discoloration of umbilicus/area surrounding
umbilicus
a. Bluish discoloration (Cullen’s sign, e.g. acute
hemorrhagic pancreatitis or ruptured ectopic
pregnancy).
b. Cherry red swelling, inflammation of Meckel’s
diverticulum.
Movements of Abdominal Wall
Normally, the abdominal wall rises during inspiration and
falls back during expiration and the movements are free,
smooth and equal on both sides.
The type of respiration varies in both sexes. It is abdominal
(also called abdominothoracic) in males and thoracic (also
called thoracoabdominal) in females.
Paradoxical Bulging of Abdominal Wall
It means that there is a rise of the wall during expiration. It
is seen in case of diaphragmatic paralysis.
Silent Abdomen (or Still Abdomen)
a. Complete absence of movements: It is seen in generalized
peritonitis. This helps to limit further spread of infection
within the peritoneal cavity and pain of peritoneal
irritation.
b. Partial movements (Restricted movements over a
particular area of abdominal wall): It is seen in localized
peritonitis.
Visible Pulsations
In normal condition, the pulsations are not visible over the
abdominal wall. Visibility of the pulsations indicates the
following pathological conditions.
a. Pulsations of aorta: They may be noticed in epigastric
region usually visible in nervous, thin and anemic
individuals and sometimes in children; also, in
pathological conditions like hyperdynamic circulatory
states as seen in thyrotoxicosis or aortic regurgitation
also visible pulsations of abdominal aorta are seen.
b. Aneurysm of aorta: The pulsation due to aortic aneurysm
should be distinguished from aortic pulsations. In aortic
aneurysm, the pulsation is more obvious and widened
aorta is felt on palpation and also the pulsation are
expansible in nature (in any position). A tumour of the

abdominal organs in the epigastric region will also
transmit pulsations from aorta in the same area. The
distinguishing point between the visible pulsation due to
aneurysm and tumor is that (i) the pulsation of aortic
aneurysm is more obvious and secondly, and (ii) pulsation
due to abdominal aortic white those due to transmission
through falls away from the aorta in that position
(However, this does not happen if the tumor is adherent
to the aorta. The distinction is best confirmed by the
abdominal ultrasonography).
c. Epigastric pulsations due to right ventricular hypertrophy:
They correspond with the apex beat.
d. Hepatic pulsations: They are seen in case of tricuspid
incompetence or due to hepatic hemangioma.
Note: To aid the recognition of pulsations over the
abdominal wall as well the abnormal movements (absent
or restricted) of the abdominal wall, throw light across
(tangentially) the patient’s abdomen. Even small move-
ments may be detected by alterations in the pattern of
shadow cast by the abdomen.
Prominent Superficial Veins
They are apparent in three situations:
a. Thin veins over the costal margin.
b. Occlusion of inferior vena cava (IVC).
c. Venous anastomosis in portal hypertension. These veins
are usually tortuous and dilated.
Thin veins over costal margins/subcostal margins: They are
common and usually of no significance. They are more
clearly visible in thin and lean individuals.
Occlusion of inferior vena cava: It causes edema of limbs,
buttocks and groin and also leads to distended veins on the
abdominal wall and chest wall. They signify dilated
anastomotic channels between the superficial epigastric and
circumflex iliac veins below, and the lateral thoracic veins
above, conveying the diverted blood from long saphenous
vein to axillary vein; the direction of flow is, therefore,
upwards. In sufficiently prominent and dilated veins, try to
detect the direction of blood flow.
Venous anastomosis in portal hypertension: Distended vein
around the umbilicus (caput medusae) are uncommon; but,
if present, indicates portal hypertension, other signs of which
include splenomegaly and ascites. The distended vein
represents the opening up of anastomoses between the portal
and systemic veins and are also seen in other sites like
esophageal varices and hemorrhoids. (Fig. 6.2, Plate 2)
Interpretation: (Direction of Blood Flow)
When the portal vein, the superior vena cava (SVC) or
inferior vena cava (IVC) is obstructed, the superficial
Alimentary System 107
abdominal veins are dilated and provide a collateral
circulation. The dilated veins that radiate from the umbilicus
are given the name caput medusae. They are typically seen
in portal obstruction in which blood flow is upwards above
the umbilicus and downwards below the umbilicus. In
inferior vena caval obstruction, the thoracoepigastric vein
open up, connecting the great saphenous vein with the axillary
vein. In superior vena caval obstruction, the blood in the
thoracoepigastric veins flows downwards.
Procedure: The direction of blood flow should be tested by
selecting a vein with no side branches and compressing it
with one finger of either hand held near each other. The
fingers are then drawn apart so that the vein collapses
(milking of vein) under them. The pressure of these fingers
is released in turn and the side from which the vein fills up
is noted.
Causes of IVC Obstruction
1. Hypercoagulable states like nephrotic syndrome.
2. Compression by massive ascites.
3. Thrombosis of femoral iliac veins.
4. Secondary to infection and prolonged intake of oral
contraceptive pills (OCPs), trauma/injuries, etc.
5. Idiopathic retroperitoneal fibrosis.
6. Congenital anomalies or tumors of the walls of the veins.
7. Thromboembolism.
Visible Peristalsis of Stomach or Small Intestine
It may be observed in the following situations:
a. Obstruction at the pylorus: This occurs due to fibrosis
following chronic duodenal ulceration or less commonly
by carcinoma of the stomach in pyloric antrum.
Peristalsis will be seen as a slow wave either passing
across the upper abdomen from left to right hypo-
chondria or if gross gastric dilatation is present, passing
down to the suprapubic region and ascending to
terminate in the right epigastrium. In pyloric obstruction,
a diffuse swelling may be seen in the left upper abdomen,
but where obstruction is long standing with severe gastric
distention, this swelling may occupy the left mid and
lower quadrants. Such a stomach may contain up to
two liters of fluid; and on shaking the abdomen, splashing
noise is usually heard (succussion splash). This is
frequently heard in healthy individuals for up to 3 hours
after a meal, so inquire when the patient last ate or drunk.
b. Congenital pyloric stenosis of infancy: Not only may
visible peristalsis be apparent but also the grossly
hypertrophied circular muscles of the antrum and pylorus
may be felt as a “tumor” to the right of midline in the
epigastrium. Both these signs may be elicited more easily
108 Essentials of Clinical Medicine
after the infant has been given a feed. Standing behind
the mother with the child in her lap may allow the child’s
abdominal musculature to relax sufficiently to feel the
walnut-sized swelling.
c. Obstruction in the distal small bowel: Peristalsis may
be seen when there is instestinal obstruction in the distal
small bowel or co-existing large and small bowel hold-
up produced by distal colonic obstruction, with an
incompetent ileocecal valve allowing the reflux of gas
and liquid into the ileum. Not only is the abdomen
distended and tympanitic (hyper-resonant) but also the
distended coils of small bowel may be visible in a thin
patient and tend to stand out in the center of the abdomen
in a “ladder” pattern (writhing movements in the center
of the abdomen).
d. Visible peristalsis: It may be a normal finding in very
thin, elderly patients with lax abdominal muscles or large,
wide-necked incisional hernia seen through an abdominal
scar.
e. Large intestinal obstruction: It can also produce
peristaltic wave in the epigastrium and here the wave is
seen passing from right to left.
All the peristaltic movements are observed more clearly
when the abdomen is viewed transversely, gastric peristalsis
in pyloric obstruction can be made more prominent if the
patient drinks a glass of water. Any cold stimulus like a
spray of ethyl chloride over the abdominal wall also
stimulates the underlying peristalsis. The peristaltic waves
may also be made more clear by applying a sharp tap with
the fingers over the abdominal wall.
Hernial Sites
The hernia is a common cause of localized swelling and
should be distinguished from divarication of rectus
abdominis. Divarication of the recti, common in multiparous,
becomes more obvious as the supine patient attempts to sit
upright, the intra-abdominal pressure rises and the region
of line alba bulges between the rectus. An umbilical hernia
bulges through the navel. It is very common in babies and
usually disappears spontaneously. An epigastric hernia is
visible as a small swelling usually not more than 1 cm in
diameter. It is due to the herniation of extraperitoneal fat
through defect in the linea alba. By gentle massage with the
fingertip, it is often possible to reduce such hernia and then
the small defect can be felt. An incisional hernia may form
at the site of an operation in the abdomen, especially if the
wound has been complicated by the sepsis. A femoral hernia
is palpable below the inguinal ligament and lateral to the
pubic tubercle. An inguinal hernia emerges from abdominal
wall through the external inguinal ring and is palpable above
and medial to pubic tubercle. It is often difficult to accurately
differentiate between direct and indirect inguinal hernias.
An indirect inguinal hernia occurs into a persistent remnant
of the processus vaginalis. It occurs in young men and
may extend to testes. Following reduction, control can be
achieved by pressure over the internal inguinal ring, just
above the midpoint of the inguinal ligament. A direct inguinal
hernia occurs directly through the weakened posterior wall
of the inguinal canal medial to the inferior epigastric artery
and lateral to the rectus muscle. It is more common in older
men and does not reach the testes. It will be controlled by
pressure over the external inguinal ring.
SKIN AND SURFACE OVER THE ABDOMEN
The skin and surface of the abdominal wall should be
observed for the presence of scar marks of injuries or marks
of any previous surgical intervention. Note their number,
site and whether they are old (white) or fresh (red or pink)
Striae atrophic or gravidarum are white or pink wrinkled
linear marks on the abdominal skin. They are produced by
gross stretching of the skin with rupture of elastic fibers
and indicate a recent change in size of the abdomen, such
marks are found in pregnancy, ascites, wasting disease and
severe dieting. Wide purple striae are characteristic of
Cushing’s syndrome and excessive steroid treatment.
Prominent superficial veins are seen as distended veins
around umbilicus (caput medusae) and they signify portal
hypertension but are rarely seen. Pigmentation of the
abdominal wall may be seen in the midline below the
umbilicus, where it forms the linea nigra and is a sign of
pregnancy. Erythema ab igne is a brown mottled
pigmentation produced by constant application of heat,
usually with hot water bottle or heat pad, on the skin of the
abdominal wall. It is a sign that the patient is experiencing
severe pain and is most commonly associated with chronic
pancreatitis. In elderly patients seborrhoeic warts, ranging
from pink to brown or black, and hemangiomas (Campbell
de Morgan spots) are so common that they could be
considered normal changes. Lineae albicantes (linea alba)
are produced by stretching of the abdomen and are evidence
of previous pregnancies, abdominal tumors or ascites. Linea
nigra is the term used to describe the black line produced
by deposition of melanin in midline and is also seen in
females who have had multiple pregnancies. The abdominal
skin may show presence of multiple small modules which
are evidence of widespread hematogenous metastasis.
However, these are rarely the result of an abdominal
malignancy. The abdominal skin appears to be smooth,
shining and stretched when there is abdominal distention
due to pathological cause.

Surgical Incisions
Non-Specific Incisions
• Vertical incisions — Midline or paramedian
(used for general — Upper, lower or full
access) length
Specific Incisions
• Subcostal — Gallbladder
• Suprapubic — Bladder, prostate, gynec-
ology
• Mc Burney’s point — Appendix
• Inguinal — Hernia.
PALPATION
Palpation forms the most important part of abdominal
examination. The patient is asked to relax his abdominal
wall and to breath quietly. You should assure the patient
that your palpation procedure will absolutely not harm him/
her.
A Word of Caution
1. Students usually start palpating from over the area which
is tender. This is absolutely a blunder. The students should
keep in their mind that the patient may guard his abdomen
(i.e. he may make the abdominal wall taut) if the area is
tender and it may lead to missing of some other very
important signs (which may provide diagnostic clues).
Therefore, you should first inquire about the site of any
pain and come to this region last.
2. Always warm your palms before palpation and try to
bring it to the temperature equal to that of the patient’s
abdominal wall. Any difference in temperature may cause
the abdominal wall to be taut.
3. Always do palpation with the knees of the patient flexed
and brought close to his buttock and arms held by the
side of the body (Fig. 6.3). This makes the abdominal
wall lax.
4. During palpation, observe the patient’s face for any
grimace indicative of local discomfort.
Sequence of Palpation
• Start in the left iliac region, palpating lightly, and going
anticlockwise to end in suprapubic region. This is
repeated with deeper palpation, and if needed, with both
the hands.
• Next palpate left kidney.
• Next palpate spleen.
• After that right kidney.
Alimentary System 109
• Next to it palpate liver.
• Feel for urinary bladder.
• Then aorta, para-aortic glands and common femoral
vessels.
• Palpate both groin.
• Region for any pulsation, and swelling, etc.
The way to palpate is to make gentle movements with
firm pressure and with the fingers held almost straight with
slight flexion at metacarpophalangeal joints. Do not try to
deeply insert your finger into the patient’s abdomen. At times,
you may need the assistance of your own left hand while
palpating. In an obese or high muscular patient, putting your
left hand over the right hand will help you to exert increased
pressure.
Methods of Palpation
1. Light palpation.
2. Deep palpation.
3. Palpation during respiration.
4. Dipping method.
5. Bimanual palpation.
Light Palpation
In this method, a very gentle pressure is applied over the
abdominal wall. It is done to elicit minimum degree of
tenderness or guarding.
Normally, the abdominal wall feels soft and yielding with
no guarding or rigidity. As mentioned above, the palpation
should be carried out from an area which is non-tender.
The gentle and light palpations provide many useful
information like underlying abdominal tumor mass, megaly
of any organ or full (distended) urinary bladder.
Deep Palpation
It is used to examine those abdominal organs which are
deeply seated. Deep tenderness also can be alicited with it.
Dipping Method
This method is useful during deep palpation in patients with
marked ascites to detect the presence of hepatic or splenic
enlargement and map the outlines of enlarged organs or of
a tumor that might otherwise have been missed because of
ascites. The sudden displacement of liquid gives a tapping
sensation over the surface of liver or spleen similar to patellar
tap.
In this method, the examiner places his hand flat on the
abdomen and makes quick dipping movements of the fingers
by flexing them at the metacarpophalangeal joints.
Bimanual Palpation
This is a method generally used to examine kidneys (and
also other retroperitoneal mass).
110 Essentials of Clinical Medicine
The examiner keeps his one hand over the loin
(posteriorly) and other hand over the anterior abdominal
wall. With the help of posterior hand, the examiner pushes
the kidney (or any mass) upwards, i.e. towards the ant.
abdominal wall and palpates it with the hand placed anteriorly.
Normally, the kidney is not palpable, but the lower pole of
right kidney may be palpable in thin and lean individuals.
Abnormal Findings
Muscle Guarding
It is done voluntarily by the patient, as a protective procedure
(self-defense mechanism) when the examiner palpates over
a tender region. It occurs due to muscle contraction. The
patient should be made relaxed and comfortable and must
be assured that there will be no harm to him/her by palpation.
Guarding is usually seen in conditions like localized
peritonitis and can be elicited over the area of actual
anatomical locations of the organ, for example:
• In appendicitis—over right iliac fossa.
• In perforated peptic ulcer—over epigastric area.
Rigidity
It is also due to muscular contraction and again self-defense
mechanism. It is also seen (elicited) over the inflamed
organs, the only difference between the guarding and rigidity
is that the guarding occurs only when the abdomen is
palpated, whereas rigidity is present all the time in order to
prevent (or minimize) the movements of abdominal organs
with respiration. Hence, the type of respiration that is seen
in case of rigidity is usually thoracic type (in males, the
respiration is generally of the abdominal type). Rigidity
occurs in the conditions like peritonitis, perforation of a
hollow organ, acute pancreatitis, cholecystitis, ectopic
pregnancy, twisted ovarian cyst or torsion of fibroid,
thrombosis of superior mesenteric artery, etc.
Tenderness
It suggests an underlying inflammatory process of abdominal
viscera and the surrounding peritoneal structure. Tenderness
over a particular area gives a clue about the organ involved.
For instance:
• Over right iliac fossa—may be appendicitis.
• Over epigastrium—may be peptic ulcer.
• Over light hypochondrium—may be hepatitis or
cholecystitis.
Rebound tenderness: Deep seated inflammation not causing
localized guarding may be revealed by rebound tenderness.
Although initial pressure of palpation may fail to elicit a
painful response, the abrupt withdrawal may cause the
sudden movements of a deeply placed, inflamed organ,
resulting in pain.
Other Abnormal Findings
• Generalized “board-like rigidity” implies peritonitis, the
abdomen does not move and respiration (respiration is
completely thoracic) and bowel sounds are
characteristically absent.
• Feces may be palpable in any part of colon in severe
constipation. Indentation of a lump by finger pressure
is evidence that it is fecal. Sometimes, however, a hard,
craggy lump of feces can only be distinguished from
malignancy by re-examination following defecation.
Liver
Procedure
The examiner places his hand flat on the abdomen so that
his fingertips point upward towards the ribs. The fingers
that mainly sense the liver (middle and index fingers) are
positioned lateral to rectus muscle so that the fingertips lie
to parallel to expected liver edge. Now the examiner presses
his hand firmly inwards and upwards and keeps it steady
while the patient takes a deep breath through the mouth.
When the inspiration reaches to its peak, the pressure
towards the upward direction is still maintained but the
pressure towards inward direction is released. By the tip of
the fingers slip over the edge of a palpable liver is palpated
using the fingertip keeping them steady in a new position
each time the patient takes a deep breath. The examiner
feels the irregularities as the liver slides under the fingertips
with each inspiration.
Alternate Method
Though this method is less accurate; in this method, the
right hand is placed below and parallel to right subcostal
margin. The liver edge is then felt against the radial border
of the index finger. The liver is often palpable in normal
patients without being enlarged. If the edge is indefinitely
felt, percuss in the right hypochondrium, keeping the hands
still as the patient breathes. Movement of lower border
Fig. 6.3: Palpation of viscera
 Alimentary System 111

together with dullness on respiration is further supporting the costal margin more towards left side. Then the patient
evidence of liver enlargement. is made to breathe deeply. The examiner presses in deeply
with fingers of right hand beneath the costal margin, at the
Points to be Noted in Palpation of Liver same time exerting considerable pressure medially and
Size downwards with the left hand. The procedure is repeated
It can be measured and expressed either in terms of with the right hand being moved more medially beneath the
centimeters, below the costal margin (in midline, midclavi- costal margin on each occasion.
cular line and in mid-axillary line) or in terms of finger breadth If the patient presents with the history and clinical
below costal margins. features of splenic enlargement and still the spleen is not
palpable, the examiner turns the patient half on to right side
Interpretation and asks him to relax back on to his left hand (which now
• Severly enlarged liver – Congestive cardiac failure, supports the lower ribs). The procedure mentioned above
(gross enlargement) malignancy, blood dyscrasias, is repeated.
amebic abscess.
Second method: The examiner stands on the left side of the
• Moderate enlargement – Alcoholic hepatitis, fatty
degeneration, obstructive patient. He curls his fingers of the left hand beneath the
hepatitis in cirrhosis. costal margin, while the patient is made to breathe deeply.
• Mild enlargement – Infective hepatitis, anemia. Third method: It is used to detect massive splenomegaly. In
this method, the examiner stands on ‘right’ side of patient
Conditions in which Hard Nodular Liver is Seen
facing towards the footend of bed. He starts palpating the
It is seen in secondary carcinoma of liver—commonest spleen from the right iliac region. The radial border of index
tumor of liver, primary arising from portal territory stomach,
finger of right hand (sensing finger) is placed parallel to left
pancreas, large bowel. Through hematogenous—breast,
costal margin (with fingertips pointing towards the pubic
bronchus, kidney, thyroid.
symphysis of the patient) and he moves his hand more
Causes of Firm Liver, Hard Liver and Soft Liver towards left hypochondrium. The enlarged spleen will be
Causes of firm liver: felt by the index finger.
• Cirrhosis of liver Fourth method: Dipping method as mentioned above.
• Amyloid
• Hodgkin’s or chronic myeloid leukemia. Interpretation
Causes of hard liver: • Mild enlargement—just palpable below the left costal
• Primary and secondary carcinoma margin.
• Hydatid cyst. • Moderate enlargement—palpable but not reaching
Causes of soft liver: umbilicus.
• CCF • Severe enlargement—up to umbilicus or beyond that.
• Infective hepatitis
Table 6.1: Differentiation between splenic lump and
• Amebic hepatitis lump due to splenic flexure carcinoma
• Fatty liver.
Splenic lump Carcinoma lump (splenic)
Spleen Moves (Not fixed) Does not move (fixed)
Not hard. Firm to hard.
Procedure No history of bowel Bowel disturbances like malena,
disturbances or malena altered bowel movements.
Normal spleen is not palpable. To become palpable, the spleen
has to be enlarged to 2-3 times of its normal size. Enlarged Differences between pancreatic lump and spleen:
spleen is felt below the left subcostal margin. Prior to its • Pancreatic lump is situated in midline, umbilicus,
becoming palpable, the spleen enlargement takes place in epigastric region.
superior and posterior direction, spleen enlarges downwards • Pancreatic pain is deep into back towards L-1 vertebra.
and towards right iliac fossa. • It is fixed and does not move.
While standing on ‘right’ side of the patient, the examiner • Cystic in nature.
places the flat of his left hand over the patient’s lowermost • Percussion is dull.
rib cage posterolaterally, and the right hand is placed beneath • No notch is felt.
112 Essentials of Clinical Medicine

Table 6.2: Differences between carcinoma fundus of be pushed from one hand to the other in an action which is
stomach from splenic mass called “balloting”.
Carcinoma fundus of stomach Spleen
Right Kidney
Fixed Not fixed
Hard Not hard The right kidney is palpated in a way similar to the left. The
UGI symptoms, like nausea No GI symptoms examiner stands on the “right” side of the patient and places
vomiting, weight loss. Fundus gas shadow his right hand horizontally in the right lumbar region
Fundus gas shadow lost in X-ray
anteriorly with the left hand placed posteriorly in right loin.
Causes of Tender Spleen The patient is asked to take a deep breath and the left
hand is pushed forwards and right hand inwards and
• Splenic abscess. upwards.
• Subacute bacterial endocarditis with splenic infarct.
Normally (unlike the left kidney), the lower pole of the
• Sickle cell anemia with splenic infarct.
right kidney is commonly palpable in lean and thin individual
• Mitral stenosis with splenic infarct.
and is felt as a smooth, rounded swelling which descends
• Subcapsular hematoma.
• Splenic rupture. on the inspiration and is bimanually palpable and may be
• Splenic vein thrombosis. “balloted”.
The kidney should be examined (palpated) for size,
Table 6.3: Differences between left kidney and spleen surface, consistency, and tenderness.
Features Left kidney Spleen Differential Diagnosis of Kidney Mass
1. Site Posteriorly L1 region Anteriorly 9th, 10th,
and 11th ribs
1. Spleen—notch, moves with respiration, interiorly
2. Notch Absent Present enlarged, renal angle free.
3. Edge Smooth and rounded Sharp edge 2. Left lobe of liver—no notch, irregular surface, moves
4. Finger insinu- Possible Not Possible with respiration.
ation between
organ and
3. Ca. fundus of stomach—fixed, hard, no notch.
costal margins 4. Omental mass—edge not clear, no notch, gap between
5. Band of colonic Present Absent costal margin and lump (due to TB/malignancy)
resonance 5. Ca. splenic flexure—hard and fixed.
6. Movement No Moves freely on inspi-
ration with respiration
6. Malignancy of tail of pancreas.
7. When organ It grows towards It grows towards right 7. Suprarenal tumor—deeply placed, can reach the sub-
enlarges lumbar region iliac fossa. costal angle.
8. Bimanual Possible (palpable) Not palpable. 8. Pancreatic tumor—no notch.
palpation
9. Ballotable Ballotability possible Not possible
9. Ca. of colon.
10. Fullness and Present Absent 10. Ovarian tumor.
dullness in loin
Gallbladder
Kidneys
The normal gallbladder is not palpable. Enlarged gallbladder
Normal kidney is not palpable. The kidneys being is palpated in the same way on the enlarged liver. When
retroperitoneal organ are palpated by bimanual technique. enlarged it is palpated as a firm, smooth, rough or globular
pear-shaped swelling with distinct borders just lateral to the
Left Kidney
edge of rectum abdomens near the tip of ninth costal
The examiner stands on the “right” side of the patient and cartilage. It moves up and down with respiration. When
places his right hand anteriorly in the left lumbar region severe enlargement, it may not be felt in the right
while the left hand is placed in the left loin. hypochordrium, but in the right lumps or region or even
The patient is asked to take a deep breath in, and the left low down as the right illiac region.
hand is pressed forwards and right hand backwards, The palpation of gallbladder is possible in the following
upwards and inwards. The left kidney is not usually palpable situations (painless swelling):
unless either low in position or enlarged. Its lower pole, • Carcinoma of head of pancreas as well as the other
when palpable, is felt as a rounded firm swelling between malignancies—obstruction of common bile duct. The
both right and left hands (i.e. bimanual palpation) and it can patient presents with clinical features of severe jaundice.

• Mucocele of gallbladder—the gallstone causes impaction
of the neck of a collapsed and empty bladder and when
the secretion starts appearing in its lumen, it leads to
gallbladder distention and it becomes palpable. The
patient does not have jaundice.
• Carcinoma of gallbladder—the gallbladder becomes
palpable as a stony, hard, irregular swelling.
Courveisier’s law: As mentioned above, the gallbladder is
palpable in carcinoma of head of pancreas. But in certain
conditions like cholelithiasis, the gallbladder wall gets
repeatedly infected and becomes thick and so is unable to
distend. This is called Courvesier’s law.
Murphy’s sign: Acute inflammation of gallbladder is called
acute cholecystitis. The patient complains of pain over the
right hypochondrium radiating to the inferior angle of right
scapula or to the right shoulder when a finger is placed just
below the costal margin, at the tip of 9th costal cartilage,
the patient feels sharp pain on inspiration. This is called
Murphy’s sign. The sign is not found in chronic cholecystitis
or uncomplicated cases of gallstones.
Urinary Bladder
Normally, the urinary bladder is not palpable. In cases of
retention of urine, a smooth, firm, regular oval-shaped
swelling is palpated in the suprapubic region and its upper
border (also called the dome) may even reach the umbilicus.
It is dull on percussion and on applying pressure over the
swelling, the patient develops a desire to micturate.
The differential diagnosis of distended urinary bladder
in case of women:
• Gravid uterus—firm, mobile from side to side, with
certain specific vaginal signs.
• Ovarian cyst—eccentric swelling on the right or left
side.
• Uterine fibroid—firm, bosselated and vaginal signs
different.
Note: Abdomen gives doughy feeling in tuberculous
peritonitis.
Percussion: Percussion of the abdomen is done with light
hands. Normally, resonant (tympanic) note is heard
throughout except over the liver, where dull note is heard.
Percussion is generally helpful in making the diagnosis of
hepatomegaly or splenomegaly.
Normal liver span: Normal liver extends, from 5th rib (or
just below the right nipple in men) to the palpable margin or
right costal margin. It is about 12 to 15 cm in height. The
hepatomegaly can also be measured in terms of centimeters
below the right costal margin at the midclavicular line or in
terms of finger breadth (again below the same right costal
margin).
Alimentary System 113
Fig. 6.4: Palpation of abdomen. Diagrammatic representation of
some findings which may be normal and are often misinterpreted
Percussing over the liver: Normally, the upper and lower
borders of the right lobe of liver can be assessed accurately
by percussion. The examiner begins anteriorly, at the 4th
intercostal space where the note is resonant over the lungs
and then he goes vertically downwards under normal
conditions, the upper border of liver is at about the 5th
intercostal space, where the note is dull. This dullness is
present up to the right subcostal margin. In certain
conditions, the dullness over the upper part of liver is reduced
or absent. These conditions are severe emphysema, presence
of large right pneumothorax and presence of gas or air in
the peritoneal cavity (indicating perforation of a viscus).
In case of hepatomegaly, percussing below the right
costal margin is useful. The patient is asked to take deep
breath which the examiner percusses lightly. The fingers
are kept parallel to the rib margin. During inspiration, the
liver descends down and change in the note from resonance
to dull signals the edge of the liver. The percussion of upper
border (margin) is also done. This gives the measure of
liver size.
Spleen: Percussion over the enlarged spleen adds confir-
matory findings to the palpation. Dullness of spleen can be
elicited from left lower ribs to left hypochondrium and left
lumbar region. Dullness of spleen gives way to the resonance
of surrounding bowel.
Urinary bladder: The percussion over the urinary bladder
differentiates it from swelling due to gases (the urinary
bladder gives a feel of cystic or solid swelling). Its superior
and lateral borders can be readily defined from the adjacent
bowel, which is resonant.
114 Essentials of Clinical Medicine

Use of percussion for detection of fluid in pertoned cavity: Contd...

Usually, palpation and percussion have to be combined to Features Gross ascites Large ovarian Intestinal
determine the presence of fluid in the peritoneal cavity. cyst obstruction
Shifting dullness: About 750 to 1000 ml of fluid should be tension like which one cannot constipation.
present to elicit this sign. The patient is made to lie supine hemoptysis, “get below” Increased and/
over bed and the examiner percusses laterally from the signs of liver or “noisy”
midline (keeping the fingers in longitudinal axis, until dullness cell failure like bowel sound
spider nevi,
is elicited). In normal individuals, dullness is detected only
flapping tre-
over the lateral abdominal musculature and the flanks are mors, etc., he-
dull (except in case of ascites or adherent bowel loops). morrhoids due
Then keeping his hands over the abdomen, the examiner to opening of
asks the patient to roll away from him (i.e. to turn laterally A-V shunts
to other side). Percussion is again performed in this new
position Puddle’s sign: It is percussion of the umbilical area in knee-
Interpretation: If the area of percussion was previously chest position. This sign is to assess the presence of minimal
giving dull note and has now become resonant, the ascitic amount of fluid (as little as 100-150 ml of ascitic fluid) in
fluid is most probably present. The confirmation is possible the peritoneal cavity. The patient is made to lie in prone
only when the procedure is repeated on the other side of position for a few minutes and then to attain the knee-chest
abdomen. This change in note occurs due to shift of the position so that the midportion of abdomen is downwards
fluid in the peritoneal cavity. (becomes dependent) and the back is horizontal. Now the
Unilateral shifting dullness: In splenic rupture this is called percussion is done around the umbilicus and dullness is
balance sign. Blood present in left flank becomes clotted elicited (as the fluid accumulates in the area around
near the spleen and does not shift to right. But blood present umbilicus). A stethoscope is placed over the umbilical region
on right side (hemoperitoneum) is shifted to left. and abdominal wall is scratched from center (umbilicus)
towards periphery. A change in the quality of sound can be
Fluid thrill: About 1,500 ml of fluid (under tension) should
auscultated very clearly.
be present to elicit this sign.
This is another way to confirm the abnormal pressure Horseshoe-shaped dullness: This is elicited in case of
of fluid in peritoneal cavity. The examiner places one hand moderate ascites. The percussion is done in various
flat over the lumbar region of one side and asks the patient directions from umbilicus towards periphery. As soon as
(or an assistant) to put the side of hand firmly over the the dullness is encountered in a particular direction that point
midline. Then the examiner taps the opposite lumbar region. should be marked. At the end, if an imaginary line is drawn,
A fluid thrill or wave of moving fluid can be felt as an impulse it will be seen to resemble the shape of a horseshoe with
by the other hand (detailing hand) held flat in the lumbar concavity upwards. This is because the fluid accumulates
region. The patient’s or the assistant’s hand is used to dampen in the dependent parts and intestine floats up.
any impulse that may be transmitted through the fat of the
abdominal wall. AUSCULTATION
Note: Absence of shifting dullness or of fluid thrill or both The auscultation is done to listen the bowel sounds (normal,
does not exclude diagnosis of ascites. increased or decreased), arterial bruits or venous hum.
Table 6.4: Common causes of abdominal distention
Principles of Auscultation
Features Gross ascites Large ovarian Intestinal
cyst obstruction
• Normal peristaltic sounds can vary from person to person
and to a certain extent depends upon the state of intestines
Flank Flank dull Resonant Resonant
Umbilicus Transverse Vertical May be everted (empty or filled with food contents).
with/without • Normal peristaltic activity of the gut creates characteristic
hernia (smiling gurgling sounds which may be heard from time to time
umbilicus) by the unaided ears without the help of a stethoscope.
Shifting dullness Positive Negative Negative
Fluid thrill Positive Negative Negative
They are called Borborygmi’s sound. Through the
Other features Features of Large swelling felt Colicky pain, stethoscope, they may be heard every 5 to 10 seconds,
portal hyper- arising out of pelvis vomiting, though the interval varies greatly and they occur more
Contd...
frequently after meals.
 Alimentary System 115

Table 6.5: Causes of palpable abdominal masses

Right iliac fossa masses Middle masses Left iliac fossa masses
• Hard or impacted feces (scybala) Lymphoma (lymphadenopathy) • Carcinoma colon, left ovary
• Psoas abscess Carcinoma—gastric, pancreatic, colonic • Transplanted
• Appendix abscess • Kidney (note any overlyng scar)
• Carcinoma—colon, right ovary Aortic aneurysm
Pancreatic pseudocyst • Diverticular abscess
• Transplanted kidney (note any overlying scar) Ovarian cyst or tumors (benign or malignant) • Psoas abscess
Horseshoe-shaped kidney • Hard or impacted feces (scybala)
• Crohn’s disease (often adherent bowel loops) Uterine masses, pregnancy, fibroid, tumors,
• Tuberculosis of illeocecal region Bladder enlargement retention of urine

• Auscultate for peristaltic sounds for at least 3 minutes • Few hours after meals.
before deciding that they are absent. • Delayed gastric emptying as in diabetic autonomic
• The stethoscope should be placed on one site on the neuropathy.
abdominal wall (just to the right of the umbilicus is the
best) and kept there until sounds are heard. It should Arterial Bruits
not be moved from site to site. Normal bowel sounds
are heard as intermittent, low or medium pitched gurgles They are harsh systolic murmurs heard due to turbulence
interspersed with an occasional high-pitched noise or of blood flow. Care should be taken not to press the chest
tinkle. piece too firmly in the epigastrium as otherwise an artificial
systolic murmurs may be produced by compressing the
Peristaltic Sounds abdominal aorta.
Peristaltic sounds are produced by the contractions of Table 6.6: The sites of bruits and their causes
muscular walls of the gut and the resultant vibration of the
Site of bruit Cause
gut wall produced by movements of a gas-fluid mixture
through the gut. • Over liver • Vascular tumor like
hepatoma or hemangioma
Causes of increased bowel sounds (hyperperistalsis): • Hepatocellular carcinoma
• Subacute intestinal obstruction (high-pitched tinkling • Acute alcoholic hepatitis
quality) • Over spleen • Vascular tumor
• Diarrhoea/Dysentery. • Over aorta • Aortic aneurysm, atheroscle-
• Severe gastrointestinal bleeding rosis, extreme tortuosity of
• Small bowel malabsorption. aorta
• Over kidneys • Renal artery stenosis
• Carcinoid syndrome (marked borborygmi) • Mid-abdomen • Hypertension due to stenosis
Causes of diminished or absent bowel sound: of renal artery stenosis
• Perforation • Over common illiac artery or • Aneurysm or stenosis
• Immediately after abdominal surgery. femoral artery
• Paralytic ileus follwing intestinal obstruction or • Over pancreas • Coeliac artery stenosis
• Carcinoma pancreas.
necrotizing enterocolitis.
• Hypokalemia.
Causes of Splenic Bruit
• Bowel atony
• Peritonitis. • Intrahepatic portal obstruction.
• Vascular tumors as angioma of spleen, angiosarcoma.
Succussion Splash
Venous Hum
It is somewhat similar to that heard in case of
hydrothoraxes. It is produced by shaking the patient and • It is a continous, softer and low-pitch sound.
auscultating over the epigastrium. It is heard in cases of: • Heard between xiphisternum and umbilicus due to
• Pyloric obstruction turbulence of blood flow in well-developed collaterals
• Severe intestinal obstruction as a result of portal hypertension. (Cruveilhier-
• Paralytic ileus accompanied with bowel distention. Baumgarten syndrome)
116 Essentials of Clinical Medicine

• Signifies portal systemic shunting of venous flow when sus (SLE), chronic alcoholism, rheumatoid arthritis,
portal flow is obstructed. thyrotoxicosis.
• Heard over liver and umbilicus.
Causes of Bilateral Parotid Enlargement
Friction Rub • Mumps
Heard in cases of perihepatitis or perisplenitis. • Portal cirrhosis.
• Fibrocalculus pancreatitis.
Common Cases in GIT Cirrhosis • Sarcoidosis.
History in a Case of Cirrhosis of Liver • Mikulicz syndrome.
• Sjögren’s syndrome.
• Ask for fatigue, weight loss, flatulent dyspepsia, anorexia
and low-grade fever Complication of Portal Cirrhosis
• History of hematemesis, malena, leg swelling, • Hematemesis
progressive abdominal swelling, drowsiness and • Anemia.
inversion of sleep rhythm in prehepatic coma cases • Hepatic encephalopathy.
• Past history of viral hepatitis • Spontaneous bacterial peritonitis (SBP)
• History of drug intake, INH, rifampicin, anabolic steroid, • Hypersplenism.
oral contraceptive pills, NSAIDs for malena • Hepatorenal syndrome.
• Past history of blood transfusion—viral hepatitis B, C • Peptic ulcer.
and D or transfusion of any blood products, recent • Infection—TB, etc.
tattooing, acupuncture, drug abuse. • Chronic cholecystitis.
• Alcohol consumption. • Pigment stone.
• Hematochezia, lower GI malignancy and hemorrhoids.
Clinical Features of Hepatic Encephalopathy
Clinical Features of Cirrhosis of Liver • Early—confusion, inversion of sleep rhythm, flaps (Aste-
a. Features of portal hypertension: rixis), constitutional apraxia, micrographia, slurred and
• Ascites monotonous speech.
• Splenomegaly. • Late—coma
• Opening of portosystemic collaterals. • Deep jaundice
b. Features of liver cell failure: • Fetor hepaticas
• Jaundice—terminal. • Liver dullness obliterated bleeding, decerebrate rigidity.
• General weakness, weight loss, muscle wasting, • Cerebellar sign
anorexia, flatulence.
• Fever low grade Causes of Enlarged Liver in Cirrhosis
– Gram-negative bacteremia • Hepatoma.
– Hepatic cell necrosis. • Fatty liver.
• Endocrine manifestation—loss of libido, spider nevi, • Postnecrotic cirrhosis.
spare hairs, palmer erythema gonadal atrophy. • Primary biliary cirrhosis.
• Bleeding diasthesis—PT increased, purpura.
• Cardiac cirrhosis.
• Anemia—microcytic, iron loss due to upper GI
• Budd-Chiari syndrome.
hemorrhage, normocytic due to hypersplenism.
• Ascites—transudate type. • Constructive pericarditis.
• Spider dilated capillaries—face, dorsum of hand, Table 6.7: Causes of anemia, fever, and exudative ascites in cirrhosis
forearm, chest.
Anemia in cirrhosis Fever in cirrhosis Exudative ascites in
Mechanism of Portal Hypertension cirrhosis
• Decreased vascular bed due to fibrosis. Upper GI bleeding Liver cell necrosis Tuberculosis peritonitis
• Distortion of vascular tree. Hypersplenism Portal bacteremia Hepatoma
• Transmission of hepatic arterial pressure to the portal Folate deficiency reaching systemic Subacute bacterial
B12 and iron deficiency blood Peritonitis
system. Melena Associated After diuretic therapy
• Compression of portal tributaries by regenerating nodule. Zieve’s syndrome malignancy Splenic vein thrombosis
Hemolyses
Causes of Palmar Erythema
Anorexia—malnutrition
• Portal cirrhosis, pregnancy, systemic lupus erythemato-
 Alimentary System 117

Endocrinal Manifestation of Cirrhosis • Plantar extensor.

Due to estrogen: • Paraplegia in chronic encephalopathy.
• Palmar erythema. • Change in handwriting.
• Gynecomastia, testicular atrophy. Circulatory Changes in Cirrhosis
• Spider nevi.
• Hyperkinetic circulation.
• Increased ADM secretion.
• Bounding pulse.
• Increased incidence of acid peptic disease and ulcer due
• Tachycardia.
to increased levels of histamine.
• Hyperdynamic apex.
• Increased aldosterone—edema and ascites. • Ejection systolic murmur at the apex.
Causes of Obliteration of Liver Dullness Complications of Alcoholic Cirrhosis
• Pneumothorax. • Bilateral parotid enlarged.
• Emphysema. • Gynecomastia.
• Acute fulminant hepatitis. • Testicular atrophy.
• Following perforation. • Wasting muscle man.
Causes of Dullness over Right Lung Base • Dupuytren’s contracture.
• Amebic liver abscess. Eye Signs in Cirrhosis
• Pleural effusion. • Icterus (terminal stage)
• Subdiaphragmatic abscess. • Pallor.
• Pleural thickening • Bitot’s spots.
• Pneumonic consolidation. • KF ring.
• Basal collapse. • Subconjunctival hemorrhage.
• Malignancy of lung over base.
Causes of Tender, Firm and Hard Liver Causes of Portal Hypertension
• Tender liver—infective hepatitis, amebic hepatitis, fatty Presinusoidal
liver, CCF. Extrahepatic
• Firm liver—cirrhosis, amyloid liver. • Umbilical sepsis.
• Hard liver—malignancy, primary and secondary • Portal pyemia.
carcinoma. • Oral contraceptive pills.
Mechanism of Ascites in Cirrhosis • Portal vein thrombosis.
• Extrahepatis obstruction.
• Portal hypertension—increased hydrostatic pressure in • Abdominal trauma.
portal capillary bed. • Portal lymphadenopathy.
• Hypoproteinemia due to diffuse liver damage. • Hyperviscosity syndrome.
• Increased ADH, estrogen. • Malignancy of liver and pancreas.
• Increased aldosterone. • Idiopathic.
• Increased hepatic lymph formation—seepage of lymph
from liver capsule. Intrahepatic
• Increased pressure of ascites over vein. • Schistosomiasis.
Differential Diagnosis of Hepatic Coma • Congenital hepatic fibrosis.
• Sarcoidosis.
• Subdural hemotoma. • Lymphoma.
• Drunkeness. • Leukemia infiltration
• Wernicke’s encephalopathy. • Primary biliary cirrhosis.
• Primary psychiatric diseases. • Arsenic, copper intoxication and vinyl chloride.
• Hypoglycemia. • Idiopathic portal hypertension.
Neurological Changes in Hepatic Coma Postsinusoidal
• Change in behavior. Intrahepatic:
• Flaps (Asterixis). • Cirrhosis.
118 Essentials of Clinical Medicine

• Alcoholism. Table 6.10: Differentiation between portal cirrhosis and

• Veno-occlusive. primary biliary cirrhosis
• Metastasis. Factor Portal cirrhosis Primary biliary cirrhosis
Extrahepatic: Sex Male Female
• Budd-Chiari syndrome. Pruritus Absent Present
• Constrictive pericarditis. Jaundice Mild Marked
Clubbing No Yes
• Pericardial effusion.
Xanthoma No Yes
Table 6.8: Causes of abdominal pain, hematemesis, Hepatomegaly No Yes
fever, and death in cirrhosis Spleen Markedly enlarged Moderately enlarged
Ascites Present Absent
Abdominal Hematemesis Fever in Death in Serum cholesterol Normal Increased
pain in cirrhosis in cirrhosis cirrhosis cirrhosis Alkaline phosphates Normal Increased
TB peritonitis Rupture eso- TB peritonitis Hepatic encepha- Antimitochondrial No Yes
phagus lopathy antibodies
Spontaneous Peptic ulcer SBP Cerebral edema Autoimmune Rare Yes
bacterial peri- Portal hyper- Hepatic failure Infection Associated disease TB Systemic sclerosis,
tonitis (SBP) tensive gastro- Chronic active- Respiratory failure rheumatoid arthritis, SLE, Lichen planus
pathy hepatitis
Chronic chole- NSAID-induced Coagulopathy
Skin Manifestations of Hepatocellular Failure
cystitis (1/3rd gastric erosion Associated pul- Renal failure
cirrhotics have Rupture gastric monary TB Hypoglycemia • Spider nevi
pigment gall- varices sclero- Others Hypokalemia
stones) pathy-induced Malaria Acid-base
• Palmar erythema
Pancreatitis ulcer Enteric fever imbalance • Diffuse pigmentation
(alcoholic • White nails (Teyy’s nails)
cirrhosis) • Clubbing in biliary cirrhosis
Zieve’s syndrome
• Loss of axillary and pubic hair
(Hemolysis,
pain in abdo- • Paper money skin (upper arms)
men, hyper- • Petechiae and ecchymosis.
lipidemia in
alcoholic Hepatic Facies
patient)
• Shrunken eyes
The WHO classification: • Hollowed temporal fossa
• Grade 0 — Not palpable. • Pinched up nose and malar prominence
• Grade 1 — Palpable and visible only with head • Parced lip
raised. • Muddy complexion of skin
• Grade 2 — Easily visible with head in normal
• Shallow and dry face
position.
• Icteric tinge.
• Grade 3 — Visible from a distance.
Table 6.9: Differentiation between extrahepatic Pathogenesis of Hepatic Encephalopathy
and intrahepatic cirrhosis
Cause Extrahepatic Intrahepatic
• Elevated gamma aminobutoyric acid.
cirrhosis cirrhosis • Elevated endogenous benzodiazepine.
Ascites No Yes • Altered amino acid level.
Hepatic encephalo- No Yes • Increased blood ammonia.
pathy • Increased false neurotransmitter—Octgopamine.
Malena Repeated May have
Liver morphology Normal Abnormal
• Increased cerebral level of glutamine, acetylcholine.
LFT Normal Deranged • Increased short chain fatty acids.
Spleen Massive splenomegaly Enlarged Fischer’s index: The ratio of aromatic amino acid (phenyl-
Prognosis Poor Grave
Wedge hepatic Normal Increased alanine, tyrosine and tryptophan) to branch chain amino
vein pressure acid (Leucine, Isoleucine and Valine) is raised.
 Alimentary System 119

ASCITES – Amebic liver abscess

– Gynecological causes like endometriosis, struma
Clinical Features
ovarii.
• Evening fever, weight loss and chronic diarrhea suggest
tuberculosis Enumerate Causes of Ascites with Jaundice
• Hematemesis, melena in cirrhosis • Gland at porta hepatis—carcinoma stomach, pancreas
• Pigmentation suggests hemochromatosis • Alcoholic hepatitis
• Abnormal distention, weakness, fatigue • Late stage of cirrhosis
• Low-grade fever due to hepatic necrosis. • Subacute hepatic necrosis.

Causes of Distention of Abdomen Signs and Symptoms of Ascites

• Fat • Symptoms
• Fluid – Increase in abdominal girth
• Flatus – Shortness of breath due to elevation of diaphragm.
• Feces • Signs
• Full bladder – Generalized distention of abdomen
• Fetal growth – Flanks become full
• Firm mass—spleen, liver, ovary, kidney. – Umbilicus is everted and stretched (laughing
umbilicus)
Enumerate Causes of Ascites – Epigastric vein may be prominent
– Shifting dullness present
• Transudate – Fluid thrill present
– CCF – Recti divarication may be seen, tense shiny skin
– Nephrotic syndrome – Puddle sign—for quantity of fluid.
– Anemia, hypoproteinemia When peritoneal fluid accumulation exceeds 500 ml,
– Beri-beri ascites can be demonstrated by physical examination.
– Portal hypertension
Table 6.11: Signs and symptoms of portal hypertension
– Cirrhosis of liver
– Epidemic dropsy Common causes Signs Symptoms
– Meige’s syndrome. Cirrhosis Ascites Hematemesis
Nutritional postnecrosis
• Exudate
Drugs Epigastric vein Melena
– Tuberculosis Idiopathic Bleeding piles Pigmentation
– Malignancy Sarcoidosis Retracted liver Abdominal distention
– Secondary deposits in peritoneum Budd-Chiari Spleen palpable
syndrome Low-grade fever
– Collagen disorder Veno-occlusive (Fig. 6.5)
Secondary malignant disease
Noncirrhotic portal fibrosis
Wilson’s disease
Hemochromatosis

Table 6.12: Differences between ascites and ovarian cyst

Points Ascites Ovarian cyst

Uniformity Symmetrical Asymmetrical
Border Never Upper border
Maximum girth Around umbilicus Below umbilicus
Spino umbilical Equal Not equal
distance
Flanks Full Not full
Xiphisternum to Greater Umbilicus to pubic
Fig. 6.5: The subcutaneous venous collateral circulation in: (A) Portal umbilicus distance symphisis distance greater
obstruction (B) Superior vena caval obstruction (C) Inferior vena caval Shifting dullness Present Absent
obstruction. Arrows indicate the direction of blood flow PV examination Normal Ovarian cyst felt
120 Essentials of Clinical Medicine

Table 6.13: Causes of chylosus and hemorrhagic ascites 2. Hepatitis B and C

Chylosus ascites Hemorrhagic ascites • H/o of vertical transmission (for this, the mother
Milky and turbid fluid • Tumor malignant ascites
has to be inquired about her health during pregnancy)
• Trauma to thoracic duct • Tuberculosis ascites • Past H/o jaundice (especially hepatitis B shows H/o
• Tuberculosis • Trauma of longstanding jaundice)
• Tumor invading thoracic duct • Thrombosis of mesenteric • In hepatitis B—signs and symptoms of kidney
artery
• Thrombosis of p. vein. pathology appear—glomerulonephritis, type of
• Tropical (filaria) neuropathies, arthritis, arthralgia.
• Tuberculosis ascites
• Trauma
3. Metabolic causes
i. Wilson’s Disease: (deficiency of enzyme cerulo-
Special Signs giving Clue to Diagnosis of plasmin)
Ascites – Age of onset—18 to 20 years of age
– H/o of recurrent jaundice (which may lead to
• Pulsatile liver with ascites—tricuspid regurgitation (TR)
hepatitis and ultimately total liver damage)
with CCF.
• Big/Soft liver with ascites—intrahepatic portal obstruc- – Clinical features of higher function abnor-
tion. malities like
• Firm shrunken liver with ascites—cirrhosis. a. Abnormal movements
• Hard modular liver with ascites—secondaries. b. Neurological deficit
c. Jaundice
Mucinous Ascites ii. Hemochromatosis
– More common in Scandinavian countries
The ascitic fluid is mucinous in character. It is seen in:
• Pseudomyxoma peritoneii. – Abnormal iron deposition starts in pancreas
• Colloid carcinoma of stomach or colon with peritoneal resulting in diabetes mellitus
implants. – Heart affected (restricted cardiomyopathy)
– Uncontrolled type 2 DM.
ABDOMINAL DISTENTION 4. Cardiac causes
Approach through History • Rheumatic valvular heart disease
• Right heart failure
• Inquire about “duration” of onset
• < 15 days—acute illness 5. Primary biliary hepatitis
• Inquire about “recurrences” of illness • Clinical feature of
• Chronic distention—> 4 months of duration. – Jaundice
Commonest cause of chronic distention is the chronic – Pruritus
liver pathology. In India, some other important causes of – Abdominal pain (upper quadrant)
chronic distention are—Koch’s abdomen (tubercular • Starts at the age of 30 to 35 years in males with
abdomen) and gases in abdomen. family H/o connective tissue disorders.
Liver Pathology Causing Abdominal Distention • May lead to primary biliary cirrhosis.
• Does not present alone, but along with other
Alcoholism, hepatitis B and C, metabolic, cardiac, auto- autoimmune diseases like SLE, Hashimoto’s
immune, and primary TB all cause hepatic congestion. thyroiditis.
Ruling out the Causes One by One • Clubbing of fingers.
1. Alcoholism 6. Koch’s abdomen
• H/o of chronic alcohol addiction • Clinical features of tuberculosis.
• Family H/o alcoholism. • Evening rise of body temperature
• Questions to be asked for alcohol addiction have • H/o weight loss (chronic type)
been described previously in this book
• Loss of appetite—severe anorexia
• H/o of features (signs and symptoms) of alcoholism
• Carotids are enlarged (due to opening of AV • (No H/o of jaundice unless liver is affected because
communications) TB of liver is not common)
 Alimentary System 121

7. Gaseous abdomen SPLENOMEGALY, HEPATOMEGALY AND

• Commonest cause is myxoedema (hypothyroidism) HEPATOSPLENOMEGALY (Fig. 6.6, Plate 3)
• Other causes are—chronic constipation, depressed 1. Mild splenomegaly—spleen is 5 cm (or less) palpable
patients, intestinal tuberculosis with chronic obstruc-
below the left costal margin.
tion of intestine. 2. Moderate splenomegaly—over 5 cm below the left costal
• Superinfection by virus may occur.
margin but not crossing beyond the umbilicus.
8. Hepatorenal syndrome 3. Severe splenomegaly—crossing the umbilicus.
• Patients will present with respiratory failure type I
and type II Table 6.14: Causes of splenomegaly
• Oliguria, anuria Mild Moderate Severe
• Peripheral edema. Enteric fever Hodgkin’s disease Chronic malaria
9. Metabolic encephalopathy Septicemia Lymphoma Kala-azar
Infective endocarditis Leukemia Chronic myeloid
• Uremic and hepatic features like:
Viral hepatitis Polycythemia leukemia (CML)
– Altered sensorium Hemolytic anemia Hemolytic anemia Extrahepatic portal
– Altered sleep hypertension
– Convulsions Weil’s disease Portal hypertension Myelofibrosis
• Anuria. Miliary tuberculosis Biliary cirrhosis Gaucher’s disease
All causes of moderate Hemochromatosis Bilharzias
10. Spontaneous bacterial peritonitis and severe splenome-
• Peritoneal cavity is immunocompromised galy, splenomegaly
• Pain in abdomen with distention in early stages.
• Fever.
Causes of Acute Splenomegaly
11. Portal hypertension
• Abdominal distension Typhoid, malaria, septicemia, splenic infarct, infective
• Upper GI bleeding endocarditis, splenic vein thrombosis, brucellosis and
• Splenomegaly toxoplasmosis and infectious mononucleosis.
• Subconjunctival hemorrhage (because coagulation
Table 6.15: Differentiation between enlarged
cascade is disturbed). spleen and enlarged kidney
12. Carcinoma of any abdominal organ: Severe and sudden Enlarged spleen Enlarged kidney
weight loss (in hepatorenal and hepatopulmonary Edge sharp Rounded
syndrome if we find severe weight loss, then always Notch felt at lower medial border Not felt
suspect carcinoma of liver). Upper border cannot be felt by Can be felt by insinuating finger
13. Sparse hair insinuating finger below the between the mass and costal margin
costal margin
• Chronic liver diseases cause congestion of whole Bimanually not palpable Bimanually palpable
GI tract Dull on percussion Colonic resonance anterior to
• Malabsorption syndrome kidney present
• Hair become sparse Bulge is forwad and inward Tendency to bulge in loin
• Koilonychia develops over nails (because of Loin on percussion is resonant Loin on percussion is dull
decreased iron absorption, iron is lost from nailbeds). Cannot be pushed back into the loin Can be pushed back into the loin

14. Skin Mechanism of Splenic Enlargement

• Spider nevi (dilated capillaries) over neck, face, palate,
upper arm, supramammary area Mechanisms of splenic enlargement are:
• More clearly visible in fair skin and lean individuals. • Reactive of lymphoma cells
15. Autoimmune causes • Infiltration with neoplastic cells
• Blood test for the presence of autoantibodies against • Extramedullary hemopoiesis
bile duct biliary system • Vascular congestion
• Associated with other autoimmune diseases like SLE, • Proliferation of phagocytic cells in response to increased
Hashimoto’s thyroiditis, etc. cell destruction.
122 Essentials of Clinical Medicine

Pathophysiological Basis of Splenomegaly Contd...

• Circulatory disturbance—increased portal venous Category Causes

pressure-prehepatic, posthepatic and hepatic causes Congestive Cirrhosis with portal hypertension
• RES system hyperplasia—hematological: anemia, Metabolic Wilson’s disease
Gaucher’s disease
leukemia, purpura Collagen-vascular disease SLE
• Blood component—hemolytic JRA
• Storage disease and infiltration—amyloid
• Cyst and hemangioma. Table 6.17: Hepatosplenomegaly + Petechiae

Hypersplenism Category Causes

Hypersplenism is a syndrome consisting of splenomegaly, Infective Viral hemorrhagic fever, dengue
viral
pancytopenia (anemia, leukopenia and thrombocytopenia).
Bacterial Septicemia
Presence of hyperactive bone marrow is seen. Increase Infective endocarditis
plasma volume due to pooling of RBC is noted. It reverses Protozoal Toxoplasmosis (IU infection)
after splenectomy. Primary hypersplenism is said to be Hematological Chronic ITP
present when there is no underlying disease. Secondary Thalassemia
Henoch-Schönlein purpura
hypersplenism occurs when there is a known identified cause
Malignancy Leukemia
like in chronic malaria, and kala-azar, etc. Lymphoma
Congestive Hemorrhagic shock syndrome
Causes of Hyposplenism (Splenic Atrophy)
Metabolic Gaucher’s disease
• Sickle cell disease. Niemann-Pick disease
• Coeliac disease. Miscellaneous Cirrhosis with hyposplenism, histiocytosis
• Dermatitis herpetiformis.
Table 6.18: Hepatosplenomegaly + Icterus
• Ulcerative colitis.
• Essential thrombocytopenia. Category Causes
• Congenital absence of spleen. Infective viral Hepatitis
• Splenic irradiation. Bacterial Disseminated Koch’s/disseminated Koch’s
on AKT
Causes of Splenomegaly with Jaundice and Anemia Protozoal Malaria
• Hemolytic anemia. Kala-azar
Hematological Thalassemia
• Cirrhosis of liver with liver cell failure.
Sickle cell anemia
• Acute viral hepatitis, acute Plasmodium falciparum Hereditary spherocytosis
malaria. Malignancy Leukemia
• Lymphoma. Lymphoma
Metabolic Galactosemia
Splenomegaly due to Portal Hypertension Neonatal hepatitis
• H/o upper GI bleeding and malena. Miscellaneous Postnecrotic cirrhosis
Cirrhosis Biliary cirrhosis
• Presence of abdominal veins (prominent vein). Drugs AKT
• Ascites transudates. Antimetabolites
• Esophageal varices as seen in barium swallow or GI Anticonvulsants
endoscopy. Antibiotics

Table 6.16: Hepatosplenomegaly + Pallor Table 6.19: Hepatosplenomegaly + Lymphadenopathy

Category Causes Category Causes

Infective Disseminated Koch’s Viral HIV
Bacterial Infective endocarditis Bacterial Disseminated Koch’s
Protozoal Malaria Protozoal Kala-azar
Kala-azar Hematological Thalassemia
Hematological Thalassemia Malignancy Lymphoma
Sickle cell anemia Miscellaneous Sarcoidosis
Hereditary spherocytosis Histocytosis
Malignancy Leukemia Drugs Phenytoin
Lymphoma Dapsone
Imferon
Contd...
 Alimentary System 123

Table 6.20: Hepatosplenomegaly + Splenomegaly Contd...

Category Causes Protozoal Amebic liver abscess

Hydatid cyst
Infective viral Hepatitis
Hematological Sickle cell disease with autosplenectomy
CML
Malignancy Leukemia
Infectious mononucleosis
HIV Lymphoma
Bacterial Typhoid Congestive AV malformation
SBE Metabolic Glycogen storage disorders (III,VI & IX)
Disseminated Koch’s Niemann-Pick disease
Protozoal Malaria Tyrosinosis
Kala-azar Mucopolysaccharidosis
Hematological Thalassemia Galactosemia
Sickle cell anemia
Chronic hemolytic anemia
Malignancy Leukemia DIARRHEA
Lymphoma
Congestive CCF
History Taking in Case of Diarrhea
Constrictive pericarditis
• Duration—acute (less than 7-14 days)
Cirrhosis with portal hypertension
Metabolic Gaucher’s disease • Chronic more than 2 to 3 weeks.
Niemann-Pick disease • With abdominal pain/without pain—in cholera there is
Glycogen storage disorder no abdominal pain.
Wilson’s disease
Collagen vascular disease SLE • Weight loss—suggests malabsorption or chronic
JRA inflammatory bowel disease, whereas in irritable bowel
syndrome weight loss is not found.
Table 6.21: Hepatosplenomegaly + Ascites
• Nocturnal diarrhea is always organic. It is seen in diabetes
Category Causes with autonomic neuropathy.
Infective Bacterial Disseminated Koch’s • Motion after each meal—suggests irritable bowel
Malignancy Hepatoma syndrome.
Congestive CCF
Constrictive pericarditis
• Fasting stops diarrhea—osmotic diarrhea—lactose
Cirrhosis with portal hypertension intolerance.
Miscellaneous Nephritic syndrome • Milk increase diarrhea—lactose intolerance.
• Stool volume large over one liter—secretory diarrhea.
Table 6.22: Hepatomegaly + Pain
• After same food consumption by several members of
Category Causes family affected—acute gastroenteritis.
Infective viral Hepatitis • Traveling and diarrhea—infection like E. coli,
Bacterial Pyemic abscess
Salmonella, Giardia.
Protozoal Amebic liver abscess
Malignancy Hepatoma • The H/o taking laxative, cholchicine, lactulose.
Congestive CCF • H/o surgery—postgastrectomy, enterostomy.
• H/o systemic illness—diabetes, scleroderma, hyper-
H/o D/D thyroiditis, pulmonary TB.
Further history on associated features along with hepato- • Presence of pus—infective diarrhea, ulcerative colitis,
splenomegaly. In the following discussion, the common bacillary dysentery.
causes of various clinical conditions are listed in the form • Blood in stool—vascular, infective, neoplastic.
of tables. • Whether diarrhea continues with fasting—secretory
diarrhea.
Table 6.23: Hepatomegaly (Fig. 6.6, Plate 3)
• Fecal incontinence, and disease or sphincter dys-
Infective function.
Viral Hepatitis • Tenesmus—colonic—bacillary dysentery.
Bacterial Pyogenic liver abscess
Typhoid
• Homosexual—AIDS.
Tuberculosis • Steatorrhea—fat malabsorption—stool floats, sticks to
toilet, bulky, foul smelling, greasy.
Contd...
124 Essentials of Clinical Medicine

Pathophysiology and Mechanism of Diarrhea • Decreased motility—increased bacteria—DM, sclero-

derma, amyloid, postvagotomy.
• Osmotic diarrhea—large amounts of poorly absorbable
• Increased colonic motility—irritable bowel syndrome.
osmotically active solutes in the gut lumen, e.g. lactose
intolerance. Causes of Diarrhea due to Pancreatic Insufficiency
• Secretory diarrhea—increased chloride and water
• Chronic pancreatitis.
secretion with or without sodium absorption, e.g.
cholera. • Cystic fibrosis.
• Exudative—mucus, blood and protein from the site of • Severe fat malabsorption.
information into the bowel lumen, e.g. Crohn’s disease. • Also in fibrocalculus pancreatic diabetes.
• Abnormal motility—abdominal intestinal motility with
Characteristic Features of Secretory Diarrhea
increased or decreased contact between lumen contents
and mucosal surface, e.g. hyperthyroidism. • Stool volume more than one liter per day.
• Drugs—laxative, magnesium, antacids, colchicines, • Stools are watery.
quinine, diuretics and antibiotics like ampicillin. • No pus or blood
• Miscellaneous—fecal impaction, diverticulitis, ischemic • Diarrhea continuous during last 24-48 hours.
bowel disease. • Osmolality of stool similar to plasma.
Systemic Disease Causing Malabsorption Medical Causes of Acute Abdomen (Non-surgical
• TB Causes of Pain in Abdomen)
• Crohn’s disease. • Diabetic ketoacidosis.
• Lymphoma. • Henoch-Schönlein purpura.
• Immunoglobulin deficiency. • Lead colic.
• Collagen vascular disease. • Acute porphyria.
• Infiltrative disease. • Tabes dorsalis.
Causes of Diarrhea due to Motility Disorders • Dissection of abdominal aorta.
• Increased motility of small bowel—hyperthyroidism, • Anterior wall myocardial infarction.
carcinoma syndrome, postgastrectomy dumping • Irritable bowel syndrome.
syndrome. • Arteritis of mesenteric artery.

Table 6.24: Causes of acute diarrhea

A. Agent B. Pathology C. Organism D. Osmotic diarrhea E. Secretory diarrhea F. Exudative diarrhea

Viral – small bowel Mucosal invasion absent. Rotavirus entro, Primary– Enterotoxin– Idiopathic-Crohn’s
Watery fecal leukocyte adenovirus, norwalk Disaccharidase V cholerae disease ulcerative
absent virus deficiency, spruce E. coli colitis
Mucosal invasion absent Vibrio cholerae S. aureus
Bacteria - small Non-inflammatory, Toxigenic E. coli Secondary– Hormonal–VIP, Infective–Shigella,
bowel fecal leukocytes absent, After gastroen- calcitonin, sero- Salmonella, Campy-
Colon mucosal invasion present. teritis, mannitol, tonin, prostaglandin lobacter TB.
inflammatory, bloody, sorbitol, lactulose Gastric hypersecre- Ischemic–vasculitis
leukocytes present. therapy, sodium tion – ZE syndrome, due to radiation
Parasitic small bowel Non-inflammatory Giardia sulfate, magnesium short bowel syn- entercolitis.
mucosal involvement sulfate, milk of drome, laxatives.
Colon Mucosal invasion present. Entamoeba histoly- magnesia con- Bile salts–ideal
Bloody, fecal, leukocyte tica taining antacids resection, bile duct
present, inflammatory obstruction.
Food poisoning Toxin induced, mucosal S. aureus Fatty acid–pan-
invasion absent, non- C. botulinum creatic insuffi-
inflammatory watery ciency, small intestine
diarrhea mucosal disease
 Alimentary System 125

Table 6.25: Diarrhea due to small bowel and large bowel dysfunction Table 6.27: Amebic and bacillary dysentery

Small bowel Large bowel Amebic dysentery Bacillary dysentery

Large amount Small amount Macroscopic
Watery Formed Number 6 to 8 motions a day Over 10 motions a day
Soapy and greasy Not so Amount Relatively copious. Small.
No tenesmus Tenesmus present Odor Offensive Odourless
Undigested food may be present No undigested food Color Dark red Bright red.
Periumbilical, right quadrant Pain in lower abdomen, pelvis, sacral Nature Blood and mucus Blood and mucus; no
intermittent crampy pain and left lower quadrant mixed with faces. faces
Weight loss more No significant weight loss Reaction Acid Alkaline
No pus and blood Mucus and blood Consistency Not adherent to the Adherent to the bottom
Pain not relieved after passing Pain relieved by passage of stool or continue of the container
stool gases Microscopic
RBC In clumps; reddish
yellow in color.
Clinical Features of Malabsorption
Pus Scanty.
• Frothy, floating, foul-smelling stool Macrophages Very few.
Eosinophils Present
• Soreness of tongue Pyknotic bodies Very Common.
• Weight loss. Ghost cells Nil.
Parasite Trophozoites of
Table 6.26: Causes of chronic diarrhea E. histolytica.
Bacteria Many motile bacteria.
Type Agent
Cl crystals Present.
Infection Giardia, E. histolytica, tubercular Culture No No
Drug Laxative, antibiotic, alcohol, antacid,
theophylline, diuretics, NSAIDs
Malabsorption a. Small bowel mucosal disease
CASE OF JAUNDICE
b. Disaccharidase deficiency History Taking
c. Pancreatic insufficiency
d. Ischemic enteritis • Age of onset—young—hemolytic
e. Short bowel syndrome
f. Bacterial overgrowth
• Old—malignancy
Endocrine causes Zollinger-Ellison syndrome, hyper- • Familial history—Gilbert’s, Dubin Johnson, Wilson’s
thyroidism, cardinoid, villous adenoma disease and hereditary spherocytosis
Motility disorders Irritable bowel syndrome, postvagotomy • In females gallstone, lupoid hepatitis and primary biliary
syndrome, postgastrectomy dumping syn-
drome, short bowel syndrome.
cirrhosis
• Fever with jaundice
Physical Signs of Diarrhea – Infective hepatitis
– Gallstones
• Weight loss – Cholangitis—chills and rigor
• Anemia – Malaria
• Edema feet – Chronic active hepatitis
• Fever
• Abdominal pain—dull right hypochondial pain—infective
• Skin rash
hepatitis
• Peripheral neuropathy
• Colicky pain—gallstones. Constant pain radiating to back
• Abdominal bruit
relieved by forward bending—pancreatic carcinoma
• Fistulae
• Painless jaundice—carcinoma ampulla of Vater
• Right iliac fossa mass
• Lymphadenopathy • Clay-colored stool—cholestasis, extrahepatic obstruc-
• Debility tion
• Tetany • Itching—obstructive jaundice, primary biliary cirrhosis
• White nails • History of pricks by needles and syringe—hepatitis B.
• Goiter virus
• Perianal abscess • History of blood transfusion, alcohol intake
• Rectal mass • Exposure to toxins and drugs.
126 Essentials of Clinical Medicine

Table 6.28: Hemolytic, hepatocellular and cholestatic jaundice Deep jaundice: When jaundice takes greenish hue due to
oxidation of bilirubin to biliverdin seen in obstructive
Haemolytic Hepatocellular Cholestatic
jaundice.
Primaquine Isoniazid Chlorpromazine
Mepacrine Halothane Anabolic steroids
Chloramphenicol Rifampicin Oral contraceptive
Conditions under which the Tissues
Nitrofurantoin Carbon tetrachloride Erythromycin estolate
are not Stained in Jaundice
Staining of tissues depends on blood flow and protein content
• Intermittent (recurrent) jaundice—gallstone, Dubin of fluid. In edematous limb, scar tissue and hemiplegic limbs
Johnson, Gilbert’s syndrome, hemolytic, recurrent staining are absent.
familial cholestasis
Table 6.29: Differences between conjugated and unconjugated bilirubin
• Jaundice with ascites—gland at porta hepatis, late stage
of cirrhosis, primary cirrhosis Properties / Features Conjugated Unconjugated
bilirubin bilirubin
• Palpable gallbladder with jaundice—carcinoma pancreas,
gallbladder • Affinity to lipids No Yes
• Water solubility Yes No
• Enlarged liver with jaundice • Renal excretion Yes No
– Soft tender—infective hepatitis, fatty liver • Vender Berg’s reaction Direct Indirect
– Firm—cirrhosis amyloid • Bound to protein Mildly Strongly
– Hard—secondary carcinoma Table 6.30: Jaundice and hepatocellular jaundice
• Hepatorenal syndrome—viral hepatitis, Weil’s diseases,
halothane Bile acids Very high Moderate increases
• Left supraclavicular gland enlargement and jaundice- Cholesterol Increased Decreased
SGOT/SGPT Slight increase Marked increase
carcinoma stomach Alkaline phosphatase more than 3 times less than 3 times normal
• Lymphadenopathy and jaundice—infectious mono- normal
nucleosis, type B hepatitis, Hodgkin’s disease Prothrombin time Yes No
response to vit K
• Anemia with jaundice—hemolytic, carcimona pancreas,
Steatorrhea Common Uncommon
secondary carcinoma liver. Splenomegaly with jaundice-
hemolytic, cirrhosis of liver, 1/3rd cases of viral hepatitis Table 6.31: Differences among hemolytic, hepatocellular
• Extrahepatic manifestations—arthralgia, rash, lympha- and obstructive jaundice
denopathy Hemolytic Hepatocellular Obstructive
• Short stature, arthritis, mild jaundice, leg ulcer—hemo- jaundice jaundice jaundice
lytic anemia • History • H/o blood • H/o contact with • H/o marked
• Parotid swelling, Dupuytren’s contracture, gyne- transfusion in patient with pruritus and
comastia, testicular atrophy family/siblings/ jaundice (hepa- abdominal pain
patient himself titis)
• Coma and jaundice—hepatic coma, hepatorenal syn- • H/o drug intake • H/o drugs (AKT) • H/o surgery/
drome. • H/o abdominal • H/o vomiting, weight loss
pain during right hypocho-
Where do You See for Jaundice? acute episode. ndriac pain
• Exami- • Pallor may be • Tenderness over • Pallor may be
• Bulbar conjunctiva, buccal mucosa, frenulum of tongue, nation present the liver may be present
nails and skin. findings present
• Ascites may be • Scratch marks
• Bulbar conjunction first gets stained yellow because it
present due to itching
is rich in elastin and elastin has high affinity for bile may be present
pigments. • Ascites may be
present
Differential Diagnosis of Yellow • Investi- • S Bilirubin–Mild • S Bilirubin-Mode- • Bilirubin-mode-
Discoloration of Skin gation increase rate-to-severe rate increase
increase
• Carotenemia—Skin • SGOT/SGPT- • SGOT/SGPT
• Mepacrine—All over except bulbar conjunctiva usually normal markedely
• Drugs—B Complex, Nitrofurantoin, Pyridium and many increased
more. Contd...
 Alimentary System 127

Contd... Alcohol
Hemolytic Hepatocellular Obstructive
jaundice jaundice jaundice Drug Toxicity
• S Alkaline Phos- • S Alkaline phos- • S Alkaline phos- • Predictable, dose dependent, e.g. acetaminophen, unpre-
phatase usually phatase phatase marked- dictable, idiosyncratic, e.g. isoniazid.
normal increased ly increased
• Urine Absent Present Present
Environmental Toxins
exami- • Vinyl chloride
nation: • Jamaica bush tea – pyrolizidine alkaloids.
• Bilirubin Present Present Absent • Wild mushrooms – Amanita phalloides or verna.
Urobilinogen
• Wilson’s disease
• Stool Present Present Absent
exami- • Autoimmine hepatitis.
nation:
sterco- Cholestatic Conditions that may
bilinogen Produce Jaundice
• Retic count Increased Normal Normal
Intrahepatic
Causes of Jaundice • Viral hepatitis:
i. Fibrosing cholestatic hepatitis—hepatitis B and C.
Causes of Isolated Hyperbilirubinemia ii. Hepatitis A, Ebstein—Barr virus, cytomegalovirus.
Indirect Hyperbilirubinemia • Alcoholic hepatitis
• Hemolytic disorders • Drug toxicity
i. Inherited: i. Pure cholestasis—anabolic and contraceptive
a. Spherocytosis, elliptocytosis G-6-PD and pyru- steroids.
vate kinase deficiency. ii. Cholestatic hepatitis—chlorpromazine, erythromycin
b. Sickle cell anemia. estolate.
ii. Acquired: iii. Chronic cholestasis—chlorpromazine and prochlor-
perazine.
a. Microangiopathic hemolytic anemias.
• Primary biliary cirrhosis.
b. Paroxysmal noctural hemaglobinuria.
• Primary sclerosing cholangitis.
c. Immune hemolysis.
• Vanishing bile duct syndrome:
• Ineffective erythropoiesis i. Chronic rejection of liver transplants.
i. Cobalamin, folate, and iron deficiencies. ii. Sarcoidosis.
• Drugs iii. Drugs.
i. Rifampicin, probenecid, ribavarin. • Inherited
• Inherited condition i. Benign recurrent cholestasis
i. Crigler-Najjar type I and II • Cholestasis of pregnancy.
ii. Gilbert’s syndrome. • Total parenteral nutrition.
Direct Hyperbilirubinemia • Non-hepatobiliary sepsis.
• Inherited condition. • Benign postoperative cholestasis.
• Paraneoplastic syndrome.
i. Dubin-Johnson syndrome
• Veno-occlusive disease.
ii. Rotor’s syndrome.
• Graft versus host disease.
Hepatocellular Conditions that may Extrahepatic
Produce Jaundice • Malignant
Viral Hepatitis i. Cholangio carcinoma.
ii. Pancreatic cancer.
• Hepatitis A, B, C, D and E. iii. Gallbladder cancer.
• Ebstein-Barr virus. iv. Ampullary cancer.
• Cytomegalovirus. v. Malignant involvement of porta hepatitis, lymph
• Herpes simplex. nodes.
128 Essentials of Clinical Medicine

• Benign Contd...
i. Choledocholithiasis. Intrinsic G-6-PD deficiency Extrinsic
ii. Primary sclerosing cholangitis. • March hemoglobin
iii. Chronic pancreatitis. uria
iv. AIDS cholangiopathy. 3. Miscellaneous
Chemical drugs,
infection, burn, lead
Causes of Ascites with Jaundice and
poisoning.
Hard Liver
• Budd-Chiari syndrome. Causes of Hepatocellular Jaundice
• Gland at porta hepatis.
• Secondary seedling peritoneum. • Active liver disease, viral hepatitis, infectious mono-
• Cardiac cirrhosis. nucleosis, yellow fever.
• Constrictive pericarditis. • Non-viral relapsing fever, septicemia.
• Drugs, anti-TB drugs, halothane, etc.
Causes of Intermittent Jaundice • Fatty liver of pregnancy.
• Chronic liver disease—primary biliary cirrhosis, primary/
• Hemolytic anemia.
secondary tumor of liver.
• Congenital hyperbilirubinemia.
• Gallstone impaction and disimpaction. Table 6.33: Causes of obstructive jaundice
• Carcinoma of ampula of Vater. Intrahepatitic cholestasis Extrahepatic jaundice
• Viral hepatitis • Porta hepatitis – ampula of
Causes of Unconjugated Hyperbilirubinemia
• Drugs –Methyl testosterone, Vater
• Overproduction—hemolysis, ineffective erythro-poiesis. chlorpromomide, anabolic, • Causes in lumen – stone,
• Decreased hepatic uptake—septicemia, starvation, drug. steroid, chlorpromiazine, parasite, stricture
PAS, oral contraceptive pills. • Causes in wall of lumen –
• Defect in bilirubin conjugation (decreased glucuronyl
• Alcoholism carcinoma bile duct, trauma,
transferase) • Jaundice in pregnancy. acute pancreatitis chronic
• Gilbert’s syndrome, Criggler-Najjar syndrome, neonatal • Dubin-Johnson and Rotor’s pancreatitis
jaundice, drug induced) (chloramphnicol, novobiocin, syndrome • Causes outside the wall –
pregnanediol). • Postoperative jaundice carcinoma head of pancreas,
• Sclerosing cholangitis pseudocyst
Table 6.32: Causes of hemolytic jaundice • Biliary atresia
(unconjugated hyperbilirubinemia)
Intrinsic G-6-PD deficiency Extrinsic Sequelae of Viral Hepatitis
• Spherocytosis • Antimalarial drugs 1. Immune mechanism • Acute fulminant hepatitis.
• Elliptocytosis • Sulfonamides • Autoimmine,
• Chronic persistent hepatitis.
• Hemoglobino- • Chloromphenicol Warm and cold
pathies. antibodies • Chronic active hepatitis.
• Sickle cell disease • Nitrofurantoin • Cold hemoglobin- • Posthepatitis syndrome.
• Hbs • Quinine uria • Cirrhosis of liver.
• Thalassemia • Drugs and chemicals
• Carcinoma of liver (hepatoma)
• Hemoglubinuria • Viral pneumonia
• Malaria • Cerebral edema, GI bleeding.
• Hypersplenism • Hepatorenal failure.
• Incompatible blood • HBs Ag carrier.
transfusion
2. Non-immune
• Rarely pancreatitis, myocarditis, atypical pneumonia,
mechanism: aplastic anemia, peripheral neuropathy, glomerulo-
• Mechanical hemo- nephritis.
lysis due to cardiac
valve Sequelae of Fulminant Hepatic Failure
• Microangiopathic
hemolytic anemia • Hepatic encephalopathy.
Contd... • Cerebral edema.
 Alimentary System 129

• Respiratory failure. Table 6.34: Distinctive features of Crohn’s disease and ulcerative colitis
• Hypothermia. Feature Crohn’s disease Ulcerative colitis
• Infection.
Macroscopic
• Bleeding, pancreatitis. Bowel region Ileum ± colon Colon ± ileum Colon only
• Renal failure. Distribution Skip lesions Skip lesions Diffuse
• Metabolic Stricture Early Variable Late/rate
Wall
– Hypoglycemic, hypokalemia, hypomagnesemia, acid- appearance Thickened Thin Thin
base disturbance. Dilation No Yes Yes
Microscopic
MAJOR CAUSES OF NEONATAL Psuedopolyps No to slight Marked Marked
CHOLESTASIS Ulcers Deep, linear Deep, linear Superficial
Lymphoid Marked Marked Mild
• Bile duct obstruction reaction
Serositis Marked Moderate Mild
• Extrahepatic biliary atresia Granulomas Yes (50%) Yes (50%) No
• Neonatal infection Fistulas/sinus Yes Yes Yes
• Cytomegalovirus Clinical
• Bacterial sepsis Fat/vitamin Yes Yes If ileum
Malabsorption No No
• Urinary tract infection Malignant Yes Yes Yes
• Syphilis potential
• Toxic drugs Response to Poor Fair Good
surgery
• Parenteral nutrition
• Metabolic disease RUPTURE SPLEEN
• Tyrosinemia
As the shock passes off, there are signs which point to
• Niemann-pick disease intra-abdominal bleeding.
• Galactosemia
• Defective bile acid synthetic pathways General Signs
• Antitrypsin deficiency
Increasing pallor, rising pulse rate, sighing respiration and
• Cystic fibrosis restlessness.
• Miscellaneous
• Shock/hypoperfusion Local signs
• Indian childhood cirrhosis
• Abdominal rigidity more in left upper quadrant.
• Alagille syndrome (paucity of bile ducts) • Local bruising and tenderness in left upper quadrant.
• Abdominal distention 3 hours after the rupture due to
INFLAMMATORY BOWEL DISEASE irritative effect of intraperitoneal blood which produces
Diagnosis in favour of irritable bowel syndrome: peritonitis and ileus.
Continuous or recurrent abdominal pain or discomfort • Kehr’s sign—pain referred to left shoulder due to blood
– relieved by defecation, or associated with altered stool in contact with undersurface of diaphragm, pain
frequency or consistency together with either or both of mediated via phrenic nerve.
• Shifting dullness in flanks.
the following features:
• Ballance’s sign—dull note in both flanks, but on right
a. Altered pattern of defecation—for at least 25 percent of
side it can be made to shift; whereas on left, it is
the time is two or more of the following:
constant. Reasons for this is that blood near the lacerated
– Altered stool frequency (> 3 / day or < 3 / week). spleen has coagulated though there is blood in peritoneal
– Altered stool form (lumpy, hard, loose, watery). cavity.
– Altered stool passage (straining, fecal urgency, feeling • Rectal examination—tenderness, soft swelling due to
of incomplete emptying). blood or clot in rectovesical pouch.
– Passage of mucus.
b. Abdominal distention or a feeling of abdominal Radiological Signs
bloating. • Obliteration of splenic outline and psoas shadow.
130 Essentials of Clinical Medicine
• Identification of left side of gastric air bubble.
• Fracture of one or more lower ribs on left side.
• Elevation of left side of diaphragm.
• Free fluid between gas-filled intestinal coils.
GIT
1. A 40-year-old male with longstanding alcohol abuse
complains of abdominal swelling which has been pro-
gressive over several months. He has a history of gastro-
intestinal bleeding. On physical examination, there are
spider angiomata and palmar erythema. Abdominal
collateral vessels are seen around umbilicus. There is
shifting dullness, and bulging flanks are noted. A
paracentesis is performed in this patient. The serum
albumin minus ascitic fluid albumin equals 1.2 gm/dl.
The most likely diagnosis is:
Portal hypertension
2. While hospitalized, the patient’s mental status
deteriorates. He has been having guaiac-positive stools
and low-grade fever. He also has received sedation for
agitation. On physical examination, the patient is
confused. He has no meningeal irritation signs and no
focal, neurological and no rhythmic flapping tremor of
the wrist. The most likely explanation for mental status
change is:
Hepatic encephalopathy
3. A 60-year-old male is noted to have mild jaundice and
weight loss. Alkaline phosphates is very elevated. He
had very pale stools. The most probable diagnosis is:
Pancreatic carcinoma
Nephrology
1. A 70-year-old male with a history of urinary tract infection
and congestive heart failure was admitted to the hospital
for sepsis and pulmonary edema. He was treated with
clindamycin and tobramycin and also received intra-
venous furosemide. After several days, the signs of sepsis
improved, but the BUN rose to 60 mg/dl and creatinine
to 5.0 mg/dl. The blood pressure changed. Weight was
unchanged throughout the hospital course. The most
likely diagnosis is:
Acute tubular necrosis
2. A young man presents to the emergency room with
cyanosis and disorientations. Blood gases show a pH of
7.2, PCO2 of 68 mm Hg., HCO3 of 35 mg/dl. There are
multiple needle tracks in the antecubital fossa. The rest
of the examination is normal. The most likely acid-base
problem is:
Acute respiratory acidosis
 Alimentary System 131

RADIOGRAPHS (Figs 6.7 to 6.15)

Fig. 6.7: Duodenal ulcer shown by barium meal Fig. 6.8: Renal artery stenosis

Fig. 6.9: Almost achalasia, but note the irregularity of Fig. 6.10: Plain radiograph showing radiopaque
the taper, which indicates carcinoma of cardia stones in gallbladder
132 Essentials of Clinical Medicine

Fig. 6.11: Retrograde ureterogram showing double ureter on the left Fig. 6.12: Radiograph showing a vescicle calculus
(no contrast has been used)

Fig. 6.13: Retrosternal goiter causing deviation of Fig. 6.14: Plain radiograph of a perforated ulcer,
a) trachea b) esophagus (barium swallow) showing air under diaphragm

Fig. 6.15: Chest radiograph showing an abcess with a fluid

level below the diaphragm secondary to a pancreatic
abscess
 7

Cardiovascular System

INTRODUCTION not be counted as a regular beat. It is indicative of low

arterial tension and is noted in fevers, congestive cardiac
Before examining the cardiovascular system (CVS) proper
(which includes peripheral vascular system and heart), a failure, cardiac tamponade, or following open heart
systematic examination of the patient must be carried out. surgery.
Certain points of particular interest should be assessed • Catadicrotic pulse: A pulse wave with two small notches
before carrying out the examination of CVS. These points in the descending portion.
are: (Fig. 7.1, Plate 3) Points to be looked for in the pulse are:
1. Pulse i. Presence or absence of pulse
2. Blood pressure ii. Equality on both sides
3. JVP iii. Rate
4. Edema of various body parts. iv. Rhythm
v. Force of the pulse
EXAMINATION OF THE PULSE vi. Tension
The term pulse has been derived from the Latin word “Pulses” vii. Volume of the pulse
meaning “Beating”. viii. Character of the pulse
ix. Radiofemoral delay
Definition x. Condition of the vessel wall
xi. Synchronicity on both sides.
The blood forced into the aorta during systole not only moves
the blood in the vessels forward but also sets up a pressure
Presence or Absence of the Pulse
wave that travels along the arteries. The pressure wave
expands the arterial walls as it travels, and expansion is All the peripheral pulses should be examined before declaring
palpable as the “pulse”. The rate at which the wave travels, the pulse to be absent. The arteries that should be routinely
which is independent of and much higher than the velocity palpated are:
of blood flow, is about 4 m/s in the aorta, 8 m/s in the large • Radial artery
arteries, and 16 m/s in the small arteries of young adults. • Dorsal pedis artery
Consequently, the pulse is felt in the radial artery at the • Popliteal artery
wrist about 0.1 sec after the peak of systolic ejection into • Femoral artery
the aorta. With the advancing age, the arteries become more • Carotid artery
rigid, and the pulse moves faster.
• Ulnar artery
• Anacrotic pulse: A pulse showing a secondary wave on
• Temporal artery.
the ascending limb of the main wave. It is best felt in
the carotids in aortic stenosis, hypertension. Pulses are absent in conditions like:
• Catacrotic pulse: A pulse showing one or more secondary • Diabetic arteriopathy
waves on the descending limb of the main wave. • Pulseless disease (Takayasu’s syndrome)
• Dicrotic pulse: A pulse with a double beat, one heartbeat • PVD (peripheral vascular diseases)
for the two arterial pulsations, or a seemingly weak wave • Peripheral embolization
between the usual heartbeats. This weak wave should • Subacute aortitis.
134 Essentials of Clinical Medicine

Equality of Pulse on Both Sides • Athlete

• Those performing meditations, yogas, etc.
Normally, the pulse are equal (both in the volume and force)
• May be a familial trait
on both the halves of the body. An inequality in these features
• Sleep.
is said to be pathological and is suggestive of:
b. Pathological:
• Aneurysms of aorta
• Vagal stimulation due to any cause
• Coarctation of aorta
• Enteric fever and viral infection
• Cerebrovascular disease (unequal carotids on both sides)
• Raised intracranial tension (ICT)
• Severe hypoxia
Pulse Rate
• Hypothermia
It is defined as number of contractions of heart per unit of • Myxoedema
time (i.e. per minute). It is detected by palpating a peripheral • Sick sinus syndrome
artery, the best being the radial artery. Normally, the rate of • Early stage of myocardial infarctions
pulse in a healthy adult is about 60 to 100 per minute. The • Obstructive jaundice
condition in which the rate is < 60 is called sinus bradycardia • Raised intraocular pressure (IOP)
and if it is > 100, the condition is sinus tachycardia. • Heart blocks.
Pulse should always be counted for one full minute by c. Drugs: Beta-blocker, verapamil, diltiazam, digoxin
palpating a peripheral artery (usually radial artery) to avoid
Apex—Pulse Deficit
missing extrasystoles or other irregularities like atrial
fibrillations. It is defined as the difference between pulse rate and heart
It should be simultaneously correlated to heartbeat, so rate when counted simultaneously for one full minute.
that any beat that is too weak to be transmitted to radial Causes are: Atrial fibrillations, ventricular premature beats.
pulse can be judged.
Rhythm
Abnormality of Pulse Rate
Pulse rate can either be fast (tachycardia) or slow Normally, the rhythm is regular. It is usually assessed by
(bradycardia) with a normal sinus rhythm. palpating the radial artery. The rhythm becomes irregular in
certain conditions both physiological and pathological.
Causes of sinus tachycardia:
i. Physiological: Sinus arrhythmia pulse becomes
1. Physiological causes:
irregular with normal respiration. During inspiration,
– In children/infants
the pulse rate gradually increases; and during
– Emotional upsets
expiration, the rate slows down. It occurs in normal
– After a hot shower
healthy individuals and is not pathological. Normally,
– Exertion/exercise.
it is seen in infants and children but may exist in adults
2. Pathological causes:
also. The origin is believed to be vagal.
Noncardiac:
ii. Pathological:
– Pyrexia/hyperpyrexia.
1. Regularly irregular pulse:
– Hyperdynamic circulatory states like anemia, thyro-
• Extrasystole appearing regularly after fixed
toxicosis, beri-beri, arteriovenous (AV) fistula, pheo-
normal beats, ventricular bigeminus, trige-
chromocytoma.
minus, quadrigeminus, etc.
Cardiac:
• Atrial tachyarrhythmias with fixed AV block.
– Tachyarrhythmias—supraventricular, ventricular.
2. Irregularly irregular pulse:
– Acute anterior wall MI
• Occasionally missed beats due to extrasystole
– Cardiac failure
(premature beats), early heartblock (Wenke-
– Cardiogenic shock.
bach’s phenomenon), sinoatrial block (rare)
Systemic/peripheral:
• Multiple ectopics (extrasystoles), atrial
– Hypotension
fibrillation
– Hypovolemia.
• Atrial flutter with varying AV blocks.
3. Drugs:
– Atropine, nefedipine, beta agonists like salbutamol, [Regular pulse: It is defined as a pulse felt when the force
thyroxine, catecholamines nicotine, caffeine. and frequency are the same. When length of the beat and
Causes of sinus bradycardia: number of beats per minute and strength are the same]
a. Physiological: (Figs 7.2 to 7.4).

Fig. 7.2
Pulsus Bigeminus (Coupling of Beats
Coupled Pulse)
Definition: A pulse in which two regular beats are followed
by a longer pause (called compensatory pause). It has the
same significance as an irregular pulse mechanism/genesis.
The type of pulse is a result of regularly repeating
extrasystoles. After every normal beat, there is an extra-
Fig. 7.3: Note that second dicrotic wave is felt during diastole
Cardiovascular System 135
Fig. 7.4
systole. Hence, on palpation, two beats are felt in succession
followed by a pause. The sequence is repeated again and
again.
In pulsus alternans, the compensatory pause is absent;
whereas in pulsus bigeminus, the compensatory pause is
present.
Conditions:
• Most common cause is digoxin toxicity
• Alternate premature beats
• AV block, every third sinus impulse being blocked
• Sinoatrial block with ventricular escape.
Force of the Pulse
Force of the pulse is indirectly an indication of systolic
blood pressure (SBP). It is defined as the amount of pressure
(which the examiner applies with his fingers) needed to
occlude the pulse.
Procedure
It is measured in the following way. The examiner keeps
his 3 fingers (index, middle and ring fingers) over the radial
artery of the patient. The finger placed most distally, (i.e.
towards the palm of the patient) is used to press the artery
tightly so as to present any back flow of blood towards the
heart. Then with the help of most proximal finger (i.e. the
finger which is towards the elbow of the patient), the
examiner slowly compresses the pulse until the pulse is no
longer felt by the middle finger. The force (or pressure)
applied in this manner is called the force of the pulse.
In abnormalities of force, the rhythm of the pulse is
normal (through the variation in force gives a false feeling
of irregularity).
136 Essentials of Clinical Medicine
The pulses which come under this category are:
a. Pulsus alternans
b. Pulsus bisferience
c. Dicrotic pulse
d. Anacrotic pulse.
Pulsus Alternans
Definition: A pulse with alternating strong and weak
pulsations. The rhythm of the pulse is normal. This differs
from pulsus begeminus where there is a distinct pause after
two beats.
Procedure: Pulsus alternans can be easily detected by
measurement of blood pressure of the patient. By using
auditory method when the SBP is measured at the highest
level, then only auditory sounds are audible. But all the
sounds become audible as soon as the pressure is lowered.
This is because the pulse wave produced by the weaker
beat is not sufficient to get recorded as the highest systolic
pressure (highest SBP). This type of pulse is best appreciated
by palpating radial or femoral pulses, rather than the carotids.
Mechanism/genesis: It is produced most probably due to
alternate rather than regular contraction of the muscle fibers
of the left ventricle. It usually indicates grave prognosis.
Conditions:
• Severe left ventricular failure
• Tonic myocarditis
• Paroxysmal tachycardia
• Several beats following a premature beat in an otherwise
normal heart.
• Coupled ventricular premature beats may also resemble
pulses alternans; but in this case, the rhythm is irregular.
Pulsus Bisferience
Definition: A pulse marked by two systolic peaks on the
pulse waveform. It has 2 systolic peaks separated by mid-
diastolic dip. In this type of pulse, every pulse beat is
distinctly felt to have a double impulse.
Mechanism/genesis:
i. Idiopathic hypertrophic subaortic stenosis: In the early
phase, there is no obstruction to outflow of the blood
and nearly more than 3/4th (i.e. about 80%) of the
stroke volume is ejected in the early part of systole.
As the systole proceeds, the obstruction occurs in
midsystole when aortic value comes close to
hypertrophied septum. Therefore, there occurs a dip,
due to sudden cessation of the blood flow followed
by a secondary rise as the left ventricle gets over the
obstruction.
ii. Severe aortic incompetence and mild aortic stenosis:
Due to severe aortic incompetence, the volume of
flowing blood initially increases during the early part
of systole. And as the mild aortic stenosis also
accompanies, it causes an extra high velocity jet to be
thrown out, giving rise to secondary rise.
iii. Conditions:
– Combined aortic stenosis and aortic regurgitation.
– Severe aortic regurgitation (without aortic
stenosis)
– HOCM (hypertrophic obstructive cardiomyo-
pathy)
c. Dicrotic pulse: See above
d. Anacrotic pulse: See above
Tension of the Pulse
Definition
An opposite to the force of the pulse, the tension of the
pulse indirectly indicates diastolic blood pressure (DBP).
Procedure
The examiner palpates the arterial pulse of the patient (usually
radial pulse). A very heavy pressure is required to feel the
high tension pulse which indicates high DBP. Accordingly,
medium or normal DBP requires moderate pressure and
low DBP requires light pressure.
Volume of the Pulse: (Amplitude of the pulse)
Definition
It indirectly indicates stroke output of the heart (i.e. left
ventricular output per beat.)
Procedure: The examiner palpates the arterial pulse of the
patient. When pulse waves pass through the artery, an uplift
is felt by the palpating finger, the extent for this uplift
(amplitude) is a rough estimate of the volume of the pulse.
– Pulse pressure between = 30-60 mm Hg – Volume normal
– Pulse pressure between < 30 mm Hg – Small (low)
volume pulse
– Pulse pressure between > 60 mm Hg – Large (high)
volume pulse
– Pulse volume depends on stroke volume and arterial
compliance.
Character of the Pulse: (Form)
Definition
Sometimes a very confusing term is used called character
of the pulse. What does the character of pulse actually mean?
The character of the pulse is a congregate description of its
“volume, force and tension”. Pulse is not only an expansion
(dilatation) and contraction (returning to original size) of
the vessels; but the whole vessel is made taut and let loose
thus undergoing a physical sinuous movement because of

wave of vibrations imparted by the ventricles at every beat.
This wave may have either a rapid (celer) or rather a
prolonged (tardus) onset. The description of the wave type
as regards the rate of onset and the energy of vibrations is
called the character or form of the pulse. It can be studied
by a sphygmograph. Clinically, it is described as “abrupt”
or “prolonged.” The abrupt pulse may be further “short
and slapping” or “thin and thready.” The prolonged pulse
may be either “full” or “bounding”.
But due to its confusing nature, the term character (or
form) of the pulse is now totally obsolete. Similarly, most
of the estimates of the force and tension usually go wrong
and do not corroborate with the blood pressure measure-
ments done by sphygmomanometer. Their separate
observations are, therefore, omitted now.
ABNORMALITIES OF VOLUME OF THE PULSE
Normally, the volume of the pulse reduces during inspiration
and increase during expiration.
Mechanism
During inspiration, a high negative pressure develops in the
thoracic cavity due to the descent of the diaphragm. As a
result of that, the chambers of the heart dilate → pressure
of blood in the heart falls → more venous return from the
periphery is favored → leading to low volume of the pulse.
Reverse of this occurs during the act of expiration.
Hypovolemic or Hypokinetic Pulse
Causes are:
• Cardiac failure
• Cardiac tamponade
• Pericardial effusion
• Constrictive pericarditis.
• Shock/dehydration (severe)
• Blood loss (severe)
• Mitral stenosis
• Aortic stenosis
• Excessive vomiting ultimately may lead to severe
dehydration
• Adhesive pericarditis
• Mediastinal tumor
• Massive pleural effusion
• Tension pneumothorax
• Massive emphysema.
Hypervolemic or Hyperkinetic Pulse
Causes are:
• Hyperdynamic (hyperkinetic) circulatory states like –
anemia, beri-beri, thyrotoxicosis, pyrexia, pheochro-
mocytoma.
Cardiovascular System 137
• Mitral regurgitation
• Ventricular septal defects.
Abnormalities of Pulse Due to Variations in
Force, Tension and Volume
Water Hammer Pulse, or Corrigan Pulse or
Collapsing Pulse or Triphammer Pulse
In its milder form, it is also called “bounding pulse”.
Definition: A pulse characterized by short, powerful, jerky
beat that suddenly collapses. The peculiar pulsation may be
distinctly visible, not only in the carotids but throughout the
brachial artery. It is diagnostic of aortic regurgitation (AR).
Mechanism/genesis: The water hammer pulse is diagnosis
of AR during the period of compensation, and its force is
due to excessive ventricular hypertrophy and due to large
amounts of blood expelled with each systole; its sudden
recession is due to incompetent valves failing to support
the column of blood.
It is a large volume pulse with a rapid upstroke (systolic
pressure is high) and rapid down stroke (diastolic pressure
is low).
Procedure: The examiner holds the forearm of the patient in
its middle portion. A distinct palpable shock is felt. If the
arm is raised, the pulse becomes more prominent (because
the radial artery comes in line with the aorta).
(Note: A water hammer is an evacuated glass-tube half-
filled with water that was a popular toy in the 19th century;
when held in the hand and inverted, it delivers a short, hard
knock)
Causes of water hammer pulse
i. Physiological:
• Fever (pyrexia)
• Pregnancy
• Chronic alcoholism
• Temporary after hot shower.
ii. Hyperkinetic circulatory states:
• Anoxia
• Thyrotoxicosis
• Beri-beri
• Cor pulmonale
• Cirrhosis of liver
• Paget’s disease
• Arteriovenous fistula
• Arteriovenous aneurysm.
iii. Cardiac causes:
• Aortic regurgitation
• Patent ductus arteriosus (PDA)
• Aortopulmonary window
138 Essentials of Clinical Medicine

• Complete heart block JUGULAR VENOUS PULSE

• Systolic hypertension
• Bradycardia The two main objectives of examination of neck veins are
• Rupture of sinus of Valsalva into the heart cham- inspection of their wave form and estimation of central
bers. venous pressure (CVP). In most patients, the right internal
jugular vein is best for both purposes. Usually, the pulsations
Thready Pulse of internal jugular vein is greatest when the trunk is inclined
The characteristics are: by < 30°. In patients with elevated venous pressure, it may
• Low volume pulse be necessary to elevate the trunk further, sometimes to as
• Low force pulse much as 90°. When the neck muscles are relaxed, shinning
• Seen in any condition producing shock of especially a beam of light tangentially across the skin overlying the
cardiogenic. vein exposes the pulsation of internal jugular vein.
Pulsus Parvus et Tardus: The normal JVP reflects phasic pressure changes in the
(See above) (Slow rise and slow fall) right atrium and consists of two or sometimes three positive
waves and two negative trough.
Pulsus Parvus
Some as pulsus parvus at tardus but slow rise and slow fall The “a” Wave
are not seen. It is commonly seen in case of severe mitral
The positive presystolic “a” wave is produced by venous
stenosis.
distention due to right atrial contraction and is dominant
PULSUS PARADOXUS: (KUSSUMAUL’S PULSE) wave in JVP, partial only during inspiration.

Definition The Large “a” Wave

A pulse that is more or less suppressed at the close end of
each full inspiration, frequently noted in adherent pericarditis.
Mechanism
Normally, the SBP falls by 3 to 10 mm Hg during inspiration
(as explained earlier) when the SBP falls more than 10 mm
Hg during inspiration, the pulse is (erroneously) called pulsus
paradoxus, though it is just an exaggeration of normal
phenomenon and not its reversal.
The situation is said to be paradoxical, because in severe
cases, the peripheral pulse disappears on inspiration; whereas
paradoxically, the heart sounds are still audible during missed
beats.
[A reverse pulsus paradoxus—in individuals who are on
continuous ventillatory support by a mechanical (artificial)
ventillation].
It indicates that the right atrium is contracting against an
increased resistance. It is seen in:
• Tricuspid stenosis (TS)
• Increased resistance to right ventricular filling pressure
(pulmonary hypertension or pulmonic stenosis)
• Tricuspid atresia
• Myxoma of right atrium
• Pulmonary stenosis (Figs 7.5A to E).
Cannon “a” Waves
They are produced when large “a” wave occurs during
arrhythmias whenever the right atrium contracts, while the
tricuspid valve is closed by the right ventricular systole.
They occur regularly (as during functional ryhthm) or
irregularly (as in atrioventricular dissociation with ventricular
tachycardia or complete heart block). They are also seen in
ventricular tachycardia and ectopic beats.

Causes Absent “a” Wave

• Atrial fibrillation
• Systemic
– Superior vena cava (SVC) obstruction There is an increased delay between “a” wave and the
• Related to heart carotid arterial pulse in patients with first degree
– Severe congestive cardiac failure atrioventricular block.
– Constrictive pericarditis Diminished “a” Wave
– Pericardial effusion.
• Prolonged PR interval
• Pulmonary
• Tachycardia.
– Airway obstruction
– Emphysema The normal jugular venous pulse and its component
– Asthma. waves (Fig. 7.6).

Figs. 7.5A to C: Waveform of jugular venous pulse. The ECG is
portrayed at the top of the illustration. Note how electrical events
precede mechanical events in the cardiac cycle. Thus, the P wave
(atrial depolarization) and QRS complex (ventricular depolarization)
precede the “a” and “V” waves of the JVP.
A. Normal JVP. The “a” wave produced by atrial systole is most
prominent deflection. It is followed by “X” descent interupted by small
“C” wave making tricuspid valve closure. Atrial pressure then rises
again (“V” wave) as atrium fills passively during ventricular systole.
The decline in atrial pressure as the tricuspid valve opens produces
the “Y” descent.
B. Giant “a” wave. Forceful atrial contraction against a stenozed
tricuspid valve or a non-compliant hypertrophied right ventricle
produces an unusually prominent “a” wave.
C. Cannon “a” wave. This is caused by atrial systole against a closed
tricuspid valve. It occurs when atrial and ventricular rhythms are
dissociated (complete heart block, ventricular tachycardia) and marks
coincident atrial and ventricular systole.
D. Giant “V” wave. It is seen in tricuspid regurgitation. The regurgitant
jet produces pulsatile systolic wave in JVP.
E. Prominent “X” and “Y” descents. These occur in constrictive
pericarditis. In tamponade only “X” descent is exaggerated.
Fig. 7.6: The normal JVP and its component waves
Cardiovascular System 139
The “C” Wave
It is position wave produced by the bulging of tricuspid
valve into the right atrium during right ventricular
isovolumetric systole and by the impact of carotid artery
adjacent to jugular vein.
It begins at the end of first heart sound and reaches its
peak shortly after the first heart sound..
The “X” Wave
The “X” descent wave during systole is after acentuation in
patients with constrictive pericarditis, but the nadirs of this
wave is reduced with right ventricular dilation and is
recovered in tricuspid regurgitation.
The “X” descent is obliterated or may be replaced by a
positive wave “S wave” in tricuspid regurgitation. The I
wave may fuse with “C” waves and V wave to produce a
giant “V” wave.
The “V” Wave
The positive, late systolic “Y” wave results from the
increasing volume of blood in the right atrium during
ventricular systole when the tricuspid valve is closed.
Tricuspid regurgitation causes the “V” wave to be more
prominent; when tricuspid regurgitation becomes severe,
the combination of a prominent “V” wave and obliteration
of the X-descent results in a single large positive systolic
wave. After the “V” wave peaks, the right atrial pressure
falls because of the decreased bulging of the tricuspid valve
into right atrium as the right ventricular pressure declines
and the tricuspid valve opens.
The “Y” Wave
The negative descending limb, the “Y” descent of the JVP
is produced mainly by the opening of the tricuspid valve
and the subsequent rapid inflow of blood into right ventricle.
A rapid, deep, “Y” descent in early diastole occurs with
severe tricuspid regurgitation. A venous pulse characterized
by sharp “Y” descent, a deep “Y” trough and a rapid ascent
to the baseline is seen in patients with constructive pericarditis
(Friedriech’s ataxia) or with severe right-sided heart failure
and a high venous pressure. A slow “Y” descent in the JVP
suggests an obstruction to right ventricular filling, as occurs
with tricuspid stenosis or right atrial myxoma.
Measurement of JVP (jugular venous pressure) (Fig.
7.7).
INSPECTION
Inspection forms a very important part of cardiovascular
system examination. The points to be examined in inspection
of cardiovascular system are:
140 Essentials of Clinical Medicine

Other Causes of Bulging of Precordium

• Mediastinal tumor
• Scoliosis.
Causes of Flattened Precordium
• Congenital deformity
• Fibrosis of lung
• Chronic case of pleural or pericardial effusion.

Apex Beat

An apex beat is the lowermost, outermost and maximum

thrust of juxta apical part left ventricle.
An apex beat (or apex inpulse) is the lowermost and
Fig. 7.7: Jugular venous pressure. In the normal subject, with the outermost point where the cardiac impulse is felt/seen up
back reclining at an angle of 45° to the horizontal, slight pulsations are till 4 years of age. Normally, the apex upon heart lies in 4th
visible in jugular vein just above clavicle. This corresponds to the to
the level of sternal angle whatever the position of thorax. The vertical
intercostal space and after 5 years of age 4 years of age.
distance between right atrium and sternal angle indicates the mean Normally, it is seen in the fifth intercostal space about 31/2
hydrostatic pressure in the right atrium. inches (9 cm.) from the midsternal line. It can also be
described in relation to the midclavicular line and the normal
1. Size and shape of precordium and thoracic cage apex beat is about ½ inch (1 cm) medial to thin line.
2. Apex beat Describing the position of normal apex in relation to nipple
3. Retraction of chest wall is incorrect as the position of nipple varies in different
4. Any visible pulsation individuals.
5. Pulsation over suprasternal notch and epigastric pulsation
6. Distended vein over precordium and chest wall Points to be Looked for in the Apex Beat
7. Scars, sinuses, etc. 1. Present or absent (i.e. visible or invisible).
2. Exact site.
Precordium: (Also called 3. Type
Antecordium or Precordia) 4. Extent
It is defined as the area on the anterior surface of the body 5. Mobility of apex beat
overlying the heart and lower part of the thorax. 6. Character of apex beat.
Size and shape of precordium and thoracic cage: Present, absent, displaced or shift apex beat: Apex beat may
a. Cardiac hypertrophy - Bulging precordium, be invisible in the following conditions:
(which may be due to - Bony cage and inter- • Apex beat behind a rib
rheumatic or congenital costal spaces both are • Thick chest wall as in obesity.
heart disease) prominent (These 2 are the commonest causes of invisibility of
b. Pericordial effusion - Bulging of only the apex beat. In case, where the apex beat lies, behind a rib
intercostals spaces. it may become visible in anterior axillary line, on turning
c. Pectus excavatum or - Funnel-shaped the patient to left lateral position).
depressed sternum deformity of anterior • Emphysema.
aspect of thorax. • Pericardial effusion.
Apex impulse is pushed • Tight cavity as in fibrosis, calcification or constrictive
laterally pericarditis
Does not alter the phy- • Decreased force of ventricular contraction as seen in
siology of hearts/lungs. inflammatory conditions, degenerative condition or
It needs no treatment. asphyxia.
d. Aortic aneurysm - Localized bulging to the • Severe dilatation of heart.
right side of sternum or • In myocardial failure.
near the sterni. • If covered by pendulous breast.
 Cardiovascular System 141

• In extreme shift to the right side when the apex beat lies Mobility of the beat: It is defined as the change in position
behind the sternum. of apex beat with the change of body position. Normally, a
• Diffuse apex beat. change (mobility of apex beat occurs with the change in
Exact site: (Exact site has been mentioned earlier) body position).
Apex beat visible but shifted or displaced: a. Mobility absent:
a. Cardiac causes: • Adhesive pericarditis.
Outward and horizontal shift (which may later on also b. Excessive mobility
go upwards) – Right ventricular hyper trophy. • Cor mobilale.
• Downwards and outwards—left ventricular hyper- • Tear drop heart
trophy. • Congenital heart disease.
• Apex impulse on right side in the 5th intercostal space
– Dextrocardia. Retraction of Chest Wall over the Precordium
b. Extra cardiac causes: • Retraction of apex along with parasternal:
There are mostly due to respiratory disorders, where – Pulsation—massive right ventricular hypertrophy
the heart (mediastinum) is pulled or pushed to one side. (right ventricular rock).
Push Pull • Prominent apex beat with retraction of parasternal.
• Pleural effusion Pulmonary fibrosis – Area (left side)—massive left ventricular hypertrophy
• Pneumothorax Pulmonary collapse (left ventricular rock).
• Hydropneumothorax • Prominent apical and left parasternal impulses with
• Massive hemothorax retraction in between—biventricular hypertrophy
– Intrathoracic tumor. (biventricular rock).
– A massive ascites may cause the shift of the
impulse upwards. Visible Pulsations
c. Deformities of thoracic cage:
• Kyphosis a. Pulsations over the precordium:
• Scoliosis Left parasternal – Right ventricular hypertrophy
• Kyphoscoliosis – Left atrial enlargement
• Pectus excavation (shifts the apex laterally by – Aneurysm of aorta.
compressing and flattening the heart). (Aortic aneurysm may be seen as a pulsating mass either
at base of heart on the right side in 2nd ICS or rarely when
Type of apex beat: it erodes through the sternum).
a. Hearing apex beat • Pulmonary area – Pulmonary hypetension
b. Hyperdynamic apex beat (rarely).
c. Tapping apex beat. • High output – Pulmonary artery dilatation,
(The above three are more a part of palpation and have states pulmonary hypercirculation
been explained there). (ASD).
d. Retraction at the site of apex beat. is seen in adhesive • Second right – Dilated pulmonary artery
pericarditis. intercostal – Aneurysm of aorta.
e. Dome-shaped apex beat—severe left ventricular space – Hyperkinetic space.
hypertrophy, which is of the following types— – Enlarged left atrium.
hypertrophy in parallel (concentric hypertrophy), b. Pulsation outside precordium:
hypertrophy in series, work hypertrophy, anoxic • Suprasternal – Hyperdynamic circulatory
hypertrophy. states like anemia, thyrotoxi-
f. Bifid apex beat—[double heart beat – due to left bundle cosis, beri-beri
branch block (LBBB)]. – Aortic aneurysm.
Extent of apex beat: Normal apex beat extends to a distance – Coarctation of aorta.
of about 2.5 cm (1 inch). If the apex beat extends > 2.5 – Abnormal thyroidea ima artery.
cm, it is called diffused apex beat. – Pulsating thyroid gland.
In hyperdynamic circulatory states, we get diffuse heart – Syphilitic aortitis.
beats. – High arch aorta.
142 Essentials of Clinical Medicine
– Abnormal course of innomi-
nate artery or anomalous sub-
clavian artery.
• Epigastric pulsation:
– Aortic aneurysm.
– Right ventricular hypertrophy.
(To differentiate between the above two, the examiner keeps
his hand flat over the epigastric area. He then slowly tries to
insert his middle and ring fingers below the xiphisternum.
If the beats come and touch the tip (little towards left) of
the fingers, then it is due to right ventricular hypertrophy;
and if the beat touches the pulp of fingers, then it is due to
abdominal aortic aneurysm).
• Aortic pulsation in is seen asthenic individual with thin
chest wall.
• Mass (or tumor) attached to or in close association to
aorta (transmitted aortic pulsation).
• Hepatic pulsation in tricuspid valve disease (either
incompetence or stenosis).
• Juxta apical pulsation – Ventricular aneurysm
pulsations.
• Right side of chest – Dextrocardia.
– Right atrial enlarge-
ment.
– Shift of the heart to
right of aorta.
• Right sternoclavicular joint – Right-sided aortic
arch
– Aortic aneurysm.
– Dissecting aneurysm
of aorta.
• In the neck:
carotid artery pulsation – Hyperdynamic
states.
– Aortic regurgitation.
– Coarctation of aorta.
– Systemic hyperten-
sion.
• Aortic regurgitation.
• Subclavian artery aneurysm
• Exophthalmic goiter
• Sternoclavicular – Aortic regurgitation.
– Aortic dissection.
– Aortic aneurysm
– Right-sided aortic
arch (TOF)
• Apical – Left ventricular or
right ventricular en-
largement.
• Over the back: – Pulmonary arterio-
interscapular region venous fistula infra-
scapular pulsation.
– Coarctation of aorta
(Suzzman’s sign).
• Ectopic pulsation – Ischemic heart dis-
ease.
– Left ventricular dys-
function or aneu-
rysm.
– Cardiomyopathies.
Distended Veins over the
Precordium and Chest Wall
• Superior vena cava obstruction
• Inferior vena cava obstruction
• Right-sided heart failure
• Intrathoracic obstruction.
Detailed Arteries over the
Precordium or Chest Wall
• Coarctation of the aorta (however, they are more
prominent on the back than in precordial region and
also when the patient bends forwards).
• Spider nevi in liver cell failure.
Scars and Sinuses
Scars: A middle sternotomy scar usually indicates previous
coronary bypass or valve replacement.
A left submammary scar is usually the result of a mitral
valvotomy.
Sinuses: Due to tuberculosis of spine (Pott’s spine). They
are now not commonly seen due to improvement in the
treatment of tuberculosis.
PALPATION
Palpation is another very important part of cardiovascular
system examination. Palpation is done to confirm findings
of the inspection.
Golden Rules for Palpation
1. Use the whole flat of the palm first.
Then fingers
Lastly single finger (tip)
2. Use palm for
– Left ventricle.
 Cardiovascular System 143

– Apex. • Retractile apical impulse—severe

– Mitral area for palpating thrills. – Pericarditis
– Parasternal area with the base of the palm in the – Severe TR.
epigastrium and central portion and fingers in the
Parasternal Impulse
left parasternal area (Dressler’s method). This gives
pulsation of right ventricle. Seen in - Right ventricular enlargement left atrial
3. Force of apex beat: enlargement.
a. Heaving apex beat:
Table 7.1: Causes of RVH and LVH
It is felt as increased thrust of the apex where the
impulse is forceful and sustained throughout systole Left ventricular hypertrophy (open Right ventricular hypertrophy
and is increased both in force and amplitude. It is beat down and out and heaving) (open beat tapping)
suggestive of: • AS • MS
• Left ventricular enlargement. • AR • PS
• Hypertension • Cor pulmonale
• Ill-sustained heave
• MR • TR
– aortic stenosis
• PDA • ASD
– aortic or mitral regurgitation.
b. Hyperdynamic apex beat: Palpable Aortic Component of Second Heart
Here although the force or the amplitude of the Sound (A2) : (Over Aortic Area)
impulse is increased, but the duration is not
• Severe hypertension
prolonged. It is felt like a quick thrust to the palpating
• Syphilitic aortitis.
hand. It is felt in:
• Aortic aneurysm provided there is no associated aortic
• Aortic incompetence. incompetence.
• Mitral incompetence. i. Mitral opening snaps
• Hyperdynamic circulatory states like anemia, ii. Aortic ejection clicks.
beri-beri, thyrotoxicosis, pregnancy, pheochro- iii. Triple rhythm including gallop rhythm
mocytoma, Paget’s disease. If palpable in the If palpable in left
apical area, then it is parasternal area, then
Differences between Hyperdynamic and left ventricular it is right ventricular
Heaving Apex Beat gallop gallop rhythm
a. Tapping apex beat: (opening snaps, ejection clicks and gallop rhythm have been
It is felt like a clear and distinct tap over the position of described in “auscultation”).
apex. In fact, it is first heart sound, which has become
palpable and accentuated. THRILLS
b. Feeble apex beat: Thrills can be defined as the vibrations felt by the palpating
• It is mostly due to weakness of: hand when it is placed over the heart or the blood vessels. A
Myocardium thrill is a sensation like the “purring of a cat” that is felt by
– myocardial infarction the hand when a murmur is palpable. A thrill is never present
– myocarditis. without a murmur.
c. Other features:
• Hypodynamic apex Table 7.2: Mechanism of production
– Obesity, acute myocardial infarction, pleural Obstruction to blood Abnormal direction Rapid and increased blood
effusion, pericardial effusion, constrictive flow in valvular of blood flow flow in normal direction
pericarditis, COPD. stenosis • Septal defects blood flow in dilated
• Diffuse apical impulse—left ventricular aneurysm, • Regurgition chamber
left ventricular dysfunction.
• Double apical impulse—HOCM (hypertropic • Thrills are palpable, low frequency vibrations associated
obstructive cardiomyopathy), infarction, pleural with heart murmurs. Usually present in stenotic lesions
effusion, pericardial effusion. of heart.
144 Essentials of Clinical Medicine

Table 7.3: Examination of thrills Contd...

(5) Carotid thrills : (carotid shudder)
Disease Site Timing of thrill
Systolic thrill
MS Apex Presystolic
• Aortic stenosis
AS Aortic Systolic
PS Pulmonary Systolic
VSD 3rd and 4th interspace Systolic (6) Apical thrills
PDA Pulmonary Continuous Systolic thrill Diastolic thrills
• MR • MS
Thrills should be examined for: • AS
• Site
• Nature Murmurs not Associated with Thrills
• Timing of thrills (it can be judged by comparing it with
apex impulse). 1. Austin-Flint murmur:
A presystolic or late diastolic heart murmur best heard
Golden Rules at the apex of the heart. It is present in some cases of
aortic insufficiency. It is due to the vibration of mitral
a. Thrills at the apex (apical thrills) are diastolic. However, valve caused by backward – flowing blood from aorta
apical thrills may be systolic (as in severe MR)
meeting the blood flowing in from the left atrium.
b. Thrills at the base of the heart (basal thrills) are more
commonly systolic. However, basal thrills may be 2. Carry Coomb’s murmur.
diastolic (as in acute severe AR).
Pericardial Rub
Reason for basal thrills being systolic: The soft diastolic
murmur which are produced by aortic or pulmonary Pericardial rush is a harsh grating palpable sound over the
incompentence are usually not accompained by thrills. precordium. Tenderness may or may not associate it. It is
Table 7.4: Thrills and their corresponding area characteristically felt in pericardial inflammation (acute dry
with underlying pathology pericarditis).
(1) Mitral area
Tracheal Tug
Systolic thrill Diastolic thrill
• mitral incompetence may be prolonged with a typical The examiner raises the chin of the patient and applied a
presystolic accentuation ending in firm pressure in the upward direction with the help of fingers
tapping apex mitral stenosis of one or both the hands kept on the cricoid cartilage.
In case of aortic arch aneurysm or mediastinal tumor, a
(2) Pulmonary area downward tug (pull) is felt by the fingers with each
Systolic thrill Continuous thrill Diastolic thrill heartbeat. It is due to downward pull on left bronchus which
• Pulmonary stenosis • PDA • Tricuspid stenosis is transmitted to trachea and cricoid cartilage.
• Atrial septal defect • Rupture of
(ASD). sinus of Valsalva
• Venticular septal
Some Interesting Facts
defect (VSD) In case of aortic incompetence, a few important signs are
• PDA noted. Some of these are:
• Head nodding with each beat heartbeat—De Musset’s
(3) Parasternal area sign.
Systolic thrill (in 3rd and 4th ICS) Diastolic thrill tricuspid stenosis • Movement of uvula, or ear pinna.
• Venticular septal defect VSD • Nailbed movement (flushing and blanching).
• Tricuspid incompetence • In anterior pericarditis—we get retraction at each heart-
beat (Broadman’s sign).
(4) Aortic area
Systolic thrill Thrill due to a flow murmur PERCUSSION (Fig. 7.8)
• Aortic stenosis • Hyperdynamic circula-
tory states. Percussion as a method of physical examination was
• Acute severe aortic regur- discovered by Aunbrugger.
gitation. Percussion has a very limited role in the modern
• Syphilitic aortic regur-
cardiology. Hence, it has been described in short here. It is
gitation
useful only in certain special situations such as:
Contd...
 Cardiovascular System 145

Fig. 7.8: Percussion of borders of heart
• Pericardial effusion (increased dullness).
• Emphysema—where there occurs enlargement of
cardiac borders (decreased cardiac dullness).
• Detecting the aortic dilatation as in aneurysm of aorta
and pulmonary artery dilation as in pulmonary
hypertension or idiopathic pulmonary artery dilation.
• Dextrocardia (which may or may not be associated
with situs invertus).
• Dilated cardiomyopathy.
Principles of Percussion
1. Always start percussing from resonant to dull area.
2. Finger should be parallel to the border being percussed.
3. No space (gap) should be left between the finger and
chest wall.
4. Scratching and stethoscope method: That is when the
stethoscope is placed over the chest wall and the chest
wall is scratched, then over the area which is dull, there
will be change in the intensity of the sounds which can
be very well detected by the stethoscope.
• Pericardial effusion—increases cardiac dullness
• Emphysema—encroachment of cardiac dullness.
AUSCULTATION (Figs 7.9 and 7.10)
Table 7.5: Conduction speed in cardiac tissue
Fig. 7.9: Diagram showing the projections of heart valves and the
auscultatory areas 1- pulmonary artery valve; P – pulmonary area; 2
– aortic valve; A – aortic area; 3 – tricuspid valve; T – tricuspid area;
4 – mitral valve; M – Mitral area
Some Interesting Facts Related to Auscultation
• Stethoscope was invented by Lennaec
• Total ideal length of stethoscope—12 inch (the
stethoscope that we generally use is 18 inch long).
• Diameter of lumen—1/8 inch (minimum)
• Thickness of diaphragm—0.003 inch.
• Diameter of diaphragm—4 cm
• Diameter of bell—2.5 cm.
Sounds Best Heard by the
Diaphragm of Stethoscope
High-pitched sounds (including murmurs also)
• First and second heart sounds
• Systolic murmurs (especially early diastolic)
• Pericardial rubs
• Opening snaps
• Clicks
Sounds Best Heard by Bell of the Stethoscope
Low-pitched sounds (including murmurs also)
• Mild diastolic murmurs
• Third heart sound
• Fourth heart sound.

Cardiac tissues Conduction speed mts/sec.

SAN 0.05
Atrial pathways 1.0
AVN 0.05
Bundle of His 1.0
Purkinje system 4.0
Ventricular muscles 1.0
Atrial muscles 1.0 Fig. 7.10: The normal heart sounds comparing duration and frequency
146 Essentials of Clinical Medicine

Sites to keep the stethoscope (areas of auscultation) auscultating beyond the point of appearance (as explained
a. Over precordium: above) we may sometimes come across another sound
(or murmur), the intensity of which (the intensity of
Table 7.6: Mitral area and cardiac apex sound) is maximum.
Mitral area Cardiac apex Significance: If an examiner does not ausculdate
• Tricuspid area Lower left parasternal area carefully, he may assume the second sound as the
• Aortic area 2nd right intercostals space close “radiation of first murmur and involvement of another
to sternum valve may be missed”. Therefore, all the students are
• Secondary aurtic area (erbs area) 3rd left intercostals space close to advised to auscultate every centimeter (or every inch)
sternum between two murmur sounds.
• Pulmonary area 2nd left intercostals space close
to sternum Principles of Auscultation
• Gibson’s murmur or murmur 1st left intercostals space close to
1. Low-pitched sounds/murmurs are best heard by the bell
of PDA sternum
of the stethoscope and high intensity sounds/murmur
by the diaphragm.
b. Other ausculatory areas: 2. Always start auscultating the chest from the aortic area.
The significance of this is that, over the aortic area only
Table 7.7: Other auscultatory areas
A2 (i.e. aortic component of second heart sound) is
Axilla (anterior mid and posterior Murmurs of mitral stenosis audible and you have no chance of getting confused by
axillary lines) the other type of murmur.
Epigastrium Abdominal cortic murmurs
3. Then you should auscultate the pulmonary area where
Carotids Carotid shudder
Inter-and infrascapular areas you auscultate only P2 (pulmonary component of second
Supra-and infraclavicular areas heart sound). Again no chance of confusion.
4. Then, go to the tricuspid area when you auscultate 1st
Auscultation can be performed at any other site of the heart sound.
body where you suspect pulsations/bruits. 5. And at last, auscultating, the mitral area. The mitral
area is auscultated at last because here you have 1st
Scratching and the Stethoscope Method heart sound as well as A2 (aortic component of second
The examiner keeps his stethoscope over the chest wall of heart sound), as the aorta originates from the left
the patient and he scratches the chest wall (either with ventricle and vibration of aortic valve closure may be
fingernails or with other solid objects). Increased intensity transmitted via blood to the area of mitral valve.
of sound will be heard over the area of dullness as compared Thus, the sequence for auscultation → aortic area
to other areas, which are normal. ↓
Triangular and hour glass auscultation: Pulmonary area
a. Triangular auscultation:
↓
Every murmur has its peculiar area of origin (exact site
of origin). It forms the base of the triangle. We all know Tricuspid area
that every murmur is heard over some extent (it may be ↓
a few millimeters or a few centimeter from the exact Mitral area
site of origin). As we go on auscultating away of murmur
(This sequence is for the beginners so that they can
sound goes on decreasing and ultimately it disappears .
differentiate various murmurs clearly. Experienced ears, of
Now, if we join, the base with this point (beyond which
the sound of murmur disappears), we get a triangular course, require no rules).
area. Purpose of Auscultation
Significance: It gives us the idea about:
1. Heart sounds (1st and 2nd)
1. Which valve is involved/affected?
2. Murmurs
2. Radiation of murmur
3. Added sounds (third heart sound, fourth heart sound,
3. The point where maximum intensity is heard.
b. Hour glass auscultation: opening snap ejection clicks, pericardial rub, plop sounds
This method is used to differentiate between two similar due to prosthetic valves, gallop, which is in fact
types of murmurs. This method is similar to the pathological HS3)
triangular method, but the difference is, if we go on • First heart sound is auscultated for:
 Cardiovascular System 147

– Absence Characteristic features:

– Accentuations
– Split Atrial muscles contract
Gallop—pathological HS3 ↓
Rise in atrial pressure
↓
Right atrial pressure rises by 4-6 mm Hg
↓
1. Atrial type 2. Ventricular type And left atrial pressure rises by 7-8 mm Hg
– Ejection click
↓
– Pulmonary
Propels 30 percent of additional blood into ventricles.
– Aortic Narrowing of orifices of IVC and SVC and pulmonary
Before coming on to the heart sounds and murmurs, orifices occurs but still some blood regurgitates because of
you should have a knowledge of the “Cardiac cycle” which absence of valves between atrial and great vessels (veins).
is very essential!!! ↓
Narrowing of orifices of IVC, SVC, and pulmonary veins
CARDIAC CYCLE (Fig. 7.11) causes decrease in VR to heart.
Atrial Systole
Ventricular Systole
Duration—0.1 sec.
Duration—0.3 sec.
a. Isovolumetric ventricular contraction (0.05 sec).
b. Ventricular systole proper (0.25 sec)
Isovolumetric Ventricular Contraction
(0.05 sec)
As the atrial contraction phase passes off, the pressure in
both, the atria and ventricles falls.
↓
Ventricular contraction begins.
↓
Ventricular pressure exceeds atrial pressure very rapidly.
↓
Closure of AV valves with 1st heart sound.
Thus 1st heart sound appears in isovolumetric ventricular
contraction phase (HS)
↓
The ventricles are now closed chambers.
↓
Myocardial pressure on blood continuously goes on
increasing.
↓
This causes bulging of AV valves into the atria.
↓
Small but sharp rise in atrial pressure.
↓
During this phase although contraction is occurring, but
Fig. 7.11: Normal resting pressures in mm mercury there is no emptying of ventricle called isovolumetric
in the chambers of heart ventricular contraction.
148 Essentials of Clinical Medicine

Ventricular Systole Proper (0.25 sec) a. Protodiastole: (0.04 sec)

When pressure in LV exceeds pressure in aorta (80 mm Due to end of ventricular systole.
Hg) ↓
and Ventricular pressure falls rapidly.
When pressure in right vent. exceeds pulmonary artery (10- ↓
12 mm Hg) Arterial pressure is better sustained due to elastic recoil
↓ of vessel wall.
Opening of semilunar valves ↓
↓ Arterial pressure exceeds the ventricle.
Ejection phase occurs ↓
Closure of semilunar valves.
↓ ↓
2nd heart sounds
(1) Rapid ejection (2) Summit (3) Slow ejection 2nd heart sounds occur during protodiastole.
phase (0.1 sec) phase (0.15 sec) b. Isovolumetric ventricular Relaxation Phase: (0.06 sec)
Begin after closure of S1 valves.
Rapid ejection phase: ↓
Intraventricular pressure rises to maximum Intraventricular pressure drops continuously.
(LV = 120 mm Hg) (RV < 25 mm Hg) ↓
↓ Ventricular muscles continue to relax without change in
ventricular volume called IVR phase.
Rapid increase in ventricular volume output
↓
(2/3rd of stroke vol. is ejected in this phase) Ends when ventricular pressure falls below atrial
↓ pressure (resulting in opening of AV valves).
Arterial pressure rises. c. Ventricular Diastole Proper:
Approx 70 percent of ventricular filling occurs.
↓ – Rapid filling of ventricles:
Opening of semilunar valve and closure of AV valves Begins with opening of AV valves (0.1-0.12 sec)
occurs. It is due to continuous relaxation of ventricular
Summit: pressure in ventricles remains low.
The summit of ventricular pressure curve is reached – Slow filling of ventricles:
when aortic or pulmonary artery pressure actually It is called diastasis (0.18-0.2 sec)
exceeds the ventricular pressure. Although due to It is due to continuous VR filling of both atrium and
momentum, the blood continues to flow for some time. ventricle and readjusting the EDV of ventricle.
Slow ejection phase: (0.15 sec) d. Last Rapid Filling Phase:
Atrial systole occurs.
Ventricular contraction begins to subside.
↓
↓ This terminates the cardiac cycle.
Ventricular pressure falls.
↓ Atrial Diastole: (0.7 sec)
Whereas flow from arteries to its peripheral branches Atrial muscle relaxes (pressure drops to zero).
continues to be high. ↓
Blood enters into it.
Ventricular Diastole: (0.5 sec) ↓
a. Protodiastole (0.04 sec). Pressure increases inside it.
b. Isovolumetric ventricular relaxation (0.06 sec) ↓
Opening of AV valves.
c. Ventricular diastole proper (0.30 sec)
↓
d. Last rapid filling phase—(0.1 sec)
Cycle continues.

Although events of the two sides of the hearts are similar,
they are somewhat asynchronous. Right atrial systole
proceeds left arterial systole, and contraction of right
ventricle starts after that of the left. However, since
pulmonary arterial pressure is lower than the aortic pressure,
right ventricular ejection begins before left ventricular
ejection. During expiration, the pulmonary and aortic valves
close at the same time. But during inspiration, the aortic
valve closes slightly before the pulmonary. The slower
closure of pulmonary valve is due to lower impedance of
the pulmonary vascular tree. When measured over a period
of minutes, the outputs of the 2 ventricles are, of course,
equal, but transient differences in output during the
respiratory cycle occurs in normal individuals.
The first event in a cardiac cycle is atrial depolarization
(p wave on the surface ECG). Followed by right atrial and
then left atrial contraction.
Ventricular activation (the QRS complex on the ECG)
follows after a short interval (the PR interval). Left
ventricular contraction starts and shortly thereafter right
ventricular contraction begins. The increased ventricular
pressures exceed the artrial pressure, and close first the
mitral and then the tricuspid valves. Until the aortic and
pulmonary valves open, the ventricles contract with no
change in volume (isovolumetric contraction). When
ventricular pressures rise above the aortic and pulmonary
artery pressures, the pulmonary valve and then the aortic
valve open and ventricular ejection occurs. As the ventricles
begin to relax, their pressures fall below the aortic valve
closure. Isovolumetric relaxation then occurs. After the
ventricular pressures have fallen below the right atrial and
left arterial pressures, the tricuspid and mitral valves open.
BASIC SOUNDS
The First Heart Sound (S1)
The first heart sound (S 1) is produced by the events
associated with closure of mitral and tricuspid valves, in
that order.
1. Normally, in (S1) is louder than (S2) at the cardiac apex.
(S1) is heard well with the diaphragm and the bell of the
stethoscope.
2. Because the sound produced by tricuspid valve closure
is much fainter than the sound produced by mitral valve
closure, audible splitting of S1 into its mitral and tricuspid
components is uncommon in normal patients.
3. Splitting of S1 into two components, about 0.03 seconds
apart, can sometimes be heard normally at the lower
left sternal border where the tricuspid valve component,
is the louder when splitting of S1 is heard at the cardiac
Cardiovascular System 149
apex, the split is usually due to mitral valve closure,
pulse on atrial sound (S4) or mitral valve closure plus an
ejection sound, and not true splitting of S1.
a. Wide splitting of S1 occurs with delayed closure of
the tricuspid valve in the right bundle branch block
(RBBB).
4. The intensity of S1 depends on the rate of pressure
development in the ventricular, the structure of the valve
leaflets, and the position of the AV valves at the beginning
of the ventricular contraction.
5. The examiner can recognize S1 of increased intensity
by noting that S1 is louder than S2 at the base of the
heart. S1 increased in intensity occurs:
a. In hyperkinetic states exhibiting increased contra-
ctility and myocardial tension development. Such
conditions include anemia, pregnancy, anxiety,
hyperthyroidism and fever.
b. In the presence of mitral valve leaflet thickening and
scarring as long as the leaflets maintain some motility.
This is characteristic of mitral.
c. When the mitral valve is wide open at the onset of
the ventricular contraction. This occurs when there
is a short P-R interval (0.11-0.13 seconds) on the
ECG and the onset of ventricular contraction
following atrial contraction occurs earlier than normal.
The mitral valve also occurs earlier than minimal.
The mitral valve is also wide open at the onset of
ventricular contraction in mitral stenosis because of
the high left atrial pressure seen in this disease.
6. The examiner will recognize S1 of decreased intensity
when S2 is louder than S1 at the cardiac apex. S1 is
decreased in intensity:
a. In states of impaired ventricular contractility and
decreased myocardial tension development. Such a
situation occurs in congestive heart failure.
b. When the mitral valve is completely immobile. This
occurs in severe cases of mitral stenosis.
c. When the mitral valve is already nearly closed at the
onset of ventricular contraction. This situation occurs
when there is a prolonged P-R interval (>0.2 seconds)
on the ECG where the onset of ventricular
contraction following atrial contraction is delayed.
As a result, the mitral and tricuspid valves to have
already floated particularly shut at the onset of
ventricular contraction.
7. S1 varies in intensity from beat to beat when the position
of the AV valves at the onset of the ventricular contraction
is variable. This occurs in atrial fibrillation, third degree
heart block and in patients with ventricular demand
pacemakers. In each of these conditions, there is no
150 Essentials of Clinical Medicine
fixed relationship between atrial excitation and ventricular
contraction. Thus, the position of the AV valves at the
beginning of ventricular systole is variable, sometimes
being particularly shut, and at other times being
completely open.
Causes of Loud S1
• Mitral stenosis, tricuspid stenosis.
• AV block, short P-R interval.
• Tachycardia.
• Hypodynamic circulation.
• Increased AV flow from left to right.
• Shunt—ASD, VSD.
The Second Heart Sound (S2)
The second heart sound (S2) is produced by the events
associated with closure of aortic and pulmonary valve.
1. S2 is normally higher pitched and shorter in duration
than S1.
2. S2 is normally louder than S1 at the cardiac base (second
intercostal spaces), and is heard well with both the
diaphragm and bell.
3. Two components of S2 are normally heard in many
patients. Although right ventricular ejection, right
ventricular ejection has a longer duration, and finishes
after left ventricular ejection. As a result, P2 occurs after
A2.
a. The first component (A2) is associated with closure
of aortic valve, and is readily heard in the second
right. ICS, the second and 3rd left ICS, and lower
left sternal border and at the cardiac apex.
b. The second component (P 2) is associated with
closure of the pulmonic valve. Because P2 is softer
than A2, P2 is normally heard only at the second or
third left intercostal spaces. P2 may increase in
intensity as a result of pulmonary hypertension, and
then may be heard along the lower left sternal border
and at the cardiac apex.
c. When S2 is increased in intensity, it will be louder
than S1 at the cardiac apex. If S2 is louder than S1 at
the apex, and if splitting of S2 is heard at the apex,
then pulmonary hypertension is likely.
4. Separation of S2 into its two components is termed S2
splitting which is more commonly heard in individuals
less than 50 years of age than in older patients. Splitting
of S2 should be assessed with the patient sitting upright.
5. Physiologic splitting of S2 characterizes the normal
occurrence of the aortic component (A 2) and the
pulmonic component (P2) widening during inspiration.
a. The mechanism responsible for widening of the split
is somewhat complicated, but related primarily to a
delay in the closure of the pulmonic valve with
inspiration.
b. During inspiration, the capacitance (volume) of the
pulmonary vascular bed increases when intra-
thoracic pressure decreases. As the smallest
pulmonary vessels pop open during inspiration, the
pulmonary vascular impedance falls.
c. The decrease in the pulmonary vascular impedance
allows forward flow from right. Ventricular ejection
persists for a longer period of time, and in effect
delays the closure of the pulmonic valve until forward
flow. Thus, P2 occurs first.
d. The S2 split widens to 0.04-0.05 seconds and is heard
as two discrete sounds (A2–P2) in the second left
ICS.
e. During expiration, the pulmonary vessels close off
due to a rise in intrathoracic pressure. As a result,
the pulmonary vascular impedance increases, thereby
shortening forward flow from right ventricular
ejection. P2 occurs earlier, and the S2 split narrows
to 0.1-0.2 seconds, and it is heard as a single sound.
6. Wide physiologic splitting of S2 is due to a delay in the
closure of the pulmonic valve (P2), or early closure of
aortic valve (A2). On inspiration, the split widens to 0.06
seconds; and on expiration, it narrows to 0.03 –0.04
seconds. Wide splitting is easily detected by nating both
components of the second heart sound during expiration.
a. Wide physiologic splittings occur in conditions that
prolong right ventricular ejection (pulmonary
stenosis), delay the onset of right ventricular ejection
(RBBB), or shorten left ventricular ejection (mitral
regurgitation, VSD).
7. Wide fixed splitting of S2 describes the situation where
splitting is detectable during both inspiration and
expiration and does not vary with breathing. It is
characteristic of arterial ventricular septal defects.
a. The left to right shunting of blood that occurs in the
septal defects causes the right ventricular forward
cardiac output to exceed the left ventricular forward
cardiac output. As a result, the pulmonary vascular
capacitance is always high and relatively independent
of breathing.
b. Because the pulmonary vascular capacitance is high,
the pulmonary vascular impedance tends to be lower
than normal, and is relatively unaffected by breathing.
The low pulmonary vascular impedance assures that
forward flow from right ventricular ejection is

prolonged, and this situation gives rise to a wide
split.
c. The splitting of S2 in fixed impedance is lower than
normal, and because it is subject to little change with
respiration, breathing has only a small effect on the
duration of forward flow from right ventricular
ejection.
d. There are two pathways for blood return to the right
heart in the septal defects. One path comes from the
great veins, and the other from the left-sided cardiac
chamber through the hole in the septum. During the
inspiration, the systemic venous return increases and
column of blood shunted through the septal defect
decreases. As a result, the final amounts to eight
ventricular ejections.
8. Reversed (paradoxic) splitting describes the condition
where the audible split of S2 narrows with inspiration
and widens with expiration. Reversed splitting results
from a prolongation of left ventricular ejection to the
extent that A2 occurs after P2.
a. The most common causes for reversed splitting is
left bundle branch block (LBBB).
b. Reversed splitting may also be observed in aortic
stenosis, IHSS, severe systemic hypertension, and
in patients having a right ventricular demand
pacemaker.
9. Narrow physiologic splitting is characteristic of severe
pulmonary hypertension, where the P2 component is
increased in intensity, and where right ventricular ejection
is shortened due to high pulmonary vascular resistance.
When the right ventricular begins to fail in pulmonary
hypertension, wide splitting of S2 will result.
S1 Split
Points 2: and 3(a) of the heading “The first heart sound
(S1)
S2 Split
Points 4; 5 (a), (b), (c), (e), 6 (a), 7(a) (b) (c-1) (c-2); 8
(a), (b); 9 of the heading “The second heart sound S2.
The Third Heart Sound (S3)
The third heart sound (S3) is a low-pitched sound that is
heard almost exclusively with the bell of the stethoscope
while S3 may occur normally in younger age groups; it is
nearly always pathologic when heard in people older than
forty. S3 occurs in early diastole, about 0.12-0.20 seconds
after S2. S3 is sometimes referred to as a protodiastolic
gallop. When originating from the LV, S3 is best heard at the
Cardiovascular System 151
apex. Turning the patient into the left lateral decubitus
position may augment detection of an S3 which is heard at
the 4th intercostal space adjacent to the sternum.
1. S3 occurs at the end of early ventricular filling when the
ventricle reaches its elastic limit. There is some evidence
that the sound heard during auscultation is due to the
impact of the heart against the chest wall.
2. S3 occurs when the ventricle reaches its elastic limit
during early diastolic filling. S3 may be produced when
normal or subnormal amounts of fluid enter an already
overfilled ventricle (congestive heart failure), or when
very rapid filling occurs in a more normal ventricle
(valvular regurgitation and high output states).
3. Maneuvers that increase venous return (leg elevation)
tend to increase the intensity of S3 and move it closer to
S3 while things that decrease cardiac filling cause the S3
to decrease in intensity move farther away from S2.
The Fourth Heart Sound (S4)
The fourth heart sound (S4) or atrial sound, is alone pitched
sound, heard almost exclusively with the bell of stethoscope.
An S4 occurs in late diastole approximately 0.04-0.12
seconds prior to S1. For this reason, S4 is sometimes referred
to as a presystolic gallop. When originating from the left
heart, S4 is best heard at the cardiac apex.
Turning the patient into the left lateral decubitus position
may augment detection of a left-sided S4. When originating
from the right heart, S4 is best heard at the 4th left intercostal
space adjacent to the sternum or at the xiphoid.
1. “An audible S4, is rare in normal subjects”. This is a
controversial statement that has been the source of much
debate. Studies from the 1970s indicate that apparently
normal men over age 50 may have audible S4 gallops.
2. An S4, when pathologic, is produced by atrial contraction
against a stiff, non-compliant ventricle. Stiff ventricles
are characteristic of ventricular hypertrophy, as such
are commonly seen in pulmonary or systemic hyper-
tension, pulmonic or aortic stenosis, and scarring
secondary to previous myocardial infarction.
3. S4 increases in intensity and moves farther from S1 with
maneuvers that increase venous return or with the
sympathetic stimulation.
4. S4 often decreases to the point of inaudibility with
standing.
5. S4 is dependent on atrial contraction and is always absent
in patients with atrial fibrillation.
6. A left-sided S4 can be distinguished from split S1 by
location (S1 is loudest at the LSB, while S4 is loudest at
the apex) and the fact that the S4 should disappear with
firm pressure on the diaphragm.
152 Essentials of Clinical Medicine
EXTRA SOUNDS
Ejection Sound (ES)
The ES is a short high-pitched sound that follows S1 by
0.04-0.06 sec. ES has been classified as:
a. Vascular—originating from the forceful ejection of blood
into great vessels.
b. Valvular—occurring when a deformed rapidly ascending
aortic or pulmonary valve reaches its elastic limit.
1. When due to pulmonic stenosis, the ES is heard in
2nd / 3rd left intercostal space and increases in
intensity with inspiration.
2. When due to aortic stenosis or bicuspid aortic valve,
the ES is heard at the apex and 2nd right intercostal
space.
3. An ES in the presence of an accompanying murmur
almost always means that the murmur is pathological.
Click
Pathogenesis of Click
a. Vascular theory:
• Both aortic and pul. clicks are usually associated
with dilation of corresponding vessels.
• Their mode of production is thought to be due to
vibrations caused by sudden distention of vessel
walls.
b. Valvular theory:
• Their mode of production is sudden opening of aortic
or that of pul. valves midsystolic click.
– Midsystolic click is a high-pitched sound that
occurs in midsystole.
– It is produced by sudden tensing of the chordae
tendinea in mitral or tricuspid valve prolapse.
– Best heard at the apex, 2nd right sternal border,
3rd left sternal border and carotid.
Pulmonary Ejection Clicks
• Best heard in pulmonary area.
• Change their charac. with phases of respiration
• Seen in:
– Dilated pul. a.
– PS.
– Pul. HTN.
– Idiopathic pul. a dilation.
Pericardial Clicks
• In chr. constrictive pericarditis (pericardial click should
not be confused with peri. rub)
• Extra sound during diastole which is again at end of
isovolumetric relaxation period.
• Supposed to be produced by rapid filling of vent against
resistance.
• Now-a-days believed to be mitral valve prolapse.
Gallop Rhythm: (Patam in 1876) (Triple rhythm)
Presystolic Gallop
• Produced due to 4th HS becoming audible.
• Lub-lub dup.
• Strong atrial contraction produced the gallop rhythm by
making the physiological HS4 audible.
• If gallop is LV—at. apex.
• If gallop is RV—left parasternal area.
• Heard much better if AV conduction time (increase PR
interval) or if there is LBBB.
• Another theory—extra sound is due to premature closure
of either the mitral valve or the tricuspid valve depending
upon whether the gallop is left or rt. vent.
Left ventricular presystolic gallop:
• Hypertensive heart disease
• AS
• MI.
Right ventricular presystolic gallop:
• Pul. stenosis.
Prognostic Valve
• With improvement in cardiac decompensation in between
extra sound and HS1 shortens.
• With deterioration, reverse takes place.
Protodiastolic Gallop Rhythm
This term is misnomer and should be replaced by diastolic
gallop rhythm.
• Protodiastolic is first part of vent. relaxation while extra
sound in this type of gallop is heard after phase of
volumetric relaxation.
• Extra sound is caused by:
– Sudden distension of ventricles.
– At end of rapid filling phase.
– More common in ventricles with dilated muscu-
lature, having no elastic recoil.
• Left vent. diastolic gallop is best heard at apex in left.
• Right vent. diastolic gallop is best heard in left 4th
parasternal area.
Common causes:
1. MI with dilatation
2. Hypertension
3. AI
4. MR
5. Cardiomyopathies.
 Cardiovascular System 153

Prognosis: • It is not affected by exercise or respiration

• Gallop rhythm is cry of failing heart for help. • Delayed in standing position.
• Presys gallop devotes a heart under stress trying to help Significance:
itself while protodiastolic gallop denotes a heart which • The S2-OS interval narrows with severity of MS S2-OS
has no further reserves left. less than 8 msec. Signifies critical MS
Summation Gallop • MS is organic and valve cusp is pliable
• High atrioventricular pressure gradient
• Marked tachycardia.
• Readily amenable to surgery
• Presystolic and HS3 can be overlapping.
• Absent when valve is calcified or ankylosed or when
• Extra sound heard in mid-diastolic.
MS is associated with MR.
• After slowing of heart rate, true nature of gallop may be
evident (either presystolic or diastolic). Conditions in Which Opening Snap (OS) is Heard
Quadruple Gallop • MS
• TS
• If presystolic gallop of one ventricle is combined with
• MI involving posterior leaflet.
diastolic gallop rhythm of other ventricles, this rare effect
of four sounds being heard in one cardiac cycle can be
Murmur
produced.
Definition
Opening SNAP: (OS) Murmur is an extra sound produced during the cardiac cycle
An OS is an early diastolic, high-pitched sound that closely usually caused by abnormal vibrations of valves or vessels
follows A2 by 0.03 to 0.15 second. An OS is produced by due to either an anatomical defect of these structures or an
opening of the mitral valve under high pressure in mitral abnormal flow of blood through them.
stenosis and by opening of the tricuspid valve under high Table 7.8: Heart murmurs
pressure in tricuspid stenosis.
Valve Abonormality Timing of murmur
1. In mitral stenosis, the OS is heard half-way between
the lower left sternal border and the cardiac apex and as Aortic or pulmonary Stenosis insufficiency Systolic
Mitral or tricuspid Insufficiency Systolic
high as the 3rd left intercostal space.
2. In tricuspid stenosis, the OS is heard in the 4th Mode of Production
intercostals space at the left sternal border.
3. It is important to differentiate splitting of S2 from an S2 1. Velocity of blood
followed by an OS. Two easy clues that may be used – Forcible ejection.
by the examiner in making this distinction are: – Dilatation
2. Calibre of blood vessels
a. If the 2nd component of a split S2 is louder at the
3. Bubbling
apex than at the 2nd left intercostals space, it is
– Of water vapor and blood gases
probably an OS.
– Called cavitation.
b. If a split second sound widens on standing, it has an
– Also produces murmur
OS as its second component.
4. The S2-OS interval has been used as a rough measure Most Accepted Theory
of severity of atrioventricular valve stenosis. The closer Formation of eddies due to:
the OS is to S2, the more severe the stenosis while not • Obstruction
always true, this statement is frequently helpful in • Back flow
estimating the degree of mitral stenosis. • Flow in dilated chambers
• Best heard between the apex left sternal border. • Abnormally rapid flow.
Snap and its Significance Physical Abnormalities Producing Murmurs
• It is a sharp, snappy early diastolic sound occurring 30- 1. Hyperdynamic or rapid flow of blood.
100 msec after 2nd heart sound 2. Obstruction due to stenosis or due to base structures
• Usually heard best at lower left sternal border and (athero. plaque or ruptured valve cusp, or vegetation as
radiating to the base of heart in infective endocarditis).
154 Essentials of Clinical Medicine

3. Regurgitation of flow of blood.

4. Flow in abnormally dilated chamber or vessels.
Description of Murmur
Timing:
• Systolic—between HS1 and HS2.
• Diastolic—between HS2 and HS1.
– Whole of systole—pansystolic murmur.
– Ejection sys. murmur—starts after HS1 (mid-systolic
murmur), gradually increases in intensity and then
fades before beginning HS 2 (diamond-shaped
mummur)
– Usually pansys. and long—indicates a disease.
– Short ejection systolic mummur—indicates a disease
process or may be innocent.
– There is no pandiastolic murmur but may be rarely
heard in severe aortic incompetence.
Early Diastolic Murmur
• 1st part of diastole.
• Immediately after HS2.
Mid-Diastolic Murmur
• Immediately after HS3.
• May be prolonged in obstruction to AV flow (i.e. mid-
Fig. 7.12: Showing duration and pattern of cardiac murmurs
dias may continue as presystolic murmur)
Late Diastolic Murmur
(presystolic) Example:
• Precedes HS1. – Presystolic murmur
• And may end at HS1 – MS.
• Usually has a crescendo or rising charac. when atria are • Decrescendo or Diminuendo murmur—decreases in
contracting normally intensity
• A sys. and dias. murmur may be present at same time Example:
called to and fro, see-saw murmur. – Early diastolic murmur of AI.
Example: • Diamond-shaped or Crescendo-Decrescendo murmur—
– AS increases and then decreases.
– AI Example:
• Continuous murmurs without interruption with an – Ejection systolic or
accentuation in early diastole is heard in patients with – Midsystolic of AS and PS
PDA (Fig. 7.12). Character
Site: – Blowing harsh
• Localized or heard diffusely. – Rumbling
• Site of max. intensity. – Cooling
Intensity and character: – Loudness.
Levine classification: 6 categories: Direction of conduction:
• Grade I—faintest audible murmur • Usually in direction of flow.
• Grade II—heard even when chest piece is slightly Therefore, MI—Lat. in axilla
removed from chest. MS—Over neck vessels.
• Grade III—and above are usually accompanied by a • Conducted murmur—same intensity at new and original
thrill. site.
• Crescendo murmur—increases progressively in intensity. • Transmitted murmur—decreases.
 Cardiovascular System 155

Effect of respiration posture, exercise and drugs: 2. Due to regurgitation: (pan. or holosystolic)
a. Respiration: a. AV valve incompetence—mitral incompetence
– Inspiration: increases blood flow through tricuspid (pathological or functional)
and pul. valves. – Tricuspid incompetence (pathological or
– Hence murmur produced by defects on right side of functional).
heart are heard louder during inspiration. b. Left to right shunt
– During inspiration, a large part of heart may be – VSD.
covered by pul. tissue and hence mechanical – Early cases of PDA.
muffling of murmurs. Diastolic:
– Murmurs on left side of heart may become softer 1. Early Diastolic
during inspiration. a. Aortic:
– Murmurs caused by right to left shunts may be softer i. Valvular incompetence
during inspiration. ii. Dissecting aneurysm
b. Posture:
iii. Bicuspid aortic valve (congenital).
Certain murmurs are heard when the patient is lying
b. Pulmonary:
down in particular pain.
i. 1° or 2° pul. hypertension (Graham-Steel murmur)
– Left lat. position—MS
ii. Pul. incompetence.
– Sitting and bending forward—AI.
iii. Aneurysm of pul. a.
c. Exercise:
2. Mid-diastolic
– Faint murmurs are better heard after exercise.
a. AV stenosis mitral or tricuspid
– May also augment a thrill which was previously
b. AV valve obstruction
doubtfully palpable.
– ball-valve thrombus
d. Drugs:
– atrial myxoma.
– Amylnitrite lowers peripheral vasculature resistance
c. Increased flow across AV valves:
and hence it makes ejection, aortic murmur
i. Across mitral valve:
prominent, and regurgitant left side murmur fainter.
1. Mitral incompetence.
– Phenylephrine and nor epinephrine increases the
2. VSD.
peripheral vascular resistance and have an opposite
3. PDA (flow murmur)
effect.
ii. Across tricuspid valve:
Non-Pathogenic Murmurs 1. ASD
1. Innocent murmurs—usually midsystolic. 2. Anomalous pul. venous drainage.
2. Flow murmurs—seen in hyperdynamic circulation. d. AV valve inflammation:
– rare in AV fistula. Carey-Coombs murmur occurs in RHD to be
different from MS murmur by the fact that in RHD,
Pathogenic heart sounds are muffled, the murmur changes its
Systolic: character from time to time. In MS, HS, at mitral
1. Due to forward flow (ejection or midsystolic) area is loud and sharp and murmur does not have
a. Aortic area: changing character.
i. Increased flow—aortic incompetence or rarely 3. Presystolic or Late Diastolic
in heart block. a. AV valve stenosis
ii. Obstruction—Aortic stenosis. 1. mitral stenosis.
– Supra-aortic stenosis. 2. tricuspid stenosis.
– Coarctation of the aorta. b. AV valve obstruction
b. Pulmonary area 1. due to ball valve thrombus or atrial myxoma.
i. Increased flow—left to right shunt. 2. due to regurgitant blood flow from aortic incom-
– VSD petence implying upon mitral valve cusp (Austin-
– ASD. Flint murmur).
ii. Obstructive: PS
iii. Dilation of distal chamber pul. artery. Holosystolic Regurgitant Murmur
Primary or secondary hypertension. Holosystolic murmurs (pansystolic) are generated by
156 Essentials of Clinical Medicine
retrograde flow from a high pressure chamber to a low
pressure chamber.
i. > Start with S1 and continue through and beyond A2
ii. > Have a blowing quality to them.
iii. > Do not exhibit post extrasystolic potentiation
following a long diastole.
Table 7.9: Causes
Patent ductus arteriosus Proximal coronary artery stenosis
Coronary AV fistula Mammary soufflé
Ruptured aneurysm of sinus of Pulmonary artery branch stenosis
Valsalva
Aortic septal defect Bronchial collateral circulation
Cervical venous hum Small (restrictive) ASD with MS
Anomalous left coronary artery Intercostal AV fistula
iv. > The murmur of mitral regurgitation is holosystolic
and plateau shaped. It is loudest at the cardiac apex
where it may completely obscure S1. It radiates to
the axilla. If the murmur is secondary to a ruptured
anterior chordae, it may radiate to the top of the
head/midthoracic spine. Anything that increases
peripheral vascular resistance (hand grip exercise)
will make the murmur louder. Anything that decreases
peripheral vascular resistance (amyl nitrate) will make
the murmur softer. The murmur increases with
Valsalva’s and inspiration.
1. Associated findings in mitral regurgitation are:
a. A brisk pulse (small water hammer pulse).
b. A wide split and left ventricular ejection is
shortened, causing A2 to come early.
c. A hyperdynamic apical impulse that is
displaced down and to the left.
d. An S3 gallop at the apex.
v. The murmur of tricuspid regurgitation is also
holosystolic and plateau shaped. It can be distin-
guished from that of mitral insufficiency by:
1. The murmur of tricuspid regurgitation is best
heard at the 4th and 5th intercostal spaces along
the left sternal border.
2. The murmur of tricuspid regurgitation does not
radiate into axilla.
3. The murmur of tricuspid regurgitation becomes
louder with inspiration (Carvallo’s sign).
4. Tricuspid regurgitation causes prominent OcvO
waves in the JVP. The ear lobe may pulsate with
each heart beat.
vi. The murmur of VSD is holosystolic but tends to be
more harsh than that of mitral or tricuspid
regurgitation. The murmur of VSD is typically heard
over the entire precordium (best at 4th, 5th and 6th
intercostal spaces to the left of the sternum) and is
often associated with a palpable thrill.
1. Unlike the murmur of MR, the murmur of VSD
does not radiate into axilla.
2. Unlike the murmur of TR, the murmur of VSD
does not increase with inspiration.
3. The murmur of VSD is associated with fixed
and sometimes wide splitting of S2.
4. Like MR, the apical in pulse is hyperdynamic
and displaced down and to the left.
Midsystolic Ejection Murmur: or
Midsystolic Murmur (MSM)
MSM (Systolic Ejection Murmur) are typically produced
by the forward flow of blood across the ventricular flow
tract.
MSM:
a. Begin after S1 and end prior to S2.
b. Are diamond shaped (crescendo-decrescendo).
c. Tend to be harsh and saw like in quality.
d. Exhibit postextrasystolic potentiation, increasing in
intensity after a long diastole when ventricular filling is
increased.
e. MSM result from one of the following situations:
1. The rate or amount of blood flow across a normal
semilunar valve. The systolic murmurs of preg-
nancy, thyroid excess states, exercise, anemia and
fever are caused by this mechanism.
2. Ejection of blood into the dilated aorta that results
from arteriosclerosis or aneurysm formation.
3. Ejection of blood past thickened valve cusps and
calcified plaque lining the wall of the aorta up to 50
people older than 50 years of age will have a murmur
related to this mechanism (aortic sclerosis). Aortic
sclerosis can be distinguished from aortic stenosis
by the fact that carotid artery pulse is normal in
patients with aortic stenosis.
4. Ejection of a blood across a narrow semilunar valve
or narrow outflow tract (semilunar valvular stenosis,
subvalvular stenosis).
f. Valvular aortic stenosis produces the classic midsystolic
ejection murmur.
1. The murmur is caused by turbulence across a
narrowed aortic valve orifice.
2. The murmur is crescendo-decrescendo in shape and
may be heard in 2nd right intercostal space, 3rd left
intercostal space and at the apex. The murmur may
radiate into the carotid arteries bilaterally and is
frequently proceeded by an ejection sound grade 3-
4/6 is common.

3. Aortic stenosis is associated with a narrow pulse
pressure and a slow, delayed carotid upstroke.
4. Chronic pressure overloading on the left ventricle
results in a sustained apical impulse characteristic
of left ventricular hypertrophy.
5. S2 may be narrowly split, singly or paradoxically
split as aortic ejection is increasingly prolonged.
6. The murmur decreases in intensity with sustained
Valsalva’s and inspiration.
g. The murmur of hypertrophic obstructive cardio-
myopathy is midsystolic in timing and occurs as a result
of hypertrophy of the interventricular septum. During
systole, the thickened interventricular septum makes
contact with the anterior leaflet of the mitral valve and
obstructs left ventricular outflow. This transient
obstruction results in a systolic pressure gradient,
turbulence and a midsystolic murmur.
1. The murmur is harsh, best heard along the left sternal
border.
2. The murmur of obstructive cardiomyopathy can be
distinguished from the murmur of aortic stenosis by
the fact that the murmur of obstructive cardio-
myopathy increases in intensity during any maneuver
that makes the left ventricle smaller (sustained
Valsalva’s standing). Maneuvers that make the left
ventricle larger, the intensity of the murmur in
obstructive cardiomyopathy.
h. The MSM of pulmonic stenosis is due to narrowing of
the pulmonic valve orifice. This murmur can be
distinguished from the murmur of aortic stenosis by the
following features:
1. The murmur of pulmonic stenosis is best heard in
2nd and 3rd left intercostal spaces and is usually of
lesser grades than that of aortic stenosis.
2. The murmur of pulmonic stenosis does not radiate
into the carotid arteries.
3. Pulmonic stenosis is associated with prominence of
the ‘a’ wave on the JVP.
4. Pulmonic stenosis produces a left parasternal
sustained impulse from right ventricular hyper-
trophy.
5. The murmur increases with increased venous return
to the right heart (inspiration).
Late Systolic Murmur: (LSM)
LSM occurs in mitral and tricuspid valve prolapse. The
murmurs start in midsystolic and are often proceeded by a
midsystolic click. The murmur may crescendo into S2 and
is rarely as loud as grade 3.
a. The murmur of atrial-ventricular (AV) valve prolapse is
made longer and louder by decreasing ventricular volume
Cardiovascular System 157
(Valsalva’s standing), by decreasing ventri-cular after
load and by increasing contractility. These same
alterations also move the click closer to S1.
b. The murmurs of mitral and tricuspid valve prolapse may
be transient, coming and going from day to day.
Early Diastolic Murmur
a. Diastolic murmurs are classified according to their
mechanism of production. Diastolic filling murmurs
(rumbles) are produced by forward flow across the AV
valves. Diastolic regurgitant murmurs are produced by
retrograde flow across incompetent semilunar valves.
b. The best example of diastolic regurgitant murmur
originating in the left heart is that associated with aortic
regurgitation. The murmur begins with A 2 , is
decrescendo and ends in late diastole. Mild forms or
aortic regurgitation may produce murmurs that end in
mid-diastole. The murmur of aortic regurgitation is heard
best at the 2nd right intercostal space, 3rd left intercostal
space and apex. It is accentuated by having the patient
forward and hold his breath in forced exhalation. The
murmur has high-pitched blowing quality. The murmur
S in intensity with maneuvers that peripheral vascular
resistance (handgrip, squatting, exercise). Other
manifestations of aortic insufficiency may include:
1. A wide pulse pressure due to elevated systolic
pressure and decreased diastolic pressure.
2. Water hammer pulse.
3. A to and fro pulsation of the blood in the proximal
fingernail bed when pressure is applied to the distal
nailbed (Quincke’s pulse). While this finding may
occur normally in some, it is more common and
often prominent in patients with aortic insufficiency.
4. De-Musset’s sign—head bobbing with each heart-
beat.
5. Duroziez’s sign—a bruit with systolic and diastolic
components auscultated over the femo-ral artery
while manual pressure is applied proximal to femoral
artery.
6. Dullness to percussion, the tactile fremitus, and
egophony at the lower tip of the left scapula
secondary to ring consolidation from the enlarged
heart. This same constellation of findings occurs in
large pericardial effusions and is termed Ewart’s sign.
7. S2 is single and snapping.
8. The apical impulse is displaced down and to the left
having a hyperdynamic quality typical of ventricular
dilatation.
9. An S 3 is common due to rapid, high volume,
ventricular filling.
158 Essentials of Clinical Medicine

10. Two additional murmurs often occur in aortic 4th intercostal space at the left sternal border or
regurgitation. xiphoid. The murmur of tricuspid stenosis
• An aortic ejection (midsystolic) murmur occurs increases in intensity during inspi-ration and
due to the volume of blood that is ejected across when firm pressure is applied over the liver. The
the aortic valve in the forward direction. JVP shows giant ‘a’ waves and slow ‘y’ descent.
• A low pitched, mid-to-late diastolic rumbling
Mid-Diastolic Murmur
murmur (Austin-Flint) at the apex that due to the
regurgitant flow impinging upon the anterior The (D) point of previous (early diastolic murmur).
leaflet of the mitral valve and partially closing it. Functional Murmur or Innocent Murmur
This situation creates a “functional” mitral • Systolic
stenosis. The presence of this murmur suggests • Best heard in pulmonary area
severe aortic regurgitation. • Not radiating
• The murmur of pulmonary regurgitation can be • Changes the character with respiration and position
distinguished from the murmur of aortic • Not associated with thrill
regurgitation by the fact that pulmonary • Seen in anemia, thyrotoxicosis.
regurgitation murmur increases in intensity with Grade Murmur:
inspiration, and is not associated with any of the • Gr-I - Faint murmur picked up phonocardio-
peripheral manifestation of aortic regurgitations graphycally. Head in quiet room
(wide pulse pressure, bounding pulses, large left • Gr-II - Easily audible but not loud
ventricle, etc.). The murmur of pulmonary
• Gr-III - Loud but no thrill
regurgitation that results from pulmonary
• Gr-IV - Murmur with thrill audible with full chest
hypertension is termed the Graham-Steel
piece of stethoscope
murmur.
• Gr-V - Loud murmur with thrill can be heard even
• The murmur of mitral stenosis is the typical
with edge of chest piece
diastolic filling murmur:
• Gr-VI - Loud murmur with thrill audible with chest
1. The murmur is low pitched and rumbling and
piece lifted off the chest.
is only heard with the bell (2). It is localized
to the cardiac apex in an area no larger than Causes of Systolic Murmur
2.5 cm2. • Ejection
2. The murmur of mitral stenosis may only be – Aortic—systemic hypertension, atherosclerotic
audible while listening to the patient in the aortic disease
left lateral decubitus position. – Pulmonary—functional
3. The murmur which may begin with an – Pulmonary stenosis—increased flow in ASD with
opening snap following S 2 decreases in hyperdynamic circulation
intensity toward mid-diastolic and then again • Pansystolic or holosystolic
S in intensity into S1. This crescendo effect – MR
into S1 is termed presystolic accentuation, – TR.
and is augmented significantly by atrial – VSD
contraction. • Late systolic—mitral valve prolapse precipitated by
4. The murmur is commonly no louder than muscle dysfunction
grade 1 or 2 and may be amplified by elevating Causes of Diastolic Murmur
the legs above the level of heart. Other findings • Mid-diastolic
of mitral stenosis include: – Obstructive lesions
i. S1 is increased in intensity. - MS
ii. A left parasternal impulse secondary to - TS
right ventricular hypertrophy. - Atrial myxoma
iii. The apical impulse is normal with respect • Increased flow across mitral valve
to its quality and location. – VSD
• The murmur of tricuspid stenosis differs from – PDS
that of mitral stenosis by being localized to the – MR.
 Cardiovascular System 159

• Increased flow across tricuspid valve Venous Hum

– ASD • Produced by turbulence of blood flow in internal jugular
– TR vein
• Other causes • Low pitch
– Carey-Coombs murmur • Best heard in medial aspect of rt. supraclavicular fossa
– Austin-Flint murmur • In sitting or standing position
– Complete heart block • Increases with deep inspiration, by turning the head to
• Early diastolic
opposite side
– AR
• Disappears on lying flat, turning head to same side or
– PR
compression of jugular vein transmission of a loud
Causes of Continuous Murmur venous hum to area below the clavicle may result in
• Both in systolic and diastolic heard without a gap mistaken diagnosis of PDA
• PDA • Seen in normal child and anemia.
• Aortopulmonary window
• Pulmonary AV fistula VALVULAR HEART DISEASE
• Rupture of sinus of Valsalva into rt. ventricle or rt. atrium
Table 7.12: Causes of murmur in mitral area
• Bronchopulmonary arterial anastomosis
• Venous hum. Causes of diastolic murmur Causes of systolic murmur
To and from Murmur • TS • MR
In to and fro murmurs the duration of blood flow reverses • MS • TR
• Flow murmur • MVP–Ejection click with late
in diastole. It does not cover 2nd heart sound. – MR systolic murmur
• AS with regurgitation – VSD • VSD
• Pulmonary hypertension with regurgitation. – PDA • Papillary muscle dysfunction
• Carey-Coombs murmur • Chordae tendinae rupture
Causes of Diastolic Murmur in Mitral Area • Austin-Flint murmur
• MS
• TS MITRAL STENOSIS [Figs 7.13A, (7.13B, Plate 3)]
• Flow murmur—MR, VSD, PDA
• Carey-Coombs murmur Clinical Features of MS
• Austin-Flint murmur. • May be asymptomatic
Table 7.10: Common sites of murmur in cases of stenosis of • Effort intolerance
(A) carotid sinus (B) common carotid (C) subclavian • PND
Site of murmur Site of stenosis • Edema
Murmur over angle neck Carotid sinus
• Abdominal distention
Low in the neck Common carotid or subclavian • Pedal edema.
Murmur over contralateral carotid Due to augmented flow on the
or over the eyeball with ipsilateral normal side
poor carotid pulsation

Table 7.11: Causes—TB, viral, uremic, traumatic, rheumatic

Pericardial rub Murmur

Friction sound arises from Arises from valve
pericardium
Strictly to and fro Blowing rumbling or musical
Increases with pressure of No change
stethoscope
Superficial Deep
No conduction May be conducted
Pain is present No localized pain
Sometimes palpable Thrill may be felt Fig. 7.13A: Chest radiograph of a patient with mitral stenosis and
Variability present (varies from regurgitation indicating enlargement of left atrium and prominence of
hour to hour or absent day to day) Absent pulmonary artery trunk
160 Essentials of Clinical Medicine

X-ray Findings of Signs of MS left atrial pressure being normal.

• ASD absence of left atrial englargement and absence of
• Pulmonary conus prominents
Kerley B lines with fixed splitting of S2 being present.
• Mitralization of left border
• Left atria prominent • Cor triatriatum—congenital malformation—fibrous
• Pulmonary arterial hypertension ring in left atrium can be recognized by left atrial
• Pulmonary venous pressure increased angiography.
• Kerley lines—presence of Kerley B lines correlates with Table 7.13: Differentiation between MS and TS
pulmonary wedge pressure greater than 20 mm Hg.
• Hemosiderosis MS TS
• Dilatation of upper lobe pulmonary views, inverted Diastolic murmur Mitral Area Tricuspid area
moustache sign JVP Prominent ‘a’ waves Giant ‘a’ waves
• Backward displacement of esophagus by enlarged left if associated pulmo-
nary hyperten-
atrium.
sion. Prominent
‘v’ waves if asso-
Changes Occurring in an Established Case of ciated with TR
MS with the Onset of Atrial Fibrillation RV hypertrophy Present Absent
Pulmonary Present Absent
• Clinically presystolic murmur disappears Hypertension None Murmur increases with
• Mid-diastolic murmur continues Relationship of inspiration
• ECG shows absent P waves which are replaced by murmur with
fibrillary waves respiration
• Chances of embolic manifestation increases
• Varying intensity of first learnt sound Table 7.14: Differentiation between Austin-Flint
• Absent “a” waves in neck murmur and murmur of MS
• Irregularly irregular pulse Austin-Flint Murmur of MS
• Apex-pulse deficit. murmur
Association With AR With MS
Disappearance of Opening Snap in MS Hemoptysis Never occurs Present
Atrial fibrillation Absent Present
It occurs in: Thrill Absent Present
• In calcified MS. Parasternal heave Absent Present
• Significant aortic incompetence. Diastolic shock Absent Present
• Significant mitral incompetence. Ventricular hypertrophy LVH RVH
First heart sound Normal Loud
Opening snap Absent Present
Differential Diagnosis of MS Left atrial enlargement Absent Present
• TS Peripheral signs Present Absent
Echocardiography LV enlarged RV enlarged calcified
• Left atrial myxoma—other systemic signs are: mitral valve may be
– Wt. loss seen, murmur increased
– Fever Amyl nitrate inhalation Murmur decreased Murmur increased
– Anemia
– Clubbing Complications of MS
– Third heart sound a. Mechanical effects of enlarged left atria (Fig. 7.14A)
– Increased gamma globulin. – Hoarseness of voice (Ortner’s syndrome)
• Ball valve thrombus – Dysphagia.
• Chronic lung disease due to recurrent – Collapse of left lung due to pressure on left bronchus.
– Pulmonary infection, exertional dyspnea in patients b. Embolic
with MS – Systemic—brain, kidney, spleen, retina.
• Primary pulmonary hypertension—opening snap, – Pulmonary due to pulmonary hypertension.
diastolic rumbling murmur absent with no left atrial c. Arrhythmias—AF, extrasystoles.
enlargement and pulmonary arterial wedge pressure and d. Infection:
 Cardiovascular System 161

Non-Rheumatic Causes of MS
• Congenital
• SLE, rheumatoid arthritis
• Mucopolysaccharoidoses
• Methysergide therapy
• Carcinoid heart disease.

Causes of Soft S1 in MS
• Calcified mitral valve
• Associate dominant MR
• Enlarged RV forming the apex.

Mitral Facies
Pinkish purple patches on cheek. Low cardiac output in
MS produces vasoconstriction, peripheral cyanosis often
on lips, lip of nose and cheeks. Seen due to vasodilatation
Fig. 7.14A: Chest radiograph of long standing mitral stenosis of molar area.
showing a massive left atrium
Causes of Muffled P1 in MS
– Bronchitis (in winter season) • Associated MR or AR
– SABE (Subacute bacterial endocarditis) • Mitral valve calcification
e. Others: • Acute rheumatic carditis (PR interval prolonged)
– CCF • Digitalis overdose (PR interval prolonged)
– LVF due to back pressure. • Acute M1
– Left atrial hypertrophy (LAH) • LAF
– Pulmonary edema • AF
– Right ventricular hypertrophy (RVH) Rotation of heart due to gross right ventricular
– TR-Rt. atrial enlargement.
hypertrophy. Right ventricle from the apex.
Pulmonary Hypertension in MS Table 7.15: Aortic stenosis, aortic regurgitation,
mitral regurgitation and septal defects
• Clinically, decreased mitral valve orifice leads to increased
left atrial pressure and left atrial enlargement and Aortic stenosis Aortic regurgitation
pulmonary congestion, thereby pulmonary hypertension. Pulse: Sinus rhythm, low volume, Pulse: Sinus rhythm, large
• Pulmonary anterior construction due to left atrial and slow rising volume, collapsing
pulmonary venous congestion leads to reactive Aortic area: Systolic thrill Blood pressure: Wide pulse pressure
Apex: Not displaced, sustained Apex: Displaced, diffuse, hyper-
pulmonary hypertension. Sounds: Ejection, click, soft A2, S4 dynamic
• Obliterative (organic) changes in pulmonary vascular Murmurs: Systolic, low pitched, Pulse: Sinus rhythm, large volume,
bed. Clinically, the signs are left parasternal heave, ejection, radiating to carotids collapsing
palpable P2, loud P2 component of second heart sound 1. High pitched, early diastolic at
and epigastric pulsations. Apex beat may be shifted up LSE
2. Ejection systolic at base and
and out due to Rt. ventricular hypertrophy symptoms into neck
are angina, syncope, hypoxia, and hypertension (due to 3. Mid-diastolic rumble at the
decreased cardiac output). apex
(Austin-Flint)
Embolic Manifestations of Mitral Stenosis Mitral regurgitation Mitral stenosis
Thrombus from the left atria may embolize to brain, kidney, Face: Mitral facies
spleen and extremities. A large pedunculated one may Pulse: Sinus rhythm, atrial fibrillation Pulse: Artrial fibrillation
RV: Hearing, substanced
suddenly obstruct the stenotic mitral orifice leading to ball Apex: Hyperdynamic, displaced, Apex: Localized, tapping
valve thrombus. systolic thrill
Contd...
162 Essentials of Clinical Medicine

Contd... • Cardiomegaly—displaced hyperdynamic apex beat

Sound: Soft S1, S3 Sounds: Loud S1 loud S2 opening • Apical pansystolic murmurs ± thrill
Murmurs: Pansystolic Murmurs: Mild-diastolic, rumbling • Soft S1, apical S3
apex • Signs of pulmonary venous congestion—crepitations,
Atrial septal defect Features of a benign or innocent pulmo-nary edema, effusions
heart murmur • Signs of pulmonary hypertension and right heart failure.
Sternal impulse : right ventricular Soft
heave AORTIC STENOSIS
Sounds: loud P2 Mild systolic
Fixed split S2 (A2- P2)) Heard at left sternalangle Causes of Aortic Stenosis
Murmurs: Mid-systolic ejection No radiation
in pulmonary area occasional No other cardiac-abnormalities Infants, Children, Adolescents
diastolic tricuspid flow murmur • Congenital aortic stenosis
• Congenital subvalvular aortic stenosis
MITRAL REGURGITATION (Fig 7.14B) • Congenital supravalvular
Causes of Mitral Regurgitation Young Adults to Middle-aged
Mitral valve prolapse, dilatation of mitral valve ring, (e.g. • Calcification and fibrosis of congenitally bicuspid aortic
rheumatic fever, coronary artery disease, cardiomyopathy), valve.
damage to valve cusps and chordae tendinae, (e.g. rheumatic • Rheumatic aortic stenosis.
heart disease, endocarditis), damage to papillary muscle. Middle-aged to Elderly
Myocardial infarction.
• Senile degenerative aortic stenosis, calcification of
Clinical Features of Mitral Regurgitation bicuspid valve.
• Rheumatic aortic stenosis.
Symptoms
• Dyspnea (pulmonary venous congestion) Clinical Features of Aortic Stenosis
• Fatigue (low cardiac output) Symptoms
• Palpitation (AF, increased stroke volume)
• Mild or moderate aortic stenosis is casually asympto-
• Edema, ascites (right heart failure)
matic
Signs • Exertional dyspnea
• Atrial fibrillation/flutter • Angina
• Exertional syncope
• Sudden death
• Episodes of acute pulmonary edema.
Signs
• Ejection systolic murmur
• Slow rising carotid pulse
• Narrow pulse pressure
• Thrusting apex beat (LV pressure overload)
• Signs of pulmonary venous congestion, (e.g. crepi-
tations) (Fig. 7.15).

AORTIC REGURGITATION
[(Figs 7.16A, (7.16B, PLATE 3)]
Causes of Aortic Regurgitation
• Congenital
• Bicuspid valve or disproportionate cusps.
• Acquired
• Rheumatic disease
Fig. 7.14B: Chest radiographic appearance of mitral regurgitation • Infective endocarditis
 Cardiovascular System 163

• Corrigan’s sign—large pulsation in neck (dancing

carotid)
• Duroziez’s sign.
• Alfred De Musset’s sign—nodding of head with each
heart beat due to large stroke volume
• Muller’s sign – pulsations in uvula
• Landolifi’s sign—change in size pupils synchronous with
cardiac cycle
• Quincke’s sign—capillary pulsations—alternate
blanching and flushing of tightly compressed skin in
nailbed.
• Scratch on flat surface of skin like interscapular region
shows dermographism synchronous with cardia cycle.
• Peripheral auscultatory signs.
– Traube’s sign—pistol shot sounds over femorals
– Hill’s sign—popliteal blood pressure exceeds
branchial by 20 mm. Hg
– Mild AR—20-40 mm Hg
– Moderate AR—40-60 mm Hg
– Severe AR—60 mm Hg
Fig. 7.15: Chest radiograph in aortic stenosis – Duroziez’s murmur
– Austin-Flint murmur (soft mid-diastolic)
• Trauma – A diastolic murmur heard in the diaphragm with a
• Aortic dilatation (Marfan’s syndrome, aneurysm, stethoscope by distal compression of femoral artery.
dissection, syphilis, ankylosing spondylitis).
Table 7.16: Differentiation between syphilic AR and rheumatic AR
give space in between them
Clinical Features of Aortic Regurgitation
Age Old Young
Symptoms Angina More Absent or less common
• Mild-to-moderate AR Peripheral signs More marked Less marked
• Often asymptomatic Diastolic murmur On right, parasternal On left parasternal area
area – musical nonmusical
• Awareness of heart beat, palpitations Austin-Flint Absent Present
• Severe AR Valve affected Single Multiple
• Breathlessness Others VDRL positive Jones criteria positive
• Angina
TRICUSPID REGURGITATION
Signs
Causes of Tricuspid Regurgitation
Peripheral signs of AR
• Water hummer or collapsing pulse Primary
• Locomotor branchialis • Rheumatic heart disease
• Endocarditis particularly in intravenous drug misusers
• Ebstein’s congenital anomaly
• Secondary
• Right ventricular dilatation due to chronic left heart failure
(functional tricuspid regurgitation).
• Right ventricular infarction
• Pulmonary hypertension (e.g. cor pulmonale).

EBSTEIN’S ANOMALY
Fig. 7.16A: Chest radiograph of patient with aortic regurgitation, • Tricuspid valve is dysplastic and displaced into RV, right
left ventricular enlargement and dilatation of ascending aorta ventricle “ atrialized”
164 Essentials of Clinical Medicine

• Tricuspid regurgitation and RA to LA shunt • DORV (Double Outlet Right Ventricle)

• Wide spectrum of severity • TOF
• Arrhythmias One of the causes of cyanosis is Eisenmenger’s syndrome
• Surgical repair possible, but significant risks which is secondary to:
• Clinical features of hypertrophic cardiomyopathy.
Causes of Central Cyanosis:
Symptoms • ASD (Atrial Septal Defect)
• Angina on effort • VSD (Venticular Septal Defect)
• Dyspnea on effort • PDA (Patent Ductus Arteriosus).
• Syncope on effort
• Sudden death. Peripheral Cyanosis
It is seen in:
Signs • CHF, (prolonged circulation time—limbs blue and cold)
• Jerky pulse and mid-systolic • Fallot’s tetrology — limbs blue and warm.
• Murmur at the base (sign of left ventricular outflow *(In heart failure, we have both central and peripheral
tract obstruction which may be augmented by standing cyanosis)
up due to reduced venous return, intropes and
vasodilators like sublingual nitrates). Differential Cyanosis
• Palpable left ventricular hypertrophy. It is seen in:
• Double impulse at the apex (palpable 4th heart sound • Eisenmenger’s PDA. The shunting of blood occurs from
due to left atrial hypertrophy). pulmonary artery to aorta and this causes upper limbs
• Pansystolic murmur (due to mitral regurgitation) at the to be pink in color and lower limbs blue. It is a rare
apex. (typical) condition. All Eisenmenger’s patients require
heart trans-plantation.
CONSTRICTIVE PERICARDITIS • If v-wave is rapidly coming down — constrictive
Clinical Features of Constrictive Pericarditis pericarditis.
• If v-waves fall down slowly — tricuspid stenosis.
• Fatigue
• Rapid, low-volume pulse Table 7.17: Categories and symptoms
• Pulsus paradoxus (excessive fall in BP during inspiration) Category Symptoms
• Elevated JVP with rapid descent Small VSD Generally asymtoptomatic. Detected inciden-
• Kussumaul’s sign (a paradoxical rise in JVP during tally on a routine examination due to the presence
inspiration) of a murmur. However, there is increased risk of
infective endocarditis
• Loud early third heart sound or “pericardial knock” Medium-sized VSD Symptoms are mild initially, but with the
• Hepatomegaly development of CCF, there is increased precordial
• Ascites activity, excessive coughing during feeds,
• Peripheral edema. excessive perspiration and inability to feed
properly due to fatigue.
Large VSD In addition to symptoms due to CCF as discussed
CYANOSIS IN HEART above, there is failure to thrive, repeated
DISEASES AND SEPTAL DEFECTS respiratory tract infections, excessive breath-
lessness and suck-rest-suck cycle (child sucks →
Cyanosis in Heart Diseases stops to take rest due to breathlessness and fatigue
→ falls asleep → wakes up early due to hunger →
1. Central (venoarterial mixing) sucks again)
2. Peripheral cyanosis Large VSD with Due to reversal of shunt, there is a reduction in
Eisenmengerization the pulmonary plethora and cardiomegaly. Thus,
3. Differential cyonosis symptoms of CCF and repeated, respiratory tract
infections abate. Instead the following symptoms
Central Cyanosis may occur:
It is seen in:  Cyanosis  Hemoptysis
 Dizziness  Arrhythmias
• TGA (Transposition of Great Arteries)
 Syncope  Sudden death
 Cardiovascular System 165

Table 7.18: Signs

Category Small VSD Medium-sized VSD Large VSD VSD with Eisenmengerization
General examination
Appearance Normal May show mild growth Cachexia + (failure to thrive) Cachexia +
retardation Small Normal/small
Pulse Normal Tachycardia + Tachypnea Normal/tachypnea
Respiration Normal Tachypnea + May be high elevated present Usually absent
Blood pressure Normal Usually normal during fits of crying or during
JVP Normal Normal feeding may be present
Cyanosis Absent Absent
Pedal edema Absent Absent
Systemic examination
CVS examination
Inspection
Precordium Normal Mild bulging Buldging Buldging
Apex impulse Normal Normal Shifted (LVH) Normal/Shifted (LVH)
Pulsations Absent Present Present Present
Palpation
Apex beat Normal Hyperdynamic Heaving Right ventricular (hearing apex,
but lateral to the apex)
Diastolic shock (palpable Absent Absent Present Present
2nd heart sound P2)
Thrill Systolic thrill in Systolic thrill + Systolic thrill + Thrill is absent
left parasternal
region
Percussion auscultation Normal Normal Cardiomegaly Normal
Heart sounds S1 drowned by S1 drowned by murmur S1 drowned by murmur S2– S1 Normal
murmur S2 - split S2 – widely split loud and widely split
Murmurs Loud Pansystolic murmur in Pansystolic murmur becomes Pansytolic murmur abolished.
pansystolic left parasternal region faint and may be silent at the No murmur heard at instead,
murmur, grade > becomes softer. end of systole. an early murmur may be at the
4/6, heard best Mild-diastolic murmur Mild-diastolic murmur at the apex (Graham murmur)
in left parasternal at the apex apex +
region

Signs
(See Table 7.18)

HYPERTENSION
Symptoms and Signs of Hypertension
Symptoms
• Due to elevated pressure itself
– Headache—in occipital region when the patient
awakens in the morning and it subsides
spontaneously after several hours
– Dizziness
– Palpitations
– Easy fatiguability
– Impotency
• Due to hypertensive vascular disease
– Epistaxis
– Hematuria
– Blurring of vision owing to retinal changes
– Episodes of weakness due to transient cerebral Fig. 7.17: Coarctation of the aorta showing a prominent ascending
ischemia aorta, double aortic knuckle and rib notching
166 Essentials of Clinical Medicine

sound, fourth heart sound present, aortic ejection click

and aortic systolic ejection murmur caused by turbulence
secondary to aortic dilatation.
• Chest examination—pulmonary rales, collateral vessels
resulting from coarctation of the aorta on the back
• Abdominal examination—auscultation for bruits in renal
artery stenosis, for enlarged kidneys of polycystic renal
disease.
• Femoral pulses—decreased or delayed in comparison
to radial pulse
• Examination of extremities for edema
• Any evidence of previous CVA or other intracranial
pathology.

Table 7.19: Clinical features that help in the diagnosis

of secondary hypertension

History Examination
1. Known renal disease 1. Femoral pulse delayed
2. Thirst, polyuria, nocturia 2. Palpable kidney
3. Dysuria 3. Enlarged bladder
Fig. 7.18: Renal artery stenosis 4. Hematuria 4. Uremic feature
5. Loin pain/renal colic 5. Edema
6. Stones 6. Abdominal bruits
– Angina pectoris, dyspnea due to cardiac failure 7. Abdominal trauma 7. Features of Cushing’s or
– Pain due to dissection of aorta or leaking aneurysm. acromegaly
• Due to underlying disease is secondary hypertension 8. Analgesic use 8. Cafe-au lait patches
– Polyuria, polydipsia, muscle weakness, secondary 9. Other drugs like oral contra- 9. Neurofibroma
to hypokalemia in patients with primary aldo- ceptive, steroids, liquorice, 10. Orthostatic hypotension
sympathomimetic, appetite
steronism suppressants, and carbenoxolone
– Weight gain and emotional liability in patients with sodium
Cushing’s syndrome
– Episodic headaches, palpitation, diaphoresis, postural Table 7.20: Renal causes of hypertension
dizziness, pheochromocytoma
Unilateral Bilateral
– Recurrent backache or UTI—chronic glomerulo-
nephritis and pyelonephritis Renal artery steroids Glomerulonephritis
Chronic pyelonephritis Interstitial nephritis
Signs Vesicoureteric reflux Pyelonephritis
TB kidney Polycystic kidneys
• General appearance—round face and truncal obesity of Obstructive uropathy Analgesic nephropathy
Cushing’s syndrome. Collagen disorder
• Muscular development in the upper extremities out of Obstructive uropathy
proportion to that of lower extremities suggesting Diabetic nephropathy
coarctation of the aorta TB kidney
Amyloidosis
• Rise in diastolic pressure when the patient goes from Irradiation to kidney
supine to standing position Chronic renal failure
– Essential hypertension. A fall in the absence of
antihypertensive medications suggests secondary Choice of Antihypertensive Agents
hypertension. • Angina with hypertension—beta blocker/diltiazem.
• Pulse feels forcible and more difficult to compress in • Tachycardia with hypertension—beta blocker / diltiazem.
diastole • Raised plasma rennin with hypertension—beta blocker/
• Hypertensive retinopathy changes in fundus diltiazem.
• Palpation and auscultation of carotid arteries for evidence • CCF with hypertension—diuretics as adjuvant, enalapril,
of stenosis amiloride.
• Cardiac examination—left ventricular hypotrophy, • LVF with hypertension—diuretics, adjuvants, enalapril,
accentuation of aortic component of second heart aniloride, spironolactone.
 Cardiovascular System 167

• Renal involvement with hypertension—hydralazine or 4. Such patients are at high risk from vascular
prazosin. complications.
• Moderate-to-severe hypertension—methyldopa.
• SVT with hypertension—verapanil. Intermittent Claudication
• Asthma with hypertension—calcium channel blockers 1. Pain on walking a distance (claudication distance)
• Hypertension with diabetes—ACE inhibitors. 2. Starts and on continued walking pain is aggravated and
• Resistant hypertension—minoxidil. compels the patient to take rest
• Malignant hypertension—diazoxide IV, hydralazine, 3. Disappears when exercise stops
sublingual nifedipine. 4. Typically occurs in calf muscles but may be felt in thighs
• Pregnancy with hypertension—methyldopa, hydralazine. and/or buttocks if obstruction to flow is sufficiently
• Pheochromocytoma and hypertension—phenoxy- proximal
benzamine. 5. Described as tightness or cramp like
• Hypertension in postmenopausal women with meno- 6. Male patients with gluteal claudication due to internal
pausal symptoms—clonidine. iliac disease are almost invariably impotent
7. Term claudication is also used to denote pain in leg on
Causes of Hyper-reninemia walking due to neurological and musculo-skeletal
• Hemangioparicytoma. disorders of lumbar spine (neurologic claudition) and
• Wilm’s tumor. due to venous outflow obstruction from legs (venous
• Barter’s syndrome. claudication). However, these are much lesser than arterial
• Renin producing undifferentiated bronchial carcinoma. claudication.
Stepwise Approach to Treatment of Hypertension Rest/Night Pain
• Step 1 — Diuretics/beta blockers 1. The patient awakens 1 to 2 hours later after falling asleep
• Step 2 — Calcium channel inhibitors, due to pain in foot, usually in instep. This is due to loss
clonidine, methyldopa. on recumbency of beneficial effects of gravity on lower
• Step 3 — Vasodilators, calcium channel limb perfusion. Also, due to decrease in heart rate, BP,
blockers. and cardiac output in sleep.
• Step 4 — Prazosin, guanethedin. 2. Pain relieved by hanging their legs out of bed or by
getting up and walking around .
PERIPHERAL ARTERIAL DISEASE (PAD) 3. When the patient returns to bed, symptoms reccur.
4. The patient feels comfortable by sleeping in a chair. This
1. Mainly in elderly > 60 years. leads to dependent edema and increased interstitial tissue
2. Mostly due to atherosclerosis affecting large and medium pressure causes further reduction in tissue pressure and
sized vessels. more pain. Rest pain usually indicates the presence of
3. Family H/o of premature arterial disease and DM. multilevel disease.
a. Limb symptoms
b. Neurological symptoms Tissue Loss (ulceration and/or gangrene)
c. Abdominal symptoms 1. When in patients with rest pain there occurs trivial
d. Vasospastic symptoms injuries, they fail to heal and provide a portal of entry
for bacteria leading to gangrene and/or ulceration .
Lower Limb Symptoms 2. Without re-vascularization, the ischemia will rapidly
i. Asymptomatic progress.
ii. Intermittent claudication Table 7.21: Signs suggesting of vascular disease
iii. Rest pain
iv. Tissue loss (ulceration/gangrene) Signs Implication
Hands and arms
Asymptomatic Ischemia 1. Nicotine stains – Smoking
1. Defined by reduced ankle 2. Purple discoloration of – Atheroembolism from a
2. Brachial pressure index is very common in middle- aged fingertips proximal subclavian aneurysm.
3. Pits and healed scar in finger – Secondary Raynaud’s syn-
and elderly
pulps drome
3. Asymptomatic because they choose not to walk very 4. Calcinosis and visible nailfold – Scleroderma and CREST
far, or because their exercise tolerance is limited by other capillary loops syndrome
pathology. Contd...
168 Essentials of Clinical Medicine

Contd... dorsum/forefoot or hand) are most important and indicate

Signs Implication nerve ischemia
5. Wasting of small muscles – Thoracic outlet syndrome 3. Once these features are present, limb will become
of hand irreversibly damaged unless the circulation is restored
Face and Neck within a few hours.
1. Corneal arcus and xanthelasma – Hypercholestrolemia 4. Calf muscle tenderness is another grave sign indicating
2. Horner’s syndrome – Carotid artery dissection or impending muscle infarction.
aneurysm 5. Common causes of acute limb ischemia are embolus
3. Hoarsness of voice and bovine – Recurrent laryngeal nerve (usually cardiac in origin) or thrombotic occlusion of a
cough palsy form a thoracic aortic narrowed atherosclerotic arterial segment.
aneurysm
4. Prominent veins in the neck – Axillary/subclavian vein
6. Acute arterial occlusion is associated with intense spasm
and over shoulder and anterior occlusion in arterial tree distal to blockage and limb will appear
chest “marble white”.
Abdomen 7. Over the next few hours, the spasm relaxes and skin
1. Epigastric/umbilical pulsation – Aortoiliac aneurysms fills with the deoxygenated blood leading to mottling
2. Mottling of the abdomen – Ruptured abdominal aortic which is light blue or purple, has a fine reticular pattern
aneurysms or saddle embolism and blanches on pressure.
occluding aortic bifurcation 8. As ischemia progresses, blood coalescing in the skin
3. Evidence of weight loss – Visceral ischemia
produces a coarser pattern which is dark purple, almost
black and does not blanch.
Chronic Lower Limb Ischemia
9. The final stage is large patches of fixed staining leading
1. In many patients the pedal pulses may be absent or to blistering and liquefaction.
diminished. However, the presence of pedal pulses at 10. Fixed mottling of an anesthetic paralysed limb, in
rest does not exclude a significant lower limb PAD association with muscle rigidity and turgor indicates
2. If history is convincing, ask the patients to walk until irreversible ischemia and amputation is the only option.
the onset of pain
3. If symptoms are vascular in origin, the pulses will NEUROLOGICAL PRESENTATION OF
disappear. VASCULAR DISEASES
4. Additional ischemic changes may be present, e.g.
absence of body hair on toes and dorsum of feet. 1. May present with multi-infarct dementia, strokes or TIA.
5. Such patients will have an ankle BP of less than 50 mm (transient ischemic attack.)
Hg and a positive Beurger’s test. 2. A stroke may be defined as focal neurological deficit of
6. This is indicated by the presence of rubor of forefoot vascular cause. If signs and symptoms last less than
(sunset foot) due to reactive hyperemia within 2 to 3 24 hours, then the event is termed as TIA.
min of leg becoming dependent.
7. Severe chronic ischemia of limb is associated with onset Internal Carotid Artery Territory
of extreme pallor of sole of foot and emptying the so-
called guttering of dorsal foot veins with leg elevated. • Strokes and TIA due to atheroembolism originating from
a tight atherosclerotic stenosis at the origin of internal
Acute Limb Ischemia carotid a.

1. Features of acute limb ischemia are 6 “Ps”. Ocular Features

Soft Signs • Loss of vision in ipsilateral eye (amaurosis fugax) often
• Pulse less described by patient as a curtain coming across the field
• Pallor of view usually lasting a few minutes due to transient
• Perishing cold occlusion of retinal a. or one of its braches.
Hard Signs • Less commonly, permanent monocular blindness occurs
• Paresthesia when embolus causes retinal infarction.
• Paralysis
• Pain on squeezing muscles Hemispheric Features
2. Of these, loss of motor (ability to wiggle the toes/ • Loss of power and/or sensation in the contralateral arm
fingers) and /or sensory functions (light touch over the and/or leg.

• If dominant hemisphere is affected, there may be also
dysphasia.
• A bruit over neck may arise from stenosis in other
vessels such as ext. carotid artery
• Or there may be so little blood flowing through a critical
int. carotid artery stenosis that no bruit is audible.
This consideration is equally applicable over other sites
(e.g. femoral and subclavian a.)
Vertebrobasilar Artery Territory
1. Less common TIA and strokes
2. Giddiness, collapse, with or without loss of conscious-
ness, transient occipital blindness or complete loss of
vision in both eyes.
Subclavian Artery Territory
1. Stenosis or occlusion proximal to origin of vertebral a.
may cause vertebrobasillar symptom as a part of
“subclavian steal syndrome”.
2. Signs of this include asymmetry of pulses and BP in
arms and sometimes a bruit over the subclavian a. in
supraclavicular fossa.
Visceral Ischemia
1. For signs and symptoms of chronic mesenteric vascular
insufficiency, there should be stenosis or occlusion of 2
or 3 major visceral a, i.e. celiac axis superior and inferior
mesenteric a.
2. Patients develop central abdomen pain (mesenteric
angina) 10 to 15 minutes after eating.
3. Diarrhea may also be a feature. This leads to fear of
eating and weight loss.
4. Acute mesenteric ischemia is surgical emergency. The
patient typically presents with severe abdominal pain,
shock, bloody diarrhea and profound acidosis.
5. Renal angle pain from renal infarction or ischemia is
rare. It is associated with micro or macroscopic
hematuria.
Abdominal Aortic Aneurysm (AAA)
1. Five percent men aged over 65 years.
2. Men 3 times > women.
3. Present with abdominal and back pain or an awareness
of pulsation.
4. Many are asymptomatic until aneurysms rupture.
5. As aortic bifurcation is at level of umbilical artery,
palpable AAA is felt in epigastrium.
6. A pulsatile mass below the umbilicus suggests the iliac
aneurysms.
7. Commonest misdiagnosis of ruptured AAA is renal colic.
Cardiovascular System 169
8. Atheroembolism may arise from AAA and cause the blue
toe syndrome characterised by purple discoloration of
toes/forefoot usually in association with a full set of
pedal pulses.
Vasospastic Conditions
Raynaud’s phenomenon (RP) describes digital ischemia
induced by cold and emotion and comprises of three phases:
1. Pallor due to digital artery spasm and/or obstruction.
2. Cyanosis due to deoxygenation of static venous blood
(this phase may be absent).
3. Rubor due to reactive hyperemia.
RP may be primary (Raynaud’s disease) owing to
idiopathic digital a. vasospasm or secondary (Raynaud’s
syndrome) because of digital a. obstruction caused by:
1. Connective tissue diseases (most commonly systemic
sclerosis).
2. Vibration injury (secondary to use of power tools).
3. Atheroembolism from a proximal source such as
subclavian a. aneurysm.
Venous Disorders
Pain
1. Patients with uncomplicated varicose veins may
complain of an aching discomfort in leg, itching and a
feeling of swelling.
2. Symptoms are aggravated by prolonged standing and
are often worse towards the end of the day.
3. Pain of DVT deep seated and associated with swelling
below the level of obstruction.
4. SVT produces a red painful area overlying the vein
involved.
5. Varicose ulceration may be painless; but if there is pain,
it may be relieved by elevation of limb.
Swelling
1. May be associated with varicose veins, deep venous
reflux and DVT.
Discoloration
1. Chronic venous insufficiency is associated with
deposition of hemosiderin in the skin leading to
lipodermatosclerosis (LDS). This may vary from deep
blue/black to purple or even bright red.
2. Typically affects medial aspects of lower third of leg
but may be laterally placed if superficial reflux
predominates in short saphenous veins.
Ulceration
Always associated with LDS.
• Question for deep venous thombosis:
1. Recent bedrest or operation (esp. to leg or pelvis)
170 Essentials of Clinical Medicine

2. Recent travel, especially long flights Chronic Leg Ulceration

3. Previous trauma to leg, especially long bone fractures, Bandaging for a leg ulceration is contraindicated unless there
plaster of Paris, splintage and immobilization. is documented evidence of adequacy of arterial circulation—
4. Pregnancy or features to suggest pelvic diseases. either by feeling the pulses or by measuring the ankle,
5. Previous DVT
branchial pressure index.
6. Family H/o thrombosis
7. Recent central venous catheterization, injection of Varicose Vein
drugs, etc. (in upper limb). 1. Pain felt in lower leg or whole of leg according to site of
Deep Vein Thrombosis varicosities.
1. Most often legs but can also affect the arm (axillary 2. Pain gets worse when the patient stands up for a long
vein thrombosis). time.
2. Sometimes life-threatening DVT may be asymptomatic. 3. Relieved by lying down.
4. Pain of varicocele of testes is of similar character.
Table 7.22: Clinical features of DVT
Venous Thrombosis
Clinical features Non-occlusive Occlusive thrombus
Patients may have pain and swelling of leg (around ankle)
Pain Often absent Usually present
Homan’s sign:
Calf tenderness Often absent Usually present
Swelling Absent Present Dorsiflexion of foot elicits pain in calf.
Temp Normal or slight increased Increased Mose’s sign:
Sup. veins Normal Distended Squeezing of calf muscle from side to side elicits pain.
Risk of pul.embolus High Low
• In superficial thrombopheblitis, there is pain and
The leg: Clinical features of DVT depend upon the site and tendeness over superficial inflamed veins.
extent and whether it is occlusive (as mentioned in Table • The above maneuvers may dislodge the thombus
7.22). resulting is pul. embolism.
The arm: Neurogenic Claudication
• DVT can occur as primary event due to repetitive trauma
of vein, e.g. TOS. 1. Symptoms of dysfunction of cauda equina appear either
• Also seen as a secondary complication around in on walking or on prolonged standing.
dwelling catheters in subclavian vein. 2. Relieved by rest.
• Arm swelling and discomfort exacerbated by activity, 3. This is due to lumbar canal stenosis which is made
especially where it involves holding the arm overhead. worse in middle age due to degenerative changes,
• Arm is swollen, skin often cyanosed and mottled, especially between L4 and L5 .
especially on dependency. 4. There is march of pain with paraesthesia and absent
• Collaterals often seen over the shoulder region and ankle jerk after exercise.
anterior chest wall. 5. Symptoms take 5 to 10 minutes to fade.

Superficial Venous Thombophlebitis CARDIOVASCULAR SYSTEM

1. Usually sterile, inflammation of superficial veins
associated with intraluminal thombosis
2. Affects up to 10 percent of patients with severe varicose
veins and appears to be commoner during pregnancy.
3. Recurrent SVT may be associated with underlying
malignancy.
4. SVT at or near the saphenofemoral junction is associated
with a high incidence of pulmonary embolism.
Chronic Venous Insufficiency
1. Produces skin changes in lower legs (varicose eczema,
lipodermaposclerosis, ulceration) due to sustained
venous hypertension which in turn is due to reflex (90%)
and/or obstruction (10%) in superficial and/or deep veins.
[Figs 7.19(1) to 7.19(33), Plates 4 to 10]
1. A 68-year-old man with a H/o hypertension, diabetes
and retention awoke feeling nauseated and light headed.
He did not respond to questions from his wife. When
the emergency medical technician arrived, his blood
pressure was 60 mm Hg by palpation. IV fluids signs
obtained in the ER (Emergency Room) were: blood
pressure 60, heart rate 120 and regular, temperature
38.9°C (102°F) and respiratory rate 30. A brief physical
examination revealed coarse rates approximately halfway
up in the chest bilaterally and inaudible heart sounds. An
indwelling urinary catheter was placed with drainage of
10 to 20 ml of dark urine, Chest X-ray revealed bilateral

interstitial infiltrates, ECG was unremarkable except for
sinus tachycardia. Antibiotics were administered and the
patient was transferred to ICU, where a right heart
catheterization was performed. Pulmonary capillary
wedge pressure was 28 mm Hg. Cardiac output was
1.9 L/min. Right arterial mean pressure was 10 mm Hg.
The most likely cause of this hypertension was:
Left ventricular dysfunction
2. A 53-year-old man presents to the emergency room after
the acute onset of chest pain. The episodes occurred
8 hr prior to his arrival and lasted for a resolved. The
patient has a long history of diabetes mellitus and
hypocholesteremia and has smoked approximately 1 to
1½ packs per day of cigarettes for the past 30 years.
On physical examination, he has a BP of 84/52, and his
pulse is 54. He has jugular venous distention to the angle
of mandible and clear lung fields. His rhythm strip reveals
a Wenkebach’s pattern, given his hypertension, a swan
ganz catheter is placed. Right arterial pressure is estimated
at 16 mm Hg (normal 0-5), pulmonary artery pressure
Cardiovascular System 171
at 20/10 mm Hg (normal 12-28/3-13) and pulmonary
capillary wedge pressure is 8 mm Hg (normal range 3-
10). What may be the possible abnormality?
Right ventricular infarction
3. A 75-year-old man presents with recurrent episodes of
shortness of breath on minimal exertion. He has no prior
significant past medical history. Physical examination
reveals blood pressure of 110/70 without pulses. Heart
rate of 110, respiratory rate of 25, and temp. of 27°C
(98.6°F) orally. Jugular veins are distended and heart
sounds are distant, but there are third and fourth heart
sounds and pedal edema is present. The liver is enlarged.
The electrocardiogram shows non-specific ST-T wave
changes and occasional premature ventricular
contractions. The chest X-ray reveals clear lung fields
and a mildly dilated cardiac silhoucteke. Echo-
cardiography reveals normal systolic function and
thickened ventricular walls with a speckled appearance.
Which condition is most consistence with the patient’s
clinical presentation?
Amyloidosis
 8

Central Nervous System

INTRODUCTION COMMON SYMPTOMS OF CENTRAL

NERVOUS SYSTEM DISORDERS
The aim of nervous system examination is to assess the
clinical illness of the patient on the basis of principles of 1. Headache
both anatomy and physiology that is both functionally and 2. Faintness, syncope, dizziness, vitiligo
anatomically. A proper approach, for instance, taking of a 3. Motor weakness, myalgia, abnormal posture, torticoils
detailed history and care for clinical examination will enable 4. Numbness, tingling and sensory loss
the clinician to localize the site of neurological lesion and to 5. Acute confusional state, mental state and coma,
establish a process of different diagnosis. This guided hallucination, delusion, illusion
approach may also help to localize the lesions even in nuclei 6. Aphasia, dysphonia, dysarthria, dysphagia and the focal
and their interconnecting pathways or other disease cerebral disorders
syndromes it reveals: 7. Memmory loss and dementia
1. Structural abnormalities like vascular diseases, multiple 8. Sleep disorders
sclerosis and tumors, etc. 9. Abnormal behavior and altered sensation, mood
2. Functional abnormalities like migraine, epilepsy, etc. changes, delusions, illusions, hallucination, phychotic
Abnormalities in the functioning of the central nervous depression, nervousness
system also require the thorough examination of structures 10. Personality disorders
and organs. 11. Abnormal visual and body perception
Different patients come with a variety of presenting 12. Apraxia
complaints depending upon the part of nervous system most 13. Hemiplegia, paraplegia, quadriplegia
affected. A thorough and detailed history taking, therefore, 14. Hemianopia
becomes a must. The reason for this is that unlike other 15. Acalculia, dysgraphia, agraphia, alexia
system of the body, the central nervous system (Fig. 8.1, 16. Ataxia
Plate 11) cannot be examined directly (except for the fundus 17. Abnormal cranial nervous function (or deficient)
of the optic nerve). The same physical sign may occur due 18. Disturbance in visual, auditory and taste sensation
to a variety of reasons, e.g. the causes of hemiplegia may 19. Facial palsy
be embolic, hemorrhagic, thrombotic or space-occupying 20. Nystagmus
lesion (SOL). Therefore, the clinician is expected to have a 21. Loss of tone, abnormal reflexes
complete knowledge of various etiological factors of a 22. Loss of coordination, abnormal movements
disease and should ask the patient some relevant questions 23. Disturbances in the functioning of autonomic nervous
and should also have the capability of interpreting them system
correctly. Before taking history, the clinician must find out
whether the patient is right handed or left handed. Bladder  Bowel
Another way in which the examination of central nervous 1 Incontinence 1 Diarrhea
system is different from that of the other system is that the 2 Hesitancy 2 Constipation
routine sequence of inspection, palpation, percussion and 3 Urgency
auscultation is not followed. It requires a completely different 4 Continence
approach and will be clear as we proceed further here. 5 Frequency

NEUROLOGICAL HISTORY TAKING
Sometimes the history may itself prove to be diagnostic as
it may give information about the onset and course of the
disorders. The aim of history taking in a neurological case
is:
1. To examine the absence or presence of any abnormal
feature of any illness.
2. To modify the idea suggested by the presentation and
complaints of the patient, for instance, history of
recurrent visual disturbance may be suggestive of
transient ischemic attacks or multiple sclerosis which
should be ruled out further. Any deterioration in thought
process, memory or behaviors of the patient may suggest
progressive dementia, or progressive focal higher level
brain disturbances such as aphasia.
It should always be kept in mind by medical students as
well as clinicians that it is especially difficult for a person
with damaged nervous system to understand the nature of
the symptoms with which he/she is suffering from because
these features are outside ordinary experiences.
History Taking in a Neurological Case
Presenting Complaints
a. Relationship to time:
• When did the symptoms first started/stopped? (note
that there is a heaven and hell difference between
the symptoms first appeared and first noticed by the
patients).
• How long do they continue?
• Special time of occurrence?
• Time internal between successive symptoms of
similar kind?
b. Localization:
• Part of the body affected?
• Is the localization pinpoint or diffuse?
• If widespread, is it symmetrical or asymmetrical?
c. Precipitating factors and relieving factors:
• Are symptoms triggered by—exercise, sleep posture,
reading, eating, coughing, micturition, renal activity,
or external stimuli like light, sound, smell, heat, cold,
etc.
• What are the relieving factors? Are they like bed-
rest, food, medicine, postponement of daily activities,
etc.
d. Associated symptoms:
• Like numbness, paresthesia, cold, warmth (sensory
system)
• Weakness, clumsiness, stiffness, unsteady gait
(motor system).
Central Nervous System 173
• Headache, nausea, vomiting
• Loss of consciousness, visual disturbances.
• Psychological changes like depression, weeping,
agitation, sleep and appetite disturbances, alteration
in energy and libido.
Past History
Some neurological illnesses show signs and symptoms after
many years of causative events. Examples of such kind are
epilepsy, hydrocephalus and sometimes migraine also.
Therefore, it becomes necessary to inquire about:
• Pregnancy (length of term, intrauterine problem).
• Delivery (normal, assisted or operative).
• Neonatal death (severe jaundice, respiratory difficulty
infections and confusions).
• Surgical operations and drug therapy.
Family History
There are two kinds of neurological disorders which can
be send to have genetic component. Firstly, there are some
disorders which are strictly genetic (e.g. muscular
dystrophy, spinocerebellar degeneration, Huntington’s
chorea. In others, genetic factors appear to influence the
development of condition (e.g. epilepsy, migraine, multiple
sclerosis, vascular diseases). Other diseases showing familial
tendencies are—stroke, cerebral aneurysm, dementia,
spinocerebellar degenerations and certain neuropathies.
Social History
a. The occupation of the patient may be either relevant in
the causation or triggering of neurologic disorders; for
example:
• Toxic chemicals, neuropathies and encephalopathy
• Recurrent overuse of certain joints leading to
entrapment neuropathy, carpal tunnel syndrome.
• Exercise and prolonged visual activity with visual
display units or overuse of artificial lights, tension,
headache and migraine.
b. Other factors which come under social history are
marital status, household dynamics, change of lifestyles,
marriage, divorce, bereavement, change of occupation,
smoking habits, alcohol intake or drug ingestion. It is
also necessary to ask about sexual orientation of the
patient and any exposure to sexually transmitted disease
including syphilis and HIV.
c. The commonest variety of neurological symptoms are:
• Headaches
• Altered consciousness—characterized by 3 F’s:
→ Fits
→ Faints
→ Funny twins.
174 Essentials of Clinical Medicine

HEADACHE 12. Radiation of headache: Is there any radiation of the

headache?
Headache is one of the commonest and frequent complaints.
Usually, the headache is a benign symptom and only – Unlimited pain radiating to throat, ear, eye, nose,
occasionally it may be the manifestation of a more serious cheek or face is suggestive of neuralgia
illness, like brain tumor of giant cell arthritis. – Facial pain extending beyond the territory of the
Sometimes, the diagnosis can be almost reached by the trigeminal nerve and which may be bilateral or involve
description of headache by the patient. Description of the tongue or mouth suggests a psychogenic cause
headache by the patient and its suggesting features are as – Radiation of pain to neck with tenderness or neck
follows: muscles is typically suggestive of tension headache
1. Throbbing headaches with tight muscles about the head, and cervicogenic headache.
neck and shoulder girdle suggest activation of intra-and Table 8.1: Causes and sites of headache
extracranial arteries and skeletal muscle surrounding the
head and neck by a generic head pain generating Cause Site of headache
mechanism. Subarachnoid hemorrhage Bilateral, generalized or nuchal
2. Majority of headaches are tension type headaches, no Tension headache Bilateral, generalized or nuchal
underlying disease or abnormal physical signs are seen. Migraine Unilateral—different sites on
separate occasions
Emotional factors often predominate. Cluster headache Unilateral: eye, nose, cheek
3. Headache may also occur non-specifically in febrile Cranial arthritis Unilateral with scalp tenderness
illness and some systemic diseases, which have been Trigeminal neuralgia Unilateral: maxillary or
mentioned earlier in the section of symptomatology. mandibular branches of the trigeminal nerve
Postherpetic neuralgia Unilateral ophthalmic branch of
Inquiry into the Complaints of Headaches trigeminal nerve

1. Type : What type of headache is described by the patient? Table 8.2: Characteristics of headache
2. Occurrence: When did it begin? It is cyclical or daily? Characteristics Disorder
3. What is the duration and progress of each attack of Feeling of tight band around head or Tension headache
headache? like a pressure over head
4. Is it unremitting? Sickening, dull aching or throbbing Migraine
5. Character of headaches: Lancinating, paroxysmal pain like Trigeminal neuralgias
– What is the intensity of headache? red-hot needles thrust through the
face
– What is the nature and quality of headache?
– Whether the patient is able to localize the exact site Table 8.3: Severity of headache
of headache?
Severity Disorder
– Does the headache radiate or does it have a spreading
Explosive and sudden onset of Subarachnoid hemorrhage
feature? severe headache associated with
– Is it associated with any other symptoms? neck stiffness
6. What are the precipitating, aggravating and relieving Slowly progressive headache Raised intracranial tension from
factors? increasing in duration and severity a cerebral tumor
7. Limitation: Are the daily activities of the patient limited Severe headache is also seen in Migraine, cluster headache and
trigeminal neuralgia
due to headache?
Sometimes the patient winces and Paroxysms of severe pain
8. Whether any medications and treatment are used and cries out momentarily due to pain
what was the response?
9. Health between the attacks: Inquire about the health of Table 8.4: Duration of headache
the patients between attacks. Whether the symptoms Long history of headache without Benign cause
persist or is the patient completely well between attacks? progression
Is there any sort of depression, fear or anxiety? Lasting 24-72 hours but occasionally Migraine
10. Does the patient tell you his idea about the causation of last < 6 hours
Cluster headache attacks Last > 1 hour
disease? Trigeminal neuralgia each paroxysm lasts only
11. Main site: What is the main site of headache? Whether it seconds recurring over several
affects the entire head, half the head or a smaller area of Tension type headache variable ranging from 15 minutes
the head, neck or face. For more details, see Table 8.1. to many weeks or even months.
 Central Nervous System 175

Table 8.5: Frequency and periodicity of headache Causes of raised intracranial tension:
Migraine, trigeminal neuralgias and Attacks are sudden or subacute • Cerebral hemorrhage
cluster headache onset occurring in reported short • Intracranial tumor
bursts with pain-free intervals • Meningitis
lasting weeks or months.
Migraine Often cyclical, occurring weekly
• Encephalitis
or monthly and frequently • Benign intracranial hypertension
premenstrual in women. In • Hydrocephalus
between the attacks, migraine • Hypoxic encephalopathy.
sufferer is usually well.
Postherpetic neuralgia and Subacute onset but are Symptoms of raised intracranial tension:
cranial arthritis continuous • Headache
Meningitis and subarachnoid Acute onset with rapid • Projectile vomiting
hemorrhage progression
• Convulsions
Table 8.6: Special times of occurrence of headache
• Altered sensorium
Signs of raised intracranial tension:
Times Type of headache
• Bradycardia
Severe pain awakening the patient in Cluster headaches and raised
early hours of the morning intracranial pressure • BP may be higher
Pain precipitated by facial movement Trigeminal or glossopharyngeal • Respiration is slow and deep eventually Cheyne-Stokes
such as eating, drinking, shaving or neuralgias breathing
brushing the teeth
• Papilloedema
Jaw pain during chewing Cranial arthritis
Headache occurring at times of Migraine • False localizing signs—unilateral or bilateral 6th nerve
stress relief (weekends and holidays) palsy
• Bilateral Babinski’s sign
Table 8.7: Aggravating factors of headache • Bilateral grasp reflex.
• Increased by bending, straining, Raised intracranial tension X-ray with raised intracranial tension:
and coughing • Silver beaten appearance in children
• Precipitated by bright light, loud, Migraine
noise, strong odors, missed meals, • Sutural diastasis (children)
intake of chocolates, cheese, • Erosion of clinoid process
alcohol, and citrus fruits, changes • Deep sella tursica
in weather, travel and by
• Enlargement of internal auditory meatus
contraceptive pills
• Sensitivity to even small amounts Cluster headache Tension headache is usually not accompanied with
of alcohols and other vasodilators nausea and vomiting.
• Headaches associated with weight Headache due to benign • Intolerance to light (photophobia), or noise (phono-
gain and use of corticosteroids, intracranial hypertension
tetracycline or OCPs
phobia), irritability, food cravings and hunger are usually
typically seen in migraine. In some patients, visual
Relieving Factors disturbances (teichopsic and fortification spectra) and
sometimes peripheral and circumoral (around the mouth)
• Acute attacks of migraine usually respond well to 5- paresthesia occur before the headache phase. It is called
HT1 agonists such as sumatriptan and are usually less aura or migrainous aura.
frequent and less severe during pregnancy. • Watery discharge from the eye or nose or even ptosis
• Tension headache, especially when chronic and is of eyelid during attack may be seen in cluster headaches.
resistant to analgesics. • Whether the patient has syncopal attacks, seizures, ataxia
• A rapid and dramatic response in cranial arthritis to dizziness or any other associated features.
corticosteroids therapy is characteristic.
Headache Symptoms which Suggest Some
Associated Features Important Underlying Pathology
• Migraine is usually accompanied by nausea and vomiting • Worst headache ever
• Vomiting without nausea seen in headache due to raised • First severe headache
intracranial tension (ICT) • Subacute worsening over days or weeks
176 Essentials of Clinical Medicine
• Abnormal neurologic examination
• Fever or unexplained systemic signs
• Vomiting preceding headache
• Induced by bending, lifting or coughing
• Disturbs sleep or presents immediately upon awakening
• Known systemic illness
• Onset after 55 years of age.
Note: Headache has been described in detail in section of
“Symptomatology and its Causes”.
BASIC COMPONENTS OF NERVOUS SYSTEM
The nervous system consists of central and peripheral motor
and sensory pathways, the cerebellar system and cerebral
hemisphere.
Another important part of nervous system is the spinal
cord in which motor and sensory pathways are in close
association with each other.
Various signs and symptoms are produced in our body
due to abnormal functioning of these structures of nervous
system. It causes some negative symptoms and signs like
weakness, loss of vision, sensory loss or difficulty in walking
or positive abnormalities such as seizures, pain or involving
movements.
MOTOR SYSTEM
The part of cerebral cortex or the frontal lobes which on
stimulation gives rise to skeletal muscle responses
constitutes the motor areas (Figs 8.2 to 8.4, Plate 11). As
this region lies anterior to central sulcus, it is also called
precentral motor cortex. Histologically, it is divided into:
• Area 4—motor cortex or motor area.
• Area 6—premotor cortex or premotor area
• Area 8—frontal eye field
The somatic motor activity depends ultimately upon the
pattern and rate of discharge of spinal motor nerves and
homologous nerves in the motor nuclei of cranial nerves.
The nerves are actually the final common pathway to skeletal
muscle and are bombarded by impulses from an immense
array of pathways. The whole system of nerves functions
with the coordination between input and output signals. The
inputs converging on the motor neurons subserve three
distinct functions. They are: (i) Bring about voluntary activity,
(ii) Adjustment of body posture to provide a stable back-
ground for movements, and (iii) They coordinate the action
of various muscles to make movements smooth and precise.
In this, the main role is played by corticospinal and
corticobulbar systems. Other areas which also hold a major
share are posture regulating systems, spinocerebellum, basal
ganglia and neocerebellum.
The motor output is of two types: (i) Reflective or
involuntary, and (ii) Voluntary.
Lesions of motor system might result in total weakness
(paralysis) or partial weakness (paresis) or involuntary
movements or ataxia due to fibers and their terminal
abnormal branches.
Area 4—Motor Cortex or Motor Area
The major portion of the motor cortex occupies almost the
entire length of the precentral gyrus. A small portion, called
supplementary motor area, extends medially beyond the
margin of the central sulcus over on to the medial surface
of the cerebral hemorrhage which lies above the cingulated
gyrus. The motor cortex is the main region of origin of the
pyramidal tracts. In the motor cortex, the body is
represented upside down in the cortex.
The size of representation of indivdual body part is
proportional to the skill with which the part is used in fine,
voluntary movements. Separate foci are present for each
of the fingers, the focus for thumb being the most inferior
and that for little finger the most superior. The structure
having bilateral representation are face, pharynx vocal cords,
and muscles for the closure of jaw. Stimulation of this part
of brain causes discrete and isolated movements of opposite
side of the body.
The neurons in the motor area also receive the input
signals from somatosensory area I (SSA-I) and II (SSA-
II). It plays a very important part in use of individual muscle
groups for the accuracy of motor control. Supplementory
motor area is engaged primarily in the volunry movements
that involve complex planning.
Area 6—Premotor Cortex
The area 6 or premotor cortex lies anterior to the area 4
(the motor cortex) of cerebral cortex. It gives rise to three
subdivisions of fibers. (i) Descending fibers to pyramidal
tract, (ii) Horizontal fibers passing posteriorly to stimulate
area 4, and (iii) Descending fibers not involved in the
pyramidal tract (therefore called extrapyramidal tract).
The major function of area 6 is to involve in complicated
motor function such as an alteration in the force or velocity
of a movement, action done in response to visual input as
spoken command, two-handed coordination to perform
more complicated tasks and postural support so as to
perform a wide variety of movements.
It also acts as an important channel for the relay of
processed information to the primary motor cortex or
directly to the descending pathways from other areas of
brain. Stimulation of this area leads to excitatory response

such as gross rotation of eyes, head and trunk to opposite
side of the body. The extrapyramidal pathways and
intracortical spread of the stimuli to pyramidal tracts also
help in such kind of movements.
Area 8—Frontal Eye Field
The area 8 or frontal eye field lies anterior to area 6 (the
premotor cortex) of the cerebral hemisphere. Its excitation
causes conjugate deviation of the eyes to opposite side giving
it the name of frontal eye field.
The neurons from the specific sensory nuclei of the
thalamus, project in a highly specific way to two somato-
sensory areas of the cortex—primary and secondary.
Primary Sensory Area
The primary sensory area [also called somatosensory area
I (SSA-I)] is located in postcentral gyrus which involves
Broadman’s area 3,1, and 2. Each area (3, 1, and 2) performs
some specific functions. Area 3 responds to the ‘light touch’
and receives a dense input from the thalamus, whereas areas
1 and 2 respond to deep stimuli. The primary sensory area
(SSA-I) receives the afferents from opposite side of the
body but from both sides of face. The thalamic projection
represents itself in such a way that the body is represented
upside down with legs on the top and head at the foot of the
gyrus. The fingers, thumb and lips occupy the largest areas
of somatosensory cortex.
Secondary Sensory Area
The secondary sensory area [also called somatosensory area
II (SSA-II)] is located in the cerebral cortex and is mostly
buried in the superior wall of the sylvian fissure (lateral
cerebral sulcus). Unlike from both sides of the body like
SSA-I, it shows a dermatomal (point to point) sequence of
representation. The posterior region receives afferents from
the legs, while the anterior parts receive afferents from the
face (the face area of SSA-II lying just adjacent to that of
SSA-I); thus, the body has two times representation in the
somatosensory cortex, in areas SSA-I and SSA-II. Neurons
in anterior part respond to touch and those in posterior part
respond to touch, auditory, visual and nociceptive stimuli.
Note: Lesions of the cortex do not disturb/destroy the
somatic sensation. However, the proprioception and fine
touch are mostly affected. Thus, perception is possible even
in the absence of cerebral cortex.
DESCENDING TRACTS: MOTOR PATHWAYS
The motor pathways play a very important role in altering
the balance between excitatory and inhibitory input that
Central Nervous System 177
converge upon the alpha-motor nerves by three mechanisms
namely:
• Synapsing directly upon the alpha-motor neurons (speed
and specificity).
• Synapsing directly on the gamma-motor neurons (control
of stretch reflex)
• Synapsing on interneurons which act as switches that
enable a movement to be turned “on and off” under the
demand of higher motor centers.
Different areas of cerebral hemispheres give rise to two
types of descending (or motor) pathways:
1. Pyramidal tracts
2. Extrapyramidal tracts.
Although these tracts are functionally different, but these
are usually considered together because lesion within the
cerebral cortex almost always involves both of them.
Pyramidal Tracts: Corticospinal and
Corticobulbar Tracts
The longest tract extending from motor cortex up to last
segment of spinal cord. It is present only in higher animals
and humans where cerebrum is highly developed. Mostly,
the fibers (85–90%) in the pyramidal tract are of small
diameter (≤ to lum diameter) making it a slowly conducting
pathway. Almost half of the fibers are without myelination
(unmyelinated).
Components of Pyramidal Tracts
(Fig. 8.5, Plate 11)
The pyramidal fibers run from motor area to spinal ventral
horn cells and to all motor cranial nuclei with the exception
of those supplying external eye muscles.
a. Corticospinal tracts—those pyramidal fibers which reach
to spinal ventral horn cells.
b. Corticobulbar or corticonuclear tracts—those pyramidal
fibers which reach to motor cranial nuclei. It starts in
cerebral cortex and ends up in the brainstem (bulbar—
brainstem)
The pyramidal cells and tracts (corticobulbar and
corticospinal tracts) constitute the upper motor neurons
(UMNs), whereas the spinal and cranial motor neurons
which directly innervate the muscles constitute the lower
motor neurons (LMNs).
The corticobulbar fibers end near the motor neurons
that innervate muscles of the face, eyes, tongue and throat.
Therefore, they act as a remote control for the voluntary
movement of the muscles of head and neck and the
corticospinal fibers control the muscle of rest of body parts.
178 Essentials of Clinical Medicine
Origin of Pyramidal Tracts
• 30 percent from motor cortex—area 4 in precentral
gyrus
• 30 percent from area 6—premotor cortex
• 40 percent from somatosensory areas I and II (SSA-I
and II) and adjacent parietal lobe—association cortex.
peripheral lobe.
Table 8.8: Damage or injury and its consequences
Structure/Area Result
Area 4 Monoplegia (one limb)
Level of internal capsule Hemiplegia (one side of the body)
Brainstem level Paraplegia (60th lower limbs)
or quadriplegia (all the 4 limbs).
Functions of Descending Motorways
Functions of corticospinal tracts:
1. Motor impulses to spinal cord → control of voluntary
movement (especially the fine) precise movements of
fingers and hands → skilled work.
2. Part of pathways for superficial reflex like cremasteric
abdominal and plantar reflexes.
3. Excitatory effect (via alpha and gamma motor neurons
or inhibitory effect or excitatory effect via the
interneurons.
4. Affect afferent system neurons by →
• Ending either presynaptically an axon termenal of
afferent neurons as these fibres enter the CNS or
• Ending directly on dendrites or cell bodies of neurons
in ascending pathways.
5. Those arising from SSA-I and II are concerned with
sensory motor coordination, e.g. aiming the hands
towards an object and manipulating it, hand-eye
coordination, etc. Lesions of these areas cause defect
in motor performance characterized by inability to
perform learned sequences of movements such as eating
with knife and fork.
Functions of corticobulbar (corticonuclear) tracts:
Responsible for voluntary control of muscles of larynx,
pharynx, palate upper and lower face jaw, eyes, etc.
Pseudobulbar palsy is a condition resulting in paralysis or
weakness of muscles which control swallowing, talking,
tongue, and lip movements due to bilateral lesion of these
tracts.
Extrapyramidal Tracts
The system consists of basal ganglia, subthalamic nuclei,
substantia nigra and other structures in brainstem. These
are those neurons which are concerned with muscular
movements and posture. Its fibers make many synapses in
their descending path with cells of nuclear masses on the
way which include—nuclei of cerebral cortex, basal ganglia,
hypothalamus and nuclei of reticular formation in brainstem.
In spinal cord, these fibers form separate groups according
to their site of origin. The extrapyramidal system plays an
important role in postural mechanisms like sitting, standing,
turning over in lying position, walking and running. The
complex movements such as reaching for an object requires
both postural adjustments and fine distal movements, which
are under corticospinal control (Figs 8.6 and 8.7, Plate 12)
Functions of Extrapyramidal Tracts
• Corticobulbar (corticonuclear) fibers control the
movements of eyeballs.
• Control of tone, posture, and equilibrium (rubrospinal
tract for tone and posture, tectospinal for visuospinal
reflex, vestibulospinal for equilibrium.
• Control of complex movements of body and limb such
as coordinate movements of arms and legs during
walking.
• They show tonic inhibitory control over the lower
centers. Their damage increases rigidity to muscles
called release phenomenon.
• In case of damage to pyramidal tracts, the extra-
pyramidal tracts carry out voluntary movements to some
extent.
Note: Both pyramidal as well as extrapyramidal tracts cause
effects on motor neurons of the opposite side of the spinal
cord. Some pyramidal fibers end an interneuron that play
important roles in posture, whereas the extrapyramidal tract
fibers sometimes end directly on L-motor neurons to control
discrete muscle movement. Due to this extra control
mechanism, loss of function resulting from damage of one
system may be compensated for by the remaining system,
although not completely. A total separation of functions
between pyramidal and extrapyramidal tract is not clear-
cut; therefore, all movements, whether voluntary, require
the continuous coordinated interaction of both the systems.
Table 8.9: Differences between pyramidal and extrapyramidal tract
Pyramidal tract Extrapyramidal tract
1. Origin of these tracts is as follows Rubrospinal tract from the red
nucleus (magnocellularis, i.e.
large nucleus located in mid-
brain)
Thirty percent from motor cortex Tectospinal and tectobulbar
area 4 in precentral gyrus tract- from superior colliculus
Thirty percent from premotor (which is an optic center)
cortex, area 6
Fourty percent from SSA-I and II Reticulospinal tract from
and adjacent parietal lobe neuron of reticular formation
association cortex in pons and medulla
Contd...

Contd...
Pyramidal tract
2. Axons pass without relay to spinal
segmental levels where they form
synapses with either interneurons
in the dorsal horn or directly
themselves
3. They have greater influence over
motor neurons that control
muscles involved in fine move-
ments, particularly those of
fingers and hand.
4. Lesions of this tract produce
“spasticity in muscles involved
Table 8.10: Differences between upper and lower motor neuron lesions
Lower motor neuron lesions
1. Due to lesion of lower motor
neurons (LMNs). The LMNs
include the spinal and cranial
motor neurons that directly
innervate muscles.
2. Usually single or individual
muscle is affected.
3. Muscles become completely
paralysed (flaccid paralysis).
It is due to complete loss of
muscle tone which depends
on integrity of reflex arc.
4. There occurs “disuse atrophy”
of muscles (i.e. shrinkage of
muscle fibers which is finally
(fibrous
muscle)
5. All reflexes (superficial or
deep) are absent as motor
pathway is damaged.
Extrapyramidal tract
Vestibulospinal tract from
lateral vestibular nucleus
located at the junction of pons
and medulla
Medial longitudinal fasciculus
(or bundle) from medial
vestibular nucleus reticular
formation, superior colliculus
and interstitial nucleus of Cajal
They have many synapses in
their descending path descend-
ing path nuclei of the straitum
(caudate and putamen), the
globus pullidus, the hypothala-
mus and nuclei of the reticular
formation
They are more involved with
coordination of large muscle
groups used in the maintenance
of upright posture, in loco-
motion, and in head and body
movements when turning
towards a specific stimulus.
Its tract lesion produces
“rigidity of the involved
muscles
Upper motor neoron lesions
1. Due to lesions of upper motor
neurons (UMNs) in the brain
that forms the pyramidal
tracts
2. Usually a group of muscles is
affected
3. Affected muscles become
hypertonic (spastic paralysis
a. Release phenomenon, i.e.
loss of higher inhibitory cont-
rol
b. Denervation hypersensiti-
vity of centers below the level
of transaction.
4. The muscle atrophy is not
severe (if present-very mild)
because muscles though not
used in voluntary movements,
they are continuously in action
to maintain posture by “refle-
xes”.
5. a. Deep reflexes are hyperacti-
ve (accentuated) because of
increased gamma motor
discharge
Contd...
Contd...
Lower motor neuron lesions
6. Babinski’s sign or Babinski’s
plantar not elicited
Note:
1. The response is obtained by
stroking (to pass gently in
one direction) outer edge of
sole of foot with firm tactile
stimuli; it produces a downward
movement (plantar flexion) of
great toe and small toes
(Babinski’s—negative)
2. Babinski’s sign appears with the
development of pyramidal
tracts; therefore, its presence
indicates the development of
these tracts. Normally, it is a
flexor response (withdrawal
reflexes)
Levels of Motor Control System (Fig. 8.8)
a. Highest level—the cerebral cortex
b. The middle level—subcortical centers
c. The lowest level—brainstem and spinal cord
Central Nervous System 179
Upper motor neoron lesions
b. Superficial reflexes, only
abdominal cremasteric and
anal reflexes are lost
6. Babinski’s sign—positive
(abnomal)—stroking outer
edge of the sole of foot with
firm, tactile stimulus produces
first an upward movement
(dorsiflexion) of the great toe
and fanning out (abduction) of
small toes. This is due to con-
traction of extensor hallucis
longus (Anatomists mislead-
ingly call it an “extensor
response”. It is physiologically
a “flexor” (withdrawal)
response. Note that all the
muscles which contract during
a flexor response are called
physiological flexors)
Note:
1. Babinski’s sign once becomes
positive, it remains positive
for the rest of the life thereaf-
ter. In some normal individuals,
it is always positive
2. Individuals with Babinski’s
positive can neither run fast
nor can travel long distances.
3. Causes of positive Babinski’s
sign:
a. Infants—pyramidal tracts
are not developed till child
starts walking
b. During deep sleep
c. Inhibition of pyramidal
tracts
d. Chyene-Stokes respiration
due to hypoxia
180 Essentials of Clinical Medicine
Fig. 8.8: Levels of motor control system
Table 8.11: The major levels of motor integration
Levels of integration
1. Spinal cord
2. Medulla
3. Midbrain
4. Midbrain, thalamus
5. Hypothalamus, limbic system
6. Cerebral cortex
Table 8.12: Differences between spasticity and rigidity
Spasticity
1. It is seen following the lesion
of the pyramidal tract (cortico-
spinal tract). The commonest
site of lesion being the inter-
nal capsule.
2. It involves only one group of
muscles either agonist or
antagonist. Usually, antigravity
muscles [the extensor muscles
of lower limb (ankle, knee, hip),
the muscles of the back and
muscles of the upper limb
(wrist, elbow, shoulder) are
antigravity muscles] are involved.
3. It describes a state of increased 3. Hypertonia described here is
tone which is of clasp knife type.
Principal function
Control of spinal reflexes
Regulation of heart, respiration
and antigravity reflexes
Regulation of righting reflexes
Regulation of locomotor reflex
Emotional function
Initiation of voluntary movement,
emotions and memory
Rigidity
1. It is seen following the lesion
of basal ganglia, therefore,
called extrapyramidal rigidity.
2. It involves both the agonist
as well as antagonist muscles,
therefore, hypertonia is more
uniform and often is so distri-
buted as to produce a “general
attitude of flexion” of limbs
and trunk.
of two types:
Contd...
Contd...
Spasticity Rigidity
a. Lead pipe rigidity: Passive
movements of an extre-
mity meets with a plastic
dead feeling resistance as if
bending a lead pipe
b. Cogwheel rigidity: The
resistance to passive move-
ment of an extremity is
regularly or irregularly
variable. This is described
as like a lever rubbing on
teeth of a cogwheel, i.e. a
series of catches passive
movements of the extre-
mity.
4. It is a form of spasticity which 4. No such phenomenon is seen
is stretch sensitive. The degree here.
of increased tone development
during any passive stretch is
proportional to the speed of
the applied stretch.
Signs of Pyramidal Tract Lesion
Signs of Upper Motor Neuron Lesions(UMNLs)
As mentioned earlier in the text, the corticospinal system
initiates voluntary and skilled motor actions, especially the
fine distal movements. The clinical features arising due to a
small infarct in internal capsular area affecting corticospinal
fibers alone, consists initially of the weakness in the contra-
lateral part of the body. Rapid actions (movements) usually
occurs. In case of pure corticospinal tract lesion, the residual
impairment consists of:
1. Loss of rapid, fine, distal movements of hand and
fingers, as on picking up small articles.
2. Weakness in shoulder movements as in adductions.
3. Weakness in hip flexion.
4. Weakness of dorsiflexion
5. Weakness of dorsiflexion of foot.
Other Important Signs of UMNLs
1. There is no wastings of muscles (however, muscle
wastings may occur in the late stages due to disuse
atrophy).
2. Increase in the tone of muscles (in the form of clasp
knife spasticity mainly affecting the antigravity muscles,
i.e. the flexor group of muscles in upper limb and exterior
muscle group in lower limb).
3. Other muscles with earlier involvement are:
– Muscles of hand grip
– Foot dorsiflexors (toe dorsiflexors)
(Besides shoulder abductors and hip flexors as
mentioned earlier).
 Central Nervous System 181

4. The extensors in upper limb and flexors of lower limb anterior horn cells). Early signs of paralysis are loss of tone
show more weakness (opposite to that of tone distri- and absent or reduced tendor reflexes. The classical sign of
bution). hypertonia and increased tender reflexes of a corticospinal
5. The muscle group which is affected first is the last to lesion appear after a few hours or days interval.
recover; for example, the distal movements of hands
are the last to recover. Signs of Extrapyramidal Lesion
6. Abdominal reflex is absent.
Lesions of extrapyramidal system cause difficulty in initiating
7. Babinski sign (as stated earlier in the text) is positive
the voluntary movements and certain other positive as well
(extensor plantar response).
as negative features.
8. Deep tendon reflexes are brisk or exaggerated and tone
is sustained. The positive or released features include:
• Alteration in muscles tone
Signs of Lower Motor Neuron • Involuntary movements.
Lesions (LMNLs)
The negative features include:
LMNLs cause weakness, with especially, absence of • Difficulty in initiating voluntary movement (as mentioned
appropriate tendon reflexes. The amount and distribution
above)
of abdominal features depend on the causative process.
• Impairment of orientating and balancing reflexes.
When the single nerve or nerve root lesion occurs, it causes
focal neurogenic weakness. Distal weakness of neurological The strength of the muscle mass is generally not affected.
origin occurs in peripheral neuropathy. Anterior horn cell Table 8.13: Signs and sites of extrapyramidal lesion
disease (amiyotrophic lateral sclerosis), includes generalized Sign Site of lesion
neurogenic weakness. Thus, generalized neurogenic weak-
Resting tremor Substantia nigra, red muscles
ness also occurs in spinal muscles atrophy. Muscles rigidity Substantia nigra, putamen
The typical signs of LMNLs are: Hypokinesia Substantia nigra, globus pallidus,
1. Weakness or paralysis of muscles supplied by the putamen
affected anterior horn cells or axons. Chorea Caudate nucleus
Hemiballismus Subthalamic nucleus
2. Hypotonia, that is decrease in muscle tone. Dystonia, athetosis Putamen
3. Absent or reduced deep tendon reflexes
4. Severe wasting of affected muscles.
HIGHER FUNCTIONS
5. Fasciculation in affected muscle groups (fasciculation
is a sign of degenerating anterior horn cells or irritative Introduction
lesions of the neuron roots or peripheral nerves).
Testing of higher functions forms a very important and
6. Flexor/absent plantar response.
unseparable part of nervous system examination. It should
The extensive lesions affecting the extrapyramidal or
be done early in the examination, because the examination
the subcortical structures, in addition to corticospinal fibers
of CNS requires full understanding and cooperation from
themselves, result in the clinical feature of severe paralysis
the patient.
of one side of the body (hemiplegia), with upper limb in
flexed position or of a single limb (monoplegia). Even in
Examination of Higher Functions
case of dense hemiplegia, movements of the head and trunk
(called axial movements of the body), are usually uninvol- 1. Consciousness
ved. The reason for this being that the pathways for such 2. Mental state, behavior, mood, thought, personality.
postural movements ate mostly under the control of 3. Attention and orientation in time, place and person.
subcortical area and have bilateral representation in the brain. 4. Alertness memory (immediate, short term and long
Virtually, most of lesions of corticospinal tract (system) term)
are not of isolate type. They usually involve neighboring 5. Intelligence.
extrapyramidal nuclei and pathways and group of 6. Calculation
corticospinal lesions. 7. Speech and language function
Sudden damage or destruction of the corticospinal 8. Abstract thought
system (due to hemorrhage or injury) is presented as 9. Spatial
neuronal shock (a temporary depressant effect on the 10. Visual and body perceptions.
182 Essentials of Clinical Medicine
There are many sophisticated tests of higher functions.
They can be applied to test intelligence as well as in disease.
However, much can be learned from simple bedside testing.
Mental State
The mental state relates to the mood and thoughts of a
patient. Abnormalities may reflect:
• Neurological illness, such as frontal lobe disorders or
dementia (memory-related disorders)
• Psychiatric disorders which may be causing neurological
symptoms (e.g. anxiety leading to panic attacks)
• Psychiatric disorders secondary to neurological disease
(e.g. depression following stroke).
Mental State Examination
It attempts to distinguish:
• Focal neurological deficit
• Diffuse neurological deficit
• Primary psychiatric illness such as depression, anxiety
or hysteria presenting with somatic symptoms
• Psychiatric illness secondary to, or associated with
neurological disease.
Appearance and Behavior
The clinician must watch the patient while taking the history.
Here are some questions you can ask yourself in assessing
the appearance and behavior.
• Are there signs of self-neglect?
– Dirty or unkempt—consider depression, dementia,
alcoholism or drug abuse
• Are there any signs of depression?
– Furrowed brow, immobile, downcast facies, slow
monotonous speech.
• Are there any signs of anxiety?
– Fidgety, restless
• Are there any signs of inappropriate behavior?
– Overfamiliar and disinhibited or aggressive—
consider/frontalism
– Unresponsive, with little emotional response-flat
affect.
• Does the patient show appropriate concern about his
symptoms and disability?
– Lack of concern in the face of significant disability
—consider hysterical disease.
• Are there any signs of rapid changes in mood?
– Crying or laughing easily—emotional lability.
Mood
Inquire about his mood:
• How are your spirits at the movement?
• How would you describe your mood?
If you consider the patient as depressed, ask:
• Are you ever able to cheer up?
• Do you see any hope in the future?
Patients with depression say they find it difficult to cheer
up and see little hope in the future.
Patients with schizophrenia often have an apparent lack
of mood—blunted affect—or inappropriate mood, smiling
when you expect him to be sad—incongruous affect.
In mania, patients are euphoric.
Vegetative Symptoms
Ask the patient about vegetative symptoms:
• Weight loss or gain
• Sleep disturbance (waking early or difficulty getting to
sleep)
• Appetite
• Constipation
• Libido
Find out symptoms of anxiety:
• Palpitation
• Sweating
• Hyperventilation (tingling in fingers, toes and around
the mouth, dry mouth, dizziness and often a feeling of
breathlessness).
Minimental State Test
Orientation
Score one point for correct answers to each of the following
questions:
• What is the time? Date? Day? Month? Year? (5 points)
• What is the name of this: Ward? Hospital? District?
Town? Country? (5 points)
Registration
Name three objects. Score up to 3 points if, at the first
attempt, the patient repeats, in order, the three objects you
have randomly named. Score 2 or one if this is the number
he repeats correctly. Endeavors, by further attempts and
prompting, to have all three repeated, so as to test recall
later.
Attention and Calculation
Ask the patient to subtract 7 from 100, and then 7 from the
result—repeat this five times, scoring one for each time a
correct subtraction is performed (5 points).
Recall
Ask for the three objects repeated in the registration test,
scoring one for each correctly recalled (3 points).

Language
Score one point for two objects (a pencil and a watch)
correctly named (2 points).
Score one point if the following phrase is correctly
repeated “No ifs, ands or buts”.
Score 3 if a three-stage command is correctly executed.
Score 1 for each stage; for example, ‘with the index finger
of your right hand touch the tip of your nose and then your
left ear’, or ‘take this piece of paper in your right hand, fold
it in half and place it on the floor’ (3 points).
On a blank piece of paper write, ‘close your eyes’ and
ask the patient to obey what is written. Score one point if
he closes his eyes (1 point).
Ask the patient to write a sentence. Score one if the
sentence is sensible and has a verb and a subject.
Construct a pair of intersecting pentagons. Each side
1 inch long. Score one if this is correctly copied (1 point).
Conclusion
Less than 23 = cognitively impaired.
NB: Does not distinguish focal from diffuse disease. Aphasic
patients do especially badly.
Note
1. Apraxia is a term used to describe an inability to perform
a task when there is no weakness or incoordination or
movement disorder to prevent it. It will be described
here though clearly requires examination of the motor
system before it can be assessed.
2. Before starting, explain that you are going to ask a
number of questions. Apologise that some of these
questions may seen very simple.
Test attention, orientation, memory, and calculation
whenever you test higher function (often best done with
MMS test).
Attention and Orientation
Orientation: Test orientation in time, place and person
• Time: What day is it? What is the date? What is the
month, the year? What is the season? What is the time
of day?
• Place: What is the name of the place we are in? what is
the name of the ward/Hospital? What is the name of the
town/city?
• Person: What is your name? What is your job? Where
do you live?
Make a note for errors made.
Attention: digit span
Ask the patient to repeat some numbers that you give
him. Start with three- or four-digit numbers and increase
Central Nervous System 183
until the patient makes several mistakes at one of the digits.
Then ask him to repeat the numbers backward; for example,
when I say one, two, three, you say three, two, one.
Note the number of digits the patient is able to recall
forwards and backwards.
• Normal : seven forward, five backwards
• Hint: use parts of telephone numbers you know (not
111 or 777).
Memory
a. Immediate recall and attention
• Name and address test:
Tell the patient that you want him to remember a
name and address, and give the patient a three-line
name and address, e.g. Amit Gupta, Tilak Nagar,
Indore. Ask immediately to repeat it back to you.
Note how many errors are made in repeating it
and how many times you have to repeat it before it
is repeated correctly.
• Normal: Immediate registration.
• Hint: Give a name and address that you use regularly
so that you do not make mistake yourself.
b. Short-term memory
About 5 minutes after asking the patient to remember
the name and address, ask him to repeat it.
Note how many mistakes are made.
Give the patient 5 minutes to do so.
c. Long-term memory
Test factual knowledge you would expect the patient to
have. This varies greatly from patient to patient and you
need to tailor it accordingly. For example, a retired soldier
should know the commander-in-chief in the Second
World War; a football fan should know the year England
won the World Cup, and a neurologist should know the
names of the cranial nerves. The following may be used
as examples of general knowledge: dates of the Second
World War, the American President, who was shot dead,
the Chernobil disaster of Russia, the year when man
first landed on the moon.
Calculation
Serial Sevens
• Ask the patient if he is good with numbers, explaining
that you are going to ask him to do some simple
calculations.
• Ask him to take seven from a hundred, then seven from
what remains.
Note mistakes and the time taken to perform calculation.
184 Essentials of Clinical Medicine
Doubling Threes
This should be used if the patient professes difficulty with
calculations. What is two times three? Twice that? And keep
on doubling
Note how high the patient is able to go and how long it
takes.
Further Tests
Ask the patient to perform increasingly difficult mental
arithmetic: 3 + 4, 20 + 6, 30 – 8, 9 × 4, 50 ÷ 10 and so on.
Abstract Thought
This tests for frontal lobe function: useful with frontal lobe
lesions, dementia and psychiatric illness.
• Tell the patient that you would like him to explain some
proverbs for you.
• Ask him to explain well-known proverbs. For example,
“Na Rahega Baas Na Bajega Basuri” or “Naach Na Jaane
Angan Tedha”.
• Does he give the correct interpretation?
Interpretation
• Correct interpretation: Normal
• Physical interpretation: For example, the stone just rolls
down so moss doesn’t stick, or throwing stones will
break the glass. This indicates concrete thinking.
• Ask him to explain the difference between pairs of
objects, e.g. a pair of socks and a pair of trousers, a
television, a radio.
• Ask the patient to estimate: the number of people in this
ward, the length of the room, the weight of a person
nearby, the height of his home.
Interpretation
• Reasonable estimates—normal
• Unreasonable estimates—indicates abnormal abstract
thinking.
Spatial
This tests for parietal and occipital lobe function. Also useful
in dementias.
Clock Face
• Ask the patient to draw a clock face and to fill in the
numbers.
• Ask him then to draw the hands on at a given time; for
example, quarter to nine (i.e. 8:45)
• Ask the patient to copy a five-pointed star.
Your Observation
• Accurate clock and star: normal
• Half clock missing: visual inattention
• Unable to draw clock or reproduce star: constructional
apraxia
N.B: This is difficult to assess in the presence of weakness.
Visual and Body Perceptions
Test for parietal and occipital lesions. Useful in dementias.
Abnormalities of perception of sensation despite normal
sensory pathways are called agnosias. Agnosias can occur
in all types of sensation but clinically usually affect vision,
touch and body perception.
The sensory pathway needs to have been examined and
found to be intact before considering a patient has agnosia.
However, agnosia is usually considered as part of higher
function and is, therefore, considered here.
Facial Recognition: ‘The Well-known Faces’
Take bedside newspaper or magazine and ask the patient to
identify the faces of famous people. Choose people the patient
will be expected to know: the Queen, the Prime Minister,
and so on.
Note mistakes made.
• Recognizes faces: normal
• Does not recognize faces: prosopagnosia.
Body Perception
• The patient ignores one side (usually left) and is unable
to find hand if asked (hemi-neglect)
• The patient does not recognize left hand if shown
(asomatagnosia)
• The patient is unaware of weakness of affected (usually
left) side—anosagnosia—and will often move the right
side when asked to move the left.
• Ask patient to show you his index finger, ring finger
and so on
– Failure—finger agnosia
• Ask the patient to touch his right ear with his left index
finger. Cross your hands and ask which is your right
hand
– Failure—left/right agnosia.
Sensory Agnosia
• Ask the patient to close his eyes and place an object,
e.g. coin, key, paperclip and ask him what it is.
– Failure—asterognosis
• Ask the patient to close his eyes and write a number or
letter on his hand and ask him what it is
– Failure—agraphesthesia
Hint: Test on the unaffected side first to ensure the patient
understands the test.
 Central Nervous System 185

Apraxia Table 8.14: Variety of focal loss

Test for parietal lobe and premotor cortex of the frontal Lobe Alteration in higher Associations
function
lobe function; very useful in dementias
Frontal Apathy, disinhibition Contralateral hemiplegia, Broca’s
Ask the patient to perform an imaginary task: show me aphasia (dominant hemisphere),
how you would light a matchstick, how would you smoke, primitive reflexes.
swimming action and act of hitting a ball with a bat. Temporal Memory Wernicke’s aphasia (dominant
Observe the patient. If there is a difficulty, give the patient hemisphere), upper quardanta-
nopia
an appropriate object and see if he is able to do it with the
Parietal Calculation, perceptual Apraxia (dominant hemisphere),
appropriate prompt. If there is further difficulty, demonstrate and spatial orientation homonymous hemianopia
and ask him to copy what you are doing. (non-dominant hemi- hemisensory disturbance. Neglect
• The patient performs the act appropriately—normal sphere)
• The patient is unable to initiate the action though under- Occipital Perceptual and spatial Hemianopia
standing the command—ideational apraxia orientation
• The patient performs the task but makes errors; for
Table 8.15: Ultimate impression that you get
example, uses his hand as a cup rather than an imaginary
cup—ideomotor apraxia. 1. Impaired attention and Occurs with diffuse disturbances of
If inability is related to a specific task; for example, orientation cerebral function
dressing, this should be referred to as a dressing apraxia. If acute, often associated with
disturbance of consciousness.
This is often tested in a hospital by asking the patient to put
If chronic, limits ability for further
on a dressing gown with one sleeve pulled inside out. The testing—suggestive of dementia.
patient should normally by able to overcome this easily. N.B: also occurs with anxiety,
depression.
Three-Hand Test
2. Memory Loss of short-term memory in
Ask the patient to copy your hand movements and alert patient—usually bilateral—
demonstrate: 1. make a fist and tap it on the table with your limbic system (hippocampus,
thumb upwards, 2. then straighten out your fingers and tap maxillary bodies) disturbances—
on the table with your thumb upwards, 3. then place your seen in diffuse encephalopathies,
bilateral temporal lesions;
palm flat on the table. If the patient is unable to perform this
prominent in Korsakoff’s
after one demonstration, repeat the demonstration. psychosis (thiamine deficiency)
• Inability to perform this in the presence of normal motor loss of long-term memory with
function—limb apraxia. preserved short-term memory,
functional memory loss.
Interpretation 3. Calculation Impaired calculation usually
Three patterns can be recognized: indicates diffuse encephalopathy.
1. Inappropriate attention If associated with finger agnosia
Tests useful to document level of function, but are of (inability to name fingers), left-
right agnosia (inability to
limited use in distinguishing focal from diffuse disease.
distinguish left from right) and
2. Patients with deficits in many or all major areas of testing dysgraphia—Gerstmann’s
Indicates a diffuse or multifocal process. syndrome—indicates a dominant
• If of slow onset—dementia or chronic brain syndrome. parietal lobe syndrome.
• If of more rapid onset—confusional state or acute brain Perverse but consistent
syndrome calculation errors may suggest
Common mistakes: psychiatric disease.
4. Abstract thought If interpretations of proverbs are
Dementia has to be differentiated from:
concrete—suggests diffuse
• Low level of intelligence—usually indicated from a encephalopathy.
history of intellectual attainment. If interpretation includes
• Depression—may be difficult especially in the elderly. delusion—suggests psychiatric
Often suggested by the patient’s demeanour. illness, with particular frontal lobe
• Aphasia—usually found on critical testing. involvement.
Poor estimates suggest frontal or
3. Patients with deficits in one or only a few areas of testing
diffuse encephalopathy or
control focal process. Identify areas affected and seek psychiatric illness.
associated physical signs. Contd...
186 Essentials of Clinical Medicine

Contd... Delusion
5. Loss of spatial appreciation (copying, drawing, astero-genosis)
—parietal lobe lesions. Delusion is a false belief in something which is not a fact,
6. Visual and body perception Prosopagnosia—bilateral and which persists even after its falsity has been clearly
temporo-parietal lesions demonstrated.
Neglect
Sensory agnosia, astereognosis Types
and agraphesthesia are signs of 1. Grandeur or exaltation: A man imagines himself to be
parietal lobe lesions. very rich while in reality he is a pauper.
7. Apraxia Ideomotor apraxia—lesion
2. Persecution: The person imagines that attempts are being
either of the dominant parietal
lobe, premotor cortex or a diffuse
made to poison him by nearest relatives like wife, sons
brain lesion. or parents. Delusion of grandeur and persecution are
Ideational apraxia—suggests often present together in the same person.
bilateral parietal disease. 3. Reference: The person believes that people, things,
events, etc. refer to him in a special way. He believes
Table 8.16: Interpretation that even strangers in the street are looking at him and
a. Diffuse or multifocal abnormalities: are talking about him, or items in the radio or newspapers
1. Common are referring to him.
• Alzheimer’s disease 4. Influence: They occur in schizophrenia. The person
• Vascular disease (multi-infarct) complains that thoughts, feelings and actions are being
2. Rare degenerative conditions
influenced and controlled by some outside agency, like
• Pick’s disease
• Huntington’s disease
radio, hypnotism, telepathy, etc.
3. Nutritional 5. Infidelity: A man imagines his wife to be unfaithful while
• Thiamine deficiency (Korsakoff’s psychosis) in fact is chaste.
• Vitamin B12 deficiency 6. Self-reproach: The person scolds himself for the past
4. Infective failures and misdeeds which are often of no importance.
• Quaternary syphilis 7. Nihilistic: The person declares that he does not exist or
• Cruetzfeldt-Jacob disease that there is no world, etc.
• HIV encephalopathy
8. Hypochondriacal: The person believes that there is
5. Structural
• Normal pressure hydrocephalus something wrong with his body, though he is healthy.
• Demyelination 9. Other types: are of jealousy, of religion, etc.
• Multiple sclerosis
b. Focal deficits Hallucination
May indicate early state of a multifocal disease
1. Vascular Hallucination is a false sense of perception without any
• Thrombosis, emboli or hemorrhage external object or stimulus to produce it. They are purely
2. Neoplastic imaginary, and may affect any or all the special senses.
• Primary or secondary tumors
3. Infective Types
• Abscess 1. Visual: A person imagines of being attacked by a lion
4. Demyelination
when no lion exists.
• Multiple sclerosis
2. Auditory: A person hears voices and imagines that a
person is speaking to him when no one is present.
Delirium 3. Olfactory: A person smells pleasant or unpleasant odor
when none is present.
Delirium is a disturbance of consciousness in which
4. Gustatory: A person feels sweet, sour, bitter, good or
orientation is impaired, the critical faculty is blunted or lost
bad taste in the mouth, though no food is actually present.
and thought content is irrelevant or inconsistent. In the early 5. Tactile: A man imagines rats and mice crawling into his
stage, the patient is restless, uneasy and sleepless. He then bed, when there are none.
completely loses self-control, becomes excited and talks 6. Psychomotor: A man will have feeling of movement of
furiously. some part of the body in the absence of such movement.

Visual hallucinations are the commonest in organic
mental disorders, while the auditory hallucinations are the
commonest in functional disorders. Hallucinations occur in
fevers, intoxications, and insanity. Visual and auditory
hallucinations are the most common. They may be pleasant,
but more often they are unpleasant. A person suffering from
unpleasant hallucinations may be incited to commit suicide
or homicide.
Illusion
Illusion is a false interpretation by the senses of an external
object or stimulus which has a real existence, e.g. when a
person sees a dog and mistakes it for lion, or hears the
notes of birds and imagines them to be human voices, or
imagines a string hanging in his room to be snake, or may
mistake the stem of a tree for a ghost in the dark. A sane
person may experience illusion, but is capable of correcting
the false impressions. An insane person continues to believe
in the illusions, even though the real facts are clearly pointed
out. Illusions are a feature of psychoses, particularly of the
organic type.
Impulse
This is sudden and irresistible force compelling a person to
the conscious performance of some action without motive
or forethought. A sane person having no judgment and no
reasoning power, and no capacity to understand the facts,
may do things on impulse. These are usually seen in imbecility,
dementia, acute mania, and epilepsy.
Types
1. Kleptomania: An irresistible desire to steal articles of
little value
2. Pyromania: An irresistible desire to set fire to things
3. Mutilomania: An irresistible desire to mutilate animals.
4. Dipsomania: An irresistible desire for alcoholic drinks
at periodic intervals.
5. Sexual impulses: including sexual perversions.
6. Suicidal and homicidal impulses.
Obsession
In this, a single idea, thought, or emotion is constantly
entertained by a person which he recognizes as irrational,
but persists in spite of all efforts to drive it from his mind.
It is a disorder of content of thought. Any attempt to resist
makes them appear more insistent, and yielding is the almost
inevitable outcome. It is a borderline between sanity and
insanity. They usually occur in neurotic people, well able to
discharge the ordinary responsibilities of life. These ideas
are usually associated with some sort of dread or fear. A
Central Nervous System 187
wife may continuously believe her husband to be unfaithful
in spite of proof to the contrary. A person may go to bed at
night after securely bolting the door of his room, but he
soon gets up to see he has done so. A sane person may
repeat it once or twice, but an insane person does not sleep,
and spends the whole night in frequently seeing whether
the door is bolted.
Phobia
Phobia is excessive or irrational fear of a particular object
or situation.
Neuroses
The patient suffers from emotional or intellectual disorders,
but he does not lose touch with reality. They occur mostly
in the form of anxiety, depression, or hysteria. The effects
may be mild or may cause considerable distress to the patient,
but they are not associated with severe affective change,
nor with disturbances of thought.
Types
(1) Anxiety neurosis, (2) Hysterical neurosis, (3) Phobic
neurosis, (4) Obsessive-compulsive neurosis, (5)
Depressive, (6) Depersonalization syndrome, (7)
Hypochondriacal, and (8) Unspecified neurosis.
Psychoses
Psychoses are characterized by a withdrawal from reality;
a living in a world of fantasy. These mental illnesses
supervene upon a normally developed mental faculty. There
is deterioration in the personality and progressive loss of
contact with reality.
Types
(A) Organic Psychoses: (1) Senile and presenile dementia.
(2) Alcoholic psychosis, (3) Associated with intracranial
infections, e.g. epidemic encephalitis, abscess, meningitis,
tuberculosis, GPI, etc. (4) Associated with cerebral
arteriosclerosis, epilepsy, intracranial tumours. Degenerative
disease, brain anomalies, etc, and (5) Associated with other
physical conditions, such as endocrine, metabolic and
nutritional disorders, systemic infections, drug intoxication,
childbirth, etc.
(B) Functional Psychoses:
1. Schizophrenia: (a) Simple, (b) Heberphrenic type, (c)
Catotonic type, and (d) Paranoid and other atypical or
unspecified forms.
2. Affective type: (a) Involutional melancholia, (b) Manic-
depressive, (c) Paranoid states, and (d) Other atypical
forms.
188 Essentials of Clinical Medicine
Psychosis Associated with
Organic Disease
• Pre-senile dementia
• Senile dementia
• Cerebral tumors
• Cerebral trauma
• Toxic psychosis
• Deficiency states
• Alcoholism—alcoholic blackouts
• Delirium tremens
• Alcoholic hallucinosis
• Korsakov’s psychosis
• Delusions of jealousy.
Functional Psychoses
Mental illnesses which have no neurological basis are called
functional psychoses. The functional psychoses are
characterized by disorders of thought which have no physical
basis. (a) In schizophrenic psychoses, disorders of the
thought process are dominant, and (b) In affective
psychoses, mood abnormality is dominant. This is a disease
of hereditary origin affecting young adults and forms a major
group of all psychiatric illnesses.
Schizophrenia
Schizophrenia is a condition of split personality, in which
the patient loses his contact with his environment. It is
primarily a disorder of thinking (cognition). This disorder
can be in form, stream, possession or content of thought.
It is characterized by splitting of different psychic functions.
1. Disorders of behavior: Withdrawal from reality, preoccu-
pation with the self (narcissism), attribution of feeling
of strangeness to outside influence (depersonalization),
and feelings that his mind and body are under control
(passivity of feelings).
2. Disorders of thought: Confused thoughts leading to
thought block, devious thinking leading to incoherence
of speech often with newly formed words (Neologism).
3. Disorders of affect: Depression; elation, inappropriate
moods, lability of mood, anxiety and blunting of emotion.
4. Delusions: Of grandeur, paranoid, hypochondriac and
influence.
5. Hallucinations: commonly auditory, sometimes visual
and tactile.
6. Personality deterioration: Affecting his work, family and
social relationship. It is the commonest type of insanity
in homicidal crimes, especially where the victim is a
stranger. The impulses are not sudden and the crime is
usually preceded by much complaining and planning.
1. Simple schizophrenia: It begins in early adolescence.
There is a gradual loss of interest in the outside world
from which he withdraws. There is an all-round
impairment of mental faculties. He becomes emotionally
flat and apathetic and has difficulty in forming social
relationship. He becomes irritable and has conflicts about
sex, particularly masturbation. Complete disintegration
of the personality occurs later.
2. Hebephrenia: It begins in adolescents or young adults.
Thinking process is disturbed. Wild excitement, illusions,
hallucinations and bizarre delusions are present. Often,
conduct is impulsive and senseless. Ultimately, the whole
personality may disintegrate completely.
3. Catatonia: This is characterized by alternating stages of
depression, excitement and stupor, impulsive, suicidal
or homicidal attacks and auditory hallucinations are
common. This phase lasts a for few hours to a few
days followed by a stage of stupor which begins with
lack of interest, concentration and general indifference.
4. Paranoid schizophrenia (paranoia, paraphrenia):
Paranoia is the mild form, and is common in males.
Paranoid schizophrenia develops insidiously in the fourth
decade. It is characterized by suspiciousness, delusions
of persecution and auditory hallucinations. At first,
delusions are indefinite; but later, they become fixed on
some person. The patient usually retains his memory
and orientation. When delusions affect his behavior, he
is often a source of danger to himself and others. In
paraphrenia, delusions and hallucinations are present,
but the personality is relatively intact.
5. Schizo-affective psychosis: This is an atypical type of
schizophrenia in which there are mood disturbances.
Attacks of elation or depression, unmotivated rage,
anxiety, panic, etc., occur.
6. Pseudoneurotic schizophrenia: It may start with over-
whelmingly permanent neurotic symptoms.
SPEECH
Abnormalities of speech need to be considered first as these
may interfere with your history taking and subsequent ability
to assess higher functions and perform the rest of the
examination.
Abnormalities of speech can reflect abnormalities any-
where along the following chain:
Process Abnormalities
Perception of sound Deafness
↓
}
Interpretation
↓ Aphasia
Thought and word finding
↓
Voice production Dysphonia
↓
Articulation Dysarthria

Aphasia
The term aphasia is used to refer to all disorders of under-
standing, thought and word finding. Dysphasia is a term
used by some to indicate a disorder of speech reserving
aphasia to mean absence of speech.
Aphasia has been classified in a number of ways and
each new classification has brought some new terminology.
There are, therefore, a number of terms that refer to broadly
similar problems:
Synonyms
• Broca’s aphasia—expressive aphasia—motor aphasia
• Wernicke’s aphasia—receptive aphasia—sensory aphasia
• Nominal aphasia—anomic aphasia.
The following patterns of aphasia can be recognized
associated with lesions at the sites as numbered:
1. Wernicke’s aphasia: poor comprehension, fluent but often
meaningless (as it cannot be internally checked) speech.
No repetition.
2. Broca’s aphasia: preserved comprehension, non-fluent
speech. No repetition.
3. Conductive aphasia: loss of repetition with preserved
comprehension and output.
4. Transcortical sensory aphasia – as in (1) but with
preserved repetition.
5. Transcortical motor aphasia – as in (2) but with preserved
repetition.
Reading and writing are further aspects of language.
These can also be induced in models such as the one above.
Dysphonia
Dysphonia is a disturbance of voice production and may
reflect either local cord pathology (such as laryngitis), an
abnormality of the nerve supply via the vagus or occasionally
a physiological disturbance.
Dysarthria
Voice production requires coordination of breathing, vocal
cords, larynx, palate, tongue and lips. Dysarthria can,
therefore, reflect difficulties at different levels.
Lesions of upper motor neuron type of the extrapyra-
midal system (such as Parkinson’s disease) and cerebellar
lesions disturb the integration process of speech production
and tend to disturb the rhythm of speech.
Lesions of one or several of the cranial nerves tend to
produce characteristic distortion of certain parts of speech.
Central Nervous System 189
Assessment of Speech Abnormalities
Aphasia
Speech abnormalities may hinder or prevent taking a history
from the patient. If so, take history from relatives or friends.
• Establish if right- or left-handed
• Discover his first language.
Assessment of his understanding ability:
Ask the patient a simple question:
• What is your name and address?
• What is/was your job? Explain exactly what you do.
• Where do you come from?
If he does not appear to understand: Repeat louder.
Test his understanding ability:
• Ask questions with yes/no answers
e.g. Is this a paper? (showing something else, then a
paper)
• Give a simple command, e.g. lift up your hand or with
your left hand touch your right ear.
If he succeeds:
• Try more complicated commands, e.g. with your right
hand touch your nose and then your left ear.
Remember if weak, he may not be able to perform the
simple tasks. Define how much is understood.
Assessment of spontaneousness in speech:
If he does appear to understand but is unable to speak.
• Inquire if he has difficulty in finding the correct words.
This often brings a nod and a smile indicating pleasure
that you understand the problem.
– If less severe, he may be able to tell you his name
and address slowly
• Ask further questions, e.g. about his job or how his
problem started
– Guess whether his speech is fluent? Does he use
words correctly?
– Does he use the wrong word—paraphasia—or is it
meaningless jargon (sometimes called jargon
aphasia)?
Assessment of word finding ability and naming:
• Ask him to name all the animals he can think of (normal
18-22 in 60 seconds)
• Ask him to give all the words beginning with a particular
letter, usually ‘f’ or ‘s’ (<12 in 1 minute for each letter
shows failure/abnormality)
These are tests of word finding. This test can be
quantified by counting the number of objects within a
standard time.
• Ask him to name familiar objects that are to hand, e.g. a
watch, watch strap, buckle, shirt, tie, buttons. Start
with easily named objects and later ask about less
frequently used objects that will be more difficult.
190 Essentials of Clinical Medicine

Assessment of repetition: • Cough lacks explosive start: a bovine cough—vocal cord

• Ask for repetition of a simple phrase, e.g. “the dog is palsy
barking”, and then increasingly complicated phrases. • The note cannot be sustained, and fatigues—consider
Access severity of impairment of speech: myasthenia.
• Does the aphasia socially incapacitate the patient? Dysarthria
Further Tests If the patient is able to give his name and address but the
Test for reading and writing words are not formed properly, he has dysarthria.
Ask him to repeat difficult phrases: “Chandu ke chacha
Check there is no visual impairment and that usual reading
ne chandu ki chachi ko chandni chowk par chandni raat
glasses are used.
mein chandi ke chammach se chatni chatayee” Or “Babu
Ask the patient to bhaiya bahut bhola hai” Or “Yellow lion”.
• Read a sentence
Listen carefully for:
• Obey written command, e.g. ‘close your eyes’
• The rhythm of the speech
• Write a sentence (check there is no motor disability to
• Are the words slurred?
prevent this)
• Which sounds cause the greatest difficulty?
• Impaired reading—dyslexia, impaired writing =
dysgraphia) Types of dysarthria
Interpretation: Before continuing your examination, describe • Spastic: slurred, the patient hardly opens mouth, as if
your findings, e.g. this man has a socially incapacitating trying to speak from the back of mouth
non-fluent global aphasia which is predominantly expressive, • Extrapyramidal: monotonous, without rhythm, sentences
with paraphasia and impaired repetition. There is associated suddenly start and stop
dyslexia and dysgraphia. • Cerebellar: slurred as if drunk, disjoined rhythm
sometimes with scanning speech (equal emphasis on
Table 8.17: Some special terminologies each syllable)
Aphasia Lesion in the dominant (usually • Lower motor neuron:
left) hemisphere – Palatal: nasal speech, as with a bad cold
Global aphasia Lesion in dominant hemisphere – Tongue: distorted speech, especially letters t, s, d
affecting both Wernicke’s and Broca’s – Facial: difficulty with b, p, m, w, the sounds avoided
areas
by ventriloquists
Wernicke’s aphasia Lesion in Wernicke’s area
(supramarginal gyrus of the – Myasthenic: muscle fatiguability demonstrated by
parietal lobe and upper part of making the patient count. Observe for development
temporal lobe). May be associated of dysphonia or lower motor neuron pattern of
with field defect dysarthria (N.B. Myasthenia gravis is a failure of
Broca’s aphasia Lesion in Broca’s area (inferior neuromuscular transmission).
frontal gyrus). May be associated with
hemiplegia. Before continuing your examination, describe your findings.
Conductive aphasia Lesion in acute fasciculus Interpretation
Transcortical sensory aphasia Incomplete leison in Broca’s area • Spastic dysarthria: Bilateral upper motor neuron
Nominal aphasia Lesion in angular gyrus. weakness—causes: pseudobulbar palsy, motor neuron
disease.
Dysphonia • Extrapyramidal dysarthria: common causes: parkin-
If the patient is able to give his name and address but is sonism
unable to produce normal volume of sound or speaks in a • Cerebellar dysarthria—common causes: alcohol intoxi-
whispher, this is dysphonia. cation, multiple sclerosis, phenytoin toxicity; rarely:
• Ask the patient to cough: Listen to the quality of the hereditary ataxias
cough. • Lower motor neuron dysarthria—causes: lesions of X
• Ask the patient to say a sustained ‘eeeeee’. Does it (palatal), XII (tongue) or VII (facial).
fatigue?
Findings and interpretation CRANIAL NERVES
• Normal cough—the motor supply to the vocal cords is Clinical Examination of the Cranial Nerves
intact
• Dysphonia + normal cough—local laryngeal problems Multiple cranial nerve abnormalities are also recognized in a
or hysteria number of syndromes:
 Central Nervous System 191

• Unilateral V, VII and VIII—cerebellopontine angle lesion • In aura phase of migraine

• Unilateral III, IV, V1 and VI—cavernous sinus lesion • Hyperemesis gravidarum
• Combined unilateral IX, X and XI— jugular foramen • Strychnine poisoning.
lesion
• Combined bilateral X, XI and XII. Causes of Parosmia (Perversion of Smell)
If lower mototr neuron—bulbar palsy • Severe nasal infection
If upper motor neuron—psuedobulbar palsy • Drugs—like antiepileptics—phenytoin
• Prominent involvement of eye muscles and facial • Hysterical
weakness, particularly when variable, suggests a • Recovery phase of traumatic anosmia.
myasthenic syndrome.
The most common cause of intransit brainstem lesions Causes of Cacosmia (Unpleasant Smell)
in younger patients is multiple sclerosis, and in older patients
• Severe upper respiratory tract infection
vascular disease. Rarer causes include gliomas, lymphomas
• Atrophic rhinitis.
and brainstem encephalitis.
A sound knowledge of the anatomy and physiology of
Olfactory Hallucination
the cranial nerves is essential in order to understand the
logic of methods employed for testing these, and the clinical • Epilepsy
significance of any abnormalities that may be detected. • Psychosis.

First or Olfactory Nerve Approach

• The patient is able to identify smells appropriately—
Take small amounts of oil of peppermint and oil of cloves in normal
two small test tubes. Bring these near each nostril separately,
• The patient is unable to recognize scents offered but
one after the order, and ask the patient if he can identify the
smell. Irritants such as ammonia and acetic acid should not recognizes ammonia—anosmia. This finding is limited
be used as they also act through the trigeminal nerve. It to one nostril—unilateral anosmia
should be confirmed before the test that the patient is not • The patient recognizes no smells including ammonia—
suffering from common cold. Loss of sense of smell is consider that the loss may not be entirely organic.
called anosmia. Ask the patient if he has any hallucinations Interpretation
of smell. The olfactory area of the cerebral cortex lies in • Anosmia in both nostrils: loss of sense of smell—
the uncus of the parahippocampal gyrus. common causes: blocked nasal passages (e.g. common
Causes of Anosmia (Loss of Sense of Smell) cold), trauma, a relative loss occurs with aging,
• Closed head injury Parkinson’s disease
• Subfrontal hemangioma • Unilateral anosmia—blocked nostril, unilateral frontal
• Previous bacterial meningitis lesion (meningioma or glioma (rare).
• HIV infection
• Sinusitis Second or Optic Nerve
• Other local nasal disorders
• Drugs (e.g. copper chelating agents, antibiotics) Any errors of refraction should first be corrected. There
• Subarachnoid hemorrhage. should be no opacity of the optic media and each eye should
• Tumors—tumors of olfactory groove, frontal lobe be tested separately. Investigate three functions—(A) Acuity
tumor. of vision, (B) Field of vision, and (C) Color vision (Fig 8.9,
• Infection—like tabes dorsalis Plate 12 and Figs 8.10 to 8.12).
• Metabolic—Refsum’s disease, Paget’s disease,
hypoparathyroidism Acuity of Vision
• Nutritional—Zn deficiency The acuteness of vision may be much decreased. Confirm
• Hysterical/Idiopathic first whether light can be perceived. If the impairment is
• Aging, Alzheimer’s disease not very gross, do the ‘finger-counting’ test. This should
Causes of Hyperosmia be done at varying distances. For more accurate assessment
(Increased Olfactory Sensation) of the acuity of vision for distant and near objects, use the
• Addison’s disease Snellen’s test charts and Jaeger’s test types.
192 Essentials of Clinical Medicine
Fig. 8.10: Visual field defects following lesions
of the visual pathway
Field of Vision
The part of the outside world which is visible to one eye,
when it is kept fixed on one object or point, is called field of
vision for that eye. It is restricted medially by the nose,
above by the orbital margin, below by the cheek bones, but
it extends more than 90° on the lateral side. An approximate
idea of the peripheral field of vision can be obtained by the
‘confrontation test’, but an accurate assessment and a
permanent record can be obtained only by a perimeter.
Confrontation test: Ask the subject to sit opposite to you at
a distance of about 3 feet. When testing his left eye, he
places his cupped right hand over his right eye; and with
the left eye he fixes his gaze on your right eye. Instruct him
not to move his eye in any direction. Cover your left eye
Fig. 8.11: Pathway for light reflex. The input from the left eye decussates
at the chiasma and reaches both oculomotor nerve nuclei
Fig. 8.12: Pathway for accommodation reflex
with your left hand. Extend your right arm full length and
hold your hand midway between yourself and the subject.
Keeping the fingers moving, bring your hand nearer until
you can yourself perceive the finger movements ‘with the
tail of your eye.’ At this time, ask the subject if he can catch
the movement. If he fails to see the fingers, continue bringing
the hand nearer, until he can. Test the peripheral field of
vision in this manner—upwards, downwards and from the
left side. Test his field for a stationary object in a similar
manner by asking the subject to indicate when he sees your
finger held at rest. Only gross changes in the field of vision
can be detected by this method. Scotomatas (blind areas
within the field of vision) are impossible to locate.
Color Vision
(i) Holmgren’s wools: Place small lengths of woolen threads
of different colors and hues in a heap on the surface of a
table (white or neutral background), in good light. Pick up
a test skin and ask the subject to pick up those wool threads
from the heap which are like the test skein, whether they
are of a darker or lighter shade (or hue). He is to match the
color only and not to name it. Test him first with a pure pale
green thread and then with a purple. Note if there is red-
green blindness (or weakness); blue-yellow blindness (or
weakness), or total color blindness;
(ii) Ishihara’s pseudoisochromatic plates: These are available
in the form of a book, and the instructions should be read
carefully before testing the color vision. The plates are so
constructed that a subject with normal color vision will
read one number, made up of dots of different colors and
size against a background of differently colored dots, while
a person with defective color vision will read a different
number on the same plate. For example, number 8 will be
 Central Nervous System 193

read as 8 by a normal person and as 3 by a subject with Inference

defective color vision. General
• Ptosis—common causes; cogenital, Horner’s syndrome
Clinical Application (always partial), third nerve palsy (often complete) rarer
causes: myasthenia gravis (prosis often variable), myo-
The visual system is of great clinical importance since most
pathy.
defects are readily noticed by the patient. Both vision and
• Exophthalmos—common causes: most frequently,
reflexes are affected by lesions anterior to the origin of the dysthyroid eye disease—associated with lid retraction;
brachia. Injuries to the visual pathway, after the brachia rarely: retro-orbital mass.
have left it, interfere with vision but not with visual reflexes. • Enophthalmos: a feature of Horner’s syndrome.
Salient Features of Lesions at Different Interpretation
Levels of Visual Pathways • The pupil on one side constricts when the light is shone
They are as follows into it repeatedly—normal.
• The pupil on one side constricts when the light is shone
• Optic nerve
into it; and the pupil on the other side dilates when the
– complete blindness on the affected side.
light is then shown into it—the side that dilates has a
– abolition of direct light reflex on the ipsilateral side. relative afferent pupillary defect (often abbreviated to
– abolition of consensual light reflex on the contralateral RAPD). This is also sometimes called the Marcus-Gunn
side. pupil.
– accommodation reflex not affected.
N.B: Lesion is always unilateral.
• Central part of optic chiasma
– bitemporal hemianopia Table 8.18: Pupils
– bitemporal hemianopic paralysis of pupillary reflexes. Anisocoria Pupils unequal but normally
The optic chiasma is in close relation to the pituitary fossa, reacting – normal variant
Senile miosis Normal age-related change
so that suprasellar extension of a pituitary tumor may press Holmes-adie pupil Degeneration of ciliary ganglion of
on the optic chiasma and interrupt input from the nasal unknown causes: may be associated
retina of both eyes to produce loss of both temporal fields with loss of tendon reflexes
resulting in ‘tunnel vision’. Afferent papillary defect Partial lesion anterior to the optic
chiasm – causes as for afferent
• Lateral part of optic chiasma papillary defects
– nasal hemianopia of the affected side. Horner’s syndrome (meiosis, partial ptosis, enophthalmos
– hemianopic paralysis of pupillary reflexes. and loss of hemifacial sweating):
lesion to sympathetic fibers. This may
This is usually due to an aneurysm of the internal carotid occur.
artery or its calcification. a. Centrally: in the hypothalamus,
• Optic tract, lateral geniculate body, optic radiation and in the medulla or upper cervical cord
visual cortex. (exits at TI) common causes: stroke
(N.B. lateral medullary syndrome),
All parts of the visual pathway posterior to the chiasma demy-elination; rarely: trauma or
result in syringomyelia
– homonymous hemianopia b. Peripherally: in the sympathetic
chain the superior cervical ganglion
– lesions of the tip of the occipital cortex result in loss
or along the carotid artery – common
of macular vision. causes: pan-Coat’s tumor (apical
• Both pretectal regions and their afferent and efferent bronchial carcinoma), trauma, rare
connections have to be destroyed to abolish the light cases: carotid dissection.
Argyll-Robertson pupil Probably upper midbrain lesion; now
reflex which would then be lost bilaterally. There will be very rare—common causes: syphilis, dia-
no interference with vision. betes mellitus; rarely multiple sclerosis.
• The pathways for the constriction of the pupil in the
light and accommodation reflex are different because Acuity of Vision
they may be dissociated in disease. This occurs in • Reduced acuity correctable by pinhole or glasses: ocular
neurosyphilis giving rise to Argyll-Robertson pupil where defect.
there is abolition of light reflex, but the convergence • Reduced acuity not correctable: classified according to
accommodation reflex is preserved. site in visual pathway.
194 Essentials of Clinical Medicine
Anterior
• Corneal lesion—ulceration, edema
• Cataract
• Macular degeneration—especially age related
• Retinal hemorrhage or infarct
• Optic neuropathy—inflammatory (MS)
– Ischemic
– Compressive
• Retrochiasmal—macula—splitting field defect (see
below)
• Bilateral occipital lesions—cortical blindness
Posterior
Defect limited to one eye.
Fields
Defect Limited to One Eye
Constricted field
• Tubular vision: Size of constricted field remains the same
regardless of distance of the test object from the eye.
• Scotoma: A hole in the visual field—described by its site;
for example, central or centrocecal (defect connecting
the fixation point to the blind spot) and shape (e.g. round
or ring-shaped).
• Altitudinal defect: A lesion confined to either upper or
lower half of visual field but crossing the vertical
meridian.
Defect Affecting Both Eyes
• Bitemporal hemianopias: Defect in the temporal fields
of both eyes. Note carefully if upper lower quadrant
more marked
• Homonymous quadrantanopias: Defect in the same
quadrant of vision of both eyes. Classified as congruous
or incongruous
• Homonymous hemianopias: Defect in the same hemifield
in both eyes. Classified as according to degree of
functional preservation in affected field (e.g. able to see
moving targets) whether congruous or incongruous and
whether macula-sparing or not.
• Others, including bilateral defects as described in defect
limited to one eye.
Before continuing your examination, describe your
findings, e.g. this man has normal pupillary response to
light and accommodation. His visual acuities are 6/6 on the
right and 6/12 on the left. He has a right homonymous
hemianopia which is congruous and macula-sparing.
Interpretation
Defect limited to one eye—indicates ocular, retinal or optic
nerve pathology
• Constricted field: chronic papilloedema, chronic
glaucoma
• Tabular vision—does not indicate organic disease—
suggests hysteria
• Scotoma—multiple sclerosis, toxic optic neuropathy,
ischemic optic neuropathy, retinal hemorrhage or infarct
• Altitudinal defects—suggest vascular cause (retinal
infarcts or ischemic optic neuropathy)
Defect affecting both eyes—indicates a lesion at or behind
the optic chiasm, or bilateral prechiasmal lesions
• Bitemporal hemianopias
– Upper quadrant > lower—inferior chiasmal
compression, commonly a pituitary adenoma
– Lower quadrant > upper—superior chiasmal
compression, commonly a craniopharyngioma
– The common causes for the lesions referred to below
are cerebral infarcts, hemorrhages or tumors.
• Homonymous quadrantanopias
– Upper—temporal lobe lesion
– Lower—parietal lobe lesion
• Homynymous hemianopias
– Incongruous—lesion of the optic tract
– Confruous—lesion behind the lateral denticulate body
– Macula-sparing—lesion of the occipital cortex (or
partial lesion or optic tract or radiation).
Optic Disk
Optic Disk Abnormalities
A swollen optic disk is often difficult to find, with the vessels
disappearing without an obvious optic disk.
The differences between papilloedema and papillitis can
be remembered:
• The clinician sees nothing (cannot find the disk) + the
patient sees everything (normal vision)—papilloedema.
• The clinician sees nothing + the patient sees nothing
(severe visual loss)—papillitis
• The clinician sees everything (normal looking disk) +
the patient sees nothing—retrobulbar neuritis.
Table 8.19: Common mistakes and problems
Blurred nasal margin Normal often mistaken for papillo-
edema
Temporal pallor Normally paler than nasal, often
misinterpreted as abnormal
Myopic fundus Myopic eye is large, so disk appears
paler, may be mistaken for optic
atrophy
Hypermetropic fundus Small eye, fundus appears crowded,
mistaken for papilloedema
Drusen Colloid bodies that may make disk
seem pale
Pigmentation on disk edge Normal—may make disk seem pale
Myelinated nerve fibers Opaque white fibers usually radiating
from disk, may be mistaken for
papilloedema.

Some Important Points
• Papilloedema: Common causes—raised intracranial
pressure (N.B: absence does not exclude this); rarer
caused: malignant hypertension, hypercapnia
• Papillitis: Common causes—MS, idiopathic
• Optic atrophy: Primary: common causes—MS, optic
nerve compression, optic nerve ischemia: rarely
nutritional deficiencies, B12, B1, hereditary
• Secondary—following papilloedema
• Deep optic cup: Chronic glaucoma—commonly
idiopathic.
Third, Fourth and Sixth Nerves
(Fig. 8.13)
The oculomotor (3rd nerve), trochlear (4th nerve) and the
abducent (6th nerve) are tested together as they innervate
the external ocular muscles which move the eyes. The 6th
nerve supplies the lateral rectus, the 4th nerve innervates
the superior oblique, and the 3rd nerve supplies all the other
extraocular muscles, along with the sphincter pupillae, ciliary
muscle (the muscle of accommodation) and the levator
palpebrae superioris.
1. Ask the patient to look at your finger held at a distance
of about 2 feet from his eyes. Notice if there is any
squint (strabismus). Ask the patient if he has double
vision (diplopia) or gets attacks of vertigo.
2. Test for pupillary light reflexes and the convergence
accommodation reflex. Notice the size, shape and
mobility of the pupil.
3. Fix the chin of the patient with left hand and ask him to
follow the movements of your right forefinger with his
eyes. Move your finger in the cardinal directions. The
eyes move normally 50° outwards, 50° inwards, 33°
Fig. 8.13: Extraocular eye muscles
The movements they produce and their cranial nerve (N) supply
Central Nervous System 195
upwards, and 50° downwards. Test the rotatory move-
ments of the eyes also. Observe if there is any limitation
of movement in any direction
Usually, the signs of involvement of one or more of
these nerves are: (i) Pupillary abnormalities, (ii) Presence
of diplopia, (iii) Defective movements of the eyeballs, and
(iv) Presence of a squint.
Skew deviation of the eye, i.e. one eye is directed
upwards and the other downwards—is seen in diseases of
cerebellum, labyrinth, and 8th nerve.
Abnormalities
Abnormalities can arise at any level.
Lesions can be:
1. Supranuclear
2. Internucler MLF
3. Nuclear
} Patients do not
perceive double vision
4. Nerve
5. Neuromuscular junction
6. Muscle
} Patients perceive
double vision
Intranuclear and supranuclear lesions rarely cause double
vision.
Rules of Double Vision
1. Double vision is maximal in the direction of gaze of the
affected muscle
2. False image is the outer image
4. False image arises in the affected eye
The Cover Test
This test is useful in the detection of latent squint (Fig.
8.14).
The patient is asked to look with both eyes at your right
eye. Then, the left eye is uncovered rapidly and cover his
right eye. Pay attention to see if the left eye has to correct
to look back at your eye. Repeat, covering the left eye and
watching the right eye.
Findings: If one eye has to correct as it is uncovered, this
indicates the patient has a latent strabismus (squint), which
is classified as divergent or convergent.
Interpretation:
Latent squint: Congenital squint usually in the weaker eye
(and myopia in childhood)—common.
Test the Eye Movements
The clinician holds a pen vertically about 50 cm away from
the patient in the center of his gaze. He asks him to follow
it with his eyes without moving his head and to tell the
clinician if he sees double. Hold his chin tightly to prevent
head movement.
196 Essentials of Clinical Medicine
Fig. 8.14: The cover test
The clinician moves the pen slowly. He asks the patient
to tell him if he sees double from side to side, up and down
from the center up and down at the extreme of lateral gaze.
Ensure the patient’s nose does not prevent the pen being
seen at the extreme of lateral gaze.
Pitfalls
• The target is too close.
• The target moves too fast.
• The patient is allowed to move his head.
In a patient with hemianopia, the target may disappear
from the patient’s view if moved too fast towards the
hemianopia. Thus, in the presence of hemianopia, the target
must be moved very slowly.
As you do this, watch the movements of the eyes:
• Do both eyes move through the full range? Estimate the
percentage reduction in movement in each direction.
• Do the eyes move smoothly?
• Do both eyes move together?
If the patient reports he sees double at any stage:
• Establish if the images are side-by-side, up and down,
or at an angle.
• Establish the direction where the images are widest apart.
In this position briefly cover one eye and ask which
image disappears: the inner or outer. Repeat this by covering
the other eye.
Test Saccadic Eye Movements
• Ask the patient to look to the right, to the left, then up
and down.
• Observe the eye movements—are they full, do they move
smoothly, do they move together?
• Look particularly at the speed of adduction.
Test Convergence
Ask the patient to look into the distance and then look at
you finger placed 50 cm in front of him and gradually bring
the eyes in observing the limit of convergence of the eyes.
Vestibulo-ocular Reflex
(Doll’s Eye Maneuvre)
Requirement: This test is performed in patients with a
supranuclear or internuclear abnormality.
Procedure: Ask the patient to look into the distance at a
fixed point, then turn the patient’s head to the left, then the
right and flex the neck and extend the neck.
The eyes should move within the orbits maintaining
forward gaze.
Result
1. The eyes are misaligned in primary gaze:
• The misalignment remain constant in all directions
for gaze = convergent or divergent concomitant
strabismus (squint).
One eye is deviated downwards and out, with ptosis
= third nerve lesion.
Eyes aligned in different vertical planes = skew
deviation.
2. The patient has double vision:
• Try to answer the following questions:
– Is there a single nerve (VI, III or IV) deficit?
– If there is all a III nerve deficit, is it medical
(pupil-sparing) or surgical (with papillary
dilation)?
• If not single nerve:
– Is there a combination of single nerves ?
– Is it myasthenia or dysthyroid eye disease?
3. Without double vision:
Compare movements on command, on pursuit and on
vestibular positional testing.
– Loss to command only—frontal lesion.
– Loss to pursuit only—occipital lesion.
– The patient does not look towards one side—lateral
gaze palsy; check response to vestibulo-ocular reflex
testing.
– The patient does not look up—upgaze palsy.
– The patient does not look down—downgaze palsy.
– Eyes do not move together, with markedly slowed
adduction and with nystagmus in the abducting eye

—internuclear ophthalmoplegia with ataxic
nystagmus.
– Eye movement falls short of target and requires a
second movement to fixate—hypometric saccades.
Table 8.20: The ultimate impression that you get
Skew deviation Brainstem lesion — common causes:
stroke, demyelination — look for
associated brainstem signs.
Single cranial nerve palsy Lesion along the course of the nerve
(III, IV or IV) or a nuclear lesion—common causes:
Medical Diabetes mellitus, athero-
sclerosis; rarely: vasculitis, Miller-Fisher
syndrome (a form of Guillain-Barre
syndrome).
Surgical (N.B. pupil involvement in III
nerve palsy) tumour, aneurysm, trauma,
a false localizing sign or uncal herniation
(III nerve).
N.B. Posterior communicating aneurysm
common cause of a surgical III nerve
palsy.
Nuclear lesions Arise from brainstem pathology including
brainstem infarction, multiple sclerosis
and, rarely, brainstem hemorrhage and
tumor.
Lateral gaze palsy: A large frontal or parietal lobe lesion when
can arise from: the patient looks away from the paralyzed
side (can be overcome by doll’s eye
maneuver)
A pontine lesion when the patient cannot
look to the non-paralyzed side and there
may be other pontine abnormalities
(facial weakness). Not overcome using
doll’s eye maneuver.
Vertical gaze palsy Lesions in the upper brainstem—
Common causes of lateral and vertical
gaze palsies — brainstem infarction,
multiple sclerosis, tumor.
Internuclear A lesion to the medial longitudinal
ophthalmoplegia fasciculus—common cause: multiple
sclerosis; rarer causes: vascular disease,
pontine glioma.
Supranuclear palsy with preserved
positional/vestibular testing: may arise in
association with akinetic rigid syndromes
then referred to as the Steele-Richardson
syndrome or progressive supranuclear
palsy and may be seen in other degene-
rative conditions.
Hypometric saccades Indicates a cerebellar lesion.
Nystagmus
Nystagmus is defined as a slow drift of eye in one direction
with a fast correction in the opposite direction. Nystagmus
is described in the direction of the fast phase.
Central Nervous System 197
Types
Nystagmus can be:
1. Physiological—oculokinetic nystagmus (as seen in people
looking out of the windows of trains)
2. Peripheral—due to abnormalities of the vestibular system
in the ear, the eighth nerve nucleus or nerve itself.
3. Central—due to abnormalities of the central vestibular
connections or cerebellum
4. Retinal—due to inability to fixate.
Procedure for the Test
Ask the patient to follow your finger with both eyes. Move
the finger in turn up and down, to each side. Hold the finger
briefly in each position at a point where the finger can be
easily seen by both eyes.
Observation:
• Whether it is symmetrical moving at the same speed in
both directions (pendular nystagmus) or if there is a
fast phase in one direction with a slow phase in the
other (jerk nystagmus).
• The direction of the fast phase. Is it in the horizontal
plane, in the vertical plane or rotatory?
• Whether it occurs in the primary position of gaze
(second degree) and if it occurs with the fast phase
looking away from the direction of gaze (third degree)?
– If it affects the abducting eye more than the
adducting eye.
• Whether it is unidirectional only?
– If it occurs in the direction of gaze in more than one
direction (multidirectional gaze-evoked nystagmus).
• To decide whether it is central or peripheral note:
– If it persists or fatigues?
– Whether associated with a feeling of vertigo?
– Whether it improves with visual fixation?
Pitfalls:
At the extreme of lateral gaze, one or two nystagmoid jerks
can be seen normally—ensure target remains within
binocular vision.
If found, repeat. If true nystagmus, it will appear at less
than extreme lateral gaze.
Special test: Optokinetic Nystagmus (OKN)
This can be tested when a striped drum is spun in front of
the eyes and normally evokes nystagmus in the opposite
direction to the direction of spin. This is a useful test for
patients with hysterical blindness.
Interpretation: See Table 8.21 to decide whether central or
peripheral.
198 Essentials of Clinical Medicine
Table 8.21: Central versus peripheral nystagmus
Sustained Fatigue Associated Reduced
symptoms by
of vertigo fixation
Central + – – –
Peripheral – + + +
Peripheral nystagmus is not associated with other eye movement
abnormalities and usually has a rotatory component.
Table 8.22: Final conclusion
1. Nystagmoid jerks Normal
2. Pendicular nsytagmus Inability to fixate—congenital,
may occur in miners.
3. Rotatory (or rotatory) Pure rotatory nystagmus—central;
nsytagmus peripheral, horizontal nsytagmus
usually has a rotatory component.
4. Vertical nystagmus (rare) indicates brainstem disease.
a. Upbeat: indicates upper
brainstem – common causes:
demyelination, stroke, Wernicke’s
encephalopathy.
b. Downbeat: Arnold-Chiari mal
formation, syringobulbia
demyelination.
5. Horizontal nystagmus a. Ataxic nystagmus—nystagmus
(common) of abducting eye >> adducting eye,
associated with internuclear
ophthalmoplegia—common
causes: multiple sclerosis; cere-
brovascular disease.
b. Multidirectional gaze-evoked
nystagmus: nystagmus in the
direction of gaze, occurring in
more than one direction. Always
central—cerebellar or vestibular
cerebellar syndrome—common
causes: drugs, alcohol, multiple
sclerosis; rarer causes: cerebellar
degenerations.
Central vestibular syndromes –
common causes: younger patients
multiple sclerosis; older patients
—vascular disease.
c. Unidirectional nystagmus:
second and third degree horizontal
nystagmus is usually central; if
peripheral, it must be acute and
associated with severe vertigo.
First degree horizontal nystagmus
may be central or peripheral:
• Peripheral: Peripheral vestibular
syndromes—common causes:
Vestibular neuronitis, Ménière’s
disease, vascular lesions
• Central: Unilateral central
vestibular syndrome—common
causes: as central vestibular
syndromes.
Contd...
Contd...
6. Unusual and rare eye Opsoclonus: rapid oscillations of
movement abnormalities the eyes in the horizontal,
rotatory or vertical direction—
indicates brainstem disease, site
uncertain.
Ocular bobbing: eyes drifting up
and down in the vertical plane-
associated with pontine lesions.
Fifth or Trigeminal Nerve (Mixed)
Both the motor and the sensory functions are tested.
Motor Functions
1. Ask the patient to clench his teeth – The masseter and
temporal muscles contract, and should become equally
prominent on either side. Confirm by placing your hands
on the muscles. The muscles with fail to become prominent
if there is paralysis on that side. 2. Ask him to open his
mouth – The jaw will deviate to the side of paralysis, The
healthy lateral pterygoid muscles pushing is to that side.
Sensory Functions
Test the sensations of touch, pain and temperature over the
entire face and over the anterior two-thirds of the tongue
(the taste sensation from this part of the tongue is carried
by the tongue is carried by the facial nerve).
Test the corneal reflex on both sides because the
trigeminal nerve forms the afferent path of this reflex. As
already mentioned, loss of corneal reflex is one of the early
signs of 5th nerve lesion (Fig. 8.15).
The Corneal Reflex
• Afferent: Ophthalmic br. of V n
• Efferent: VII n.
The patient is asked to look up and away from you.
Bring a piece of cotton wool twisted to a point in to touch
the cornea from the side. Watch both the eyes when they
close. In unilateral facial palsy, the sensation of cornea is
demonstrated if the opposite eye is observed.
Pitfalls:
1. The conjunctiva is touched instead of cornea (Fig. 8.15)
2. Slightly depressed in contact lens wearer.
3. If cotton wool is brought close to the eyes too quickly,
it automatically causes a blink.
Fig. 8.15: Corneal reflex: Touch the cornea and not the conjunctiva

Interpretation of corneal reflex:
After corneal stimulation:
1. Failure of either side of face to contract—V1 lesion
2. Failure of only one side to contract—VII lesion
3. Subjective reduction in corneal sensation—partial V1
4. Absent corneal reflex can be an early and objective sign
of sensory trigeminal lesion.
Trigeminal Nerve: Interpretation
Motor
• Wasting of temporalis and masseter: rare causes:
myotonic dystrophy, motor neuron disease, facio-
scapulo-humeral dystrophy
• Weakness of jaw closure—rare
• Jaw opening: jaw deviates to the side of the lesions—
causes: unilateral lesion of motor V.
Jaw Jerk
• No movement—absent jaw jerk
• Minimal movement—present normal jaw jerk
• Brisk movement—brisk jaw jerk
Sensory
Impairment or loss in one or more divisions on one side of
light touch to pinprick and temperature or both.
• Unilateral facial loss: one or all modalities.
• Muzzle loss of pinprick and temperature.
• Unilateral area of sensory loss not in distribution of whole
division.
• Trigger zone that produces facial pain.
N.B. 1. Angle of jaw is not supplied by the trigeminal but by
the greater auricular (C2).
2. The trigeminal innervates the scalp to the vertex not just
to the hair line.
Interpretation
1. Loss of all modalities in one or more divisions:
– Lesion in sensory ganglion—most commonly herpes
zoster
– Lesion of division during intracranial course-V1
cavernous sinus (associated III, IV, VI) or orbital
fissure, V2 trauma, V3 basal tumors (usually
associated motor V).
2. Loss of sensation in all divisions in all modalities:
– Lesion of the gasserian ganglion, sensory root or
sensory nucleus—lesions of cerebellopontine angle
(associated VII, VIII), basal meningitis (e.g. sarcoid,
carcinoma).
3. Loss of light tough only:
– With ipsilateral hemisensory loss of light touch—
contralateral parietal lobe lesion.
– With no other loss – sensory root lesion in pons.
Central Nervous System 199
4. Loss of pinprick and temperature with associated
contralateral loss of these modalities on the body—
ipsilateral brainstem lesion.
5. Loss of sensation in muzzle distribution: lesion of
descending spinal sensory nucleus with lowest level
outermost syringomyelia, demyelination.
6. Area of sensory loss on cheek or lower jaw: damage to
branches of V2 or V3 infiltration by metastases.
7. Trigger area: trigeminal neuralgia
Seventh or Facial Nerve (Almost Purely Motor)
Components of 7th Cranial Nerve Examination
• Motor facial muscles, sensory-taste sensations in anterior
2/3rd of the toungue, reflex-corneal reflex.
Motor
• Ask the patient to close eyes—orbicularis oculi
• Raise eyebrows—frontal belly
• Frown—corrugator
• Retreat angle of mouth/smile/purse the lips—
zygomaticus
• Blow out the check—buccinator
• Whistle—buccinator
• Draw down the angle of mouth while tightening neck
muscles—platysma
• Purse the lips—orbicularis oris.
Sensory
Taste of anterior 2/3rd. Hold the tongue with gauze. Apply
salt, bitter/sugar on either side of tongue. Ask the patient to
show symbols 1, 2, 3. Before testing, explain to the patient
that if sweet, he may show (1) finger, etc.
Reflex
• Corneal
– Afferent: Opthalmic division of 5th cranial nerve
– Efferent; 7th nerve.
Procedure
1. Ask the subject to wrinkle the skin on his forehead.
2. Ask him to shut his eyes as tightly as possible; try to
open his eyes, first one and then the other. If the
orbicularis oculi is normal it is impossible to open the
eye against the subject’s wish. In lesions of 7th nerve,
the patient cannot close the affected eye at all, or if the
eye is closed, the eyelashes are not so deeply buried in
the face as on the normal side. Normally, as the eyes are
tightly shut, the corners of the mouth are drawn
upwards. But in paralysis of the lower part of the face,
the corner of the face is not drawn up.
When one attempts to shut the eyes tightly, the
eyeballs roll upwards – this is a normal response and is
200 Essentials of Clinical Medicine

called Bell’s phenomenon. In Bell’s palsy (see below) as and the semicircular canals, the upper part is affected and
the patient is asked to close his eyes, the upward is concerned with posture and equilibrium.
movement of the eyeball becomes obvious because
closure of the affected eye is not possible. Case: Facial Nerve Palsy
3. Ask the subject to smile or show his upper teeth, or to Sites of lesion in the following conditions:
whistle. When there is paralysis of the facial muscles • Acoustic neuroma—CP angle
on one side, the angle of the mouth is drawn towards • Ramsay-Hunt syndrome—geniculate ganglion
the healthy side. • Bell’s palsy—at the exit from stylomastoid for a men.
4. Ask him to inflate his mouth with air and below out his
Causes of Infranuclear 7th Nerve Palsy
cheeks; then tap each inflated cheek with a finger; air
escapes more easily on the affected side. • CP angle tumor
5. Taste sensation: Though the seventh nerve is almost • Acoustic neuroma
• Ramsay-Hunt syndrome—secondary to herpes zoster
entirely a motor nerve, the taste fibers from the anterior
of geniculate ganglion
two-thirds of the tongue pass from the lingual nerve
• While mastoidectomy 7th nerve may be damaged
into the chorda tympani and then througn the geniculate
• Infective polyneuritis
ganglion of the facial nerve and the nervus intermedius • Leprosy
of Wrisburg into the medulla to enter the tractus • Diabetes mellitus
solitarius. It has been suggested that these taste fibers • Parotid tumor
sometime run in the maxillary division of the trigeminal • Tetanus—cephalic tetanus
nerve; this, however, is rare. The sensation of taste • Hypertension
should always be tasted whenever a lesion of a cranial • Bell’s palsy
nerve is suspected. • TB—basal meningitis.
How to test the taste sensation: Use strong solutions of
Nuclear 7th Nerve Palsy
sugar and common salt and weak solutions of citric
acid and quinine in order to test the sensations of ‘sweet’, • Associated with 6th nerve palsy—7th and 6th lower
motor ipsilateral
‘salt’, ‘sour’ and ‘bitter’ respectively. Ask the subject
• Contralateral hemiplegia
to protrude his tongue and dry the surface with clean
• No taste involvement
cloth. Apply a small amount of sugar solution, on one
• Fovile syndrome—crossed hemiplegia plus ipsilateral
side of the midline, with a clean toothpick, and ask him: paresis of conjugate gaze
Is this ‘salt’? If the taste sensation is normal he will • Millard-Gubler syndrome—crossed hemiplegia with
shake his head. Try salt and then the others in the same internal strabismus, due to abducent nerve palsy.
manner, rinsing the mouth each time. The tongue should
be kept out during the test and not withdrawn. This is Causes of Bilateral 7th Nerve Palsy
to avoid the spreading of the test substance into the • Diabetes mellitus
posterior part of the tongue since taste from this region • Infective polyneuritis—Guillain-Barré syndrome
is carried by the 9th cranial nerve. Test the taste sensation • Sarcoidosis (parotid fever—Heerfordt’s syndrome)
on the posterior part in similar manner. If the subject • Leprosy
can write, then he should write down the taste • Bulbar lesion
• Mobius syndrome.
accordingly. The loss of sense of taste is called ageusia.
The patient should always be asked whether he Muscular Causes of Facial Palsy
experiences any abnormal test sensations. These, like • Myopathy
hallucinations of smell, may form the aura of an epileptic • Myasthenia gravis
fit, especially in cases of temporal lobe epilepsy. • Dystrophica myotonia.
Supranuclear and Infranuclear Seventh Nerve Taste Sensation will be Affected
Lesions of Facial Nerve • Lower motor facial proximal to point at which chorda
The chief difference between supranuclear and infranuclear tympani leaves the facial nerve.
lesions of the facial nerve is that in the former, the lower • In post-fossa-C.P. angle tumor where pars intermedia
part of the face is chiefly affected, while in the vestibule and 8th nerve will be damaged in addition to 7th nerve
 Central Nervous System 201

palsy, e.g. fracture base of skull, spread of middle ear • Surgical decompression of facial nerve if there is no
infection, leukemic deposits and CP angle tumor. recovery after 2 months
Table 8.23: Differentiation between lower motor and • Usually recover spontaneously within 2 to 12 weeks.
upper motor facial palsy
Complication of Bell’s Palsy
Description Bell’s palsy Upper motor • Deformity
infranuclear facial palsy
• Contracture of facial muscle
• Involvement of face One half of face Lower half of face,
• Facial tics and spasms
forehead spared
• Taste sensory loss Can be No • Crocodile tear
• Bell’s phenomenon Yes No • Jaw winking.
• With emotion
paralysis increases Poor Prognostic Signs of Bell’s Palsy
• Usually associated No Yes • Extremes of age
with hemiplegia with
same side facial palsy • If delay in blinking reflex occurs in recovery stage
• Corneal-reflex Lost Preserved • EMG evidences of denervation after 10 days
• Plantar response Flexor Extensor with • Severe 7th nerve palsy with axonal degeneration there
hemiplegia is slow recovery.
• Facial muscle atrophy Yes No
Some Important Facts
Case: Bell’s Palsy (Fig. 8.16) • Unilateral LMN Weakness: Lesion of the facial nerve or
About Bell’s Palsy its nucleus in the pons—common cause—Bell’s palsy:
more rarely: pontine vascular accidents, lesions at the
Cause not known. It is due to non-suppurative inflammation
cerebellopontine angle, herpetic infections (Ramsay-Hunt
of 7th nerve. Site within stylomastoid foramen, always
syndrome—note vescicles in external auditory meatus),
unilateral, 80 percent recover in 3 weeks time. More seen
lesions in its course through the temporal bone, parotid
in males. In the differential diagnosis, polio and disseminated
tumors.
sclerosis are to be kept in mind.
• Bilateral LMN weakness: Common causes—sarcoidosis,
Treatment of Bell’s Palsy Guillain-Barré syndrome: rarer causes: myasthenia gravis
• Prednisolone one mg. per kg × 2 weeks. can produce bilateral fatiguable facial weakness
• Electrical stimulation (Galvanic) on every day after 2 (neuromuscular junction); myopathies can produce facial
weeks weakness (N.B. Dystrophia myotonica and fascio-
• Massage upwards of facial muscles 5 to 10 minutes/ scapulo-humeral dystrophy).
twice a day • Unilateral UMN—cerebrovascular accidents, demy-
• Infra-red therapy elination, tumors—may be associated with ipsilateral
• Tarsorrhaphy to prevent exposure keratitis hemiplegia (supratentorial lesions) or contralateral
• Vasodilator therapy. Nicotinic acid 100 mg three times a hemiplegia (brainstem lesions).
day • Bilateral UMN—pseudobulblar palsy, motor neuron
disease.
• Emotional paralysis—Parkinsonism.

Eighth or Vestibulocochlear Nerve (Sensory)

Fig. 8.16: Bell’s palsy of right side
This nerve has two components; the cochlear division, which
is concerned with hearing, and the vestibular division, which
supplies the vestibule and the semicircular canals, and is
concerned with posture and equilibrium.
Tests of hearing: Test each ear separately. Confirm that the
external auditory canal is waxfree. Use the whisper test and
the tuning fork tests as described earlier in this book.
Tests of vestibular functions: The semicircular canals can
be stimulated easily.
202 Essentials of Clinical Medicine
Barany’s Caloric Test
Barany’s caloric test syringe the external auditory meatus
with water at 30°C or 44°C, while the head is tilted back
60° and pointing to the opposite side, and up to the ceiling
(the horizontal canal is placed vertical). The endolymph in
the canal moves down by convection currents produced
by cold-water syringing. Note the following:
1. Nystagmus.
2. Past pointing. If the subject is asked to touch a given
point on a tape held in front of him (when the eyes are
closed), the arm deviates out towards the stimulated
side.
3. If asked to stand, there is a tendency to fall towards the
stimulated side. The subject complains of giddiness and
nausea, and may even vomit. All these reactions indicate
normal functioning of vestibular apparatus. A patient
suffering from vestibular disease complains of paroxys-
mal attacks of vertigo, tinnitus, nausea and vomiting.
Interpretation:
a. Conductive deafness—common causes: middle ear
disease, external auditory meatus obstruction, e.g. wax.
b. Sensorineural deafness:
i. Lesions of the cochlea—otosclerosis, Ménière’s
disease, drug or noise-induced damage.
ii. Lesions in the nerve—meningitis, cerebellopontine
angle tumors, trauma.
iii. Lesions in the nucleus in the pons—vascular or
demyelinating lesions.
Table 8.24: Tuning fork tests and their interpretation
Tests Normal Conductive deafness SN deafness
Rinne AC>BC BC>AC AC>BC
(Rinne positive) (Rinne negative)
Weber Not lateralized Lateralized to poorer Lateralized to
ear better ear
ABC Same as Same as examiner’s Reduced
examiner’s
Vestibular Gait
Always test heel-toe walking. Gait is unsteady, veering to
the side to the lesion.
Nystagmus
Vestibular nystagmus is associated with vertigo, horizontal
and unidirectional. It may be positional.
Caloric Test (Normally Performed in a
Test Laboratory)
The patient is lying down with head on a pillow at 30° so
the lateral semicircular canal is vertical.
Cool water (30°C) is instilled into one ear over 40 seconds
(usually about 350 ml). The patient is asked to look straight
ahead and the eyes are watched. This is repeated in the
other ear, and then in each with warm water (44°C).
Findings/Observation
Normal responses:
1. Cold water—nystagmus fast phase away from
stimulated ear.
2. Warm water—nystagmus fast phase towards stimulated
ear.
3. Reduced response to cold and warm stimuli in one ear;
canal paresis.
4. Reduced nystagmus in one direction after warm stimuli
from one ear and cold stimuli from the other—directional
preponderance
N.B: In the unconscious patient, the normal responses are
as follows:
• Cold water—tonic movement of the eyes towards the
stimulus.
• Warm water—tonic movement of the eyes away from
the stimulus.
(The fast phase of nystagmus is produced by the
correction of this response which is absent in unconscious
patient).
Interpretation:
• Canal paresis: Lesion of the semicircular canal (Ménière’s
disease) or nerve damage (causes as for sensorineural
deafness, plus vestibular neuronitis)
• Directional preponderance: Vestibular nuclear lesions
(brainstem)—common causes: vascular disease,
demyelination.
Additional Tests of Vestibular Function
Hallpike’s Test
Procedure: Used in patients with positional vertigo.
• Sit the patient on a flat bed so that when he lies down
his head will not be supported.
• Turn the head to one side and ask the patient to look to
that side.
• The patient then lies back quickly till he is flat with his
neck extended with his head supported by the examiner.
• Watch for nystagmus in the direction of gaze. Note if
this is associated with a delay, whether it fatigues when
the test is repeated and if the patient feels vertigo. Repeat
for the other side.
Table 8.25: Hallpike’s test: Interpretation
1. No nystagmus Normal
2. Fatiguable rotatory Peripheral vestibular syndrome,
nystagmus with delay usually benign positional vertigo.
3. Non-fatiguable nystagmus Central vestibular syndrome.
without delay
 Central Nervous System 203

Turning Test 2. Uvula does not move on saying ahh or gag : bilateral
• Ask the patient to stand facing you. palatal muscle paresis.
• Ask him to point both arms straight out in front of him 3. Uvula moves on saying ahh, but not on gag, with
towards you. reduced sensation of pharynx: IX palsy (rare).
• Ask him to walk on the spot and when he is doing this Larynx
to then close his eyes. Observation
• Watch his position. 1. Gradual onset cough: Bovine cough—suggests vocal
Interpretation and palsy.
• He gradually turns to one side, and may turn through 2. Bubbly voice and cough—suggests combined cord palsy
180°. This indicates a lesion on the side he turns towards. and pharyngeal pooling due to tenth nerve lesion.
3. Swallow followed by coughing indicates aspiration due
Ninth or Glossopharyngeal Nerve (Mixed) to poor airway protection—suggests tenth lesion.
4. Unilateral cord palsy—recurrent laryngeal palsy or vagal
This nerve is motor for the middle constrictor of the pharynx lesion.
and the stylopharyngeus muscle, and sensory for the Interpretation
posterior third of the tongue (taste fibers also) and the Tenth nerve palsy is caused by lesion in the medulla—
mucous membrane of the pharynx. Paralysis of 5th nerve observe for associated ipsilateral cerebellar signs, loss of
alone is rare. pain and temperature in the face on the same side and on
1. Test the pharyngeal reflex. the body on the opposite side and an ipsilateral Horner’s
2. Test the taste sensation of the posterior third of the (lateral medullary syndrome).
tongue. Extramedullary and intracranial observation to confirm
associated XI cranial, IX cranial nerves.
Table 8.26: Mouth: Interpretation
Left-sided recurrent laryngeal palsy may arise from
• Gum hypertrophy Phenytoin therapy mediastinal or intrathoracic pathology.
• Red, ‘beefy’ tongue Vitamin B12 deficiency. Bilateral lower motor neuron X occurs in progressive
• Large tongue amyloidosis, acromegaly,
congenital hypothyroidism. bulbar palsy (a variant of MND)—be observant for
• Small tongue With fasciculations—bilateral associated tongue fasciculations and mixed upper and lower
lower motor neuron lesion; motor motor neuron signs without sensory loss in the limbs.
neuron disease (progressive bulbar
palsy type), basal meningitis, Tenth or Vagus Nerve (Mixed)
syringobulbia.
• Small tongue With reduced range of movements It is motor for the soft palate except tensor palati, pharynx
—bilateral upper motor neuron and larynx. It is also motor and sensory for the respiratory
lesion—often associated with
labile emotions, increased jaw jerk: passages, the heart and most of the abdominal organs (motor
pseudobulbar palsy parasympathetic). Paralysis of this nerve is evident clinically
• Tongue deviates to one side Weakness on the side it moves only through its palatine and laryngeal branches.
towards. 1. Ask for the history of regurgitation of fluids through
– With unilateral wasting and Unilateral lower motor neurone the nose during swallowing. This is due to total paralysis
fasciculation (rare)—causes : syringomyelia,
basal meningitis, early motor of the soft palate. Use a tongue depressor to watch the
neurone disease, foramen magnum movements of palate when the patient is asked to say
tumour. ‘Ah.’ If one side is paralysed, the soft palate on that side
– With normal bulk Unilateral upper motor neuron will remain flat and immobile. In bilateral paralysis, the
weakness (common)-associated entire soft palate remains motionless. Conclusions drawn
with hemiparesis: strokes, tumors.
• Tongue moves in and out on Cerebellar disease, essential from the position of uvula are usually unreliable, since it
tremor, protrusion (‘trombon’ may normally be deviated to one side.
tremor) extrapyramidal syn- 2. Laryngoscopy is done to note the position of true vocal
dromes. cords.
Pharynx and Gag Reflex
Eleventh or Accessory Nerve (Motor)
Interpretation
1. Uvula moves to one side: upper or lower motor lesion This nerve is motor to sternomastoid and upper part of
of vagus on the other side. trapezius muscle.
204 Essentials of Clinical Medicine

1. Press on the shoulders from behind and ask the patient Contd...
to shrug his shoulders. Note any weakness or paralysis 3. Temporal bone—fracture 7th nerve lower —
of the upper part of the trapezius. base of skull infection motor paralysis
2. Ask the patient to turn his head first to one side and then of middle ear—mastoid
surgery
to the other, against resistance, by placing your hand on
4. Geniculate ganglion— Ramsay-Hunt Rash over palate
either side of the chin alternately. Herpes zoster syndrome Rash over external
Interpretation ear
5. Over face after exit Lower motor Lower motor 7th
1. Weakness of sternocleidomastoid and trapezius on the from facial canal 7th nerve palsy nerve palsy
same side indicates peripheral accessory palsy. Look a. Sarcoidosis
for associated ipsilateral IX and X lesions—suggests a b. Leprosy
jugular foramen lesion (glomus tumur or neurofibroma). c. Parotid tumor
d. Trauma to face
2. Weakness of ipsilateral sternocleidomastoid and e. Parotid surgery
contralateral trapezius—upper motor neuron weakness 6. At exit of facial canal 7th nerve lower Bell’s palsy
on ipsilateral side. within stylomastoid motor palsy
3. Unilateral delayed shoulder shrug—suggests contralateral foramen
upper motor neuron lesion.
Table 8.28: Syndromes of cranial nerve palsies
4. Bilateral wasting and weakness of sternocleidomastoid
indicates myopathy (such as dystrophia myotonica, Syndrome Cranial nerves Clinical features
involved
fascio-scapulo-humeral dystrophy or polyositis) or
motor neuron disease (look for associated bulbar Weber’s Nerve 3rd nerve palsy with contralateral
hemiplegia lesion at midbrain
abnormalities).
Benedict’s 3rd nerve 3rd nerve palsy with contralateral
5. Unilateral sternocleidomastoid abnormalities: indicate hemiplegia lesion at midbrain, and
unilateral trauma, unilateral XI nerve weakness or upper tumor with rigidity and cerebellar
motor neuron weakness (check opposite trapezius). ataxia due to red nucleus involve-
ment in addition.
Tolosa-Hunt, 3,4,5,6 nerves Lesion in cavernous sinus
Twelfth or Hypoglossal Nerve (Motor)
Milliard-Gubler- 6,7th nerves Nuclear type of facial palsy with
It is purely motor to the muscles of tongue, and depressors and Foville 6th nerve involvement and
contralateral hemiplegia. In foville
of the hyoid bone. gaze palsy is to the side of the
1. Ask the patient to push out his tongue as far as possible. lesion
If the 12th nerve is paralysed, the tongue is pushed over Vemet’s (jugular 9,10,11 Loss of taste in posterior 1/3 rd
to the side of the lesion by the contraction of the muscles foramen) tongue, vocal cord palsy, palate,
sternomastoid, paralysis.
on the healthy side. Ask him to move the tongues from Schemidt’s 10,11 nerve
side to side, over the lips and against the walls of the Tapia’s 10,12 nerve Paralysis of larynx, pharynx,
cheeks. A finger may be placed on a cheek while the tongue atrophy
Jackson’s 10,11,12 nerves
patient presses against it with tongue through the wall Collect Sicard 9,10,11,12 nerves
of the cheek. Villaret’s 9,10,11,12 nerves Homer’s syndrome along with
2. Note if there is any fasciculation wasting, or tremor. and cervical sym- 9,10,11,12th nerves involvement
Wasting and tremor indicate a nuclear of infranuclear pathetic nerves
lesion (lower motor neuron).
EXAMINATION OF MOTOR SYSTEM
Table 8.27: Site of lesion in the cranial nerve palsy (Fig. 8.17, PLATE 13)
1. Pons—neoplastic, 6th and 7th Lateral rectus palsy, The examination of the motor system is covered under the
syringobulbia, multiple nerve affected 7th nerve palsy, following subheadings:
sclerosis, poliomyelitis, conjugate deviation 1. Muscle strength and movements (power)
motor neuron disease affected
2. Posterior fossa— 7th nerve, Deafness, loss of taste,
2. Bulk of muscles (nutrition)
cerebellopontine 8th nerve and lower 7th nerve palsy 3. Muscle tone
angle tumor pars intermedia 4. Reflexes testing
5. Gait pattern
Contd...
6. Involuntary movements.

MUSCLE STRENGTH AND
MOVEMENTS (POWER)
Power (or Strength of Muscle)
Power is defined as the force of contraction that can be
generated voluntarily by the muscle. While assessing the
muscle power, it becomes important to understand the
relation between the strength of muscles to the patient being
tested. For instance, if the patient is a hard working laborer,
then in spite of his complaints of muscle weakness, the
examiner will feel the muscle to be very strong. Whereas in
case of an elderly patient, there may be no symptoms despite
being generally paretic. The muscle strength can be
determined by isometric as well as isotonic exercises.
However, the isometric (in which the length of muscle fibers
remains the some) is more sensitive than isotonic (in which
the muscle tone remains the some) in detecting the subtle
degree of weakness.
a. Isometric testing of muscles: The patient is made to
contract a group of muscles as powerfully as possible
and then to remain in that position while the examiner
tries to overpower the muscle group being tested.
b. Isotonic testing of muscles: The patient is made to put
the joint through a range of movement while attempting
to halt movement progression.
In infants and young children, it is not possible to test
the power of individual muscles or muscle groups due to
inability of the child to comprehend what the examiner wants
to do. An indirect assessment of the power in all the limbs
can be done by observing the spontaneous movements of
the child while in bed, when he gets up from the supine to
the setting position (whether he supports himself with the
arm or not), how he holds the objects, whether he refuses
to use a particular hand (hemiplegia or monoplegia), how
he walks (e.g. circumduction gait in case of hemiplegia).
Testing of muscle strength and the movements
performed by them form a very important part of
neurological examination [Figs 8.21(1) to 8.21(31), Plates
13 to 18]. It can give us many significant hints regarding
the neurological deficits of the body. A rough assessment
can be made by observing the patient’s activities like walking
and standing, observing the patient while dressing or
undressing, jumping action to get down from the bed and
so on. The clinician should try to make assessment regarding
the strength of individual muscle groups. Always try to make
a comparison between movements made by the patients
and your (examiner’s) movements or you can also compare
movements of the counterparts of patient’s own body (if
you suppose those counterparts to be normal). Note that,
Central Nervous System 205
no significant result will be obtained on observation if the
counterparts of patient’s body are both abnormal (for
example, comparing the movements of both the knee joints
of patient, if when they both are affected by similar severity
of arthritis).
Abdominal Weakness
Displacement of the umbilicus provides very important clue
in the diagnosis of weakness (paralysis) of anterior
abdominal wall. When the patient tries to lift himself from
the pillow (against resistance), there occurs displacement
of umbilicus in case of paralysis of anterior abdominal wall.
When the paralysis is present over the lower segment, the
umbilicus moves upwards; and when the upper segment is
paralyzed, the umbilicus is displaced downwards. It
indicates the level of lesion in the thoracic region in spinal
cord disease. Another important maneuver is in which the
patient is made to sit up from the lying (supine) position of
spastic paralysis of leg. The affected limb will rise first, but
in hysterical paralysis, this does not occur.
Diaphragm
The diaphragm receives nerve supply from upper vervical
segments (the phrenic nerve). It is usually unaffected in
cervical cord disease except in motor nerve disease
(amyotrophic lateral sclerosis), some muscular disorders
and sometimes in brachial neuritis. The patient is asked to
take a deep breath and to count slowly in a single breath . It
is generally, noticed that if there is weakness of muscles of
diaphragm, then it will prevent a brisk sniff (i.e. a respi-
ratory movement that requires a sudden manimal diapharag-
ments contraction). An important sign is that the patient
gets dyspnasic when he lies supine. The patient may also
be insomnic due to oxygen desaturation in supine position.
Spinal extensors: (Testing of erector spinal muscle and other
muscle of the back).
The patient is asked to lie down in prone position. He is
then made to extend the head from the bed by extending
(lifting) the neck and back. Healthy muscles will be seen to
stand out prominently during this procedure.
Grading of Muscle Strength
(Power Testing)
The power (strength) of all muscle should be tested at each
joint in both upper and lower limb both against gravity and
resistance.
There are five patterns of muscular weakness:
1. Hemiplegia
– Paralysis of one side of the body involving the arm
and leg, and usually also of the face (fascio-brachial-
crural hemiparesis).

Muscle Cord segment
Abductor pollicis brevis
Opponens pollicis
First dorsal interosseous
Interossei
Lumbricals
Flexors of the fingers:
• Flexor digitorium
profundus
• Opponens digit
• Flexor minimi
• Flexor digitorium
sublimes
• Flexor pollicis longus
• Flexor digitorium
• Flexor pollicis brains
• Opponens pollicis
Extensor of the wrist:
• Extensor carpi radialis
longus
Table 8.29: Muscle strength testing of upper limb and lower limb
Nerve supply Procedure Inference
C8 – T1 Median n Patient is asked to abduct the thumb in a Muscle is seen and felt to contract
plane at right angle to the palmar aspect
index finger against the resistance of exami-
ner’s thumb
C8 – T1 Median n Patient asked to touch the tip of little finger If muscle is normal, the the examiner
with the point of thumb of the same hand thumb/index finger feels great pulling
and examiner opposes with his thumb or force
index finger
C8 – T1 Ulnar n Patient is asked to abduct the index finger Examiner feels greater pushing force
against the resistant offered by examiner
206 Essentials of Clinical Medicine
C8 – T1 Ulnar n Patient made to flex the metacarpophalangeal • When these muscles are paralyzed and
C8 – T1 Ulnar and joints and to extend the distal interphalangeal power is retained in long flexors and
median n joints extensors of two fingers, as in ulnar
palsy, a claw-hand deformity is prod-
uced
• The proximal phalanges are overexten-
ded and distal two are flexed. The fing-
ers are slightly separated
C8 – T1 Ulnar n Asking the patient to squeeze the examiner’s Examiner can feel the crushing of his fin-
fingers can test all the flexors. gers between fingers of the patient
C7 – T1 Ulnar n Allowing to squeeze only the index and middle
fingers is sufficient to assess the strength
C7 – T1 Ulnar n
C7 – T1 Median n
C7 – C8 Median n
C7 – T1 Median n
C8 – T1 Median n
C8 – T1 Median n
C6 – C8 Radial n Ask the patient to make a first (this causes It is very difficult to overcome the wrist
contraction of both flexors and extensors of extensor of a healthy man
wrist). Examiner should try to forcibly flex
the wrist against patient’s efforts to maintain
posture • Weakness of extensors may be tested
by asking the patient to grasp someth-
ing firmly in his hands. Weakness of
the extensors will cause the wrist to
Contd...
Contd...
Muscle Cord segment Nerve supply Procedure Inference
flex because flexors are stronger than the
extensors (in case of extensor weakness)
• Weakness or paralysis of extensors of
wrist as in radial palsy
Flexors of the wrist:
Flexor carpi radialis C6 – C7 Median n First allow the patient to squeeze the fingers With normal muscle strength, it is almost
of the examiner. Ask the patient to make a impossible
fist and try to overcome his wrist flexion
Brachioradialis C5 – C6 Radial n Patient is made to place the arm midway Healthy muscle (normal) will be seen and
between the prone and supine positions. The felt to stand out prominently at its upper
patient is then made to bend up the forearm, part
while the examiner opposes the movement
by grasping the hand
Biceps brachi C5 – T1 Musculo- Patient is asked to bend up the forearm against The muscle will stand out clearly.
cutaneous n resistance with the forearm in full supination
Triceps C6 – C8 Radial n Patient is asked to straighten the forearm
against the resistance offered by the examiner
Supraspinatus C5 – C6 Suprascap- Patient is asked to lift the arm straight out at
ular n right angle to the side. The first 30° (one-third)
of the movement is carried out by the supra-
spinatus and remaining 60° (two-thirds) is
produced by deltoid
Deltoid C5 – C6 Axillary n Deltoid helps in abduction of arm, therefore, In case of paralyses of deltoid, abduction,
patient is asked to abduct the arm against flexion, medial rotation, extension and
resistance. Acrominal fibers are powerful lateral rotation all are affected at shoulder
abductors of arm. Anterior fibers are flexors joint (intramuscular injections are given in
and medial rotators of arm. And the posterior the lower half of deltoid to avoid injury to
fibers are extensors and lateral rotators of arm axillary nerve)
Intraspinatus C5 – C6 Supracap- Patient is asked to move (tuck) the elbow into The muscle can be seen and felt to contr-
ular n the side with the forearm flexed at right angle. act. In case of paralyses or weakness,
Then ask the patient to rotate the thumb out- there movements are severely affected
wards against your resistance the elbow being
at the side throughout the procedure
Pectorals pectoralis C5 – T1 Pectoral n Patient is asked to stretch the arms out in Paralysis of pectoralis major:
(major and minor) front and then to clasp out in front and then • Adduction and medial rotation of shou-
to clasp the hands together while the examiner lder, flexion of the arm, extension of
efforts to hold them apart flexed arm against resistance and clim-
bing all become impossible
Contd...
Central Nervous System 207
Contd...

Muscle Cord segment Nerve supply Procedure Inference

Paralysis of pectoralis minor:
• Pushing if punching the movements
become difficult
• Forced inspiration is not possible
Serratus anterior C5 – C7 Long thor- Patient is asked to apply force against some • In case of paralysis there occurs
acic n unmovable objects like walls, etc. “winging of scapula” with the vertebral
border projecting posteriorly
• The patient is unable to elevate the arm
above the right angle, the deformity
208 Essentials of Clinical Medicine

becomes more severe and apparent as

he tries to do so and medial border
becomes more prominent
• Pushing and punching movements are
impossible
• Weight carrying becomes difficult
• Forced inspiration is affected (though
recently has disappeared, the popular
view that severation anterior in an acces-
sory muscle of respiration)
Latissimus dorsi C6 – C8 Thoracod- Patient is asked to clasp the hand behind his • In case of damage of paralysis, the addu-
orsal n back while the examiner standing behind the ctions, extension and medial rotation of
patient, offers passive resistance to the down- the shoulder as in swimming rowing,
wards and backward movement. Alternatively, climbing, pulling, folding the arm behind
the two posterior ancillary fields can be felt as the back are severely affected
the patient coughs
• Violent expiratory efforts like coughing,
sneezing, etc. are not possible
Trapezius C6 – C8 Thoracod- The upper part of trapezes is tested by asking In case paralysis elevation is not possible
orsal n the patient to shrug his shoulder, while the Retraction of scapula and abduction of arm
examiner tries to press it and down from beyond 90° becomes difficult
behind. The lower part of muscle can be
tested bu asking the patient to approximate
the shoulder blades
• Dorsiflexion by L5, S1 Deep pero- These are tested by asking the patient to ele- “Foot drop”
tibialis ant. neal n vateor depress the distal foot against
resistance

Contd...
Contd...
Muscle Cord segment Nerve supply Procedure Inference
• Plantar flexion of feet S1 S 2 Tibial n
and toes by gastroc- (both)
nemius and soleus
Extensors of the knee
a. Quadriceps femoris L2,3,4 Femoral n Patient is asked to bend up the knee then he Look for the atrophy of quadriceps musc-
is made to straighten the knee against the ulature
resistance offered by the examiner (over the
skin)
Flexors of the knee
a. Biceps femoris L5, S1, S2 a. Long head Patient is asked to raise one of the legs from Normally the muscle is stronger so that
by tibial part the bed, while the examiner supports the thigh examiner is unable to overcome its stre-
of sciatic with his left hand and holding the ankle with ngth
nerve his right. Then patient is made to bend the
b. Short knee against the resistance
head by per-
oneal part of
sciatic nerve
b. Semitendinosus L5, S1, S2 Tibial part
of sciatic
nerve
c. Semimembranosus L5, S1, S2 Tibial part
of sciatic
nerve
Extensors of the hip
a. Gluteus maximus L5, S1, S2 Inferior gl- Patient is made to extend his knee and to lift Normally the examiner is unable to over-
uteal n his foot off the bed, then he is made to push come this movement
it down against the examiner’s resistance
Flexors of the hip
a. Psoas major L2, L3 and Branches The patient is made to extend his legs raise
sometimes L4 from (roots) off his leg off the bed against resistance
of spinal n
L2 L3 and L4
b. Iliacus L2, L3 Branches Alternatively, the related movements of flexion
from femo- of the thigh, with the thigh already flexed to a
ral n right angle, can be tested

Contd...
Central Nervous System 209
Contd...
Muscle Cord segment Nerve supply Procedure Inference
Adductors of thigh
Adductor longus, L2, L3, L4 Obturator Patient is asked to abduct the limb first and then
brevis and magnus nerve made to bring it back towards midline against
resistance
Abductors of thigh
Gluteus medius L5, S1 Superior After placing the patient’s legs together. The
and minimus L5, S1 gluteal n (to patient is asked to separate them against
both) resistance
210 Essentials of Clinical Medicine

Rotators of thigh
a. Medial rotation
• Tensor fascia L4, L5 Sup. gluteal After extending the limb of the patient, he is
latae n asked to roll it outwards or inwards against
• Ant. fibers of L5, S1 Sup. gluteal resistance
gluteus medius n
and minimus
b. Lateral rotation
• Obturator L5, S1 Nerve to
obturator
internus
• Quadratus femoris L5, S1 Nerve to
quadratus
femoris
• Gemelli L5, S1 Nerve to
obturator
internus and
quadratus femoris
 Central Nervous System 211

– It is always due to corticospinal pathway lesion. and radiculopathy and lumbar radiculopathy (with sensory
Therefore, it is an upper motor neuron lesion. abnormalities).
(UMNL)
2. Crossed paralysis FUNCTIONAL WEAKNESS
– Weakness in an ipsilateral cranial muscle group with This should be considered when:
a contralateral hemiparesis. 1. The weakness is not in a distribution that can be
– It is branistem disease sign. understood on an anatomical basis.
3. Paraplegia 2. When there are no changes in reflex or tone.
– Paralysis of both the lower limbs. 3. The movements are very variable and power erratic.
– Almost always due to spinal cord lesion. Therefore, 4. There is a difference between the apparent power of
it is upper motor neuron lesion (UMNL) moving a limb voluntarily and when power is being tested.
4. Monoplegia Power when tested is graded conventionally using the
– Paralysis of one limb. It may affect arm (brachial Medical Research Council (MRC) scale. This is usually
monoplegia) or the leg (crural monoplegia). amended to divide grade 4 into 4 + and 4–, as below:
– It is due to root or plexus disease. • 5 = Normal power
5. Quadriplegia • 4+ = Submaximal movement against resistance
– Paralysis of all the four limbs. • 4 = Moderate movement against resistance
– A feature of cervical cord disease. • 4– = Slight movement against resistance
Other Patterns of Muscular Weakness • 3 = Moves against gravity but not resistance
• Myasthenic weakness • 2 = Moves with gravity eliminated
• Neurogenic weakness • 1 = Flicker
• Peripheral neuropathy • 0 = No movement.
• Myopathic weakness Power should be graded according to the maximum
• Myotonia. power attained, no matter how briefly this is maintained.

Another Way of Classifying Muscular Weakness Approach to Weakness

There are five patterns of muscular weakness: Consider distribution and whether upper or lower motor
1. Upper motor neuron (UMN)—increased tone, increased neuron or muscular.
reflexes, pyramidal pattern of weakness (weak extensors
in the arm, weak flexors in the leg). Weakness in General
2. Lower motor neuron (LMN)—wasting, fasciculation, (Limbs and Cranial Nerves)
decreased tone and absent reflexes. Diffuse disease of:
3. Muscle disease—wasting, decreased tone, impaired or • Nerve Polyradiculopathy
absent reflexes • Neuromuscular junction Myasthenia gravis
4. Neuromuscular junction—fatiguable weakness, normal • Muscle Myopathy
or decreased tone, normal reflexes. Weakness all Four Limbs
5. Functional weakness—normal tone, normal reflexes
• Upper motor neuron Cervical cord lesion
without wasting with erratic power.
Brainstem lesion
The level of the nervous system affected can be
Bilateral cerebral lesions
determined by the distribution and pattern of the weakness
• Lower motor neuron Polyradiculopathy
and by associated findings (see Table 8.29).
Peripheral neuropathy
Examples of brainstem sign (all contralateral to the upper
• Mixed upper and lower Motor neuron disease
motor neuron weakness): third, fourth and sixth palsies,
motor neuron
seventh lower motor neuron loss, nystagmus and dysar-
• Myopathy
thria.
Hemisphere signs: aphasia, visual field defects, inattention Unilateral and Leg Weakness
or neglect, higher function deficits. • Upper motor neuron Hemisection of cervical
Mixed UMN and LMN lesions: motor neuron disease cord
(with normal sensation), or combined cervical myelopathy N.B. sensory signs
212 Essentials of Clinical Medicine

Brainstem lesion • Calf tenderness.

Weakness Both Legs
• Upper motor neuron
• Lower motor neuron
Single Limb
• Upper motor neuron
• Lower motor neuron
Patchy Weakness
Upper motor neuron
Lower motor neuron
Variable Weakness
Non-anatomical
distribution
PERIPHERAL NEUROPATHY
N.B. brainstem signs
Cerebral lesion
N.B. hemisphere signs.
Spinal cord lesion
Cauda equina lesion
N.B., sphincter involve-
ment in both
Lesion above highest
involved level
N.B. other signs may
help localize
Single nerve =
Mononeuropathy
Single root =
Radiculopathy
Multiple CNS lesions
Polyradiculopathy
Multiple single nerves =
mononeuritis multiplex
Consider functional
weakness
• Flaccid paralysis (weakness) especially in lower limb
with foot drop.
• Pes cavus in early onset, familial neuropathies.
• Vasomotor and tropic changes like edema, dryness,
desquamation, etc.
• High steppage gait.
• Enlargement of peripheral nerves in chronic
demyelinating neuropathies, as in leprosy (Hansen’s
disease)
• Distal burning pain in small fibers neuropathies, e.g.
diabetes mellitus.
Table 8.30: Classification of peripheral neuropathy
Type Evolution Causes
I. Axonal
1. Acute Days to weeks Porphria
Massive intoxications (Arse-
nic inhalation)
Mostly toxic or metabolic
polyneuropathies
2. Subacute Weeks to months < 5 yr, consider toxic/meta-
bolic causes.
3. Chronic Months to years > 5 yr, consider toxic/meta-
bases, also diabetic and dys-
proteinemic causes
II. Demyelinating causes
1. Acute Days to weeks Almost all are the common
form of GBS
2. Subacute Weeks to months Mostly relapsing form of CIDP
3. Chronic Months to years Many possibilities including
hereditary inflammatory autoi-
mmune dysproteinemia, other
metabolic and toxic causes of
neuropathies

Definition An injury to peripheral nerves is classified according to the

A disorder of peripheral nerves, either sensory, motor
autonomic mixed, symmetrical and affecting the distal parts
of limbs more than the proximal. It is general term indicating
peripheral nerve disorders of any cause.
Clinical Features of Peripheral Neuropathies
• Bilaterally symmetrical distal weakness and wasting.
• Symmetrical distal sensory deficit.
• Loss of tendon reflexes, the generalized loss occurs in
demyelination neuropathies and distal loss of reflexes
occurs in axonal (dying back) neuropathies.
• Tingling and numbering sensation at the onset, superficial
sensory.
• Anesthesia is especially of glove and stocking (i.e.
present over the distal part of the extremities).
• Tremor of outstretched fingers in chronic neuropathy.
degree of involvement.
1. Neuropraxia: Characterized by no structural change of
axon and quick recovery within days weeks (conduction
block)
2. Axonotmesis: Characterized by loss of axon continuity
and slow recovery (month and years)
3. Neurotmesis: Entire separation of nerve and connective
tissues due to injury. The recovery is incomplete and
poor.
Another way of classifying peripheral neuropathy is as
follows:
1. According to mode of onset and rate of progression
a. Acute onset (< 1 week, e.g. Guillain-Barré
syndrome)
b. Subacute onset (1 week – 1 month)
c. Chronic onset (> 1 month CIDP)
d. Relapsing (multiple episodes after acute and subacute
onset)
 Central Nervous System 213

2. According to types of nerve fibers involved Along with JPS, and two point discrimination the
a. Motor disorders of touch, pain and temperature perception
b. Sensory (hypoesthesia, dysesthesia and hyperesthesia) are also
c. Autonomic common in peripheral neuropathies and nerve injuries,
d. Mixed discogenic radiculopathies and spinal injuries.
3. According to size of nerve fibers In case of individual peripheral nerves or sensory nerve
a. Large (posterior column) root lesion, the subjective feeling of membrane and
b. Small (pressure and temperature) diminution of all sensory modalities develop in their areas
c. Mixed of distribution. An incomplete or partial lesion of peripheral
4. According to distribution nerve causes pain of a burning, unpleasant quality, as in
a. Proximal
causalgia, a condition occurring infrequently after injury to
b. Distal
either the median or the sciatic nerve. In polyneuropathies
c. Diffuse
the numbness or paresthesia and objective sensory features
5. According to clinical pattern of involvement
a. Mononeuropathy affect the distal parts of the limbs and often involve the legs
b. Mononeuritis multiplex before the arms.
c. Radiculopathy
d. Symmetrical sensory motor neuropathy General Assessment in Case of
e. Symmetrical sensory neuropathy Peripheral Neuropathy
f. Autonomic neuropathy (DM) (or inquiries made into a case of peripheral
g. Secondary to systemic disorders neuropathy)
6. According to pathology You should inquire about:
a. Axonal • Diabetes
b. Demyelination • Alcohol intake (addition)
c. Mixed.
• Drug consumption like amiodarone, vincristine
Usually, the vibration sense over the bony prominences
• Renal symptoms
gets impaired as the age advances and is often lost at the
• Travel
ankles over the age of 70. However, in certain cases, the
loss of vibration sense is seen in some patients at a stage • Weight loss
earlier than impairment of JPS. A very good example of it is • Dietary inquiry like folate deficiency.
diabetic peripheral neuropathy. Joint position sense (JPS) is You should examine for:
most commonly impaired in patients with large fiber • Diabetic retinopathy.
peripheral neuropathies and spinal and disorders • Butterfly rash over the face.
(myelopathies) affecting the dorsal columns. JPS disturbance • Smooth tongue.
may occur without paresis also. • Goiter
In such patients, the following findings may be noted: • Carcinoma of bronchus.
• Impairment of fine-finger function and alterations of • Liver and spleen pathology.
gait as a result of loss of feedback concerning muscle • Nerve thickening (leprosy—Hansen’s disease)
activity and joint position. • Small kidneys
• When finger nose test is carried out with the eyes closed, • Bone marrow dysfunctions
the sensory ataxia is noted. • Clubbing of fingers.
• Rhomberg’s test is positive. • Burns/ulcers/scars/injuries
• The patient may fall when he is required to perform • Vascular bruits
movements that require complex postural adjustments • Ulcer over the foot
such as walking in the dark room. • Distal muscle wasting in any of the four limbs.
• When the patient is made to close his eyes with his
hands outstretched, his fingers may make small slow Ruling out Myasthenia Gravis
movements (pseudoathetosis)
In certain peripheral neuropathies, especially those Diagnosis of Myasthenia Gravis
involving large sensory fibers, and in cervical mylo- History of:
radiculopathies, the two-point discrimination test in the • Diplopia, ptosis, weakness
fingers is impaired. • Weakness in characteristic distribution
214 Essentials of Clinical Medicine

• Fluctuation and fatigue, which worsens with repeated 3. Infiltration

activity and improved by rest – Neoplastic
• Effects of previous treatments. – Amyloidosis
Physical Examinations – Xanthomatosis
• Ptosis diplopia 4. Immune reactions
• Motor power examination, muscle strength testing – Vaccinations
• Forward arm abduction time (5 min) – Foreign proteins and sera
• Vital capacity (breathing) 5. Injury
• Absence of other neurological signs. – Trauma
Laboratory Testing 6. Idiopathic
• Anti-ACh R radioimmunossay—90 percent positive in – Brachial plexopathy
generalized MG, 50 percent in ocular MG, definite Causes of Polyneuropathies
diagnosis of positive, negative result does not exclude
MG. • Alcohol
• Edrophonium chloride (Tensilon) 2 mg + 8 mg, highly • Vit. B. def. (B1, B6 and B12)
probable diagnosis of positive. • Connective tissue disease—RA, SLE, PAN
• Repetitive nerve stimulation test—decrement of >15 • Drugs—INH, methotrexate, dapson, nitrofurantoin,
percent at 3 hertz (Hz) is highly probable. vincristine, phenytoin.
• For ocular or cranial MG—exclude intracranial lesions • Endocrine and metabolic causes—DM, acromegaly,
by CT or MRI uremia, porphyria, CRF, amyloidosis
• Familial—peroneal muscular atrophy, hereditary,
Some Basic Terminologies sensory, Déjérine-Sottas, familial hypertrophic poly-
neuropathy.
1. Mononeuropathy—process affecting a single nerve. • Growth—malignant disorders, lymphoma, myeloma.
2. Mononeuritis multiplex—process that affects several or • Heavy metals—arsenic, lead, gold, silver, mercury.
multiple nerves asymmetrical. • Inoculations and injections—antisera
3. Polyneuropathy—diffuse symmetrical disease process • Infections—leprosy, diphtheria
usually progressing proximally. It may be motor, sensory, • Acute idiopathic polyneuritis, chronic idiopathic poly-
sensor motor (mixed or autonomic). neuritis, HIV infection.
4. Radiculopathy—a process affecting nerve roots.
History Taking in a Case of Peripheral Neuritis
Causes of Mononeuropathy
1. Entrapment: Median nerve in carpal tunnel, lateral Signs and Symptoms of Peripheral Neuritis
cutaneous nerve at inguinal ligament. Symptoms
2. Compression: Saturday night palsy, compression of radial • Pin and needle prick sensation.
nerve against humerus. • Burning sensations over hands and feet.
3. Others causes: Injection, trauma, fracture, operation, • Difficulty in walking in the dark.
penetrating injuries. • Muscle weakness with wasting, which is peripheral in
Causes of Mononeuritis Complex distribution.
1. Inflammatory Signs
– Leprosy • Areflexia ankle jerk is the first one to be affected.
– Sarcoidosis • Stock and glove anesthesia.
2. Insufficiency (vascular) • Posterior column affected.
– Diabetes • Bilateral 7th cranial nerve involvement (GBS)
– Rheumatoid arthritis • Rhomberg’s sign is positive.
– Polyarteritis nodosa (PAN) • Gait is of high stepping type.
– SLE • Trophic changes due to loss of protective pain sensation
– Systemic sclerosis which ultimately leads to ulcers, neuropathic joint,
– Wegener’s granulomatosis degenerations.
 Central Nervous System 215

Table 8.31: Causes of acute and chronic axonal polyneuropathy • Alcoholism

Causes of acute axonal Causes of chronic axonal • Carcinoma
polyneuropathy polyneuropathy • Amyloidosis
• Porphyria (commonest) • Diabetes mellitus • Tetanus
• Uremia • Uremia • Shy-Drager syndrome
• Hypoglycemia • B12 deficiency • Multiple sclerosis
• Aurothioglucose (antirheumatic • Primary billary cirrhosis • Taber dorsalis
drug) • COPD
• Disulfiram • Malabsorption syndrome Clinical Features of Autonomic Neuropathy
• Arsenic • Lymphoma
• Polycythemia Negative Phenomenon (Loss of Certain Functions)
• Drugs – Dafsone, Disulfiram,
• Dry mouth and dry eyes due to failure of salivary and
Hydralazine, INH, Phenytoin,
Pyridoxine
lacrimal secretion.
• Inorganic lead • Anhydrosis
• Hypothermia
Causes of Subacute Axonal Polyneuropathy • Faintness or syncope due to postural hypotension
• Bladder atony
• Uremia • Blurring of vision due to lack of pupillary and ciliary
• Hypoglycemia reflexes.
• Vitamin deficiency exclude B12 • Impotence
• Carcinoma • Retrograde ejaculation.
• Lymphoma including Hodgkin’s
• Cisplatinum, disulfiram, vincristin Positive Phenomenon
(Exaggeration of Certain Conditions)
• Arsenic
• Thallium (rat poison). • Hypertension
• Tachycardia
Causes of Acute Demyelinating • Bradycardia
Polyneuropathy • Hyperhydrosis (?)
• Diarrhea.
• Lymphoma
• Aurothioglucose (antirheumatic drug) Differential Diagnosis of Thickened
• Buck thorn (toxic berry) intoxication Nerves and Neuritis
• Diphtheria. 1. Charcot-Marie-Tooth disease peroneal muscular
atrophy heriditary motor sensory neuropathy type I
Causes of Carpal Tunnel Syndrome and II are collectively called Charcot-Marie-Tooth
syndome.
• Occupational causes and condition
2. Amyloidosis (primary)
• Pregnancy
3. Leprosy
• Acromegaly
4. Acromegaly
• Hypothyroidism
5. Neurofibromatosis
• Rheumatoid arthritis
6. Diabetes mellitus
• Tenosynovitis arthritis
7. Déjérine-Sottas disease
• Amyloidosis.
8. Idiopathic
9. Refsum’s syndrome
AUTONOMIC NEUROPATHY (DYSAUTONOMIA)
10. Sarcoidosis.
The condition of autonomic neuropathy may be acute, sub- * Note - Synonyms of Guillain-Barré Syndrome (GBS)
acute (viral) or chronic. Chronic condition is more common. • Acute infective polyneuritis.
• Acute inflammatory demyelinaling polyradiculoneuro-
Causes pathy.
• Diabetes mellitus • Acute idiopathic polyneuritis.
• GBS • Acute immune-mediated polyneuritis.
216 Essentials of Clinical Medicine

• Ascending paralysis of Landry. Unilateral:

• Landry-Storhl-Guillain-Barré syndrome. – In wrist—carpal tunnel
Guillain-Barré syndrome is probable cell-mediated – In shoulder—thoracic inlet syndrome
immune response (CMI) directed at myelin sheath. There – Local pathology of an individual nerve.
is a genetic predisposition to HLA DR – 3 in acute condition. Tingling in Lower Limbs
Bilateral:
Diagnosis of a Case of Alcoholic Neuropathy – Glove stocking—peripheral neuropathy
Patients gives a history of alcoholic, polyneuritis associated – Tingling move on exertion, lumber canal stenosis.
with alcoholic hepatic cirrhosis, parotid swelling, alcoholic Unilateral:
gastritic. The condition is more common in middle-aged – Lumbar disk prolapse
males. It results from both thiamine deficiency and direct – Tumors
– Comprehensive lesion.
effects of ethanol and/or acetaldehyde. The presenting chief
complaints of the patients is usually bilateral limb numbness, Tarsal Tunnel Syndrome
tingling, paresthesias, more distally than proximately,
A type of mononeuropathy due to involvement of posterior
generally, the association with other neurological deficit like
tibial nerve (L5 S2). Near medial malleolus, clinically pain,
Wernicke’s encephalopathy, delirium tremens, Korsakoff’s
numbness of sole and weak toe flexors are present.
psychosis and alcoholic dementia is also seen.
Table 8.32: Differences between polyneuritis and myelopathy
Nigerian Ataxic Neuropathy Polyneuritis Myelopathy
It is a type of peripheral neuropathy in which features other Sensory changes Stock and glove Upper level
Reflexes Lost Present, lost lately when
than neuropathy are also present such as posterior column muscle atrophy occurs
degeneration, sensory neural deafness and optic atrophy. Weakness Distal Proximal
The basic pathology suggested behind it is the interference
with vit. B12 metabolism by cyanide derived from cassava Table 8.33: Differences between axonal and segmental myelopathy
in diet along with nutritional deficiency. Axonal Segmental
Nerve cell body and axon Schwann cell degeneration
Neuropathies Occurring with Pregnancies degeneration demyelination with intact axons
Wallerian degeneration following Rapid recovery
• Bell’s palsy crush injury Recovery slow
• Carpal tunnel syndrome Crush injury, ischemia, nutritional, Diphtheria, diabetes, GBS are the
• Maralgia paresthetica [It is an entrapment neuropathy lead, thalium are causes causes
No nerve thickening Hypertrophy of nerves may
resulting from compression of cutaneous nerve of thigh
occur
(L2,3) as it passes under the inguinal ligament commonly
seen in obese people].
POEMS SYNDROME
• Injury to pelvic nerve during vaginal hysterectomy or
lower abdominal surgery. This syndrome is associated with solitary plasmacytoma
• Obturator neuropathy related to difficult labor. and myeloma with osteosclerotic features.
• Foot drop due to peroneal nerve lesion at the level of • P — Polyneuropathy
knee or due to proximal lumbosacral compression after • O — Organomegaly
prolonged labor or instrumental delivery. • E — Endocrinology
• M — M-protein
Differential Diagnosis of • S — Skin changes.
Tingling and Numbness This neuropathy which occurs with solitary plasma-
It usually transits in a normal person after prolonged hours cytoma is different from those related with multiple myeloma
of sitting (due to neuropraxia). with lytic or diffuse osteoporotic bone lesion, i.e. the above-
mentioned neuropathy.
Tingling in Upper Limb • Responds to radiation or removal of primary lesion
Bilateral: • Are frequently demyelinating
– Along cervical roots—cervical spondylosis • Associated with monoclonal proteins and light chains
– Glove stocking—polyneuropathy peripheral (Kappa)
 Central Nervous System 217

• Occurs in association with other systemic findings

(POEMS syndrome).

CLINICAL FEATURES OF RADIAL NERVE INJURY

• Radial nerve — Root value C 5, 6, 7, 8
— Innervates
– Triceps
– Brachioradials
– Extensor Carpi
– Radials longus
— Through posterior interosseous n:
– Extensor carpi radialis
– Supinator
– Extensor of thumb
– Extensor indicis
• Sensation — Lower half of radial aspect of arm
and middle of posterior aspect of
forearm and radial aspect of dorsum
of hands
• Sites of —
injury — At axilla
— Mid-third of arm
— Posterior interosseous nerve
• Compression at axilla
Cause:
– Use of crutch
– Arm of an anesthetized patient allowed to be drawn Fig. 8.18: Branches of radial nerve
over edge of operation table
C/F: — Most muscles of thenar eminence
– Paralysis of all muscles supplied by radial nerve — 2 Radial lumbricals
mainly triceps leading to loss of extension at elbow Clinically — Inability to flex index finger, distal phalanx
• Compression of nerve in mid-third of arm against of thumb
humerus- Saturday night palsy. Triceps is spared but
— Flexion of middle finger, distal phalanx
brochioradialis, supinator and forearm extensors
of thumb
paralyzed.
— Opposition of thumb is defective
• Lesion of posterior interosseous nerve—weakness
— Ulnar deviation with index and middle
confirmed to abduction and extension of thumb and
finger more extended and thumb lies in
extension of index finger (Fig. 8.18).
same plane as fingers. Pronation is
CLINICAL MANIFESTATION OF MEDIAN incomplete, defective.
NERVE INJURY Ochsner’s
clasping test— Is inability to flex interphalangeal joint of
(Laborer’s nerve injury) index finger when hands clasp each other
Median nerve root value—C6,7,8 and T1 Sensory — Involves lateral three and a half digits and
• Lesion in forearm (at elbow) loss lateral aspect of palm
• Lesion at wrist (crapel tunnel syndrome) — Vasomotor and trophic changes are seen
• Lession in forearm (at elbow): • Lesion at wrist—carpal tunnel syndrome:
Motor — Paralysis of pronator teres, radial flexor – Compression of median nerve as it passes deep to
of wrist, long flexor of fingers except flexor retinaculam. Usual presentation is acroparae-
ulnar half of deep flexor thesia, i.e. numbness, tingling, burning sensation felt
218 Essentials of Clinical Medicine

in hand and fingers, it occurs more at night and is extension of metacarpophalangeal joint along with flexion
relieved by shaking hand at interphalangeal joint.)
– Sensory loss—occurs over tips of median innervated Froment’s sign: Consist of thumbs flexion excessively at
fingers (Fig. 8.19). interphalangeal joint when the patient attempts to pinch.
Sensory loss: Dorsal and palmar aspects of medial side of
CAUSES AND CLINICAL MANIFESTATIONS OF hand and half fingers.
ULNAR NERVE INJURY (MUSICIAN’S NERVE)
Lesion at the Wrist or Hand
Lesion at Elbow
Cause
Causes • Compression by ganglion.
• Entrapment of nerve in cubital fossa in heavy manual • Repeated occupational trauma.
workers.
Clinical Features
• Tordy—ulnar palsy occurs due to excessive carrying
Motor:
angle at elbow following previous malunited supra-
• Damage to nerve at wrist spares the dorsal branch so
condylar fracture of humerus.
that cutaneous sensations over dorsum of hand and
• Osteoarthritis elbow. fingers are spared.
Clinical Features • But lesion just proximal to wrist gives rise to sensory
1. Ulnar flexion of wrist aspect of hand and fingers alone along with weakness
2. Paralysis of flowers of terminal phalanges of the ring of all ulcer innervated intrinsic hand muscles (Fig. 8.20).
and ulnar finger (flexor digitorum profundus). • Right upper brachial plexus birth injury leading to right-
3. Muscles of hypothenar eminence (is abductor flexor sided Erb’s palsy. There is a paralysis of shoulder
and opponens minimi digiti) are paralyzed. abduction, external rotation of the arm, and paralysis of
4. Abductor pollicis muscle it also affected. forearm supination leading to a characteristic “porter’s
5. Palmaris brevis is also involved. tip” (or policeman’s tip) position of the right hand.
6. Involvement of all interosseous and inner two lumbricals Difficult delivery is a common cause of acute injury to
involvement results in claw hand deformity (i.e. peripheral nerves.
Table 8.34: Differences among myelopathy, neuropathy and myopathy
Myelopathy Neuropathy Myopathy
Age Any age Any Age Childhood
Tingling and Rare Present Never seen
numbness
Bladder and Occurs Usually absent Never occurs
bowel affect
Atrophy and Only atrophy Only atrophy Both present
pseudoatrophy
Bilaterally May be Usually Yes
symmetrical
Cranial nerve None GBS, Diphtheria Yes, 7th n affec-
involvement ted in some
Girdle-like Present Absent Absent
sensation
Sensory Upper level seen Stock and glove No sensory
involvement change seen
Motor According to Distal Proximal
involvement level of
involvement
occur
Tone Spastic Hypotonia Hypotonia
Deep reflexes Exaggerated Lost Normal
Plantar Extensor Flexor or no Flexor
response
Confirmation Myelography N.conduction EMG
Fig. 8.19: Branches of median nerve studies
 Central Nervous System 219

hypertrophied. He should also see for fasciculation at the

same time. Fasciculation indicates a chronic degeneration
of anterior horn cells or motor neuron supplying the muscles
and is very helpful in localization of site of lesion. It is seen
in motor neuron disease, syringomyelia, cervical spondylosis,
thyrotoxic myopathy and peroneal muscular atrophy.
Wasted or atrophic muscles are not only smaller, but
also softer and more flabby than normal when they are in a
contracted state. When fibrosis accompanies the muscular
wasting (as in case of muscular dystrophy or polymyositis)
the muscles feel hard and inelastic. They may show
contractures.
If there seems to be any asymmetry, then the muscles
should be measured on both sides by noting the circum-
ference of the limb at an equal distance from a fixed bony
symmetrical point on both sides.

Hypertrophy of Muscles

Fig. 8.20: Branches of ulnar nerve

In some cases of Duchenne’s muscular dystrophy (DMD)
hypertrophy of muscular, especially calf muscle, buttocks,
Table 8.35: Causes of motor and sensory neuropathy i.e. gluteus muscles, and infraspinati is seen; in spite of
Motor neuropathy Sensory neuropathy hypertrophy, these muscles are weak in strength (pseudo-
• Acute idiopathic polyneuritis • Amyloidosis hypertrophy).
• Lead poisoning • Vit. B, def.
• Peroneal muscle atrophy • Diabetes Muscle Wasting
• Porphyrias • Hereditary
• Infection like diphtheria sensory neuropathy Generalized Muscle Wasting
• CRF heavy metals like gold • Advanced motor neuron disease
leprosy
• Myopathies
• Spinal muscular atrophy.
Table 8.36: Differences between somatic and neuropathic pain
Somatic pain Neuropathic pain
Wasting of Proximal Group of Muscles
1. Nociceptive stimulus is usually No obvious nociceptive stimulus • Fascio-scapulo-humeral dystrophy.
evident • Limb girdle atrophy.
2. Pain is well localized, visceral Poorly localized • Myotonia dystrophica affecting the facial muscles,
pain may be referred sternocleidomastoids and quadriceps are mainly involved.
3. Pain is similar to other somatic Pain is unusual, dissimilar from
• Syringomyelia (due to spinal cord lesions)
pains somatic pain
4. Relieved by anti-inflammatory or Only partially relieved by • Compression of cervical cord causing the atrophy of
narcotic analgesics narcotic analgesics shoulder girdle muscles and compression of corres-
ponding roots in cauda equina syndrome causes atrophy
EXAMINING THE BULK OF THE of glinted muscles.
MUSCLE (NUTRITION) Wasting of Distal Groups of Muscle
Before carrying out the details of neurological examination, (in upper limb and lower limb)
the clinician should spend some time in general inspection Upper limb: Wasting of small muscles of hands and forearm.
of musculature of the body [Figs 8.21(1) to 8.21(31), Plates a. Lesion of anterior horn cells
13 to 18]. Muscle bulk is best assessed clinically by – Motor neuron disease
inspection and palpation both. Muscle nutrition testing – Syringomyelia
should be carried out not only in the lying down position, – Compression of cervical cord
but if possible in both sitting as well as standing positions. – Poliomyelites
Then the examiner should try to determine whether the – Progressive muscular atrophy
muscle being tested is normal, wasted/atrophied or – Spinomuscular atrophy
220 Essentials of Clinical Medicine

b. Spinal cord lesion Contd...

– Motor neuron disease Etiology Associated features Common cause
– Syringomyelia Hypokinesia
c. Vertebral lesion 3. Myopathies Muscle wasting • Hereditary conditions
– Craniovertebral anomalies (usually proximal) (e.g. muscular dystrophy)
– Vertebral metastasis. Hypotonia • Alcohol and other toxins
Tenderness (myositis)
d. Root lesion (radicolopathy) 4. Psychological Inconsistent weakness • Stress
– Cervical spondylitis No associated • Anxiety
– Cervical cord tumor features • Compensation claims
– Cervical hypertrophic pachymeningitis
– Neurologic amyotrophy TONE OF MUSCLES (OR TONUS)
e. The brachial plexus
It is defined as the state of slight contraction usually present
– Injury
in muscles that contribute to posture and coordination. It is
– Cervical rib compression of brachial plexus.
an ability of the muscles to resist a force for a considerable
f. Peripheral nerve lesions (neuropathies)
period or time without change in length.
– Leprosy
The degree of tone is assessed by handling the limbs
– Carpal tunnel syndrome
and moving them passively at various joints. The maintenance
– Lead paralysis
of tone is the function of a spinal reflex arc (formed by
– Diphtheria
afferents from primary and secondary endings of muscles
g. Myoneural junction
to anterior horn cells and efferents back to the muscles.
– Eaton-Lambert syndrome
Tone is lost/damaged if this reflex arc is damaged. Muscle
h. Muscle disease
tone is mainly regulated by the corticospinal and
– Muscular dystrophy
extrapyramidal tracts.
– Polymyositis
If the motor nerve to a muscle is cut, the muscle offers
– Myotonia
very little resistance and is said to be flaccid. A hypertonic
i. Disuse atrophy
(spastic) muscles is one in which the resistance to stretch
– Therapeutic immobilization—fracture, etc.
is high because of hyperactive stretch reflexes. Some of
– Arthritic: Rheumatoid arthritis (RA)
the states of flaccidity and spasticity is the ill-defined area
– Postparalytic
of normal tone. The muscles are generally hypotonic when
j. Wasting due to systemic causes
the rate of referent discharge is low and hypertonic when it
– Tuberculosis
is high.
– Malignancy
– Thyrotoxicosis
Lengthening Reaction
– HIV infection or AIDS
– Addison’s disease. When the muscles are hypertonic, the sequence of modern
Peripheral wasting in both upper and lower limbs is seen stretch—muscle contraction, strong stretch—muscle
mainly in chronic peripheral neuritis (alcoholic, diabetes, or relaxation is clearly seen; for example, passive flexion of
vitamin deficiency being the main causes) and in peroneal elbow meets immediate resistance as a result of stretch
muscular atrophy. reflex in triceps muscles. Further stretch activates the
inverse stretch reflex. The resistance to flexion suddenly
Table 8.37: Causes of muscle weakness
collapses and arm flexes. Continued passive flexion stretches
Etiology Associated features Common cause the muscle again, and the sequence may be repeated. This
1. Lower motor Muscle atrophy • Peripheral neuropathy sequence of resistance is followed by when limb is moved
neuron Fasciculation • Radiolopathies passively, and is called clasp knife effect because of its
Reflexes absent or • Ant horn cell damage
resemblance to closing of a pocket knife. The physiologic
diminished
Hypotonia • Motor neurone disease name for it is the lengthening reaction because it is the
2. Upper motor “Patterned” • Cerebrovascular like response of a spastic muscle (in the example cited above,
weakness hemiplegia the triceps) to lengthening.
Little or no muscle • Spinal injury or disease
washing (e.g. paraplegia) Clonus
Hyper-reflexia • Multiple sclerosis
Hypertonia, Another finding, characteristic of status in which increased
Contd... or afferent discharge is present, is clonus. This neurological
 Central Nervous System 221

sign is the occurrence of regular, rhythmic contractions of in Table 8.39. Spasticity in the upper limb is frequently
a muscle subjected to sudden, maintained stretch. Ankle more obvious in attempted extension; whereas in
clonus is a typical example. This is initiated by brisk. the lower limb, it is more obvious with attempted
maintained dorsiflexion of the foot, and the response is flexion.
rhythmic plantar flexion at the ankle. The stretch reflex b. Rigidity: Refers to sustained resistance to passive
inverse stretch reflex sequence described above may movements. It is more frequently encountered in
contribute to this response. However, it can occur on the patients with Parkinson’s disease (who have other
basis of synchronized motor neuron discharge without golgi manifestations of this disorder such as bradykinesia,
tendon organ discharge. The spindles of the tested muscle tremor, gait and postural abnormal). The rigidity may
are hyperactive and burst of impulses from them discharge be of lead type or the cogwheel type.
all the motor neurons supplying the muscle at once. The 2. Hypotonia: In the upper limb, the hypotonia is evident
consequent muscle contraction stops spindle discharge. from the posture of the outstretched hands, with slow
However, the stretch has been maintained, and as soon as flexion at wrist and extension of the fingers (dinner fork
the muscles relaxes, it is again stretched and the spindle deformity). It is a feature of LMNL, cerebellar disorders
stimulated. and in chorea. The causes of hypotonia are described in
Although a few beats of clonus are present in some Table 8.39. It is associated with hyporeflexia, muscle
normal people, sustained clonus indicates damage to the wasting and paresis. Hypotonia is also seen transiently
upper motor neurons and is a sure-shot neurological sign. in the initial phase following capsular cerebrovascular
accident in which the plegic (weak) limb is atonic prior
Examination of Tone to becoming spastic and hyper-reflexes.
Clonus: Described earlier.
The patient is asked to relax the muscles. Then the examiner
Dystonia: The patients maintain posture at extreme of
passively flexes and extends each joint in turn, slowly at
movement with contraction of agonists and antagonists.
first and then more rapidly to get a feel of muscle tension.
Percussion myotonia: It is demonstrated when a muscle
In the upper extremities the muscle tone is tested at shoulder,
dimples following percussion with patellar hammer. Most
elbow joint and wrist joint and in the lower limbs, by
commonly seen in abductor pollicis brevis.
internally and externally rotating the resting leg and by briskly
raising the patient’s knee off the bed and observing whether Table 8.38: Tests
the ankle is also raised off the bed. Tests Normal Hypotonia Hypertonia
Palpation of muscles Normal Flabby Rigid
Examination of Knee Clonus Posture of limb Normal Limp Stiff
Resistance to passice Normal Decreased Increased
The examiner sharply pushes the patella towards the foot
movements
while the patient lies supine and relaxed with knee extended Range of passive Normal Increased Decreased
following the initial jerk, exert sustained pressure with the movements
thumb and index finger in a downwards direction on the
patella. Table 8.39: Causes of hypertonia and hypotonia
Hypotonia Hypertonia
Examination of Ankle Clonus
Lower motor lesion Upper motor lesion
The examiner supports the flexed knee with one hand in the Cerebellar lesion Extrapyramidal lesion
popliteal fossa so that the ankle rests gently on the bed. Rheumatic chorea Hysterical
Using the other hand briskly dorsiflex the foot and sustain Hysterical Tetanus
Posterior column lesions tabes dorsalis Strychnine poisoning
the pressure. Deep sleep
Abnormal Findings Drugs—anesthetic, sedatives, hypnotics
Hypokalemia
1. Hypertonia: Manifests itself as rigidity or spasticity. Hypercalcemia
a. Spasticity: Characterized by increased resistance
during the first few degree of passive movements; REFLEXES
and as the movement is continued, the resistance
suddenly decreases. It is a feature of UMNL and is Testing of Reflexes
usually associated with increases deep tendon The term reflex is derived from a Latin word “reflexus”
reflexes, clonus, an anterior plantar reflex and typical meaning “bend back”. Reflex is an involuntary response to
pattern of weakness. Causes of hypertonia are given stimulus (an involuntary action) (Fig 8.22). Reflexes are
222 Essentials of Clinical Medicine

Fig. 8.22: The reflex arc

specific and predictable and are usually purposeful and

adaptive. They depend upon the integrity (completeness)
of neural pathway between the stimulation point and
responding point (a muscle of gland). This path is called
reflex arc in a simple reflex, it includes:
1. A sensory receptor
2. Afferent or sensory neuron
3. Reflex center in the brain or spinal cord
4. One or more efferent neurons and
5. An effector organ (a muscle or a gland). Fig. 8.23: The reflex arc and higher connections
Most reflexes are, however, complicated and include,
internuncial or associature neurons intercalated between
efferent and afferent neurons. which only one synapse is present between the afferent
and efferent neurons; for example, all the stretch reflexes
Note: The efferent neurons enter via the dorsal root or cranial like biceps, triceps or knee jerks are included in this
nerves and have their cell bodies in dorsal root ganglia (DRG) category.
or in homologus ganglia of cranial nerves. The efferent fibers b. Polysynaptic reflexes: Reflexes in which one or more
leave via the ventral root or corresponding motor cranial interneurons are present between afferent and efferent
nerves. neurons. For example, withdrawal reflexes, gross flexor
reflexes and gross extensor reflexes.
Bell-Magendie Law
In the spinal cord, the dorsal roots are sensory and ventral Monosynaptic Reflexes (or Tendon Reflexes)
roots are motor (Fig. 8.23). When a skeletal muscle with an intact nerve supply is
stretched, it shows contraction. This response (or
Classification of Reflexes
phenomenon) is called “the stretch reflex”. The time interval
Reflexes are classified as: between the application of stimulus and response production
a. Monosynaptic reflexes (The Stretch Reflex): Reflexes in is called “reaction time”. For a stretch reflex such as a knee

Fig. 8.24: Relationship of reflexes with sympathetic and
parasympathetic nervous system
jerk, it is usually 19 to 24 milliseconds (msec). Another
term that must be included here is the “central delay” which
is defined as the time taken for reflex activity to transverse
the spinal cord. The central delay for knee jerk is 0.6 to 0.9
msec; therefore, only it is clear that only one synapse could
have been traversed for this reflex activity. Thus, the stretch
reflexes are called monosynaptic reflexes (Fig. 8.24).
The most important feature of stretch reflex is that it is
highly developed in the antigravity muscles (like extensor
groups of muscles of legs and flexor group of muscles of
arms). Therefore, it plays a very important role in maintaining
body posture.
Short Description of Muscle Spindle and its
Neural Connections
Significance of Stretch Reflex in
Physiological Terms
1. Passive stretching of muscles causes the muscle spindles
to be stretched.
• Setting up of an action potential in sensory fibers.
• Frequency of action potential is in proportion to
degree of stretch.
• As a result, harder a muscle is stretched, the stronger
is the reflex contraction.
Central Nervous System 223
2. When whole of the muscle is stretched during stimu-
lation of afferents, additional action potentials are
generated in the sensory nerve due to further stretch on
central positions. The sensitivity of spindle fibers varies
with rate of (gamma) efferent discharge. Spindle
sensitivity increases to the rate of change of stretch due
to stimulation of efferent fibers (phasic or dynamic
component). Therefore, fibers are called dynamic
efferent fibers. And, spindle sensitivity increases to a
steady, maintained stretch when efferent fibers are
stimulated (tonic or static component). Therefore, fibers
are also called static efferent fibers. The rale of efferent
discharge is controlled by higher centers, receiving both
excitatory and inhibitory impulses.
Mechanisms by which Stretch Reflexes
Maintain the Body Posture
1. Length servo mechanism: (Negative feedback system)
It maintains posture by maintaining the muscle length
during body movements.
Normal muscle spindle length.
↓
Generation of action potentials (AP) in the sensory nerve
proportionate to the degree of stretching.
↓
Increase in the muscle fiber length.
↓
Stretching of muscle spindle.
↓
Increase in the discharge from the spindles.
↓
Stimulation of sensory nerve group (Ia) fibers.
↓
Stimulation of alpha-motor neurons in the spinal cord.
Decrease in muscle length due to muscle contraction.
↓
Muscles regain their normal shape.
2. Follow-up servo mechanism: Muscle spindle acts in
maintaining body posture by sustained contracton of
muscle. This occurs by the phenomenon of alpha-
gamma.
Coactivation
This is explained as follows:
Signals transmitted form the motor cortex or any other area
of brain
↓
reach to alpha-motor neuron
↓
Stimulation of alpha-motor neuron
224 Essentials of Clinical Medicine

↓ D. Fibers from cerebral cortex, and cerebellum reflexly

Also leads to stimulation of gamma-motor neurons inhibit the stretch reflex by stimulating inhibitory
[because both alpha and gamma motor neurons are reticular formation.
located in the (some) ventral horn, i.e. anterior horn of In normal healthy individuals the balance between
spinal cord. Therefore, they are called anterior motor facilitatory and inhibitory impulses converging on
neurons] gamma-efferent neurons shifts towards facilitation
↓ and stretch reflex remain facilitated.
Gamma-motor neurons supplies the peripheral part of
intrafusal fibers of muscle spindles Phenomenon of Reinforcement
The causes of contraction of intrafusal fibers:
Excitation of receptor zone (central area) of the intrafusal Jandressik’s Maneuver (Figs 8.25 and 8.26)
fibers from this central area, arise in the Ia In some cases, it is formal that the deep tendon reflexes like
↓
Fibers primary or annalo spinal endings
↓
This leads to information to the spinal cord and via the
motor supply to the muscles, then back to extrafusal
fibers of muscle spindles.
↓
Thus, by the initial contraction of intrafusal fibers, the
extrafusal fibers also come to contract.
↓
Contraction of muscles for action.
Brain areas for controlling gamma-efferent system: The
gamma-efferent system is excited primarily by the bulbo-
reticular facilitatory region of the brainstem, and
secondarily by the impulses transmitted into their area
from (a) cerebellum, (b) basal ganglia, and (c) cerebral
cortex. Since the bulboreticular facilitation area is
concerned with the antigravity contractions and also
because the antigravity muscles have especially high
density of muscle spindles, emphasis is given to the
possible or probable important role of gamma-efferent
mechanisms in controlling muscle contraction for
positioning the different parts of the body and for
damping the move-ment of the different parts of the
body.
Higher control of stretch reflex:
As the connection between the afferent and efferent
neuron is in the CNS (brain or spinal cord); therefore,
the activity in the reflex arc can be modified (inhibited
or facilitated) by higher centers.
A. Facilitatory reticular formation: Increases the dis-
charge of gamma-motor neurons and stretch reflex
become hyperactive.
B. Inhibitory reticular formation: Acts by inhibiting the
gamma-efferent neuron discharge thereby causing
decrease in spindle sensitivity.
C. Vestibular muscles: Acts by a direct action on the Fig. 8.25: Jandressik’s maneuver in relation to
alpha-motor neuron. higher centers of CNS

Fig. 8.26: Jandressik’s maneuver
knee jerk reflexes do not elicit without applying
reinforcement (also called Jandressik’s maneuver).
In this, the patient is asked to perform strong voluntary
muscular effort with the upper limb; for instance, he is
made to hook the fingers of the two hands together and
then pull them against one another as hard as possible or he
may be asked to clench fist with the ipsilateral hand.
Mechanism of action of the reinforcement maneuver is to
increase the excitability of alpha-motor neurons and to
increase the sensitivity of the muscle spindle primary sensory
ending to stretch (by increased gamma-efferent drive).
Inhibition of Stretch Reflexes
It occurs with the inhibition of alpha-motor neurons. The
inhibition is brought out by 2 mechanisms:
1. Reciprocal innervation (or reciprocal inhibition): Perfor-
mance of a stretch reflex (by stimulation) causes the
afferent fibers from spindle to excite the motor neurons
supplying the muscles (from which the impulses were
generated) and simultaneously inhibiting the fibers
supplying its antagonist. The phenomenon is called
reciprocal innervations. It is an example of postsynaptic
inhibition.
2. Inverse stretch reflexes (an autogenic inhibition):
Stretching a muscle
↓ 1. Superficial reflexes.
Reflex contraction of muscle
↓ Superficial Reflexes
Further increase in stretch
↓
Reflex relaxation of muscle
↓
This phenomenon is mediated by receptors called Golgi
tendon organ.
Central Nervous System 225
Clinical Importance of Stretch Reflex and
Inverse Stretch Reflexes
1. Lengthening reaction of clasp knife effect.
2. Clonus.
Both have been already described in the earlier pages.
Polysynaptic Reflexes
(Withdrawal Reflexes)
They are those reflexes in which there are many synaptic
connections between afferent and efferent neurons. Such
complex pathways (reflex pathways) including the rever-
berating circuits are common in the brain and spinal cord.
Other complex of polysynaptic reflexes are chelo-minal
and cremasteric reflexes.
Definition
It is a type of polysynaptic pathway that occurs in response
to a various or painful stimuli.
The withdrawal reflex is a protective reflex, as the “flexor
responses” can be produced either by non-damaging
stimulation of skin or by stretch of the muscle, but strong
flexor response with withdrawal are produced only by
nociceptive stimuli. Therefore, while the stimulated limb is
withdrawn to get away from the source of stimulus, the
extension of other limb supports the body.
Performing Reflex Testing
Usually, the reflex testing is done while the patient lies supine
on the bed. But neurologists also prefer to assess the tendon
reflexes with the patient sitting on the edge of the bed facing
the examiner. This sitting position in usually preferred in
case of female patients while testing their knee jerks
especially. By doing this, the patient feels relaxed and it
indirectly helps the examiner in the proper elicitation of the
reflexes.
Types of Reflexes
Reflexes (8.27) have been divided into two types.
They are:
2. Deep reflexes
They are cutaneous reflexes caused by irritation of the skin
or areas depending on the spinal cord as a motor center.
For example:
• The scapular
• Epigastic
• Abdominal
226 Essentials of Clinical Medicine

• Cremasteric
• Gluteal and
• Plantar reflexes
or on center in the medulla; for example:
• Conjuctival and corneal
• Pupillary
• Palatal reflexes.
Superficial reflex is induced by a very light stimulus, such
as stroking the skin gently with a soft cotton wad.
Deep Reflexes
The reflex caused by the stimulation of parts beneath skin,
such as tendon or bone.
For example:
• Elbow
• Wrist
• Triceps
• Biceps Fig. 8.27: The figure of “8” position (Patient in supine position on
• Knee bed). It is the best position of body in which all the reflexes (both
• Ankle jerk reflexes (Fig 8.28) superficial and deep) can be beautifully elicited
(courtesy: Dr Kumar Saurabh Gaur)
Some Special Points Contd...
1. May be extensor bilaterally. This is a normal response in tially flexing the quadriceps muscle
infants. However, unilateral extensor plantar response knees and supporting
is definitely pathological. them with the hands
in the supine position
2. The deep tendon reflexes are elicited in older children Ankle Sciatic nerve Tap the tendo-Achi- Plantar flexion of
by tapping at specific points/sites with the help of a (S1-2) lles after partially the ankle and visi-
hammer. In infants and younger children the reflexes flexing the knee and ble contraction of
are elicited with the finger or the edge of diaphragms of externally rotating the gastroenemius
stethoscope instead of hammer. the leg. muscle

Table 8.40: Deep tendon reflexes and their Table 8.41: Superficial reflexes and their methods of elicitation
mode of elicitation
Superficial Method of Response
Reflex Nerve and Elicitation Response reflexes elicitation
spinal level Plantar reflex*(S1) Stroke the lateral Normal response is
Biceps Musculocutaneous Tap the biceps ten- Further flexion of border of the sole of plantar flexion of all the
(C5-6) don after partial the elbow and the foot from the toes. In pyramidal lesions
flexion and prona- visible contraction heel to the toes there is dorsiflexion of the
tion of the elbow of the biceps muscle big toe with fanning of
Triceps Radial (C7-8) Tap the triceps ten- Extension of the the others toes.
don just above the elbow and visible Abdominal reflexes Stroke the skin of the Contraction of the abdo-
elbow after flexing contraction of the (D6-12) abdomen from the minal muscles of the same
the elbow above the triceps muscle lateral end towards side of stimulation.
chest the midline
Supinator Radial (C7-8) Tap the brachio- Further of the knees Cremasteric reflex Stroke the skin of the Contraction of cremas-
radialis tendon at and visible contra- (L1,2) medial side of the teric and elevation of the
the lower end of the ction of the quad- thigh from above testicle on the stimulated
radius after partial riceps muscle downwards side.
flexion and pro- Anal reflex (S4-5) Stroke the skin in the Contraction of the anal
nation of the elbow perianal region sphincter
Knee jerk Femoral (L3-4) Tap the quadriceps Extension of the
tendon just below knees and visible * In infants less than 2 years of age, the plantars may be extensors
the knee after par- contraction of the bilaterally. This is a normal response in infants. However, unilateral
extensor plantar response is definitely pathological.
Contd...
 Central Nervous System 227

Table 8.42: Grading of reflexes

Absent reflexes 0
Sluggish reflexes (seen with reinforcement*) 1+ (+)
Normal 2+ (++)
Brisk 3+ (+++)
Brisk with clonus 4+ (++++)

Table 8.43: Causes of absent and brisk deep tendon reflexes

Absent deep tendon reflexes
• Lower motor neuron lesions
• Severely spastic children
• Contracture of the muscles
• Stage of neuronal shock in upper
motor neuron lesions
Brisk deep tendon reflexes
• Upper motor neuron lesions (pyramidal lesions)
• Tetanus or strychnine poisoning
• Hysteria
• In small children, the reflexes may
frequently be exaggerated with any reason

Table 8.44: Summary of reflexes tested clinically

Reflexes How elicited Response Afferent path Center Efferent path
Superficial reflexes
a. Skin reflexes
1. Plantar Scratch on medial Plantar flexion of Tibial S-1, 2 Tibial
aspect of sole toes
(In Babinski, dorsiflexion
of toes)
2. Epigastric Scratch on chest down Drawing in of epigastrium Th-7,8 Th-7,8 Th-7,8
from nipple on same side
3. Upper Scratch on upper Contraction of the Th-8,9,10 Th-8,9,10 Th-8,9,10
abdominal abdomen abdominal muscles
4. Middle Scratch on abdomen Contraction of the Th-9,10,11 Th-9,10,11 Th-9,10,11
abdominal near umbilicus abdominal muscles
5. Lower Scratch on lower Contraction of the Th-10,11,12 Th-10,11,12 Th-10,11,12
abdominal abdomen abdominal muscles
6. Cremasteric Scratch on upper Drawing upwards of Femoral L-1 Femoral
medial thigh the testicle
7. Gluteal Scratch on buttock Contraction of gluteus muscle L-4,5 L-4,5 L-4,5
8. Anal Scratch on skin near anus Contraction of anal sphincter Pudendal S-4,5 Pudendal
b. Mucous membrane reflexes:
1. Corneal or Touch on cornea or Closure of eye Cranial V Pons Cranial VII
conjunctival conjunctiva with caution
2. Pharyngeal Touch on pharynx Constriction of pharynx Cranial IX Medulla Cranial X
3. Palate Touch on soft palate Elevation of palate Cranial IX Medulla Cranial X
Deep reflexes
1. Maxillary Tapping on middle of jaw Closure of mouth Cranial V Pons Cranial V
(jaw)
2. Biceps Tapping on biceps tendon Flexion at elbow Musculo- C-5,6 Musculo-
cutaneous cutaneous
3. Triceps Tapping on triceps tendon Extension at elbow Radial C-6,7 Radial
4. Radial Tapping on styloid Flexion and supination
supinator process of radius of forearm
5. Wrist Tapping on flexor Flexion of wrist Median C-6,7,8 Median
(flexion) tendons of wrist
Wrist Tapping on extensor Extension of wrist Radial C-7,8 Radial
(extension) tendons of wrist
6. Patellar Tapping on patellar Extension at knee Femoral L-3,4 Femoral
tendon
7. Ankle Tapping on Achilles Plantar flexion of Tibial S-1,2 Tibial
(Achilles) tendon foot

Contd...
228 Essentials of Clinical Medicine

Contd...
Reflexes How elicited Response Afferent path Center Efferent path
Visceral reflexes
a. Pupillary reflexes:
1. Light (direct) Shining of light Constriction of pupil Cranial II Midbrain Cranial III
on retina in one eye on that side
2. Light (indirect Shining of light on Constriction of pupil Cranial II Midbrain Cranial III
or consensual) retina in one eye on other side
3. Accommodation Subject looks on finger Constriction of pupil Cranial II Occipital Cranial III
held in front of one eye in that eye cortex
4. Ciliospinal Pinching of skin on back Dilatation of pupil Sensory Th-1,2 Cervical
of neck nerve sympathetic
b. Oculocardiac Pressure over eyeball Slowing of heart and fall Cranial V Medulla Cranial X
with thumb in blood pressure
c. Carotid sinus Pressure over carotid Slowing of heart and fall in Cranial IX Medulla Cranial X
reflex sinus on one side blood pressure
d. Bulbocavernosus Pinching dorsum of glans Contraction of bulboca- Pudendal S-2,3,4 Pelvic
penis vernosus autonomic
e. Sphincter Distension of bladder Emptying of bladder or Pudendal S-2,3,4 Pudendal and
reflexes or rectum rectum autonomic

Clinical Significance of Reflexes

Some Abnormal Findings
1. Hyporeflexia: Due to lesion affecting the afferent
pathways, the ant horn cells or the efferent pathways
(lesions of lower motor neurons)
For instance:
A. In tabes dorsalis—posterior roots are affected
B. In poliomyelilis—anterior horn cells are affected
C. In most peripheral neuropathies—both efferent
(motor) and afferent (sensory) nerve fibers are
affected.
D. Myopathies.
2. Hyper-reflexia: Seen in:
– UMNLs (upper motor neuron lesions)
– Anxious and nervous people
– Tetanus.
3. Pendular reflexes: In cerebellar disease.
4. Myotonic reflexes:
– In hypothyroidism where both the contraction and
relaxation phases of a tendon reflex are prolonged
– In hypothermic patients
– The relaxation time of ankle jerk can be estimated
by simple observation with surprising accuracy
in relation to normal, and is a sensitive and reliable
clinical index of hypothyroidism.
5. Diminution of ankle jerks may be present in some of
the healthy people.
6. In some patients or myotonic pupils some of the deep
tendon reflexes may be absent. It is called Holmes-
Fig. 8.28: The ankle reflex—three ways to get it Adie syndrome.

7. When there is a loss of reflex alone without any other
pathology, it indicates radioculopathy of that segment.
8. Symmetrical (bilateral) loss of reflexes may show in
isolated or generalized peripheral neuropathy.
9. While eliciting Hofmon’s sign, the thumb will flex
excessively if there is hyper-reflexia.
10. Inverse stretch reflex may be seen with combined
spinal cord and root pathology (myeloradiculopathy)
11. Crossed extensor reflex may be seen in spinal cord
lesion; for example, the elicitation of knee jerk on one
side may produce reflex response on the contralateral
side.
12. If the abdominal reflexes easily get fatigued in a young
person, then it may be a sign of early pyramidal
disease. The reflexes may not be elicited in patients
who are very fat (obese), after multiple pregnancies,
after repeated or major abdominal surgery or in very
tense patients who cannot relax their abdominal
muscles.
13. In case of corneal reflex, elication, if there is VIIth n
lesion, then there is no response from paralysed side
but there is blink reflex from the normal side.
Wartenberg’s Sign
The patients hand is held by the examiner in supinated
position and the fingers of the patient and examiner are
interlocked. Both of them are then made to flex the fingers
against each other’s resistance. Normally, the thumb and
terminal phalanges may bend slightly. In pyramidal tract
lesion, the thumb adducts and flexes strongly. It may be
taken as an equivalent of Babinski’s sign in case of
amputation of both the lower limbs.
Supinator Reflex
A misnomer for this reflex because the muscle involved is
brachioradialis.
Ankle Reflex Alternative
• With legs straight, place your hand on the ball of the
foot with ankle at 90° strike with your hand, watch the
muscles of the calf
• Ask the patient to kneel an a chair so that his ankles are
hanging loose over the edge. Strike the Achilles tendon
directly.
VARIOUS METHODS OF TESTING PLANTAR
• Babinski’s reflex on outer border of the sole
• Oppenheim’s reflex, over the skin of tibia pressure is
applied
Central Nervous System 229
• Gordon’s reflex, press tendon Achilles.
• Chaddock’s on lateral border of feet.
Absent Abdominal Reflex
Obesity, previous abdominal operations or frequent
pregnancy, age, a pyramidal tract involvement above of that
level or a peripheral nerve abnormality.
Conclusions Drawn from the Babinski’s Sign
• Flexion of all toes—flexor plantar response—Babinski’s
sign negative—normal.
• Extension of hallux and spreading of other toes—
extensor plantar response—Babinski’s sign positive.
• Extension of hallux, extension of other toes and flexion
of ankle—withdrawal response, repeat more gently or
try alternative stimuli.
• No movement—indicating no response
• Babinski’s sign positive—upper motor neuron lesion
• Babinski’s sign negative—normal
• No response—may occur with profound upper motor
neuron weakness (toe unable to extend), may occur if
there is a sensory abnormality interfering with the
afferent part of reflex.
• Common mistake —the examiner should not place too
much weight on the plantar response in isolation. A
negative Babinski’s sign may be found in upper motor
neuron lesion (UMNL). A positive Babinki’s which
surprises an examiner needs to be interpreted with
caution, could it be a withdrawal response?
Alternative Stimuli
• Stimulion lateral aspects of foot—Chaddock’s reflex
• Thumbs and index finger run down the medial aspect
of the tibia—Oppenheim’s reflex
Primitive Reflexes (Release Signs)
They are those reflexes which are present at birth or in
early infancy. These reflexes gradually disappear as the age
advances and as the cortical system develops.
In the later stages of life, there may be reappearance of
these reflexes when there is diffuse cortical damage because
the areas below the cortex (in the subcortical areas) are
released from the inhibitory control exercised by the higher
(cortical) center.
1. Grasp reflex: When the patient palm is touched, the radial
border between the thumb and index finger with any
object or with the examiner’s own finger, the patient’s
230 Essentials of Clinical Medicine
fingers involuntarily reflex slowly and group the object/
finger. It is seen in contralateral frontal lobe lesion.
2. Groping reflex: When an examiner shows an object to
the patient (or touches the object on the hands of the
patient) and then takes the object away from the patient
on seeing or feeling the object, tries to catch (or grope)
it is seen in contralateral frontal lobe lesion.
3. Palmomental reflex: On stroking the skin of flexor
examiner of the hand, of the patient, with a blunt object
(such as back of the hammer), a sort of puckering of
the skin over the chin on the same side is produced by
the contraction of the ipsilateral mentalis muscle.
4. Sucking reflex: When the angle of the mouth or borders
of lips of the patient is touched with the examiner’s
index finger, an involuntary opening of mouth occurs,
as if the patient is trying to suck the finger.
5. Snout reflex: On keeping a finger on the upper lip and
tapping lightly over it causes puckering and protrusion
of the lips.
6. Glabella tap reflex: When the examiner gives a tap over
the glabella (root of the nose) of the patient repeatedly
with his index finger, (from above and behind the patient’s
head), the patient is seen to blink his eyes with each tap.
Normal individuals respond by blinking to the first 2 to
3 taps and then there is no response. It is seen in
parkinsonism and diffuse degenerative disease of the
brain.
MOTOR SYSTEM REFLEXES
Further Maneuvers
Demonstration of Clonus
At the ankle: Dorsiflex the ankle briskly, maintain the foot
in that position, a rhythmic contraction may be found. More
than three beats is abnormal.
At the knee: With the leg straight, take the patella and bring
it briskly downwards; a rhythmic contraction may be noted.
Always abnormal.
INTERPRETATION
Increased reflex or clonus—this indicates upper motor
neuron lesion above the root at that level.
• Absent reflexes:
– generalized—indicates peripheral neuropathy.
– isolated—indicates either a peripheral nerve or, more
commonly, a root lesion.
• Reduced reflexes (more difficult to judge)—occurs in a
peripheral neuropathy, muscle disease and cerebellar
syndrome.
N.B. Reflexes can be absent in the early stages of severe
upper motor neuron lesion—‘spinal shock’.
• An inverted reflex—the reflex tested is absent, but there
is spread to a lower level. The level of the absent reflex
indicates the level of the lesion. For example, a biceps
reflex is absent but produces a triceps response. This
indicates a lower motor neuron lesion at the level of the
absent reflex (in this case C5) with upper motor neuron
lesion below indicating spinal cord involvement at the
level of the absent reflex.
• Pendular reflex—this is usually best seen in the knee
jerk where the reflex continues to swing for several
beats. This is associated with cerebellar disease.
• Slow relaxing reflex—this is especially seen at the ankle
reflex and may be difficult to note. It is associated with
hypothyroidism.
COORDINATION
Introduction
A coordinated combination of a series of motor actions is
needed to produce a smooth and accurate movement. This
requires integration of sensory feedback with motor output.
This integration occurs in cerebellum.
The coordination of groups of muscles is a function of
various factors, such as efferent impulses coming from the
muscles and joint receptors, cerebellar function and
corticospinal tract function.
In the pressure of weakness, tests for coordination must
be interpreted with caution and are unlikely to be informative
if there is significant weakness.
Loss of joint position sense can produce some incoordi-
nation (sensory ataxia). This is made more worse when the
eyes are closed. Joint position sense should be tested before
coordination. Sensory ataxia occurs typically in sensory
neuropathies posterior column lesions, when position sense
is impaired in the legs. Proximal weakness of muscle may
be seen in cerebellar ataxia, but this can usually be recognized
easily by testing of muscular strength.
Testing the Coordination
1. Testing the gait: (See section for “GAIT”) Expect the
right hand to be slightly better (in a right-handed person.)
2. a. Testing the coordination in the arms: The patient is
asked to hold his arms outstretched and to close his
eyes. Ask the patient to maintain this position. Then
push his arm up or down suddenly. In normal person,
the arm will again regain the original position; whereas
in case of abnormalities of coordination, this may
not be so.

Interpretation: The arm oscillates several times before
coming to rest which indicates cerebellar disease. If
they return rapidly to normal position—normal
b. Finger-nose test: Hold your finger out about an arm’s
length in front of the patient. Ask him to touch your
finger with his index finger and to touch his nose
with the sense finger. When he has done this
correctly, ask him to repeat this faster.
Interpretation: The patient is able to complete the
task quickly, accurately—normal
• The patient develops a tremor as his finger
approaches its target—intention tremors; finger
overshoots the targets—past pointing or
dysmetria.
• Coordination of fingers in rapid movements (e.g.
rapidly touching each finger in turn with the
thumb, or the thumb and index) are specially
useful tests. In cerebellar ataxia, the error of
movements tend to occur at light angles to the
intended direction of movement. In anxious
subjects, errors tend to occur in direction of
movement itself.
c. Repeated movements: The patient is asked to pat one
hand on the back of the other quickly and regularly.
(The examiner should first demonstrate this to the
patient.)
• The patient is asked to twist the hand as if opening
a door or unscrewing a light bulb (demonstrate).
• The patient may be asked to tap the back of his
right hand alternately with the palm, and then
back of his left hand. Repeat with right hand
(demonstrate).
Interpretation:
• Disorganization of the movements of the hands
and elbows taking wide excursions than expected,
irregularity of the movements which are
performed without rhythm. Compare the two
sides—these changes indicate cerebellar
incoordinations often the abnormal is heard as a
slapping sound rather than normal tapping noise.
• Mild upper motor neuron weakness would impair
fluency of the fast repeated movement, but the
movements will not be of wide excursion or
irregularly.
• When there is disorgainsation of tapping the hand
and then turning it over, this is referred to
dysdiadochokinesia.
d. Watch the patient while he is dressing or undressing,
handling an object or doing some fine type of work.
Central Nervous System 231
(which requires greater coordination). There complex
and practiced everyday movements offer very
sensitive way of assessing the coordination.
3. Testing the coordination in the legs:
a. Heel-shin-ankle test: The patient is made to lie down
supine ask him to lift his leg and place the point of
his heel on his knee and then run it down the sharp
part of his shin (Fig. 8.29).
Common mistake: Allow the patient to run his instep
along his shin.
Interpretation:
• Disorganization of movement with the heel falling
off the anterior part of the skin, knee falling from
side to side.
• In cerebellar ataxia, a characteristic, irregular,
side to side series of errors in the speed and
direction of movement occurs. The test should
also be performed with the eyes open.
b. Making circle in air: The patient is asked to draw a
large circle smoothly and accurately, with the help
of leg.
Interpretation: In cerebellar ataxia, the movements
are generally “squared off” irregularly.
Note: The finger-nose test and heel-shin test can be
used as an indication of loss of joint position sense.
The movements are accurate but when repeated with
the eyes closed, are substantially worse. This
indicates impairment of joint position sense (JPS).
c. Rhomberg’s sign: This test is used to diagnose the
loss of position sense (sensory ataxia) in the legs,
not of cerebellar function.
Fig. 8.29: The heel-shin test
232 Essentials of Clinical Medicine
In this test, the patient is asked to stand with his
feet close together, and to maintain this posture with
his eyes closed.
If the patient begins to sway (or may fall) then
Rhomberg’s sign is said to be positive. In case of
defective position sense in the legs (as seen in sensory
neuropathy or tabes dorsalis), the patient is unable
to stand without visual fixation. The same is the case
with labyrinthine lesion with cerebellar ataxia. If a
person has labyrinthine lesion, he suffers from
positional nystagmus and in cerebellar ataxia there is
ataxia (defective muscular coordination), especially
that manifested when voluntary muscular move-
ments are attempted) of limbs. Another confirmative
test that whether Rhomberg’s sign is due to
labyrinthine disease is to ask the patient to jump
quickly up and down on both feet with his legs kept
together, hands outstretched and eyes closed
(Unterberger’s test) if the patient has any labyranthine
lesion (or disease), he will gradually progress across
the floor, or fall to one side, the side of labyrinthine
leision.
d. Tendem walking test: In this test, the patient is made
to walk along a straight line by placing the heel of
one foot immediately adjacent to the toe of the one
behind. A patient with ataxia (in coordination) is
unable to do so and will or deviate towards the
affected side (in case of unilateral cerebellar
diseases). In case of bilateral or midline cerebellar
diseases his gait will be drunken and patient will sway
to either side.
e. Toe finger test: The patient is made lie in the supine
position, he is then asked to lift his toe and touch it
to the examiner’s finger held at some distance.
Interpretation: In case of cerebellar lesions there will
be overshooting of leg with incoordination. The
patient will not be able to perform the test in posterior
column lesions with his eyes closed.
4. Special tests for in coordination: (showing cerebellor
involvement)
a. Dysdiadochokinesis of adiadochokinesis: In case of
cerebellar involvement, the patient will either show
dysdiadochokinesis or adiadochoikinesis (i.e. inability
to perform repetitive alternative movements quickly).
b. Rebound phenomenon: The patient is asked to flex
his forearm at the elbow and to pull his forearm
against the resistance affixed by the examiner. The
examiner then, suddenly releases the forearm. In case
of cerebellar lesion, the patient is unable to stop his
hand and may hit his own face; whereas in normal
individuals, it does not happen so.
c. Dysmetria: The patient is asked to close his eyes and
hold his one upper lower limb in particular position.
Then he should put other limb in the some position.
The patient is unable to do so because of the inability
of judgment of the range of movements.
(The term dysmetria has been derived from the
Greek words, dye meaning bad and metron meaning
measure. Thus, dysmetria is the inability to fix the
range of movement in a muscular activity. Rapid
and brusque movements are made with more force
than necessary. Dysmetria is due to cerebellar lesion).
d. Pointing and past pointing test: The patient is first
asked to touch the examiner’s finger (held at a
distance from the patient) by his own finger. He is
then made to repeat this action twice or thrice. The
patient is made to close his eyes and made to perform
the same action keeping the examiner’s finger at the
fixed position.
In case of cerebellar lesion, the finger of the
patient past points the examiner’s fingers (on the
affected side).
e. Barony’s pointing test: The patient is made to fully
outstretch his both upper limbs and set parallel to
each other. In cerebellar lesion/disease the patient is
unable to keep his hands (arm) parallel to each other,
rather the ipsilateral limb will deviate outwards. He
is then made to close his eyes and asked to bring his
arm to the same original position again. It is found
that he is unable to do so on the affected side.
f. Merry-go-round test: In this the patient is made to
go round a chair are for some time. In case of
unilateral cerebellar disease, the patient will come
nearer and nearer to the chair if the affected side is
towards the chair. This is called centripetal type.
And if the affected side is on the opposite side, the
patient will move in circles of increasing diameter
(wide and wide). It is called centrifugal type of merry
- go-round test.
g. Pointing in a circle test: In this test, the examiner
draws a circle on paper (usually of 1 cm in diameter)
and the patient is made to mark dots within the circle.
In any ataxia, the patient will spread the dots
irregularly over a wide area, outside as well or inside
the circle.
h. Coordination testing of the trunk: Ask the patient to
sit up from the lying position without using hands.
Observe whether he falls on one side.
Interpretation: The patient is unable to sit from lying
position without falling to one side—truncal ataxia.
It is usually associated with gait ataxia.
 Central Nervous System 233

Table 8.45: Special terminology regarding coordination

1. Unilateral incoordination
2. Bilateral incoordination
3. Truncal atomic, gait ataxia
without limb incoordination
4. Unilateral cerebellar
syndrome
5. Bilateral cerebellar syndrome
6. Midline cerebellar syndrome
7. Hypotonia
— Ipsilateral cerebellar synd.
— Bilateral cerebellar synd.
— Midline cerebellar
syndrome.
Common causes –
— Demyelination, vascular disease, rare causes – trauma, tumor or abscess.
— Common causes – drugs (anticonvulsants) alcohol, demyelination, vascular disease, rare causes, heredi-
tary cerebellar degenerations, para-neoplastic disorders hypothyroidism.
— Lesion of the cerebellar various–causes = as for bilateral cerebellar syndrome.
d. pendular reflexes e. Tremor.

GAIT
Gait is defined as the manner of walking. The examination of the patient’s gait is of great importance in the diagnosis of
the neurological disease process. Gait is a coordinated action requiring integrations of sensory and motor function.
Various types of gait disorders are: hemiplegias, parkinsonism, marche a petits pas, ataxic unsteady gait. In order to test
the gait, the patient is made to walk and while doing so his lower limbs should be adequately exposed. The examiner
should also make the patient to walk on a straight line while the patient has a walk, the examiner should look out for
certain things like “Is the patient able to walk? Does he need any assistance from somebody? Is he able to walk on a
straight line? Whether the patient feels that he may fall while walking and on which side (this may provide hint for the side
affected)?
While investigating the underlying causes of an abnormal gait, the examiner should try to rule out the local causes like
osteoarthritis, pain in the leg or pelvis.
Table 8.46: Causes of unilateral gait defects and bilateral gait defects
Unilateral Bilateral
Hemiplegic Spastic
High stepping Scissor
Limping Ataxic
Hysterical Toppling
Festinant Waddling
Jaunting Stamping

Table 8.47: Interpretation of various types of gaits

Gait
1. Shuffling gait, festinant gait, Patient shows a series of start small shuffles
parkinsonian gait, kinesia
paradoxa, flexion dystonia
How the patient walks? Interpretation
Basal ganglion dysfunction. Causes are:
during which the patient slides rather than Parkinson’s disease, major tranquilizers
lifts one foot after the other. Natural swings of
arms is lost when the patient is pushed
forward, he goes on walking progressively
rapidly propulsion until he hits an object or
if he is pushed backwards, he goes on
walking backwards more and more rapidly
(retropulsion). Kinesia paradoxa is a term given
to peculiar type of movements seen in
parkinsonism. In this disease, if the patient is
in a hurry, he may be able to run quite fast;
but when he starts walking, he cannot do so
normally and has to revert to his shuffling
gait. It gives thus, as if the patient is malin-
gering. In the Parkinson’s disease, the gait
appears as though the patient is trying to
catch up with the center of gravity.
Contd...
234 Essentials of Clinical Medicine
Contd...
Gait
2. Marche a petit pas (Russian
Ballet Master)
3. Scissoring spastic gait
Bipyramidal gait (involving
both the lower limbs)
4. Sensory ataxic gait or
stamping gait
5. Cerebellar ataxia or
drunken or reeling gait or
ataxic gait
6. Waddling gait
7. Apraxic gait
8. Hemiplegic gait
9. Foot drop or high
stepping gait
How the patient walks? Interpretation
The gait resembles to the rapid steps of Bilateral diffuse cortical dysfunction.
ballet dance on points. Common causes are: Diffuse cerebrovascular
disease “Lacunar State”.
The gait is such that the legs of the patient UMNL accompanied by spasticity. Common
cross in walking. It is due to bilateral adductor causes are: Cerebral palsy, multiple sclerosis,
spasm and weakness of dorsiflexors of legs. cord compression.
Patient usually walks looking down to the Indicates loss of joint position sense (JPS)—
ground or to his feet all the time, as if he has Rhomberg’s positive. Common causes are:
fear of falling down. He may show slight Peripheral neuropathy, posterior column loss
swaying movements. He shows stamping gait (tabes dorsalis)
or legs are raised too high and thrown
outwards waved about before bringing them
down in a stamping fashion. The heel come
in contact with the ground first.
Patient walks on a broad base, the feet planted Common causes—drugs (e.g. phenytoin)
widely apart, and placed irregularly. Ataxia is alcohol, multiple sclerosis, cerebrovascular
equally severe whether the eyes are open disease.
or closed. Other signs of cerebellar disease
are usually present.
The patient walks in a zig-zag manner, and
sways on any side in reeling or staggering
fashion. This gait is also seen in patient with
Friedreich’s ataxia and multiple sclerosis.
The body is often lifted backwards (walking A feature of proximal pelvic girdle muscular
like a duck) with an increased lumbar lordosis, weakness especially of myopthies and
the feet are placed rather widely apart and the muscular dystrophies. Common causes are:
body sways from side to side. As each step is Lordosis, congenital bilateral dislocation
taken weakness of glutes, especially gluteus of hip (CDH)
medius, causes the hip to drop when the
affected leg is held off the ground in erect
posture accept Trendelenburg’s position.
Loss of concept of walking, often associated Indicates that cortical integration of the
with tiny rapid steps. movement is abnormal, usually with frontal
lobe pathology. Common causes are normal
pressure, hydrocephalus, cerebrovascular
disease
While walking, the patient drags his foot Unilateral UMNL. Common causes are stroke,
on the affected side. The resultant multiple sclerosis, hemiparesis.
obstruction to walking is avoided by
throwing the whole leg outwards from the
hip with bending forwards the opposite
side circumduction of leg to clear the
ground. Arm is flexed across the body and
does not take part in normal walking
movements. The affected arm is adducted
at the shoulder and flexed at the elbow,
wrist and fingers.
The patient raises the foot high in order to Common causes are:
overcome the foot drop and on keeping the a. Unilateral: Common peroneal palsy. Pyramidal
Contd...
 Central Nervous System 235

Contd...
Gait How the patient walks? Interpretation
foot down the toe hits the ground first. lesion L5 radiculopathy. b. Bilateral: Peripheral
There is not ataxia. neuropathy.
10. Functional gait It is variable, may be inconsistent with rest —
of the examination worse when watched.
May be mistaken for gait in chorea (esp.
Huntington’s disease), which is shuffling,
twitching and spasmodic and has associated
findings on examination. It is usually asso-
ciated with hysteria. The patient does not fall.
11. Gait in chorea dystonia In chorea of any etiology the patient has a In disorders of chorea.
wide based, lordotic gait in which he lurches
from side to side on his heels and has
tendency to fall. In chorea and hysteria the
involuntary movements are usually exag-
gerated during walking, and unusual foot
placement responses may occur so that the
toes may extend away from the floor (avoiding
response) or the feet may appear glued to the
floor (grasping response).

GAIT ABNORMALITIES (Fig. 8.30)  Bilateral : Scissor like

• Cerebral – Extrapyramidal—festinant
– Pyramidal • Cerebellar
 Unilateral: spastic circumduction of affected – Lateral - Pendular (ataxia)
lower limb – Midline - Truncal ataxia
• Spinal cord
– Lateral column - Spastic
– Posterior column - Sensory ataxia stamping
• Peripheral nerves - High stepping
Disorders of Gait
Upper Motor Neuron
• Hemiplegia
• Paraplegia and quadriplegia.
Lower Motor Neuron
• Foot drop.
• Quadriceps weakness
• Proximal weakness
• Peripheral neuropathy
Cerebellor Sydrome
• Ataxia

Extrapyramidal Syndromes
• Parkinson’s disease
• Dystonia
Fig. 8.30: Figure showing various types of abnormal gaits • Involuntary movements
236 Essentials of Clinical Medicine

Sensory Ataxia – Infarct

• Cerebellar like ataxia – AV malformation
• Infiltration (neoplastic tumors)
Apraxic Gait – Astrocytoma
• Loss of concept of walking, often associated with many – Meduloblastoma
rapid steps. – Secondary neoplasm
– Compression by acoustic neuroma
Hysteria • Metabolic—toxic
• Bizarre, functional gait disorder – Chronic alcohol abuse
Some Other Gait Disorders – Anticonvulsant drugs, carbon monoxide poisoning,
lead
• Truncal gait • Miscellaneous
• Tottering gait – Multiple sclerosis
• Titubation (head nodding movements)
– Guillain-Barré syndrome
Clinical Features of Cerebellar Lesion – Hydrocephalus, postinfective
• Cerebellar ataxia – Cerebellar syndrome of childhood
• Intention tremors – Hypothyroidism.
• Involvement of limbs, trunk and external ocular • Causes of cerebellar degeneration
movement (nystagmus) – Paraneoplastic syndrome
• Past pointing – Heat stroke
• Rebound – Postviral demyelination
• Impaired ability to generate alternating rhythmic – Drugs like phenytoin.
movements.
Clinical Features of Cerebellar Lesions
Non-Neurological Gaits 1. Of localising value:
1. Painful gaits: Causes are arthritis, trauma. • Postural disorders
2. Orthopedics gait: Causes are – shortened, limb, previous – Poor tone
hip surgery, trauma. – Post pointing
– Pendular knee jerk
Differences between Midline Lesion and
– Barany’s test
Cerebellar Hemispheric Lesion
• Gait disorders
Damage to midline structures, e.g. vermis, results in – Truncal gait
disturbance of equilibrium with unsteadiness on standing. – Tottering gait
Truncal ataxia and titubation are seen. There are no other – Turning towards side of lesion
signs of cerebellar dysfunction like limb ataxia or nystagmus. – Titubation is rhythmic nodding of head from side
Hemispheric damage leads to ipsilateral arm to the side to side and to and fro associated with distal limb
of lesion, e.g. ataxia of limbs, nystagmus is present and tremors.
there are gait disorders. Paralysis is not a feature of cerebellar • Movement disorders
disease. • Dystonia—intension tremors is tremors increasing
Disease Involving (Affecting) the Cerebellum on reaching the object.
• Development • Dysmetria—Overshooting the target during finger
– Arnold-Chiari malformation. nose test.
– Basilar investigation • Dys-synergia—is decomposition of movements, act
– Cerebral palsy is broken into its component parts.
• Infection • Dysdiadochokinesia—failure to perform rapid
– Abscess alternating movements.
• Inherited • Rebound phenomenon—Failure of antagonist to
– Friedreich’s ataxia counter overshoot movement totally.
– Ataxia telengiectasia 2. Of no localizing value
• Insufficiency • Skew deviation—ipsilateral eyes turn down and
– Hemorrhage control contralateral eye up and out.
 Central Nervous System 237

• Staccato speech or scanning speech—words broken Causes of Intermittent Ataxia

into component syllables, dysarthria may result along • Refsum’s disease
with explosive speech. • Hartnup’s disease (metobolic condition associated with
• Static tremors—due to hypotonia
cerebellar ataxia, skin eruptions, mental retardation and
• Sluggish jerks.
amino acidosis)
• Stereognosis defective.
• Nystagmus due to disease affecting cerebellar • Maples disease
connection to vestibular nucleus. • Hyperammonia syndrome.
• Myoclonic jerks and choreiform involuntary Causes of Ataxia with Cranial Nerve Involvement
movements occur with extensive cerebellar disease
• Ataxia with optic atrophy
involving deep nucleus.
• Hereditary ataxia
• Ataxia—defined as clumsiness or unsteadiness of
gait despite good muscle power. • Subacute combined degeneration
• Multiple sclerosis
Causes of Ataxia
a. Sensory ataxia Ataxia with 3rd, 4th, 6th Cranial Nerves Involvement
• Posterior column—subacute combined degeneration, • Wernicks encepholopathy
syringomyelia, multiple sclerosis. • Miller-Fisher syndrome
• Posterior roots—tabes dorsalis • Multiple sclerosis
• Posterior nerve—peripheral neuropathy
Ataxia with 5th Nerve Involvement
• Postcentral convolution—diseases of parietal lobe.
b. Vestibular lesion • Multiple sclerosis
• Acute viral labyrinthitis • Trigeminal neuralgia
• Drug-induced labyrinthitis, e.g. streptomycin, Ataxia with 7th Nerve Involvement
phenytoin, barbiturate, carbamazepin.
• Infection spreading to labyrinthine region. • CP angle tumor
c. Cerebellar lesions Ataxia with 8th Nerve Involvement
• Hemmorhage
• Postinfective demyelination • CP angle tumor
• Abscess • Refsum’s disease
• Infarct Ataxia with 9th and 11th Cranial Involvement
• Hysteria
• Nerve involvements
Table 8.46: Causes of cerebellar ataxia of acute onset and gradual onset • Craniovertebral anomaly.
Acute onset Gradual onset
Syndrome of Slowly Developing Ataxia
Infection – Cerebellar abcess Congenital
encephalitis This condition is characterized by progressive unsteadiness
Hereditary – in standing and walking along with impaired coordination
Friedriech’s ataxia of limbs.
Mark ataxia
Sanger brown
Pathologically, they are characterized by degeneration
Trauma Degeneration – of cerebellum and/or its related fibric system.
Vascular Primary cerebellar Hereditary transmission is an important feature; hence,
– PICA Oligorubra cerebellar they are also referred to as hereditary ataxia.
AICA Olivo ponto cerebellar
Sup. Cerebellar It includes three main categories:
Artery thrombosis 1. Cerebellar cortical degeneration.
Vestibobasilar insufficiency
2. Olivopontocerebellar atrophy (OPCA)
Demyelinating disease dissemi- Familial –
nated sclerosis 3. Spinocerebellar degeneration, Friedriech’s axaxia.
Drugs Refsum’s disease
Alcohol Abeta lipoproteinemia Conditions in Children which are Mistaken for Ataxia
Barbiturate Leukodystrophy • Intrusion of choreiform movements
Bromide
Piperazine Neoplastic
• Myoclonic jerks.
Phenytoin CP angle tumor cerebellar tumor. • Status petit mal.
238 Essentials of Clinical Medicine

Lateral Medullary or Wallenberg’s Syndrome PICA

Occlusion of any of the following five vessels may be
responsible for this syndrome:
• Vertebral artery
• Posterior-interior cerebellar commonest
– Superior cerebellar
– Middle cerebellar
• Interior lateral medullary arteries.
Characteristics
It is characterized by:
a. On the same side of lesion:
– 5th, 7th, 9th, 10th cranial affection
– Cerebellar sign
– Facial anesthesia Fig. 8.31: Trendelenburg’s test. (A) When both feet are supporting
– Horner’s syndrome the body weight, the pelvis (anterior superior iliac spine) on the two
sides lies in the same horizontal plane. (B) When only the right foot is
b. On the other side of lesion: Sensory change involving
supporting the body weight, the unsupported side of the pelvis is
the thalamic tract. normally raised by the opposite glutei medius and minimum. (C) If the
right glutei medius and minimus are paralysed, the unsupported left
Differences beween Intention Tremor of side of the pelvis drops. This is a positive Trendelenburg’s test.
Cerebellar Origin from that of Parkinsonism
The cerebellar intention tremor is a terminal intension tremor, to body, slightly forwards, hands face down (Fig. 8.31).
i.e. on finger-nose test, there is a tendency for the tremor They insist on a relative walking behind. However, they do
to be accentuated just before fingers touch the nose; while not fall. It is entirely a functional disorder.
in parkinsonism tremor, the movement is accurate and
constant, present even at rest and decreasing with Table 8.47: Abnormal movements
movements of pin rolling type at a rate of 3.6/second.
Movement Disease Site
Important Note Tremor Parkinson’s disease Substantia
1. The patient’s writing typically enlarges in parkinsonism, Hypokinesia nigra
and in cerebellar dysfunction the writing becomes Rigidity Corpus striatum
smaller. Chorea Rheumatic chorea Caudate nucleus
Athetosis Putamen
2. Cerebellum receives afferent supply from all the somatic
Dystonia corpus straitum
sensory system and from special senses, yet symptom
Hemiballismus Subthalamic nucleus of Luy’s
of cerebellar disease are exclusively motor because the
Spasmodic Not known
inflow does not reach consciousness but modification torticollis
of the cortical control movements is the evidence of Tardive dyskinesia Drug induced –Do–
localization of function within the cerebellum. Tics –Do–
3. von Hippel-Lindau syndrome or cerebellum retinal
hemanginoblastosis is autosomal dominant and associated
with other visceral pathologies like renal angioma, renal SENSORY SYSTEM
cell carcinoma, pheochromocytoma, pancreatic adenoma Introduction
or cyst, polycythemia.
Table 8.48: Five basic modalities of sensation
3F SYNDROME
Modality Tract Fiber size
It is an important gait abnormality often misdiagnosed as Vibration
ataxia in elderly females. 3F syndrome is the fear of further
falling, occurs after an elderly female had an attack of vertigo, Light touch
}
Joint position sense Posterior column Large fiber

syncope or drop attack. They walk pushing one foot forward Pin prick
while leaning right back on other. The arms are held at 90° Temperature } Spinothalamic tract Small fiber
 Central Nervous System 239

The posterior column remains ipsilateral up to the medulla

where it crosses over. The spinothalamic tract mostly
crosses within one to two segments of entry.
Vibration sense, joint position sense, and temperature
are often lost without prominent symptoms.
Light touch and pin prick are rarely lost without
discernible symptoms.
Sensory examination should be used:
1. As a screening test.
2. To assess the symptomatic patient.
3. To test hypotheses generated by motor examination (for
example, to distinguish between combined ulnar and
median nerve lesions and a T1 root lesion).
Examination of Sensory System
The examination of sensory system requires a considerable
attention on the part of both patient and examiner. Vibration
sense and joint position sense are usually quick and easy
and require little concentration so always test these first.
In all parts of sensory testing it is essential first to inform Fig. 8.33: Sensory loss in arm: Axillary nerve
the patient about the test. Then perform the test. Finally
check that the patient has understood and carried out the nerve, sciatic nerve, the dermatomes which are most
test appropriately. With all testing, move from areas of frequently affected are L4, L5 and S1. These are illustrated
sensory loss to areas of normal sensation. in Figs 8.34A to D.
Arms Vibration Sense
Four individual nerves are commonly affected in the arm.
Use a 128 Hz tuning fork. Those of higher frequency (256
The relevant sensory loss is illustrated in the fingers for the
or 512 Hz) are not adequate.
median nerve, ulnar nerve, radial nerve and axillary nerve.
Be sure that the patient understands that he is to feel a
Middle finger to the hand is supplied by C7. This is illustrated
vibration, by striking the tuning fork and placing it on the
in Figs 8.32 and 8.33.
sternum or chin.
Legs
Procedure
Sensory deficit is most commonly seen in the following
Ask the patient to close his eyes, place the tuning fork on
individual nerves:
the bony prominence, ask if he can feel the vibration. Place
Lateral cutaneous nerve of the thigh, common peroneal
nerve (also referred to as the lateral popliteal nerve), femoral initially on the toe tips then, if this is not felt, on a metatarsal
phalangeal joint, medial malleolus, tibial tuberosity, anterior
superior iliac spine, in the arms, on the fingertips, each
interphalangeal joint, the metacarpal phalangeal joint, the
wrist, the elbow and the shoulder. If sensation is normal
distally there is no point in proceeding proximally.
Check the patient reports feeling the vibration and not
just the contact of the tuning fork. Strike the tuning fork
and stop it vibrating immediately and repeat the test. If the
patient reports that he feels vibration, demonstrate the test
again.
Figs 8.32A and B: Sensory loss in the hand: A. Median and
ulnar nerves B. Radial nerve Remember: Start distally and compare right with left.
240 Essentials of Clinical Medicine

Figs 8.34A to D: Sensory loss in the leg: A. Lateral cutaneous nerve of the thigh;
B. Common peroneal nerve; C. Femoral nerve; D. Sciatic nerve

Sense of Joint Position
With the patient’s eyes open, show him what you are going
to do. Hold the distal phalanx between your two fingers
Ensuring that your fingers are at 90º to the intended direction
of movement, move the digit, illustrating which is up and
which is down.
Procedure: Ask the patient to close his eyes; move the toe
up and down. Start with large movements in either direction;
gradually reduce the angle moved until errors are made.
Test distal joints first and move more proximally.
Joints to be tested in the arm: Distal proximal interphalangeal
joint, middle proximal interphalangeal joint, metacarpal
phalangeal joint, wrist, elbow, shoulder.
Joints to be tested in the leg: Distal interphalangeal joint,
metacarpal phalangeal joint, ankle, knee and hip. N.B.
Romberg’s test is a test for joint position sense (Fig. 8.35).

Fig. 8.35: Testing the joint position sense (JPS)
Pin Prick Test
Use a pin, a disposable neurological pin, dressmakers or
safety pin, not a hypodermic needle or a broken orange
stick. If a hypodermic needle is used (to be discouraged), it
must be blunted before use. Dispose of the pin after use.
Stimulus should be of equal intensity every time.
Explanation: Show the patient what you are going to do.
Explain that you want him to tell you if the pin is sharp or
blunt. Touch an unaffected area with the pin and then touch
an unaffected area with the opposite blunt end of the pin.
Procedure: Ask the patient to close his eyes then apply
randomly sharp and blunt stimuli and note the patient’s
response.
Approach
Start distally and move proximally. Aim to stimulate points
within each dermatome and each main nerve.
a. Assessment of a Lesion
Always start from the area of altered sensation and move
towards normal to find the edges.
b. Assessment of a Hypothesis
Test within the areas of interest with great care, particularly
noting any differences between the two sides.
Caution: Intermittently using a blunt stimulus that needs to
be recognized correctly allows you to check that the patient
understands the test.
Central Nervous System 241
Light Touch
A piece of cotton wool is generally used. Some people prefer
to use a fingertip. Try to ensure a repeatable stimulus. Avoid
dragging it across the skin or tickling the patient.
Explanation: With the patient’s eyes open show him that
you will be touching an area of skin. Ask him to say ‘yes’
every time he is touched.
Procedure: Ask the patient to close his eyes, test the areas
as for pinprick, apply the stimulus at random intervals.
Caution: This is done by noting the timing of the response
to the irregular stimuli. Frequently, a pause of 10 to 20
seconds may be useful.
Temperature Sensation
It is usually adequate to ask a patient if the tuning fork feels
cold when applied to the feet and hands.
Bed Side Easy Testing
Fill a tube with warm water and cold water. Ideally, these
are controlled temperatures though normally the warm and
cold tap is adequate. Dry both bottles.
Explanation
‘I want you to tell me if I touch you with the hot tube’
(touch unaffected area of skin with the cold tube). Apply
hot or cold at random to hands, feet or an affected area of
interest.
The random order allows assessment of concentration.
Other Modalities
The other modalities to be tested in sensory system
examination are as follows.
Two-Point Discrimination
This requires a two-point discriminator—a device like a
blunted pair of compasses.
Explanation to the Subject/Patient
‘I am going to touch you with either two points together’
(touch an unaffected area while the patient watches with
the prongs set widely apart) or ‘one point’ (touch with one
point). ‘Now close our eyes’.
Procedure
Gradually reduce distance between prongs, touching either
with one or two prongs. Note the setting at which the patient
fails to distinguish one prong from two prongs.
Caution: Random sequence of one or two prongs allows
you to assess testing.
Normal: index finger <5 mm; little finger <7 mm; hallux
<10 mm. Compare right with left.
242 Essentials of Clinical Medicine
ADDITIONAL TESTS
Sensory Inattention Test
The patient is asked to tell you on which side you are going
to touch (either with cotton wool or pinprick). Touch him
on the right side and then on the left side. If he is able to
recognize each independently, then touch him on both sides
at the same time.
Observation
• Recognize right, left and both normally—normal.
• Recognize right and left correctly but only one side,
usually the right, when both stimulated—sensory
inattention.
Interpretation
Sensory inattention usually indicates a parietal lobe lesion,
more commonly seen with lesions of the non-dominant
hemisphere.
The Ultimate Impression that You Get
• Patterns of sensory loss.
Table 8.49: Sensory deficits can be classified into
eight levels of the nervous system
1. Single nerve Sensory loss within the distribution of a single
nerve, most commonly median, ulnar,
peroneal, lateral cutaneous nerve to the thigh
2. Root or roots Sensory deficit confined to a single root or a
number of roots in close proximity: common
roots in the arm C5, C6 and C7 and in the leg
L4, L5 and S1.
3. Peripheral nerve Distal glove and stocking deficit
4. Spinal cord Five patterns of loss can be recognized
a. Complete trans- Hyperesthesia (increased appreciation of
verse lesion touch/pinprick) at the upper level with loss
of all modalities a few segments below the
lesion
b. Hemisection of the Loss of joint position sense and vibration
cord (Brown-Se- sense on the same side as the lesion and pain
quard syndrome) and temperature on the opposite side a few
levels below the lesion
c. Central cord Loss of pain and temperature, sensation at
the level of the lesion, where the
spinothalamic fibers cross in the cord, with
other modalities preserved (dissociated
sensory loss)—seen in syringomyelia
d. Posterior column Loss of joint position sense and vibration
loss sense with intact pain and temperature.
Anterior spinal syndrome—loss of pain and
temperature below the level with preserved
joint position sense and vibration sense
5. Brainstem Loss of pain and temperature on the face
and on the opposite side of the body—
common cause: lateral medullary syndrome
Contd...
Contd...
6. Thalamic sensory loss Hemisensory loss of all modalities
7. Cortical loss Parietal lobe: the patient is able to recog-
nize all sensations but localizes them
poorly—loss of two-point discrimination,
astereo-
gnosis, sensory inattention.
8. Functional loss This diagnosis is suggested by a non-
anatomical distribution of sensory deficit
frequently with inconstant findings.
Table 8.50: Causes of sensory loss
1. Single nerve lesion Common causes are entrapment neuropathy.
More common in diabetes mellitus,
rheumatoid arthritis, typothyroidism. May
be presentation of more diffuse neuropathy.
Multiple single nerve lesion: mononeuritis
multiplex—common cause: vasculitis, or
presentation of more diffuse neuropathy.
2. Single root lesion Common causes are compression by
prolapsed intervertebral disks; rare causes :
tumors (e.g. neurofibroma).
3. Peripheral nerve Common causes are diabetes mellitus,
alcohol-related vitamin B1 deficiency, drugs
(e.g. vincristine); frequently no cause is found;
rarer causes: Guillain-Barré syndrome,
inherited neuropathies (e.g. Charcot-Marie-
Tooth disease), vasculitis, other vitamin
deficiencies.
4. Spinal cord.
a. Complete Common causes: trauma, spinal cord com-
transection pression by tumor (usually bony secondaries
in vertebra), cervical spondylitis, transverse
myelitis, multiple sclerosis; rare causes:
intraspinal tumor (e.g. meningiomas), spinal
abscess, post-infectious (usually viral).
b. Hemisection Common causes: as for transection.
c. Central cord Common causes: syringomyelia, trauma
syndrome (rare) leading to hematomyelia.
d. Posterior column Any cause of complete transection but also
loss the rare subacute combined degeneration of
the cord (vitamin B12 deficiency) and tabes
dorsalis
e. Anterior spinal Anterior spinal artery emboli or thrombosis.
syndrome (rare)
5. Brainstem pattern Common causes: in young patients—
(rare) demyelination, in older patients—brainstem
stroke; rare causes: brainstem tumors
6. Thalamic and Common causes: stroke (thrombosis, emboli
cortical loss or hemorrhage), cerebral tumor, multiple
sclerosis, trauma
7. Functional May indicate hysterical illness. N.B. this is a
difficult diagnosis to make in the absence of
appropriate psychopathology.
ABNORMAL MOVEMENTS
Introduction
Abnormality in movements are best appreciated by seeing
affected patients.
 Central Nervous System 243

There is frequently a considerable overlap between Ask the patient to:

syndromes and several types of abnormal movements are
often seen in the same patient—for example, tremor and
dystonia in a parkinsonian patient on treatment.
The anatomy of the basal ganglia is complicated and the
wiring diagrams illustrating the connections between the
various structures get more complicated as more research
is done. Neuro-anatomical correlations are of limited clinical
value as most movement disorders are classified as
syndromes rather than on anatomical grounds. Correlations
of significance include unilateral parkinsonism due to lesions
of contralateral substantia nigra and unilateral hemiballismus
due to lesions of the contralateral subthalamic nucleus or
its connection.
Interpretation
Try to Interpret
Patient’s face:
• Are there any additional movements?
• Is the face expressionless?
• Look at the patient’s head position
Arms and the legs:
• Note the position
• Are there any abnormal movements?
The patient is asked to:
• Smile
• Close his eyes
• Hold hands out in front of him with wrist cocked back
• Lift his elbows out sideways and point his index fingers
at one another in front of his nose perform finger-nose.
If there is a tremor, note the frequency, the degree of
the excursion (fine, moderate, large), note body parts
affected. Look for a tongue tremor. Test eye movement.
• Test tone: When testing tone in one arm, it is sometimes
useful to ask the patient to lift the other arm up and
down.
• Test fast repeating movements.
Also, ask the patient to:
• Rapidly bring thumb and index finger together
(demonstrate)
• Rapidly touch the thumb with each finger in turn
(demonstrate)
• Tap his toe as if listening to fast music
• Observe the speed of the movements and whether they
break up.
Gait
• Writing
• Write his name and address
• Draw an Archimedes’ spiral. Ask the patient to perform
any maneuver that he reports may trigger the abnormal
movement.
Your Observation
• Lipsmacking and twisting of mouth—orofacial
dyskinesia
• Flickering of muscles particularly around eye—facial
myokymia
• Intermittent spasm of muscles around the eye—
blepharospasm
• Intermittent spasm of muscles of one side of the face—
hemifacia spasm
Abnormalities of Head
a. Position
• Head twisted to one side—torticollis
• Head bent forward—anterocollis
• Head bend backwards—retrocollis
b. Movement
• Rhythmical movement of head—titubation: described
as yes-yes (shaking forward-backward) or no-no- (side
to side)
Abnormal Movements of Head
Arms and legs:
a. Tremor
• Present when limb (particularly hand) is at rest—
rest tremor
• Present when limb is maintained in a position—
postural tremor
• Present during an action, (e.g. finger-nose testing)
—action tremor
• Present and increasing as the finger reaches its target
—intention tremor
Commonly more than one type of tremor co-exist.
b. Position
• Limb maintained, often only transiently, in abnormal
position with contraction of both agonists and
antagonists—dystonic posturing. Commonly, the arm
is abducted at the shoulder, extended at the elbow,
pronated to an extreme position with the fingers
extended. The leg is usually extended at the hip and
knee and inverted at the ankle with the toes flexed.
Latent Phenomenon
a. On walking, the following may occur or increase:
• Rest tremor
• Dystonic posturing
244 Essentials of Clinical Medicine
• Chorea
b. Finger-nose testing may reveal:
• Action tremor
• Intention tremor (see above)
• Myoclonus—action myoclonus
c. Exacerbate
• Choreic movements
d. Fast repeating movements
• Slowed or break up easily—bradykinesia
e. Tone
• Cogwheel rigidity may be found only when the arm
is lifted up and down (activated)
f. Writing
• Writing becomes progressively slower, the hand may
go into spasm, the patient often holds pen in unusual
way—writer’s cramp
g. Archimedes’ spiral
• Spiral very tight, ending up as a circle—suggests
parkinsonism
• Spiral very large with tremor—suggests cerebellar
syndrome
h. Negative phenomena
• Rigidity—lead pipe or cogwheel
• Bradykinesia—slowness in intiating movements
• Reduced arm swing on walking.
Some Descriptions in Brief
Akinetic—Rigid Syndromes (Parkinsonism)
1. Key features—rigidity, bradykinesia and tremor.
Features include reduced facial expression (mask like),
rest tremor, stooped posture with reduced arm swing
and increased on walking. Gait may be festinant (section
4). Bradykinesia on fast repeating movements and
walking. Extrapyramidal dysarthria. May be limitation
of convergence. Glabellar tap positive (not useful).
2. Common causes—Parkinson’s disease, major tranquil-
lizers (e.g. chlorpromazine, haloperidol).
3. Rare causes—Steele-Richardson syndrome (akinetic—
rigid syndrome associated with progressive supranuclear
palsy), multiple systems atrophy (akinetic rigid
syndrome associated with autonomic failure), Wilson’s
disease.
Tremors
1. Rest tremor—feature of akinetic rigid syndrome (see
above).
2. Postural and action tremor—common causes: benign
essential tremor (also called familial tremor if there is a
family history), exaggerated physiological tremor (may
be caused by hyperthyroidism, beta-agonists)—rarer
causes: liver failure, renal failure, alcohol withdrawal.
3. Intention tremor—indicates cerebellar disease.
Chorea
a. Common causes
Drug therapy of Parkinson’s disease (excess treatment).
b. Rare causes
• Wilson’s disease (look for associated liver disease
and Kayser-Fleisher rings on cornea).
• Huntington’s disease (trace family history).
• Post-pill or pregnancy chorea
• Sydenham’s chorea
• Stroke.
Hemiballismus
Lesions of the contralateral subthalamic nucleus or its
connections—common causes: stroke.
Dystonia
Affected only one part of the body—facial dystonia.
• Isolated torticollis
• Isolated writer’s cramp
• Affecting two or more adjacent part of the body—
segmental dystonia. For example:
– Torticollis and dystonic posturing in the same arm
– Affects part of the body that are not adjacent
– Generalized dystonia: as for chorea above—rare
causes: dystonia musculorum deformans.
Superficial Reflexes
Cremasteric Reflex
This reflex can be performed in men. The inner aspect of
the upper thigh is stroked downward. The movement of
the testicle in the scrotum is watched. Cremasteric
contraction elevates the testicle that side.
• Afferent : femoral nerve L1, L2
• Efferent : L1, L2
Your observation:
The cremasteric reflex is absent in:
• May occur with non-neurological local pathology or
previous local service
• Lesion in reflex arc
• Pyramidal lesion above L1.
Anal Reflex
Make the patient to lie on his side with knees flexed.
Lightly stroke the anal margin with a stick.
You will find visible contraction of the external anal sphincter
Interpretation
This tests the intergrity of the reflex arc with

segmental innervation of S4 and S5 for sensory and motor
components.
Tests for Meningeal Irritation
i. Neck Stiffness
(Not to be performed if there could be cervical instability,
e.g. following trauma or in patients with rheumatoid
arthiritis).
• The patient should be lying flat.
• Place your hands behind the patient’s head.
• Gently rotate the head—moving the head as if the
patient was indicating no. Feel the stiffness.
• Gently lift the head off the bed—feel the tone in the
neck.
• Watch the legs for hip and knee flexion.
Interpretation
• Neck moves easily in both planes, with the chin easily
reaching the chest on neck flexion—normal.
• Neck rigid on movement—neck stiffness
• Indicates: meningeal irritation—common causes: viral
and bacterial meningitis, subarachnoid hemorrhage—
rarer causes: carcinomatous, granulomatous, fungal
meningitis.
• May also occur in : severe cervical spondylosis,
parkinsonism, with tonsillar herniation
N.B. proceed to test for Kernig’s sign.
• Hip and knee flexion in response to neck flexion—
Brudzinski’s sign. This indicates meningeal irritation.
Hint: Cervical lymphadenopathy and severe
pharyngitis may simulate neck stiffness—but
stiffness is usually only on flexion and appropriate
physical signs of these pathologies are easily found.
ii. Testing for Kernig’s sign
• The patient is lying flat on the bed.
• Flex the leg at the hip with the knee flexed.
• Then try to extend the knee
• Repeat on the other side
Interpretation
• Knee straightens without difficulty—normal
• Resistance to knee straightening—Kernig’s sign :
indicates meningeal irritation or, if unilateral, may
occur with radiculopathy (cf straight leg raising).
N.B. Kernig’s sign is absent with other causes of
neck stiffness.
iii. Straight leg raising test
Test for radicular entrapment:
• With the patient lying flat on the bed, lift the leg,
holding the heel.
• Note angle attained and any difference between the
two sides
Central Nervous System 245
• Normal > 90°, less in older patients
• Limitation with pain in back—nerve root entrapment.
Palpation of Nerves
Causes of Thickening of Nerves
• Leprosy
• Amyloidosis
• Some hereditary neuropathies
• Neuropathies
• Recurrent variety of CIDP (chronic inflammatory
demyelinating polyneuropathy)
• Refsum’s disease.
Nerves Palpable in Leprosy
1. Ulnar nerve
2. Dorsal cutaneous branch of radial and ulnar n.
3. Several n (behind lateral malleolus)
4. Greater auricular n
5. Lateral popliteal n.
HEMIPLEGIA
Past History in Hemiplegia
• Similar attacks with full recovery indicate TIA.
• Head injury with waxing and wanning neurologic deficit
indicate subdural hematoma.
• History of exposure to STD during young age and
adulthood hemiplegia after a few decades suggest
neurosyphilis.
• Hypertensive history suggests cerebral thrombosis and
hemorrhage.
• Diabetes history suggests accelerated atherosclerosis and
hypertension.
• Past history of rheumatic fever with valvular heart
disease suggests cerebral emboli.
• With epilepsy and migraine in past history, think of Todd’s
palsy, which recovers in 24 hours.
• With past history of TB arteritis, TB meningitis and
tuberculoma.
• History of oral contraceptive pill use for more than
5 years may predispose to stroke in females.
• Anticoagulant therapy and stroke occurring simul-
taneously think of cerebral hemorrhage.
• Fever in hemiplegia suggests meningitis, cerebral abscess,
encephalitis, leukemia, lymphoma.
• Pain in chest with recent or past myocardial infarction
can get embolic stroke from mural thrombosis.
• Intermittent claudication suggests atherosclerosis.
• History of severe headache in subarachnoid and cerebral
hemorrhage.
246 Essentials of Clinical Medicine

Pronation Drift 9, 10, 11, 12th cranial nerve’s sympathetic affection on

It is a sign which is elicited in case of hemiparesis (mild same side with opposite side sensory loss and same
grade). When the patient is asked to hold his arm straight in side cerebellar signs.
front of his body, while keeping his eyes closed, there occurs • If basilar artery is involved, all the four limbs affected
slight pronation of arms/forearm. with bulbar palsy motor, sensory and cerebellar signs
with bilateral plantar extensor along with vertigo, atonia,
Localization of Site of Lesion in Hemiplegia paresis, paresthesia.
1. Cortical: Clinical Features of Posterior Cerebellar
• No sensory loss Artery Occlusion
• Patchy weakness in opposite side of face/upper limb/ • Weber’s syndrome—3rd nerve with contrateral hemi-
lower limb. plegia.
• Cortical sensory loss • Thalamic syndrome with chorea/hemiballismus with
• Focal seizures hemisensory loss. Visual defect with cortical blindness
• Aphasia. is present.
Subcortical (corona radiate) patchy.
2. Capsular (internal capsule) dense hemiplegia with upper Common Sites for Hemmorhages
motor facial palsy, hemplegia with hemianesthesia. • Basal ganglia and thalamus.
3. Mid-brain—3rd nerve palsy and red nucleus involvement. • Lenticulostriate branch of middle cerebral artery (most
Ipsilateral 3rd n. can be associated with contralateral commonly artery affected).
pyramidal sign with tremors or rigidity. Weser’s Diagnosis of Hysterical Hemiplegia
syndrome (3rd nerve same side) hemiplegia of opposite
side. Benedikt’s—hemiplegia with rigidity and tremor • Common in females.
on opposite side. • Acute onset.
4. Pons—(Millard-Gubler syndrome) Ipsilateral lower 6th • Bizarre sensory, motor and psychoface escape the
and 7th n. palsy with contralateral hemiplegia. hemiplegia
5. Medula oblongata (PICA) same-sided cerebellar sign with • Deep tendon reflexes normal
9th, 10th and 12th cranial n. palsy of same side, along • Limbs flaccid
with opposite side hemianesthesia (Temperature, pain • Plantar flexion
• Hysterical gait.
sensation lost).
6. Spinal cord (cervical cord) Brown-Sequred syndrome— Clinical Features of Anterior Cerebral
opposite side of hemianesthesia with same side pyramidal Artery Occlusion
and cerebellar signs no cranial nerve lesion. • Expressive aphasic
7. Atonic hemiplegia lesion at—contralateral basis pontis— • Lower limbs move weak
affected side shows hemiplegia with cerebellar atonia. • Cortical sensory loss
8. Foville’s syndrome—6th n, 7th n. paralysis with • Forced grasping and groping
contralateral hemiplegia. • Bladder affection very common
Clinical Features of Internal Carotid • Frontal lobe release sign present.
Artery Occlusion Clinical Features of Middle Cerebral
• Ipsilateral blindness with Horner’s syndrome partial. Artery Occlusion
• Contralateral hemiplegia and hemianesthesia. • Extensive aphasia
• Bruit over the same side carotid or opposite carotid • Upper limbs more weak
artery. • Hemianesthesia.
• Jaw classification.
Clinical Features of Intravenous Sinus Thrombosis
Clinical Features of Vertebrobasilar
• Defect is bilateral
Artery Occlusion • Delta sign in CT
• Giddiness, vertigo, vomiting in a hypertensive elderly • Negative Queckensted’s test
man. • Non-filling of venous sinuses in levo phase of cerebral
• If PICA (posterior interior cerebellar artery syndrome angiography
or Wallenberg’s syndrome), the patient develops 5, 7, • Fifty percent have convulsions.
 Central Nervous System 247

Causes of Recurrent Transient Hemiplegia • Depression

• Disseminated sclerosis • Normal pressure, hydrocephalous following SAH
• Cerebral embolism • Cortical blindness.
• Migraine Poor Prognostic Features in Patients with CVA
• Hypertensive encephalopathy.
• Altered sensorium
Muscles receiving bilateral innervation and hence escaping
• Chyne-Stokes respiration
paralysis in hemiplegia (UMNL)
• Pupillary changes
• Upper half of the face
• Absent brainstem reflexes
• Masticating muscles
• Uncontrolled diabetes mellitus
• Muscles supplied by 9th, 10th and 11th
• Massive cerebral edema.
• Cranial nerves
• All trunk muscles Causes of Death in Patients with Stroke
• Diaphragm. • Massive cerebral edema
Differences between Bulbar and • Pontine hemorrhage involving vital centers
Suprabulbar Hemiplegia • Aspiration pneumonia
• Cardiac arrhythmias
Suprabulbar palsy
• Massive pulmonary embolism from deep vein throm-
• Paralysis of palati, tongue and pharynx
bosis
• Pinpoint pupil • Septicemia due to nosocomial (hospital acquired)
• Hyperpraxia infection.
• Glycosuria due to pontine lesion.
Differential Diagnosis of Strokes
Bulbar palsy
(Stroke Mimics)
• Paralysis of tongues palals and vocal cord
• Horner’s syndrome 1. Infections
• 5th nerve face involvement • Encephalitis, meningitis, abscess, cerebral malaria,
• Alania due to medullary lesion. fever with rigors.
2. Hematoma:
Causes of Cerebral Thrombosis • Subdural—especially in cases of head injury, but
• Atherosclerosis usually missed (neglected by the patient) and the
• Cerebral thrombophlebitis patient goes into lucid interval and may present
• Arteritis with hemiparesis/hemiplegia sometimes later in his
• Hypotension and shock. life.
• Hypoxia. • Extradural—injury is usually not missed (i.e. it is
• Hemotological disease like sickle cell disease, poly- remembered) by the patient.
esthesia, purpura, etc. 3. Tumor
• Benign or malignant
Causes of Cerebral Hemorrhage • Primary or secondary in nature
• Hypertension • Bleeding inside the tumor mass (if blood vessels
• Anticoagulant therapy rupture)
• DIC (disseminated intravascular coagulation) • Pseudoacute onset, i.e. the pathology/abnormality
• Head injury occurred earlier but was neglected by the patient.
• Subarachnoid hemorrhage 4. Post-ictal condition
• Hemorrhage disorders like leukemia, purpua, hemophilia • After the attack of seizures/convulsion passes off.
• Viper snake bite. 5. Metabolic encephalopathy
• Features of hypoxia
Sequelae of Stroke (Consequences) • Hypercarbia
• Residual disability • Hypoglycemia
• Scar epilepsy • Hyperglycemia
• Multi-infarct dementia • Ketoacidosis
• Septicemia
248 Essentials of Clinical Medicine

• Toxemia – Same sided lesion with opposite side sensory

• Uremia changes
• Hepatic encephalopathy. – Lesion at medulla.
Causes of Congenital Hemiplegia and Predisposing Factors for Hemiplegia
Infantile Hemiplegia • Hypertension
• Congenital cerebral deformity • Diabetes mellitus
• Intracranial angioma • Arteritis
• Infective disorder of childhood • Smoking
• Whoophing cough • Obesity
• Complication of meningitis. • Hyperlipidemia
• Contraceptive pill
Causes of Gradual Onset of Hemiplegia • Polycythemia
• Cerebral tumors • Valvular heart disease
• Chronic subdural hematoma • Pregnant lady
• Cerebral abscess • Cardiac disease
• Meningitis and encephalitis. • Hereditary
• Hyperviscosity syndrome.
Facial Clues to Localize Site of Hemiplegia
Table 8.51: Disturbances associated + Hemiplegia
• UMN 7th nerve on the same side of hemiplegia lesion is
at internal capsule on the opposite side Type of defect Site of lesion
• LMN type 7th nerve with contralateral hemiplegia— Mono-ocular blindness with Internal carotid artery below the
Lesion is at pons 7th nucleus as the side of 7th palsy contralateral hemiplegia branching of ophthalmic artery
• No facial involvement—below the level of pons. Transient visual disturbance and a. Disseminated sclerosis
hemiplegia b. Brain tumor
Causes of Monoplegia Hormonymous hemianopia with Posterior limb of internal capsule
hemiplegia
• Cortical or subcortical lesion Quadrantic hemianopia with Involvement of parietal or tem-
• Multiple sclerosis hemiplegia poral lobe due to expanding intra-
• Encephalitis cranial lesion
• Poliomyelitis Complete blindness or homonymous Basilar artery occlusion
hemianopia
• Neuropathy
• Hysterical.
Table 8.52: Causes of hemiplegia
Hemiplegia + Hemianopia—Causes Thombosis Embolism Hemorrhage

• Internal carotid occlusion—homonymous hemianopia Atherosclerosis Cyanotic heart Thombocytopenia

disease
• Optic radiation—parietal fiber Arteritis Cardiac DIC
• Optic radiation—temporal fibers catheterization
• Calcarine cortex—posterior cerebral artery occlusion Sickle cell anemia Infective endocarditis Vit K deficiency
Homocystinuria Acquired valvular Aneurysm
of cortical branch.
disease
Infection Vascular tumor AV malformation
Hemiplegia + Sensory Loss—Causes Polycythemia Cardiac tumor Hypertension
Leukemia Trauma
• One half of body including face and half of the body Thrombocytosis Hemorrhage within a
– Thalamic syndrome tumor
– Hysterial
• Face spared but hemiplegia with hemianesthesia—due Paraplegia
to lesion of the opposite side capsular lesion History in Cases of Paraplegia
• Opposite side hemianesthesia with same side pyramidal • Young age
cerebral lesion. Brown-Sequard lesion (spinal cord) – Childhood causes.
– Lateral medullary syndrome (PICA) – Hereditary spastic paraplegia
– Lower cranial nerve affected 9th,10th,11th and 12th – Spina bifida with spastic paraplegia
 Central Nervous System 249

– Myelodysplasia of lumbosacral cord flexion is said to occur with the damage to reticulospinal
– Friedriech’s ataxia tract and vestibulospinal tract. Reflux evacuation of bladder
– Birth injuries and bowel occurs. Mass reflex may be present.
– Primary muscle atrophy
– Marasmic child Table 8.54: Causes of lower motor type of paralysis
– Thrombosis of superior sagittal sinus Ant. horn Polio/Motor neuron disease
• Old age –MND Ant. root, post root, and post Radiculitis—cervical / lumbar
– Neoplasm ganglions spondylosis
• Middle age—Pott’s disease Peripheral nerve, myoneural Herper zoster
junction, muscle.
Diabetic, alcoholic, beri-beri,
Table 8.53: Causes of paraplegia leprosy
Gradual onset Acute onset Myasthenia gravis, myopathy.

• Pure motor • Trauma

– Motor neuron disease
– Hereditary spastic. paraplegia
– Disseminated sclerosis
– Lathyrism
• Posterolateral column
Lesion—Subacute combined
degeneratoin
– Pellagra.
– Friedriech’s ataxia
– SMON
• Miscellaneous
– Acute infective myelopathy
– Syringomyelia
Causes of Motor Paraplegia with
No Sensory Changes
• Infection
– Viral
– Meningovascular
– Syphilis
• Prolapsed intervertebral disk
• Vascular—Ant. spinal artery
thrombosis
• Leriche’s syndrome
• Demyelinating disease
– Disseminated sclerosis
– Devic’s disease
• Metabolic—Acute porphyria
• Iatrogenic –
– Metabolic—Acute
porphyria
• Miscellaneous
– Hysteria
– Bleeding in spinal tumor
A Few Diseases in which both Upper and
Lower Motor Neuron Paralysis are Together
• Amyotrophic lateral sclerosis (C5, 6, 7, 8)
• Syringomelia (C6, 7, 8)
• Cervical compression (9, 7, 8)
• Hematomyelin
• MND (motor neuron disease)
• Cervical spondylosis
• Cervical cord tumor.
Causes of Recurrent Paraplegia
• Familial periodic paralysis
• Disseminated sclerosis
• Recurrent spinal artery insufficiency
• AV malformation with edema or minor bleed in spinal
cord
• Spinal angiomas.
Table 8.55: Differences between flaccid and spastic paraplegia

• Cortical tumor situated over superior sagittal sinus. Flaccid Spastic

• Motor neuron diseases. Type Lower motor neuron except during Upper motor
neuronal shock of upper motor
• Lathyrism.
Causes Polio, Peripheral neuritis, Intra/extramedullary
• Hereditary spastic paraplegia. myopathies, cauda equina spinal cord tumor, Pott’s
• Erb’s spastic paraplegia. spine
Tone Decreased Increased
Plantar Down going or unelicitable Up going
Paraplegia in Extension Bladder Bladder not affected except in Usually affected with
cauda equina where dribbling retention of urine then
The lower limbs are spastic and fully extended. Initially it is of urine occurs. Patient is not overflow
a case of spastic paraplegia in extension. aware of bladder sensation.

Paraplegia in Flexion ABNORMAL MOVEMENTS

With longer duration of paraplegia, there is flexor spasms Three Main Components of
occurring spontaneously. It is called paraplegia in flexion. Parkinson’s Disease
This carries poor prognosis. Even a surgical intervention to • Tremor
remove a spinal cord tumor is attempted, paraplegia will • Muscular
not improve. Neurological defect persists. Paraplegia in • Hypokinesia (Bradykinesia).
250 Essentials of Clinical Medicine

Parkinson’s Tremors Disease of Muscles and

Neuromuscular Junction
Seen at rest, diminishing during action and sleep. They are
at 4 to 6 Hz in frequency. And may affect tongue, leg, arm, Clinical Features of Myasthenia Gravis
feet. There may be rolling tremor. • Ptosis bilateral, diplopia, nasal regurgitation, dysphagia,
loss of facial expression and jaw drop, neck muscle
Clinical Features of Parkinsonism weakness, girdle muscle weakness, distal muscle
Non-Specific Symptoms weakness.
• Weakness increases during repeated use and improves
• Tiredness
with rest. Sustained upward gaze produces gradual
• Aching limbs
ptosis of eyelid—curtain sign.
• Mental slowness
• Depression Differential Diagnosis of Myathenia Gravis
• Micrographia. • Drug-induced myasthenia—penicillamine
Specific Symptoms • Lumbert-Eaton myasthenic syndrome
• Neurasthenia
• Tremor
• Hyperthyroidism
• Hypokinesia.
• Botulism
• Rigidity of muscular tone.
• Progressive extrinsic ophthalmoplegia.
– To start with unilateral later becomes bilateral
– Plantar flexor Table 8.57: Causes of muscle weakness
– Glabellar tap positive Proximal muscle weakness Distal muscle weakness
– Eye movements impaired in upward gaze and
• Muscular dystrophy • Polyneuritis
convergence. • Polymyositis or dermato- • Distal goner’s type
myositis myopathy
Role of Surgery in Parkinsonism • DM-amyotrophy • Myotoxic dystrophy
• GB syndrome • Charcot-Marie-Tooth
• Stereotactic thalamotomy in unilateral tremor not • Porphyric neuropathy disease
responding to therapy. • Fulminant myasthenia gravis
• Implantation of facial midbrain. • Cushing’s syndrome
• Metabolic myopathy hypokalemia
• Implantation of adrenal cells into basal ganglia. • Thyrotoxic

Parkinsonism Plus Syndrome Table 8.58: Myasthenia gravis and myasthenic syndrome

When the symptoms of parkinsonism are present along with Myasthenia gravis Myasthenic syndrome
the following disorders, it is called parkinsonism plus Sex Female Male
Age Young and middle age Old age
syndrome. These disorders are: Muscle affected Ocular, facial, bulbar, Pelvic girdle, proximal
• Shy-Drager syndrome proximal muscles muscle of neck, middle
• Wilson’s disease (late) trunk
• Huntington’s chorea Etiology Antibodies against Defective release of acety-
muscle endplate lcholine from terminals
• Steele-Richardson-Olzewik syndrome Muscle power on Deteriorates Increases
• Progressive supranuclear palsy exercise
• Normal pressure hydrocephalous Treatment Anticholinergic drugs Removal of tumors,
• Striato niagral degeneration. quinidine hydrochloride
20-30 mg/kg/day in divided
Table 8.56: Differention between classical and doses
arteriosclerotic parkinsonism
Table 8.59: Distinguish between cerebellar and sensory ataxia
Classical parkinsonism Arteriosclerotic parkinsonism
Feature Cerebellar Sensory
1. No UMNL sign UMNL sign present
Lesion Cerebellum or its connec- Mainly of local reflexes
2. Onset is gradual Onset is acute, condition worsens
tion including vetibule
in between attackes
Muscle atrophy Absent May be present
3. Upper limbs affected first Gait and lower limbs affected first.
Tone Decreased Markedly diminished
4. Levo dopa improves the Effect of levo dopa is doubtful
Power Normal Usually decreased
condition
Contd...
 Central Nervous System 251

Contd... • Postinfective demyelination

Feature Cerebellar Sensory • Abscess
Jerks Pendular Absent • Infarct
* Feature of Absent Present • Hysteria
posterior
column lesion
* Segmental Present
Tests Used to Assess Cerebellar Function
sensory • Scanning speech—words are broken, dysarthria, speaks
impairment
* Impaired Present
slowly with scanning syllables, pronounces Calcutta as
vibration sense CAL-CUT-TA
Features of Present Absent • Nystagmus
cerebellar dys- • Rhomberg’s test
function • Tandem walking, the patient is asked to walk along a
Gait Staggering High stepping
Walking in No change Impossible to walk
straight line
darkness • Finger-nose test
Romberg’s Negative Positive • Knee-heel test
Ataxia with eyes Open Close • Dysdiadochokinesia test- the patient is asked to alternate
Diseases causing Hereditary ataxia, vascular Tabes dorsalis, subacute
pronation and supination movements of hands
lesions of cerebellum, neo- combined degeneration,
plasm, multiple sclerosis syringomyelia • Rebound test of Gordon-Holmes—the patient is asked
to flex his elbow against resistance offered by observer,
then resistance is suddenly withdrawn- in cerebellar
Table 8.60: Distinguish between cerebellar and sensory ataxia lesion flexion cannot be arrested by instant contraction
Peripheral Central of triceps (antagonist muscle) and the patient strikes his
Conjugate Conjugate or disassociated face with the hand.
Affected equally Abducted eye predominantly
affected MUSCLE PAIN OR WEAKNESS OR WASTING
Unidirectional Bidirectional
Enhanced by loss of fixation Abolished by loss of fixation 1. Necrosis—myoglobin may appear in urine after acute
Horizontal or rotatory Horizontal, rotatory or vertical muscle necrosis (rhabdomyolysis) causing brown-red
Transient and associated Persistent and unassociated with discoloration of urine.
with vertigo vertigo
2. In ulnar paralysis—the hand becomes deformed by
overextension of the wrist, combined with excessive
Ataxia flexion of ulnar two digits, so that claw-like attitude is
produced. Wasting of small muscles of hand; for
Defined as clumsiness or unsteadiness of gait despite good
example, due to median or ulnar n lesion, cervicle root
muscle power.
(T1) disease or loss of anterior horn cells at same level,
Causes of Ataxia gives the hand a flattened appearance.
a. Sensory ataxia 3. Wasting of small hand muscles in a chronic neuropathy.
• Posterior column—subacute combined degeneration, a. There is marked wasting of abductor pollicis brevis
syringomyelia, multiple sclerosis. b. Guttering of dorsal surfaces of the hand indicating
• Posterior roots—tabes dorsalis atrophy of dorsal interossei.
• Posterior nerve—peripheral neuropathy 4. Symptomatic muscular weakness in the absence of
• Post-central convolution—diseases of parietal lobe. neurological disease is a feature of several metabolic
disorders including thyrotoxicosis, Cushing’s syndrome
b. Vestibular lesion
and Vit. D deficiency
• Acute viral labyrinthitis
5. In all these conditions, the metabolic myopathy causes
• Drug-induced labyrinthitis, e.g. streptomycin,
symmetrical proximal weakness, mainly involving the
phenytoin, barbiturate, carbamaze, muslin.
shoulder and hip girdle musculature. There is usually
• Infection spreading to labyrinthine region.
associated muscle wasting. The major symptom is
c. Cerebellar lesions difficulty in climbing upstairs, boarding a bus or rising
• Hemorrhage from sitting position.
252 Essentials of Clinical Medicine
6. Conditions in which metabolic myopathy is a feature:
• Painless:
– Hyperthyroidism (Proximal weakness)
– Cushing’s syndrome including iatrogenic steroid
myopathy.
– Acromegaly
• Painful:
– Vit D deficiency
– Osteomalacia
– Hypothyroidism
7. The differential diagnosis of painful proximal muscular
weakness includes polymyositis and polymyalgia
rheumatica as well as spinal root or plexus disease.
8. Proximal weakness with or without wasting of shoulder
and hip girdle musculature (proximal myopathy) is a
typical feature of thyrotoxicosis, glucocorticoid excess
and Vit D deficiency. Osteomalacia myopathy is often
associated with myalgia.
Patterns of Weakness
1. Pattern of weakness and disability described by the
patient and observed on examination is of great help in
considering diagnosis.
2. Try to work out pattern of weakness when watching
the patient coming in your consulting room and observe
the gait and posture and capacity for movement of upper
limb.
i. Hemiplegia
1. Paralysis of one side of body involving arm and
leg and also of face (fascio–brachio-crural
hemiparesis)
2. Virtually always due to a lesion in corticospinal
pathway and is therefore an UMNL.
ii. Crossed paralysis:
1. Weakness in an ipsilateral cranial muscle group
with a contralateral hemisparesis.
2. It is a sign of brainstem disease.
iii. Paraplegia:
1. Paralysis of both legs
2. Nearly always due to a spinal cord lesion and so
UMNL in type.
iv. Monoplegia:
1. Is a paralysis of one limb which may be arm
(brachial monoplegia) or leg (crural monoplegia)
2. This may be due to root or plexus disease.
iv. Quadriplegia:
1. Feature of cervical cord disease.
2. Weakness of all limbs.
v. Corticospinal lesion:
1. As in spastic hemiparesis, there is weakness, in
the leg in hip flexion and in dorsiflexion of foot
and in arm, in abduction of shoulder and in
dorsiflexion of wrist.
2. There is supranuclear (UMN) facial palsy.
3. Face and arm or leg may be particularly involved
depending on location of lesion in hemisphere.
4. Slowness and clumsiness of rapid finger fine
movement is a feature of spastic hemiplegia
5. Gait is characteristically affected with a slow,
dragging rolling gait on affected side, the hip and
foot not being lifted up to clear the ground so
that toe of shoe wears quickly.
6. Antagonistic movements such as hip extension
and plantar flexion of foot are strikingly less
involved than extensor muscle in early stages.
7. This characteristic pattern of weakness is
important in diagnosis.
vi. Detection of hemiplegia in a comatose patient
1. If the paralysis is of recent onset, hypotension
may be detected in the paralyzed limbs. If arm,
e.g. is raised from side and allowed to drop, it
falls, it is paralysed, as if it is not a part of body
of patient, the sound arm also falls, but not in
such an utterly limb fashion.
2. Face is asymmetrical, the angle of the mouth
more open on paralyzed side and affected cheek
moves loosely outwards and inwards with resp.
3. Abdo. and tendon reflex may be absent on both
sides, but an extensor plantar response can usually
be obtained on hemiplegic side.
vi. Myasthenic weakness:
1. Usually affects external ocular and bulbar
muscles more than rest of skeletal musculature.
2. Worsened or provoked by repeated contraction
of affected muscle (myasthenic fatigue).
3. In Lambert-Eaton myasthenic syndrome (LEMS-
“carcinomatous myopathy”) there is weakness
initially; but during continued contraction of a
muscle or continued exertion, strength improves
at first followed by weakness if exertion is
continued.
4. During the phase of increased strength, the tendon
reflexes which are often difficult to elicit in this
condition and diagnosis is made by EMG.
5. LES was first described in association with small
cell ca. of bronchus; but in about ½ the people
with the syndrome, it occurs as an idiopathic
autoimmune disorder
 Central Nervous System 253

vii. Neurogenic weakness: symmetrical and often affects the pelvifemoral

1. In LMN lesion weakness is associated with muscles more severely than pectoral girdle mus.
muscular atrophy, reduced tone and absent 2. Affected muscles are atrophic and may feel firmer
tendon reflex. These are features of LMNL. than normal.
2. Weakness and atrophy may be localized as in 3. In Duchenne’s muscle dystrophy (Xp21
peripheral nerve or root disease or generalized as dystrophy) pseu-dohypertrophy of some weak
in anterior horn cell disease, e.g. motor neuron muscle develops.
lesion. In latter and to a less extent in other types 4. In inflammatory muscle disease, the muscles are
of neurogenic weakness, fasciculation may tender to palpation and may be swollen. Fascicu-
occur. (spontaneous contraction of groups of lation do not occur in myopathic weakness.
muscle fibers probably representing enlarged, 5. Progressive proximal muscle weakness and
reinnervated motor units or parts of such motor atrophy, calf hypertrophy and male childhood
units and may also occur in fatigued normal onset suggest Duchenne’s disease.
subject. In chronic neurogenic weakness action x. Myotonia:
fasciculation may be noted. This occurs during 1. In some inherited muscular disorders, of which
initial contraction of a muscle, the muscle is seen myotonic dystrophy is commonest, relaxation is
to undergo rhythmic fasciculation-like con- impaired following contraction of a muscle.
traction as motor units are recruited into 2. In some myotonic disorders, affected muscle
muscular effort. Fatigue is a common feature of may be weak.
neurogenic weakness, but also occurs in some 3. Phenomenon of myotonia is most evident when
myopathies. muscles are cold and it is, therefore often best
viii. Peripheral neuropathy: demonstrated in hand.
1. Distal tendon reflexes are diminished in axonal 4. Ask the patient to grip your hand firmly and then
neuropathies; and in demyelinating neuropathies, let go suddenly. The grasp is maintained for a
these may be areflexia. moment and then slowly and gradually released.
2. In disease of individual peripheral n. (mononeuro- 5. Myotonia can be demonstrated in tongue and
pathies), the c/f are restricted to distribution of other muscles (e.g. in thenar eminence) by lightly
affected n. and in brachial plexus lesions to wider striking the muscle with a small patellar hammer.
motor and sensory distribution of cervical roots. A dimple of contraction appears that relax only
3. Mononeuropathies: Disorders of single nerves: slowly.
a. Motor and sensory involvement in distribution Table 8.61: Causes of muscle weakness
of affected n.
b. Acute mononeuropathies are often painful Anatomical etiology Associated features Common causes
c. Multiple nerves may be affected (mono- 1. Lower motor Muscle atrophy Peripheral neuropathy
neuron fasciculation Radiculopathies
neuritis multiplex)
Reflex absent or Ant. horn cell damage
4. Causes of brachial plexus lesion: decreased (e.g. poliomyelitis)
a. Brachial neuritis Hypotonia Motor neuron disease
b. Infiltration by tumor, e.g. Ca. of breast may 2. Upper motor Patterned weakness
infiltrate the brachial plexus, lymphoma may neuron little or no muscle CVD (e.g. hemiplegia)
wasting
infiltrate nerve root Hyperreflexia Spinal injury (e.g. para-
c. Radiation plexopathy (rarely follows radio- plegia)
therapy for breast ca.) Hypertonia Multiple sclerosis
d. Vasculitis 3. Myopathies Muscle wasting Hereditary (e.g. muscular
(usually proximal) dystrophy)
e. Trauma, especially in traffic accidents or at
Hypotonia Alcohol and other toxins
work direct or stretch injuries Tenderness
f. Compression, e.g. by cervical rib or tumor. (myositis)
ix. Myopathic weakness: 4. Psychological Inconsistent weak- Stress
ness
1. In myopathies, dystrophies and polymyositis, No associated features Anxiety
mus. weakness is strikingly proximal usually Compensation claims
254 Essentials of Clinical Medicine

xi. Wasting or weakness: c. Cervical hypertrophic pachymeningitis

1. Wasting or weakness of trapezius muscle will d. Neuralgic amyotrophy
produce a flaring of vertebral border of scapula 6. Peripheral nerve lesions (neuropathies)
which will be displaced away from spine in its a. Leprosy
upper part and rotated towards the spine at its b. Carpal tunnel syndrome
lower end. The point of shoulder will appear c. Lead paralysis
dropped and arm will appear lower. d. Diphtheria
2. Wasting is also seen in RA 7. Myoneural junction
• Also seen in LMNL a. Eaton-Lambert syndrome
• Causes include: 8. Muscle diseases
– Syringomyelia a. Muscular dystrophy
– Poliomyelitis b. Polymyositis
– Lesion of first thoracic nerve root c. Myotonia
– Peripheral neuropathies and motor neuron 9. Disuse atrophy
disesase a. Therapeutic immobilization: fracture
– Ulnar and median nerve lesion will affect b. Arthritis: RA
muscle group, e.g. in leprosy c. Post-paralytic
• In carpal tunnel syndrome median n. com- 10. Systemic wasting
pression may result in selective wasting of a. TB
the thenar muscle b. Malignancy
• This may occur in RA, autoimmune hypo- c. Thyrotoxicosis
thyroidism and acromegaly or may be d. HIV infection or AIDS
associated with premenstrual fluid retention e. Addison’s disease.
or pregnancy.
MUSCULAR DYSTROPHY
• Bilateral facial weakness can be due to UMNL
or LMNL as well as disorders of muscle and Types of Muscle Wasting
NMJ (neuromuscular junction).
Muscle wasting is usually a sign of lower or primary muscle
• Progressive supranuclear paresis will cause
disease.
a bilateral facial paresis associated with a
lability of emotional expression and a disso- Generalized Wasting
ciation between emotional (well preserved)
and voluntary (poorly preserved/movements). a. Advanced systemic illness (CVS, RS, Renal, IDDM)
b. Thyrotoxicosis
Causes of Wasting of Muscles c. Malignancy
d. Advanced stages of crippling neurological diseases
1. Parietal lobe lesions
(motor neuron diseases, muscular dystrophies)
2. Vertebral lesions
a. Craniovertebral junctional anomalies. Muscle Wasting in Upper Limbs
b. Vertebral metastasis.
3. Spinal cord lesions Predominantly Proximal Muscle Wasting
a. Motor neuron disease. a. Spinal muscular atrophy
b. Syringomyelia. b. Motor neuron disease
4. Anterior horn cell lesions c. Syringomyelia
a. Poliomyelitis d. Compressive lesion of C5-C6 (cervical spondylosis)
b. Peroneal muscular atrophy e. Lesion of upper brachial plexus (Erb’s palsy)
c. Progressive muscular atrophy f. Late stages of muscular dystrophies (facio-scapulo-
d. Spinomuscular atrophy humeral dystrophy, proximal limb girdle dystrophy,
5. Root lesion—radiculopathy Duchenne’s dystrophy, dystrophia myotonica.
a. Cervical spondylitis g. Inflammatory muscle disease (neuralgic amyotrophy,
b. Cervical cord tumor poliomyelitis, polymyositis)
 Central Nervous System 255

Proximal muscle wasting and weakness are signs of 6. Peripheral nerve lesion
primary muscle disease except myotonic dystrophy, a. Hansen’s disease (especially hypothenar)
mitochondrial myopathy, inclusion body myositis and distal b. Carpal tunnel syndrome (especially thenar)
muscular dystrophy of Gower. c. Lead poisoning (wrist drop)
Predominantly Distal Muscle Wasting 7. Muscle diseases
a. Distal muscular dystrophy
a. Motor neuron disease b. Polymyositis
b. Syringomelia
c. Myotonia
c. Cervical cord tumors (affecting segmental levels C8-
d. Distal myopathy of Gower.
T1)
8. Disuse atrophy
d. Lesion of lower brachial plexus (Klumple’s paralysis)
a. Therapeutic immobilization (fracture)
e. Cervical ribs
b. Arthritic (RA)
f. Cervical glandular enlargement
c. Postparalytic (hemiplegia)
g. Pancoast syndrome (superior pulmonary sulcus
e. Volkmann’s ischemic contracture (tight improper,
tumors)
plaster application).
h. Traumatic lesions of radial, median and ulnar nerves.
i. Peroneal muscular atrophy (Charcot-Marie-Tooth
Muscle Wasting in Lower Limbs
syndrome or hereditary sensory motor neuropathy
types I and II) Isolated wasting of muscles in lower limb is less common
j. Peripheral neuropathies. than in upper limb. The wasting usually occurs in
Distal muscle wasting and weakness are signs of the combination with that of upper limb.
peripheral neuropathy except porphyric neuropathy,
Conditions Producing Wasting in Lower Limb
diabetic amyotrophy and Guillain-Barré syndrome.
a. Cauda equina lesion
Both Proximal and Distal Muscle Wasting b. Peripheral neuropathy
a. Motor neuron disease c. Peroneal muscular atrophy (Charcot-Marie-Tooth
b. Syringomyelia. syndrome or hereditary motor-sensory neuropathy types
Small Muscle Wasting of Hand (C8-T1) I and II)
d. Poliomyelitis
1. Vertebral lesions e. Peripheral nerve trauma (lateral popliteal nerve)
a. Craniovertebral anomalies f. Tarsal tunnel syndrome.
b. Vertebral metastasis
2. Spinal cord lesion Conditions Causing Wasting in
a. Syringomyelia Both Upper and Lower Limbs
b. Cord compression by tumor
3. Anterior horn cell lesion a. Peroneal muscular atrophy (Charcot-Marie-Tooth
a. Motor neuron disease syndrome or heriditary motor-sensory neuropathy types
b. Poliomyelitis I and II)
c. Spiral muscular atrophy b. Chronic polyneuropathy.
4. Root lesion c. Spinal muscular atrophy (Werdnig-Hoffman’s disease
a. Cervical spondylitis in childhood later stages of Kugelberg-Welander
b. Cervical cord tumor syndrome)
c. Cervical hypertrophic pachymeningitis d. Distal myopathy of Gower
d. Pancoast tumor e. Hansen’s disesase.
e. Peroneal muscular atrophy
f. Cervical disc prolapse HYPERTONIA
5. Brachial plexsus lesion
Definition
a. Cervical rib
b. Klumpke’s paralysis (avulsion of lower brachial Increased resistance to passive movements, a heightened
plexsus) salience of muscles and increased firmness on palpation.
256 Essentials of Clinical Medicine

Causes 7. Gegenhalten phenomenon

• Here there is stiffening of a limb in response to
1. Pyramidal disorders
control and a resistance to passive changes in position
2. Extrapyramidal
and posture. The strength of antagonists increases
3. Hysterical
as one increases force to change the position off the
4. Tetany
limb. It can be mistaken for hysterical rigidity.
5. Tetanus
Causes: Encephalopathy, toxic (manganese, carbon
6. Decerebrate rigidity
monoxide), drugs (Reserpine, phenothiazine) and
7. Strychnine poisoning
extrapyramidal (dystonia, athetosis and spasmodic
8. Stiffman syndrome
torticollis).
9. Continous muscle fiber activity (ISAAC) disease.
8. Myotonia
• Increased muscles tone and contraction
Types of Hypertonia
• Tonic preservation of muscular contraction and
1. Clasp knife spasticity relaxation occurs slowly
• Increased tone in flexors of upper limb • Sudden movement may be followed by marked
• Resistance is increased only at the beginning or at spasm and inability to relax
end of passive movements • Repeatition of movements often brings about ease
• Seen in pyramidal lesions of relaxation and gradual decrease in hypertonicity
2. Lead pipe rigidity • Percussion myotonia can be elicited by mechanical
• Increased tone both in flexors and extensors stimulation
• Resistance present throughout the range of move- • Abrupt tapping of thenar eminence with hammer is
ment followed by opposition of thumb, which persists for
• Result from failure of straital regulation of tonus several seconds before relaxation begins. It can be
controlling centers in the midbrain and brainstem elicited by tapping on the tongue, deltoid or other
• Seen in EP lesions. muscular masses, which produces a “dimple” that
3. Cogwheel rigidity disappears slowly.
• Throughout entire range of passive movement
• Rhythmically jerky because static tremors which are HYPOTONIA
marked by rigidity emerge faintly during mani-
• Inspection: Muscle groups are lax and show pendulous
pulation.
shape when allowed to hang freely.
4. Decerebrate rigidity
• Palpation: Hypotonic muscle groups are flabby to feel
• Marked contraction of all extensor muscles
• There is decreased resistance to passive movements of
• Limbs are stiff, extended, head is erect and jaw
the joints, thus widening the range of movement at the
closed.
joint.
• The righting reflexes are abolished but the twice neck
and labyrinthine reflexes are retained and tender
Causes of Hypotonia
reflexes are exaggerated
• Due to release of vestibular nuclei from higher 1. Lesion of motor side of reflex arc:
extrapyramidal control and may result from lesion • Poliomyelitis
of brainstem at any level between superior colliculi • Polyneuritis
and vestibular nuclei • Peripheral nerve injuries
5. Hysterical rigidity 2. Lesion of sensory side of reflex arc:
• It is of wide distribution i. Tabes dorsalis
• It is of long duration ii. Herpes zoster
• Precipitated by alarm, excitement or fatigue with iii. Carcinomatous neuropathies
resistance usually increasing with increased force 3. Combined motor and sensory lesions:
or passive movement of the limb. i. Syringomyelia
6. Reflex rigidity ii. Cord or root compression
• Muscle spasm in response to pain, e.g. board-like iii. Gross cord destruction
rigidity of the abdomen in peritonitis, neck rigidity in 4. Lesion of muscle (myopathies)
meningitis. 5. State of spinal shock in UMNL

6. Cerebellar lesion
7. Chorea
8. Periodic paralysis (potassium disorders).
MYOTONIA
A state in which muscle contraction continues beyond the
period of time required for a particular movement to be
made.
• Best seen in face and hand muscles
• On face, a feature called “transverse smile”
• When the patient is asked to grip the examiner’s finger
and then let go immediately, a delay in the relaxation of
grip is noted.
Causes
a. Myotonic dystrophy
b. Myotonias congenita
c. Paramyotonia congenital (myotonia occurs on exposure
to cold).
MYASTHENIA GRAVIS
At any age, more common in young adults, more common
in females, predilection for extraocular muscles, muscles
of mastication, facial, pharyngeal and laryngeal muscle,
respiratory and limb muscles may also be affected.
1. Insidious onset
2. Exacerbation occurs in pregnancy or before menses
3. Cardinal symptom is abnormal fatigue of muscle and
intensification of symptoms towards the end of the day
or following vigorous exercise
4. The first symptoms are intermittent, ptosis or diplopia
but weakness of chewing, swallowing, speaking or of
moving the limb also occurs.
Fig. 8.36: Hemmorhagic infarction (stroke) unenhanced axial CT
showing density in Rt. anterior cerebral artery territory (arrows)
Central Nervous System 257
5. The muscle groups commonly involved in a decreasing
order are bulbar, neck, limb, girdle, distal limbs and trunk.
6. Sustained activity of muscle leads to temporary increase
in weakness as evidenced by:
a. Sustained upgaze for 2 min leads to increased ptosis.
Power increased after brief rest.
b. On counting aloud, the patient’s voice gradually
weakens.
7. The other features are brisk DTR and normal pupillary
response.
8. Mild atrophy of muscles occur in advanced stage.
EATON-LAMBERT SYNDROME
(Myasthenic Syndrome)
Associated with bronchial small cell carcinoma or rarely
with autoimmune disease (pernicious anemia)
1. Weakness is mostly in proximal muscles of limbs and
trunk.
2. The extraocular muscles and bulbar muscles are rarely
affected.
3. The power of muscles is steadily increased if contraction
is maintained.
4. Tendon reflexes are reduced and show a slight response
to edrophonium.
5. Autonomic disturbances are present (dry mouth,
constipation, impotence).
Neurology
(Figs 8.36 to 8.44; see also Plate 18)
1. A 30-year-old male complains of leg weakness and
paresthesia of arm and leg. Five years previously, he
had an episode of transient visual loss. On physical
Fig. 8.37: MR angiography
258 Essentials of Clinical Medicine

Fig. 8.41: MRI hemangioma of cerebellum demonstrating a sharply

marginated ovoid hyperintense mass in superior aspect of left
cerebellar hemiparesis on the superior margin of this cystic mass, a
flat nodule that is isointense to adjacent gray matter is identified (arrow)
(Fig. A only)

promised limb and neck muscle weakness with minimal

atrophy, normal sensory findings, intact deep tendon
reflexes. The most likely diagnosis is:
Fig. 8.38: Acute right hemiparesis—fluid attenuated inversion recovery
(FLAIR) MR image showing high signal in periventricular regions (small
Polymyositis
arrows) and posterior limb of left internal capsule (arrow)
EXAMINATION OF UNCONSCIOUS PATIENT
examination, there is hyper-reflexia, bilateral Babinski’s
Introduction
sign and cerebellar symmetric with poor finger-nose
test. When asked to look right, the left eye does not Level of Consciousness
move normally past in the middle. There is nystagmus The assessment of the unconscious and confused patient:
noted in the abducting eye. A more detailed history The reticular activating systems in the brainstem maintain
suggests the patient has had episodes of gait difficulty normal consciousness. Process that disturbs its functions
that has resolved spontaneously. He has no systemic will lead to altered consciousness.
symptoms of fever or weight. The most likely diagnosis
is: Conditions
Multiple sclerosis This may be seen in the following conditions:
2. Three weeks after an upper respiratory illness, a 25- 1. Diffuse emephalopathy: Generalized disturbances of
year-old male develops weakness of his arms and legs brain function affecting the whole brain, including the
over several days. On physical examination, he is reticular activating system.
tachypneic, with shallow respirations and symmetric
muscle weakness in both arms and legs. There is no
obvious sensory deficit, but motor reflexes cannot be
elicited. The most likely diagnosis is:
Guillain-Barré syndrome
3. A 45-year-old woman presents to her physician with an
eight-month history of gradually increasing limb
weakness. She first noticed difficulty climbing stairs,
then problem rising from chairs, walking more than half
a block, and finally, lifting her arms above the shoulder
level. Aside from some difficulty in swallowing, she
has no ocular, bulbar or sphincter problems and no
sensory complaints. Family history is negative for Fig. 8.42: Mature cerebral abcess (MRI) with hypointense rim,
neurological disease. Examination reveals significant central cavity and adjacent surrounding edema
 Central Nervous System 259

Fig. 8.43: Thymoma in a patient with myasthenia gravis. A.

Posteroanterior chest radiograph shows mass in right cardiophrenic
angle (arrowheads) B. Contrast-enhanced CT confirms well
circumscribed heterogeneous cardiophrenic angle mass (arrowheads)

2. Supratentorial lesions: Either massive leision or those

associated with distortion of brainstem—coning.
3. Infratentorial lesions: Producing direct damage to
brainstem
Assessment of patients with altered consciousness will be
divided into:
a. Resuscitation: (including same examination to allow you
to know how to resuscitate).
b. Examination: The examination of unconscious patient
must:
– Describe in a repeatable way the level of con-
sciousness, so it can be compared with other
observer’s results.
– Distinguish the three syndromes 1-3 above
– Attempt to define a cause—frequently requires
further investigations.

Herniation or Coning
Coning is what occurs when part of the brain is forced
through a rigid hole—either:
1. The uncus and the temporal lobe through the cerebellar
tentorium (which separates the cerebrum from the
cerebellum)—uncal herniation row
2. The cerebrum is pushed centrally through the tentorium
—central herniation.
There is a characteristic progression of signs in both
types of herniation.
N.B. The signs of herniation are superimposed on top of
signs due to the supratentorial mass causing the coning and
are progressive.
Uncal Herniation
Fig. 8.44A to C: CT – TB in a patient with advanced AIDS. A woman
A unilateral mass forces the ipsilateral temporal lobe through with status positive for HIV was shown at autopsy to have bilateral
the tentorium compressing the ipsilateral third nerve and pulmonary infiltrates. (A) Extensive lymphadenopathy, (B arrows)
later the contralateral upper brainstem, and eventually and multiple lytic bone lesion, (B-C) (arrowheads)
260 Essentials of Clinical Medicine

the whole brainstem. Once CSF flow is interrupted, Table 8.62: Glasgow coma scale
the process is accelerated by an increase in intracranial Score
pressure. Eyes open
Never 1
Physical signs: To pain 2
• Early - Ipsilateral dilated pupil and signs of supra- To verbal stimuli 3
tentorial mass lesion Spontaneously 4
• Later - Ipsilateral hemiplegia Best verbal response
- Progressive ptosis and third nerve palsy No response 1
Incomprehensible sounds 2
- Cheyne-Stokes respiration
Inappropriate words 3
• Later - Tetraparesis Disorientated and converses 4
- Bilateral fixed dilated pupils Orientated and converses 5
- Erratic respiration Best motor response
- Death No response 1
Extension (decerebrate rigidity) 2
Progression is usually rapid
Abnormal flexion (decorticate rigidity) 3
Flexion—withdrawal to pain 4
Central Herniation Localizes pain 5
A supratentorial lesion forces the diencephalon (the thalamus Obeys commands 5
and related structures between the upper brainstem and 15
cerebral hemispheres) centrally through the tentorium. This
compresses first the upper midbrain, later the pons and The three categories of information required in the GCS
medulla. assessment require no special skills and are thus particularly
suited for special observations by relatively untrained staff.
Physical signs The GCS is much used in the manage-ment of head injury.
• Early - Erratic respirations This simple non-timers clinical rating scale enables relatively
- Small reactive pupils accurate assessment of improvement or deterioration in a
- Increased limb tone patient’s conscious state by physicians, nurses and ambu-
- Bilateral extensor plantars lance staff alike. The best score is 15, worst is 3, representing
• Later - Cheyne-Stokes respiration “none in” all the categories assessed. Abnormal extension
- Decorticate rigidity implies decerebrate posturing.
• Later - Fixed dilated pupils Look at the Patient
- Decerebrate posturing
This is best of ten done from the end of bed.
Progression usually slower. • Is the patient lying still or moving? If there is movement:
Terms used to Describe the Levels – Are all the four limbs moved equally?
of Unconsciousness – Is the patient lying symmetrically?
– Are there any abnormal movements?
Drowsiness, confusion, stupurous, coma lose, are in
everyday language and are used in different senses by Inference
different observers. It is, therefore, better to subscribe • Arms flexed at elbow and wrist and legs extended at
the level of consciousness individually in terms described knee and ankle
below: – Decorticate posturing
• Change in the level of consciousness and associated • Arms extended at elbow, promoted and flexed at wrist
physical signs are very important and need to be and legs extended at knee and ankle
monitored. Always record findings. – Decerebrate posturing
• The Glasgow coma scale (GCS) is a quick, simple, • Head falls to one side, with flexion of the arm
reliable method for monitoring level of consciousness. – Hemiparesis
It includes three measures—eye opening, best motor • Brief spasms, lasting less than a second, of arms or legs
response and best verbal response. – Myoclonus
 Central Nervous System 261

Best Verbal Responses Pitfalls

Try to arouse the patient. Aphasia, either receptive or expressive, may be missed—
• It is patient rousable ? going a false level of consciousness and missing a focal
↓ dominant hemisphere sign.
If yes
↓ Head and Neck
Ask—“What is your name” ? • Inspect the head for evidence of trauma.
↓ • Percuss the skull (as for chest percussion) a fracture
If you get a reply may be associated with a “cracked pot sound”.
↓ • Look at ears and nose for evidence of CSF or bleeding.
See if he is oriented Examine for evidence of perforation, or otitis media?
a. In time • Test the neck for stiffness.
Ask Do not test, if there is evidence of trauma, until cervical
• What is the time by your watch? injury is excluded.
• What time of day is it now—morning, noon, evening
or night? Eyelids
• What day is it?
• What is the date today? Look at the eyelids:
• What is the season? • Do they open and close spontaneously?
• What is the month, year? • Tell the patient to open and close his eyes
b. In place • Assess the response to pain—do the eyes close?
Ask • Is there ant eyelid movement?
• Name of the place where you are in? • Is the eyelid movement symmetrical?
• What is the name of the Hospital or number of the • Is there a ptosis?
Ward? Where the patient is? And what is the floor • Is there a facial weakness?
number?
Pupils
• What is the name of the town/city?
c. In person Look at the pupils:
Ask • Note the size in mm.
• What is your name? • Test direct and consensual light reflex.
• What do you think I am? (pointing to your white
apron and stethoscope)? Table 8.63: Interpretation
• Name of the relatives standing nearby (whether the 1 2 3 4
patient recognizes them) Pupils Equal Pinpoint Opiates or pontine
Make a note of the errors made. lesion
Small Reactive Metabolic encepho-
↓
lopathy
If you get no reply Mid-sized Fixed Midbrain lesion
↓ Reactive Metabolic lesion
Try other questions like: Pupils Unequal Dilated Unreactive IIIrd N palsy
• What happened to you? Small Ractive Horner’s syndrome
• Where do you live?
• To which place do you belong to? Fundi
Make a note of the responses made. Examine the Fundi
Note the best level of the response:
Look especially for the optic new head swelling (rare) or
• Oriented
subhyloid hemorrhages.
• Confused conversation–using long or short sentences
• Inappropriate words Common Mistakes
• Incomprehensible sounds Absence of papilloedema does not exclude raised intracranial
• None. pressure.
262 Essentials of Clinical Medicine

Eye Movements • Directional preponderance: Vestibular nuclear leisons

(brainstem)—common causes—vascular disease
Watch the Eye Movements
demyelination.
• Do they look at you?
• Do they follow a moving object, like a torch or a hanging CORNEAL REFLEX
bulb?
• Do they move together (conjugately), or independently See in the section of “REFLEXES”.
(disconjugately).
GAG REFLEX
• Do they move at all?
• What is their position? • Afferent—glossopharyngeal (IXth) nerve
• Efferent—vagus (Xth) nerve
Interpretation – Touch the pharyngeal wall behind the pillars of the
• Deviation—brainstem lesion faucets
• Test eye movements – Watch the uvula—it should lift following the stimulus
• Evidence of 3rd, 4th or 6th nerve palsies, lateral gaze – Ask the patient to compare the sensation between
palsy. two sides.
CALORIC TEST Interpretation
The patient is lying down with head on a pillow at 30° so • Uvula moves to one side—upper or lower motor neuron
the lateral semicircular canal is vertical. lesions of vagus on the other side.
Cool water (30°C) is instilled into one ear over 40 seconds • Uvula does not move on saying aah or gag—bilateral
(usually about 250 ml). The patient is asked to look straight palatal muscle paresis
ahead and eyes are watched. This is repeated in other ear, • Uvula moves on saying aah, but not on gag, with reduced
and then in each ear with warm water (44°C). sensation of pharynx (IX palsy) (rare).
Interpretation of Caloric Test MOTOR SYSTEM ASSESSMENT
• Normal response
• Assess the tone in all the 4 limbs:
– Cold water—nystagmus fast phase away from
– Is it symmetrical?
stimulated ear.
• Assess the movements in each limb
– Warm water—nystagmus fast phase towards the
– Look at the spontaneous movements of the limbs
stimulated ear.
– Reduced response to cold and warm stimuli in one – Are they symmetrical?
ear—canal paresis • Ask the patient to move the limbs
– Reduced nystagmus in one direction after warm – If he cooperates—test power more formally
stimulation from one ear and cold stimuli from – If no response:
other—directional preponderance  Press the knobble of your thumb into the
sternum
Note: In the unconscious patient, the normal responses are
 Is there a purposeful movements to site of pain?
as follows:
 Do arms flex with this pain?
• Cold water—tonic movements of eyes towards the
 Is there asymmetry in there response?
stimulus
 If no response to this stimulus:
• Warm water—tonic movements of eyes away from the
1. Apply pressure to inner and of eyebrow note
stimulus
The fast phase of nystagmus is produced by the response
correction of this response, which is absent in uncon- 2. Squeeze the nailbed of a digit in each limb—
scious patient. does the limb withdraw?

Caloric Testing: What It Means TENDON REFLEXES

• Canal paresis—Lesion of semicircular canal (Ménière’s (See in section of neurological examination)
disease), or nerve damage causes as for sensory neural • Are they symmetrical ?
deafness, plus vestibular neuronitis. • Plantar response—extensor or flexor.
 Central Nervous System 263

CAUSES OF COMA Contd...

Features History suggestive of
A. Metabolic
– Hypoglycemia Seizures of recent onset, whether abscess or trauma)
focal or generalized
– Diabetes mellitus Drug-induced coma
– Renal failure Search of patient’s clothings Presence of drug containers or
– Hypatic failure alcohol in the home of the patient
– Hypothermia Hospital outpatient attendance
card, unfilled prescriptions, drugs
– Hypothyroidism or even syringes. Diabetic or
– Cardiorespiratory failure epileptic patients may carry some
– Hyponiz encephalopathy form of identifications.
B. Drug overdosage (including alcohol)
C. Structural Basic Management of Head Injury
i. Diffuse: • Exclusion of intracranial hemorrhage by CT scan
• Meningitis
• Controlling circulation
• Encephalitis
• Controlling intracranial pressure
• Other infections (e.g. cerebral malaria)
• Subarachnoid hemorrhage • Controlling ventilation
• Epilepsy • Obtaining neurological/neurosurgical opinions.
• Head injury
• Hypertensive encephalopathy Causes of Coma with Neck Stiffness
ii. Focal (In deeply comatose patients, neck stiffness may be relatively
Supratentorial lesions inapparent)
• Cerebral hemorrhage • Subarachnoid hemorrhage
• Cerebral infarction with edema • Encephalitis
• Subdural hematoma • Cerebral malaria
• Extradural hematoma
• Meningitis—viral, bacterial
• Tumor
• Intracerebral hemorrhage.
• Cerebral abscess
• Pituitary apoplexy
Comma with Hyperventilation
Subtentorial lesions
• Cerebeller hemorrhages • Brainstem lesion, e.g. stroke
• Pontine hemorrhages • Metabolic acidosis
• Brainstem infarction • Rising acidosis
• Tumor • Diabetic ketoacidosis
• Cerebellar abscess • Rising intracranial pressure
• Secondary effects of transtentorial herniation of • Bacterial meningitis
brain due to cerebral mass lesions.
• Liver failure
Table 8.64: History taking in case of coma • Pneumonia complicating brain lesion
Features History suggestive of • Renal failure.
Comma occurring suddenly in Subarachnoid hemorrhage or
vascular disorders stroke (cerebellar hemorrhage) Causes of Coma with
H/o trauma with concussion Extradural hematoma Focal Neurological Signs
followed a few days later by
fluctuating drowsiness and stupor • Epilepsy (post-ictal state)
Concussion followed by brief lucid Intracranial space-occupying • Encephalitis
interval before rapidly deepening lesions (SOLs) of any cause
coma
• Subarachnoid hemorrhage
A H/o headache before coma Cerebral disease (which may be • Cerebral abcess
supervenes due to a tumor, encephalitis, • Bacterial meningitis with cortical infarction
Contd... • Cerebral venous sinus thrombosis.
264 Essentials of Clinical Medicine

Investigations to be Done in a Case of Coma Spinal reflex activity in response to peripheral stimulus
• Cervical spine X-ray (e.g. pressing the toe nailbed) is usually absent but may be
• CT head scan preserved in brain-death. EEG testing is not necessary to
• Chest X-ray diagnose brain death but usually shows a flat, isoelectric
• X-ray of suspected fractures/bruised limbs trace.
• Blood for cross-matching The brain death tests should be performed by two
• Check hemoglobin, hematocrit, WBC count experienced clinicians either together or separately. The tests
• Drug screen are then repeated, after an interval, prior to the declaration
• Electrolytes and liver function tests of brain death.
• Blood gases and pH.
THE AUTONOMIC NERVOUS SYSTEM (ANS)
Table 8.65: Important papillary signs The various components of autonomic nervous system
Abnormal features of pupil Suggestive of pupil includes—afferents, postganglionic sympathetic and para-
Bilaterally dilated and fixed pupil Bilateral 3rd nerve (owing to sympathetic neurons in the periphery, together with the
massive brain swelling and tentorial herniation or midbrain damage) central prepanglionic components of these systems in
and following ingestion of the intermediolateral cell columns in the spinal cord, and
anticholiner- gic drugs [e.g. magic rostal connections in the brainstem and cerebral hemispheres.
mushrooms, tricyclic antidepressants
The various important functions of ANS include—
(TCA)]
Unilateral fixed dilated pupil Ipsilateral intracranial mass lesion modulation of function in cardiovascular and gastro-
(e.g. spontaneous intracerebral intestinal systems, with temperature regulation, secured
hemorrhage, traumatic hematoma) reflexes, bladder and bowel control, detrusor and sphincter
causing a 3rd nerve palsy. control and pupillary and respiratory reflex control
Pinpoint pupil Pontine vascular lesions and
mechanisms.
after narcotic overdose.
Metabolic Pupils are normally reactive to light.
Clinical Features of Disorders of ANS
Unconscious patients are unable to fixate and will, • Postural hypotension
therefore, have roving “eye movements”. Not infrequently • Retention and incontinence of urine
the ocular access will not be conjugate. • Constipation, and fecal incontinence
Assessing the Brain Death • Importance and erective failure
Prior to testing for brain death, it is necessary that the cause • Poor urine stream (failure of detrusar muscles)
of irreversible brain damage has been established, (e.g. • Esphageal and gastrointestinal dysmotility
intracerebral hemorrhage, encephalitis), and that reversible • Immobility of pupils
conditions such as hypothermia, drug intoxication and • Snoring and sleep apnea
metabolic defects have been excluded. In patients who have • Impairment of sweating.
been previously neuromuscularly paralyzed, respiration of Rare syndromes like “program autonomic
normal neuromuscular function requires to be tested electri- failure” involves the degeneration of both pregonglionic and
cally by elicitation of deep tender jerks. Brain death post-ganglionic neurons which in turn results in various
can only be diagnosed in the absence of the following abnorma-lities of autonomic nervous system functioning
functions: such as:
• Pupil reflex to light • Incontinence of urine
• Corneal reflex • Constipation and other disorders of gastrointestinal
• Oculovestibular reflex using iced-water irrigation of the motility
external ear canal • Inability to maintain blood pressure in the erect posture
• Gag reflex (orthostatic hypotension)
• Cough reflex • Impotence
• Spontaneous respiration when Pa CO2 > 6.6 kPa or > • Pupillary areflexia
50 mm Hg • Loss of cardiovascular reflexes
• Response to painful stimuli, within the cranial nerve • Syncope due to orthostatic hypotension
territories. • Disturbances of sweating
 Central Nervous System 265

Table 8.66: Evaluate autonomic functions the SBP falls > 30 mm Hg. The 30th : 15th pulse ratio >
Proceedure Normal response Inference 1.03 normal subjects and ≤ 1.0 in case of autonomic
Standing – Decrease in systolic Excessive response indi-
disturbances
BP less than 20 cates:
– Moderate tachy- – Adrenal dysfunction Loss of Cardiovascular Reflexes—Causes
cardia—Increase – Endorgan refractoriness
in plasma nordre- • Tachycardia at rest
naline level • Absence of normal slowing of pulse in response to
Deep breathing – Variation in pulse Impaired vagal function
Valsalva’s maneuver
rate of 10 beats or
more/min • Absence of normal slight increase in the pulse rate and
Hyperventilation – Reduction in sys- blood pressure on standing
tolic BP by • Absence of normal increase in blood pressure during
10-20 mm Hg. hand grip
Valsalva’s man- 4 phases or stage res- Disorder of sympathetic
euver ponse system • Absence of BP increase with stressful tasks such as
Cold pressor Tachycardia in res- Sympathetic lesion central mental arithmetic.
ponse to systemic or efferent
Test immersion arterial hypertension Sympathetic lesion either Bladder and Bowel Function
of an extremity central or efferent
in ice-cold water Patterns of Abnormality
for 1-3 minutes
Amynitrate Tachycardia in res- Sympathetic lesion either a. Frontal bladder: Urinary urgency, precipitant and
inhalation ponse to systemic central or efferent uncontrolled voiding of large volumes without residual urine.
arterial hypotension Periods of urinary control. Normal anal tone. Frontal release
Induction of Sweating –do–
hyperthermia
signs.
Occurs in dementia, normal pressure, hydrocephalus,
Assessing the Functions of ANS frontal tumors.
• The papillary response to light and accommodation b. Spinal bladder: Initially urinary retention + overflow
• Skin—normal or dry (due to absence of sweating) incontinence. Later bladder contracts and voids small
• Tachycardia at rest—present or absent volumes of urine automatically and precipitantly.
• Change in pulse rate with deep inspiration Constipation. Normal anal tone. May develop reflex
• Trophic changes in distal skin—absence of hair growth. penile erections—called priapism (after the Greek god
Priapus).
Standing Test for Orthostatic Hypotension (OH) Occurs in spinal cord lesions—common causes: trauma,
The patient is made to lie supine for about 15 minutes (with multiple sclerosis, spinal tumor.
sphygmomanometer, cardiac rate meter or lead 1 ECG c. Peripheral neurogenic bladder: Painless distention of
attached). Check the resting blood pressure. Then the patient flaccid bladder with overflow in continence and large
is made to stand. Then the pulse rate from RR interval at residual volumes. Fecal incontinence. Reduced anal tone.
the 15th and 30th beats after standing are noted and BP There may be saddle anesthesia. Impotence.
taken one and three minutes after standing. Occurs in cauda equina lesions—common causes:
central lumbar disc protrusion; rarer causes: spina bifida,
Interpretation ependymomas, cordomas, metastases—or peripheral nerve
In normal individuals, the SBP should not decreases by more lesions—common causes: diabetes mellitus, rarer causes:
than 10 mm Hg. In patients with autonomic dysfunction, pelvic surgery, malignancy.
 9
Examination of the Spine
GENERAL EXAMINATION OF
VERTEBRAL COLUMN
Inspection
Examine the patient in standing and sitting in the erect
posture. The normal shape of thoracolumbar spine is S-
shaped curve. In case of any abnormality, you should try to
point out the vertebrae involved or are there any projections
(i.e. the most prominent portion) seen over the spine.
Palpation
The most prominent landmark seen over the spine is the
spinous processes of C7 (called the vertebra prominence).
Another major landmark is the last rib which articulaties
with 12th thoracic vertebra. However, the last rib palpation
does not hold much importance, as this rib cannot be
distinctly felt in all the individuals.
You should note any curvature of the spinal column,
whether a whole or a part of it. The curvature may be in
anterior, posterior or lateral direction.
• Anterior curvature—lordosis
– Natural lordotic curves are present in the cervical
and lumbar regions.
• Posterior curvature—kyphosis
– The thoracic spine usually exhibits a slight kyphosis,
which increases in the elderly and especially in
osteoporosis. It must be differentiated from a
localized angular deformity (called gibbus) caused
by fracture, by Pott’s disease (spinal tuberculosis)
or by a metastic malignant deposit.
• Lateral curvature—scoliosis
– It may be towards either side. It is usually always
accompanied by rotation of the bodies of the verte-
brae in such a way that posterior spinous process
come to point towards the concavity of the curve.
a. Scoliosis due to muscle spasm (e.g. lumbosacral
disk protrusion syndromes)
 the spinal curvature and rotational deformity
decreases flexion.
b. Scoliosis due to inequality of leg length
 Scoliosis disappears on sitting because the
buttocks then become level.
c. Scoliosis secondary to skeletal anomalies.
 In spinal flexion it shows as a “rib-hump”
due to rotation.
• Kyphosis and scoliosis are often combined, particularly
when the cause is an idiopathic spinal curvature,
beginning in adolescence.
Examination of Cervical Spine
• Posture of the neck should be noted for any abnormality
like loss of lordosis, a torticollis (wryneck) or cock robin
deformity (unilateral flexion).
• Perform the palpation of bony contour for any tender-
ness in the spine, trapezius, interscapular and paraspinal
muscles.
• The patient is made to look right and left (80 degrees
rotation each way) and then to tilt the head to the right
and left (45 degrees of lateral flexion each way) and to
flex (75 degrees) and extend (60 degrees) the neck, you
should note any assymetrical movement.
• You should also perform sensory and motor examination
of upper and lower limbs.
• In rheumatoid arthritis, particular care is necessary in
examining the neck as atlantoaxial instability may lead
to damage to the spinal cord when the neck is flexed or
extended.
Common Abnormalities of Cervical Spine
• Local tenderness in the cervical region.
• Regional and paraspinal muscle tenderness is commonly
associated with neck pathology.
• Widespread muscle tenderness may be a feature of
psychological distress.

• Loss/impairment of movement.
• Torticollis, associated with acute neck pain.
• Loss of cervical lordosis, associated with chronic
neck pain.
• Loss of sensation in upper limb dermatomes, associated
with nerve root irritation.
Causes of Abnormal Neck Posture
• Loss of lordosis or flexion deformity—acute lesions,
rheumatoid arthritis.
• Increased lordosis—ankylosing spondylitis.
• Torticollis (wryneck)—sternomastoid contracture.
• Lateral flexion (cock robin position)—erosion of lateral
mass of atlas in RA.
Examination of Thoracic Spine
The main movement at the thoracic spine is the rotation.
• You should examine the patient (while he is standing
erect) from front, back and side and note any deformity
like increased kyphosis (curvature in anteroposterior
plane) or scoliosis (curvature in coronal plane).
• You should note the bony countour as well as areas of
tenderness.
• Make the patient to sit and then observe the range of
rotation from behind.
• Note whether the scoliosis is corrected or not by the
spinal flexion movements.
• Chest expansion should be measured (normal—5 cm
minimum).
Common Abnormalities of Thoracic Spine
• Tenderness in any localized area over the thoracic spine.
• Presence of kyphosis/kyphoscoliosis.
Examination of Lumbar Spine
It includes:
1. Inspection for the presence of any deformity.
2. Assessment of movement of the spine.
3. Assessment of the effects of lumbar spinal pathology
on the spinal cord or nerve roots.
• You should note the posture of the patient (with the
patient in both, sitting as well as standing position).
• Any abnormal lateral curvature – scoliosis.
• Note any area of tenderness over the lumbar spine.
• The patient is asked to keep his legs straight (while
he is in standing posture), and then make him to
bend backwards, then forwards and to each side.
Note the range of movements and contour of spine.
Examination of the Spine 267
• The normal lumbar cordosis should be abolished in
the flexion. The extent of lumbar flexion can be
assessed more accurately by marking a vertical,
10 cm line on the skin overlying the lumbar spinous
processes and sacral dimples, and measuring the
increase in the line length on flexion (modified shober
test), this should normally be 5 cm or more. Pain-
full restriction of spinal movements is an important
sign of cervical and lumbar spondylosis, but may
also be found in vertebral disk disease or other
mechanical disorders of the back or neck. A useful
clinical aphorism is that a rigid lumbar spine should
always be investigated for serious pathology such
as infection (e.g. staphylococcal or tuberculosis
discitis), malignancy or inflammation (e.g. ankylo-
spondylitis).
Common Abnormalities of Lumbar Spine
• Loss of lordosis—advanced age, ankylospondylitis,
acute disk prolapse.
• Scoliosis—acute disk prolapse
– If lateral to nerve root, the patient leans away from
lesion.
– If medial to nerve root, the patient leans towards the
lesion.
Examination of Sacroiliac Joints
Movement of these joints usually cannot be demonstrated
clinically. During and immediately after pregnancy, laxity
of the pelvis may occur causing instability in the pelvic
girdle. This may allow a small amount of movement to be
detected.
Pain arising from the sacroiliac joints may radiate into
the buttocks and posterior thighs, but unlike sciatica, rarely
entends below the knee. Local palpation over the sacroiliac
joints is often not helpful and may give rise to false-positive
and false-negative results. Inflammation of these joints may
cause pain in the buttocks when pelvis is stressed upon.
Examination of Sacrum
• Firm pressure with the side of the hand over the sacrum.
• Inward pressure over both the iliac bones in an attempt
to distort the pelvis. Flex the hip to 90 degrees and exert
firm pressure at knee through the femoral shift.
Common Abnormalities
• Restriction of spinal movements.
• Pain exacerbated by movements of the spine.
• Neurological sign associated with acute nerve root
compression.
268 Essentials of Clinical Medicine

TESTS Femoral Nerve Stretch Test

Test for Nerve Root Compression The patient is asked to lie prone or on the unaffected side if
there is painful flexion deformity of the hip. Flex the knee
Compression of nerve root results into various complicated
slowly and the patient is asked to report onset of pain. If
neurological disorders. Neurological abnormalities arising
this fails to produce pain, in the thigh or back, gently extend
due to nerve root involvement are called “radiculopathies”.
the hip with the knee still flexed.
Prolapse of intervertebral disk also causes compression of
nerve roots. Prolapse of intervertebral disk most frequently
PAIN
occurs at L4/L5 or L5/S, level producing compression of L5
and S1 nerve roots respectively. Causes of Referred Pain in the Arm
• Cervical spine pathology
Straight Leg Raising Test (SLRT) • Cervical rib
Tension can be applied to the nerve roots by flexing the hip • Apical lung neoplasm (pancoast lesion)
with the knee straight. Normally, about 90 degree of hip • Cardiac ischemia
flexion should be possible (but it varies considerably from • Hiatus hernia.
70-120 degrees). When the root is stretched over a prolapsed
disk, straight leg raising will be restricted and pain is usually Causes of Pain in Thoracic Spine
felt in lumbar region, not just in the leg. When this limit is Adolescent and Young Adults
reached, gently dorsiflex the ankle, thereby applying further • Ankylosing spondolytis
tension to nerve root (Bragaard’s test). • Scheuermann’s disease
• Disk protrusion (rare).
Bowstring Sign
Middle Age and Elderly
Perform straight leg raising test and at the limit flex the
• Osteoporotic fracture
knee, reducing tension on the sciatic roots and hamstrings.
• Degenerative change.
Now further flex the hip. Now gently extend the knee until
pain is reproduced once again (Laségue’s sign). The Any Age
posterior tibial nerve is now stretched like a bowstring across • Tumor
the popliteal fossa. Firm pressure is then applied with the • Infection.
thumb, first over the nerve in the middle of the popliteal
fossa and finally over the other hamstring tendon. Ask the SPINAL CORD
patient to which maneuver exacerbated the pain. Lesions of the Spinal Cord
Interpretation The extent of the spinal cord lies from foramen magnum to
The test is said to be positive if the second maneuver is the interspace between T12 and L1 spines and below this
painful and if the resultant pain radiates from the knee to level lies the cauda equina.
the back. The spinal segments do not correspond exactly with
the vertebrae overlying them. Thus, it is important in
Flip Test assessing patients with spinal cord compressions due to
vertebral disease. To determine which spinal segment is
The patient is asked to sit on the edge of the bed with the related to the given vertebral body:
hips and knee flexed to 90° and then you test the knee
reflexes. Then extend the knee, and examine the ankle jerk • For the cervical vertebrae — Add one level
• For the thoracic 1-6 — Add two levels
relieve, the sudden increase in the tension on the nerve roots.
• For the thoracic 7-9 — Add three levels
Interpretation • The 10th thoracic arch — Over L1 and L2
When there is root irritation, the patient “flips” backwards segments
to relieve the sudden increase in tension on the nerve root. • The 11th thoracic arch — Over L3 and L4
In the absence of significant nerve root irritation, the patient, segments.
distracted by attention to the ankle jerk test, may permit full • The 12th thoracic arch — Over L5 segment.
extension of the knee, which is the equivalent of full 90 • The first lumbar arch — Over sacral and
degree straight leg raising. coccygeal segment
 Examination of the Spine 269

Tracts of Spinal Cord Table 9.1: Sensations and their pathways

A collection of nerve fibers that connects two masses of Class Sensations Pathway
gray matter within the central nervous system is called a Exteroceptive i. Pain and temperature Lateral spinothalamic
tract. Tracts may be ascending or descending. They are tract
(conscious) ii. Touch and pressure Ventral spinothalamic
usually named after the masses of gray matter connected tract
by them. Some tracts are called fasciculi or lemisci or Proprioceptive
funiculi. a. Conscious i. Position and movement
(muscle and joint sense)
Descending Tracts ii. Vibration sense Gracilis and cuneatus
iii. Light touch Fasciculi in the dorsal
1. The corticospinal tract descends from the cerebral cortex column
to the spinal cord. It consists of two parts (i) the lateral iv. Two-point discrimi-
corticospinal tract, which lies in the lateral funiculus, nation
b. Unconscious Proprioceptive impulses Anterior and posterior
and (ii) the anterior corticospinal tract which lies in the for coordination spinocerebellar tracts
anterior funiculus. The corticospinal tracts are also called function of cerebellum
the pyramidal tracts.
2. The rubrospinal tract.
3. The olivospinal tract.
4. The vestibulospinal tract.
5. The tectospinal tract.
6. The lateral and medial reticulospinal tracts.
7. The medial longitudinal bundle tract.
Ascending Tracts (Figs 9.1 and 9.2)
1. Tracts in the posterior funiculus
a. Fasciculus gracilis (medially).
b. Fasciculus cuneatus (laterally)
The fasciculus gracilis and cuneatus are also called
posterior column tracts.
2. Tracts in the lateral funiculus
a. Lateral spinothalamic tract.
b. Anterior and posterior spinocerebellar tract.
c. Spino-olivary tract.
d. Spinotectal tract.
3. Tracts in anterior funiculus
a. Anterior spinothalamic tract.

Functions of the Spinal Cord

The functions of the spinal cord can be divided into—
sensory, motor and autonomic functions.
Sensory Functions
All the sensations after entering the spinal cord in dorsal
nerve root are conveyed to the brain (post-central gyrus)
by ascending tract either in the:
i. Dorsal column of the same side which covers the
fine touch, tactile localization and discrimination,
pressure, proprioception and kinesthetic sensation, i.e.
sensation of body position in space and joint move-
ments and vibration sense. Fig. 9.1: Ascending tracts and lemnisci
270 Essentials of Clinical Medicine
Fig. 9.2: Ascending tracts—spinocerebellar
ii. Spinothalamic tracts of the opposite side: the anterior
(ventral) tract conveys gross (crude) touch and tactile
localization, whereas lateral tract conveys pain and
temperation sensations.
Motor Functions
The spinal cord controls the:
i. Tone and power of the muscles.
ii. Movements of the muscles and joints.
iii. Deep (tendon) reflexes.
iv. Superficial reflexes.
The motor functions are conveyed to the spinal cord by
pyramidal and extrapyramidal tracts.
Autonomic Functions
The spinal cord regulates the:
i. Body temperature.
ii. Visceral functions regulate the cavity of smooth
muscle, in heart glands of the GIT, sweat glands,
adrenals, etc.
TRANSACTION OF SPINAL CORD
Spinal cord transaction, i.e. cut across the cord can be
divided into 3 types—complete, incomplete and hemisection
of the spinal cord.
Complete Transaction of Spinal Cord
Commonest site of involvement is at midthoracic level.
Clinical features of complete transaction has been divided
into 2 stages.
Stage of Spinal Shock or Stage of Flaccidity
Characteristic features:
• The patient feels as if he is cut into 2 portions, whole of
the body below the level of section is deprived of all the
activities.
• Muscles are completely paralyzed (flaccid paralysis) and
lie in any position imposed on them by gravity:
– Paralysis of both the lower limbs—paralplegia.
– Paralysis of all the 4 limbs—quadriplegia.
– Paralysis of muscles decreases the venous return to
the heart producing cold and blue extremities, skin
becomes dry and scaly and bedsores develop.
• Muscle tone is completely lost.
• All the reflexes (superficial and deep) are markedly
decreased or lost.
• All the sensations below the transaction are lost.
• The urinary bladder and rectum are generally paralyzed,
however, the sphincter vesicle recovers very rapidly
resulting in retention of urine.
• Penis is flaccid and erection is impossible.
• All the sympathetic vasoconstrictor fibers leave the spinal
cord between T1 to L2. As result:
– A transaction below L2 produces no effect or very
little fall of BP.
– A transaction at T1 level cuts off all thoracolumbar
sympathetic neurons from medullary cardiovascular
center producing marked fall in mean BP from a
normal resting value of 100 to 40 mm Hg.
– Fall of BP is much less marked as the section shifts
more distally towards L2.
• If the lesion is at a level of T6, all the impulses coming in
from the abdominal viscera are cut off from the brain,
gripping sensation or distention of viscera are thus not
appreciated.
Stage of Reflex Activity
Intermediate grey column of spinal cord are rich in
Norepinephrine and 5-HT (5-hydroxy tryptamine-serotonin);
therefore, after one week of cord transaction, when the
autonomic reflexes are hyperactive, NE and 5-HT content
of cord below the transaction are markedly reduced.
Autonomic reflexes: Within days or weeks of cord
transaction, spinal sympathetic cell bodies appear to recover
some toxic discharge and, moreover, are capable of
responding by increased activity to noxious stimulation;
therefore:
• Return of functional activity first occurs in the smooth
muscle as the stage of shock passes off. As a result of
that, the sphincter vesicle shows early recovery (in
compression to smooth muscle of urinary bladder, i.e.

the detrusor muscle which shows slow recovery). The
favorable consequence of this is the urine. After some
time, the evacuation of urinary bladder is gradually
established in a perfectly normal manner. The regain of
anal sphincter activity also occurs in the same way.
• Paralyzed blood vessels also regain their normal tone
(as the connector cells in the spinal cord begin to act
independently of VMC):
– Sweating restarts from the skin (which was lost
earlier) and also skin appears to be more healthy.
– Rapid healing of ulcers occurs.
– As the circulation becomes better in the limbs, they
become warm and also gain good color.
• BP is normal at rest but may show wide fluctuations.
Muscle tone:
• Return of tone in the skeletal muscle occurs after
2 to 3 weeks.
– Flexor muscles show early and better return of tone
as compared to extensor muscles.
• All the muscles (including the flexors) are hypotonic
because stretch reflexes which are responsible for
muscle tone are feebly mediated by the spinal cord alone
and need reinforcement from brainstem centers.
• Limbs show paraplegia in flexion.
• Wasting of muscle do not occurs because although they
are paralyzed for voluntary movement they are in
constant reflex activity.
Reflex movements: The body takes a period of about 2 weeks
from the time when transaction of spinal cord has occurred
till the beginning of return of reflexes. Recovery of reflex
excitability occurs due to phenomenon of “denervation
hypersensitivity” to the mediators released by the remaining
spinal excitatory endings, and development of collaterals
from the existing neurons with the formation of additional
excitatory endings on interneurons and motor neurons.
i. Flexor reflex: (or withdrawal reflex): Spontaneous
involuntary reflex movements of the limbs is the first
reflex response to appear. This can be best elicited by
positive Babinski’s sign.
ii. Mass reflex: It appears several months after the original
lesion. It is due to irradiation of afferent stimuli from
one reflex center to another. The mass reflex can be
elicited by scratching any point on the lower limb or
anterior abdominal wall below the level of lesion. The
mass reflex consists of:
a. Flexor response of both the lower extremities and
contraction of anterior abdominal wall.
b. Evacuation of urinary bladder due to hyperactive
reflex activity and abdominal compression which
Examination of the Spine 271
increases intravesicle pressure to threshold level,
similarly reflex evacuation of rectum also occurs.
c. Profuse sweating below the level of lesion, the
sweat fibers to head and neck arises from T1 and
T2 and those to arms from T5-9, therefore, a lesion
at T2 level causes sweating of whole of the body
when mass reflex is obtained as all the sympathetic
fibers leave the cord below the level of the lesion.
iii. Deep (tendon) reflex: The knee or ankle jerk returns
about 1 to 5 weeks later than the flexor response
– The ankle jerk may return still later.
– About 6 months after the transaction has
occurred, marked activity appears in the extensor.
This results in exaggerated extensor reflexes with
the appearance of extensor spasms.
Note: The mass reflex can also be used as a therapy (a sort
of exercise) for the patient. It can be used to give paraplegic
patients a degree of bladder or bowel control. They can be
trained to initiate urination and defecation by stroking or
pinching their thighs thus producing on intentional mass
reflex.
Coitus (or Sexual) Reflex
The coordinated sexual activity depends upon a series of
reflexes integrated at many neural levels and is absent after
spinal transaction. Human experiments have shown that
genital manipulation in male with spinal cord transaction
produces erection and even ejaculation. A similar type of
response in (sexual excitation) also occurs in case of fender
when their external genital parts are stimulated.
Failure of Reflex Activity
There are conditions in which the reflex activities fail to
appear, some of these conditions are infection, malnutrition
and toxemia. The important features are:
1. The reflexes become increasingly difficult to obtain
because the threshold of reflex activity is highly
increased.
2. The receptive field is narrowed down to the optimum
areas from which reflexes can be obtained.
3. The mass reflex disappears.
4. The threshold of all the reflexes is increased and a few
group of muscles are involved in the motor response.
5. The muscles get wasted and become flaccid and bed
sores also develop, which further decrease the general
state of well being of the patient.
Incomplete Transaction of the Spinal Cord
In this type of lesion of the spinal cord, few tracts escape
injury and are prevented from being cut.
272 Essentials of Clinical Medicine
i. Stage of spinal shock is similar to that of complete
transaction of spinal cord.
ii. Stage of reflex activity:
As the transaction of the spinal cord is not of complete
type, therefore, some of the descending tracts in the
ventrolateral columns of the spinal cord (especially vestibulo-
spinal and reticulospinal tracts) may escape injury and some
connections persist between the brain and spinal cord. These
tracts mainly reinforce the activity of the extensor motor
neurons producing extensor hypertonia, i.e. paraplegia in
extension. As a result, the legs lie extended at hip and knee
and knee with toe pointing slightly downwards.
Characteristic Features
• All features of UMNLs are seen (They have been
described in section of “Neurological Examination”).
• Involuntary movements are relatively infrequent, but
when they occur, they involve an increase in the extensor
tone, producing downward movement of toes and feet.
• Extensor thrust reflex:
This reflex can be elicited by passively flexing the lower
limb and allowing it to rest on the bed, the patient’s foot
is then pressed up with the palm of the hand. Active
contraction of quadriceps and posterior calf muscles
occurs, and the limb straightened out. Physiologically it
is an extensor response because all the muscles which
contract during an extensor response are called
physiological extensor. This reflex is absent in complete
transaction of the spinal cord.
• Cross extensor reflex:
Stimulus to the sole of the foot produces withdrawal
(flexor) reflex extending up to the knee only. It is usually
accompanied by active and forcible extension of opposite
limb.
• Phillipson’s reflex:
Gentle flexion of one limb causes extension of opposite
limb. The flexed limb then becomes extended and
opposite one flexed, the response alternate in each limb
producing a steppage movements in which the legs are
lifted abnormally high, occurring due to foot drop.
Failure of Reflex Activity
Similar to that of “stage of spinal shock”.
Hemisection of Spinal Cord:
(Brown-Sequard Syndrome)
In this type of lesion, only one lateral half of spinal cord is
affected. The autonomic functions are usually normal. The
other functional changes which occur are listed into 3
categories.
Changes below the Level of Hemisection:
On the Same Side
Sensory changes:
• Loss of fine touch, tactile localization and tactile
discrimination, vibration sense and kinesthetic sensation,
i.e. sensation of movement and position, due to damage
of dorsal column.
• Unaffected pain temperature and crude touch as the
spinothalamic tracts (anterior and lateral) carrying these
sensations cross to the opposite side and escape injury.
Motor changes:
• Extensive paralysis of UMNL due to damage of cross
pyramidal tracts. Since some fibers of direct pyramidal
tract of opposite side (which and in the same side) escape
injury, therefore, some muscles on the same side of
lesion may not be paralyzed.
• Temporary loss of vasomotor tone due to damage to
the descending fibers from the vasomotor center (VMC)
in the medulla to the lateral horn cells. This leads to the
dilatation of blood vessels and fall in BP. Later, intact
lateral horn cells start acting as supplementary VMC
and tone returns.
On the Opposite Side
Sensory changes
• Complete loss of pain, temperature and crude touch due
to damage to spinothalamic fibers which come from
the opposite side.
Motor changes
• Complete LMNL type paralysis is seen due to damage
to anterior horn cells.
• Complete and permanent vasomotor paralysis occurs
due to damage of the lateral horn cells.
Hemisection: On the Opposite Side
1. Sensory changes: Some loss of pain sensation due to
injury of pain fibers of spinothalamic tract which cross
horizontally in the same segment and may be caught up
in the lesion.
2. Motor changes: Nil or very slight due to damage of some
pyramidal tract of the same side.
Changes the Same Side
A band of hyperesthesia present due to irritation of upper
cut end of damaged fibers.
On the Opposite Side
Hyperesthesia may be referred.

Hemisection in Cervical Region
• Constriction of pupil on same side because pupillary
dilator fibers coming from medulla and passing via T1,2,3
anterior roots are damaged.
• If L4,5,6 segments are involved, it results in loss of biceps,
triceps, supinator and pronator jerks.
• Paralysis of diaphragm on the same side due to phrenic
nerve (C4,5,6) involvement.
Hemisection in the Lumbar Region
If it involves the L3,4 loss of knee jerk and disturbances in
the micturition occurs.
Hemisection in Lumbosacral Region
This leads to control over the sphincters of urinary bladder
and anus.
Complications Arising due to
Transaction of Spinal Cord
• Immobilization in case of paraplegia and quadriplegia
causes increased catabolism of large amounts of body
protein, ultimately leading to negative nitrogen balance.
• Decubitus (postural) ulcers which heal poorly due to
depletion of body proteins.
• Hypercalcemia, hypercalciuria and calcium stones in the
urinary tract due to increased breakdown of protein from
bone matrix.
• Stones may lead to urinary retention, urinary tract
infection, septicemia, uremia, coma, and ultimately
patients demise may occur (Fig. 9.3).
CLINICAL APPLICATIONS
Lesions of Motor Neurons and
Corticospinal Tracts
• Upper motor neuron lesions are caused by transaction
of the corticospinal tract or destruction of the cells of
origin in the cortex. Spastic paralysis results with
pyramidal signs (Babinski’s sign).
• Lower motor neuron lesions are caused by damage to
motor neurons. Flaccid paralysis occurs with loss of
reflexes. Poliomyelitis results from damage to motor
neurons in the anterior horn.
• Combined upper motor neuron and lower motor neuron
disease is caused by damage to the corticospinal tract
and motor neurons in the anterior horn. An example is
afforded by amyotrophic lateral sclerosis.
• Direct injury to conus medullaris destroys segmental
neurons (conus syndrome). It results in weakness of
Examination of the Spine 273
movement in the feet and loss of sensation in the buttocks
due to the involvement of anterior and posterior gray
horns, paralysis of bladder and rectum due to involve-
ment of intermediolateral cell column. The syndrome is
usually caused by injury to vertebra L1 or prolapse of
intervertebral disc between L1 and L2 since the sacral
segments lie against these.
Lesions of Sensory Tracts
• Degeneration of dorsal column (fasciculus gracilis and
fasciculus cuneatus) is seen in tabes dorsalis. There is
loss of sense of position and vibration and two-point
discrimination in the extremities. Patients have a positive
Rhomberg’s sign, i.e. when the patient stands with his
feet together and closes his eyes, he begins to sway and
perhaps loses his balance and falls indicating loss of
sense of position in the legs. By opening his eyes, he
can partially compensate by the visual knowledge of
uncrossed fibers of the posterior column. This selective
disturbance of sensation is known as ‘dissociated
sensory loss’.
If the cavitation round the central canal enlarges to
include the motor cells in the anterior horn, then there is
flaccid paralysis of the intrinsic muscles of the hand as
the disease usually involves the lower cervical and upper
thoracic regions of the cord.
• Intractable pain can be treated by cutting the spino-
thalamic tract in the operation known as cordotomy. A
needle is inserted into the lateral column of the cord.
When the needle is in the spinothalamic tract, the patient
reports tingling on the opposite side of the body. The
tract is then destroyed electrolytically. The pain fibers
are superficially placed in the tract, while the temperature
fibers are deeply situated.
Brown-Sequard Syndrome (Fig. 9.3)
It is characterized by the following signs:
• On ipsilateral side—spastic paralysis (lateral cortico-
spinal tract interruption); loss of position sense, tactile
discrimination and vibration sense (interruption of dorsal
column); Horner’s syndrome (interruption of hypo-
thalamospinal tract).
• On contralateral side—there is loss of pain and
temperature sensation one segment below the lesion
(interruption of lateral spinothalamic tract).
– Complete transaction of the cord results in total loss
of sensations in the region below the level of injury
(interruption of all sensory tracts), flaccid paralysis
(interruption of corticospinal tracts).
274 Essentials of Clinical Medicine
Fig. 9.3: Brown-Sequard (hemiparaplegic) syndrome.
Result of lesion at segment T10 on left side is shown
– The posterior column tracts and lateral corticospinal
tracts undergo bilateral degeneration in pernicious
anemia (vitamin B12 neuropathy) resulting in loss of
position and vibration sensations and tectile
discrimination (posterior column lesion) and bilateral
spasticity, exaggerated tendon reflexes, extensor
plantar response (corticospinal tract lesion).
Brainstem lesions occur quite frequently and may
represent an immediate or a delayed threat to the patient’s
life. The symptoms are often complex but arise directly
from the regional anatomy, they are referable to involvement
of the motor and sensory pathways passing through it and
particularly to involvement of the nuclei of the cranial nerves
which lie within it.
Signs and Symptoms due to
Involvement of Tracts
Most of the ascending and descending tracts are present at
all levels of the brainstem and their involvement will produce
the following signs and symptoms:
• Contralateral hemiplegia (corticospinal tract).
• Contralateral loss of pain and temperature sensation from
trunk and limbs (spinal lemniscus).
• Contralateral loss of position sense in limbs (medial
lemniscus).
• Involuntary movements of the limbs (rubrospinal
tract).
• Loss of pain and temperature sensation from face, loss
of corneal reflex (spinal tract of trigeminal).
• Conjugate deviation of the eyes may be affected (medial
longitudinal bundle).
• Movement of the head towards the source of sound or
light may be affected (tectospinal tract).
• Incoordination of movements (spinocerebellar tracts).
• Progressive cerebellar ataxia, impaired gait and
equilibrium (cerebellar tracts).
• Drooping of the eyelid (ptosis), a small pupil (meiosis)
inability to sweat on the ipsilateral side of the face
(anhydrosis), a recession of the eyeball into the socket
(enophthalmos) occur due to paralysis of the sympa-
thetic supply to the eye. These signs constitute Horner’s
syndrome.
Signs and symptoms related to cranial nerves are
ipsilateral and will depend upon the level of brainstem
involved. Hemiplegia (pyramidal tract) and hemianesthesia
(spinothalamic tract) and loss of position sense (medial
lemniscus) associated with various lesions of brainstem are
contralateral.
Medulla Oblongata
• Respiratory and cardiac failure and postural hypotension
(vital centers, viz. respiratory, cardiac and vasomotor
are situated in the reticular formation of medulla). An
injury to medulla is usually fatal.
• Vertigo, vomiting, nystagmus (vestibular nuclei).
• Dysphagia, hoarseness of voice (nucleus ambiguus).
• Syncope (dorsal nucleus of vagus).
• Paralysis of tongue with thick speech (hypoglossal
nucleus).
Paralysis of the last four cranial nerves is known as
bulbar paralysis in which vital centers also get involved.
Pons
• Anesthesia of face and weakness of jaw muscles
(trigeminal nuclei).
• Internal squint with diplopia (abducent nuclei).
• Paralysis of muscles of facial expression (facial nerve).
• Persistent tinnitus, progressive deafness and vertigo
(vestibulocochlear nerve).
Midbrain
• Divergent squint (external ophthalmoplegia), dilated
pupil, loss of light and accommodation reflex (internal
ophthalmoplegia) (oculomotor nerve).
• Internal squint and diplopia (double vision) on looking
down (trochlear nerve).
• Paralysis of upward gaze of the eyes (nucleus of
superior colliculus).
• Involuntary movements and rigidity (red nucleus,
substantia nigra and reticular formation). The
disorder most frequently affecting the extrapyramidal
system is Parkinson’s disease — a combination of
tremor, rigidity bradykinesia (immobility of facial
expression, slowness of movements).
• Between the red nucleus and substantia nigra is the
ventral segmental area of Tsai. It contains neurons

identical to those of substantia nigra, the dopaminergic
neurons from this area enter the mesolimbic pathway
which supplies the limbic structures of the forebrain.
Excess activity in the mesolimbic pathway is thought to
be related to the onset of schizophrenia characterized
by thought disturbances and delusions.
Localization of the Site of Lesion in
Spinal Cord Lesion
• Localization is made from:
– Sensory level
– Motor reflex level
– Vibration sensation level.
For sensory level determination:
• add 1 to cervical segment
• add 2 to upper dorsal segment
• add 3 to lower dorsal segment (9th to 12th).
Sensory motor level landmarks correspond to spinal
cord segments.
• What is the syndrome of foramen magnum?
Weakness of shoulder, arm followed by weakness of
ipsilateral leg than contralateral leg, finally contralateral
arm constitutes the foramen magnum syndrome. Mass
in this region can produce suboccipital pain spreading
to neck and shoulders.
• High cervical compression C 1, C 2, C 3 sensory C2
interaural vertex meatal line. Motor C1-4 muscles of hand
and neck C1, C2 vasomotor and respiratory center in
addition can have cranial nerve involvement:
– Papilloedema
– Ophthalmic division of trigeminal is affected because
spinal tract of trigeminal nerves are affected
– Spinal accessory affected by 11th cranial nerve.
• C4 diaphragmatic paralysis
• C5-6 sensory radial division of arm, forearm and hand.
Motor paralysis of rhomboid supraspinatus, infra-
spinatus, teres major and minor, deltoid, biceps and
brachioradialis. Arms adducted and internally rotated.
Inversion of supinator jerk, i.e. brachioradialis contrac-
tion is absent but finger flexion seen.
• C7—paralysis of triceps with flexion, extension of wrist
and fingers. Loss of tricep reflex or paradoxical response
leading to flexion of forearm instead of extension.
• C8 to T1—sensory ulnar side of forearm and hand. Motor
atrophic paralysis of small muscles of hand. Finger
flexion reflex is decreased or lost.
• T4—sensory nipple level
• T 6—motor loss of all abdominal reflexes below
umbilicus. Beevor’s sign is present, i.e. umbilicus
Examination of the Spine 275
position shifts upwards on making the patient to get up
against resistance from bed.
• T12 to L1- Sensory-Groin. Motor T12-Abdominal reflexes
intact. L1-Muscles of lower limb involved including hip
flexion. Lower abdominal muscles may be weak, with
absent cremasteric reflex and exaggerated knee and ankle
reflex.
• L1 to L3- Sensory-anterior aspect of thigh, motor L2
same as L1 but knee reflex may be decreased. No
weakness of abdominal muscles. At T12 vertebra and
below as cord ends at L1 root involvement occurs, e.g
cauda equina is involved. Saddle anesthesia over gluteal
region with lower motor paraplegia.
• L4- Sensory level anterior lower aspect of thigh and
medial aspect of leg. Motor hip flexion, adduction, knee
flexion, leg extension preserved. Knee jerks not elicitable.
Ankle jerks exaggerated.
• L5- Lateral aspect of leg and medial aspect of foot from
the sensory level. Motor level is formed by normal knee
jerk but exaggerated ankle jerk.
• S1-Sensory little toes, most of sole of interior and lower
border of foot. Motor weak gastrocnemius with weak
small muscles of foot with absent ankle reflex.
• S2-Sensory posterior aspect of thigh and leg. Motor
paralysis of small muscles of foot.
• S3,4,5 Sensory –anal, scrotal, perineal anesthesia. Motor
paralysis of rectum, bladder, sphincters with impaired
erection.
NECK PAIN AND SHOULDER PAIN
Trauma to Cervical Spine
• (Fractures, subluxation)
• Motor vehicle injury (87%)
• Violent crimes, and falls
Whiplash Injury
1. Due to trauma (automobile accidents)
2. Causes cervical musculoligamental sprain or strain due
to hyperflexion or hyperextension
3. Objective data on pathology of neck soft tissue injuries
is lacking.
Cervical Disk Disease
1. Herniation of a lower cervical disk is common cause of
neck, shoulder, arm or hand pain.
2. Neck pain (worse with movement), stiffness and limited
range of neck motion are common.
3. With nerve root compression, pain may radiate into
shoulder or arm.
4. Extension and lateral rotation of neck narrows the
intravertebral formation and may reproduce radicular
symptoms (Spurling’s sign).
276 Essentials of Clinical Medicine
Cervical n. Pain distribution
Roots
C5 - lat. arm, medial scapula
C6 - lat. forearm, thumb, index finger
C7 - post arm dorsal forearm, lat. hand
C8 - 4th and 5th finger, medial forearm
T1 - medial arm, axilla
Cervical Spondylosis
1. Osteoarthritis of cervical spine may produce neck pain
that radiates into back of head, shoulder, and arms
2. Arthritic or other pathological condition of the upper
cervical spine may be source of headache in posterior
occipital region (supplied by C2-C4 n. root).
3. Cervical spon. with osteophyte formation in lateral recess
or hypertropic forced joints may produce a mono-
radiculopathy.
4. In some, a combination of radiculopathy and myelopathy
occurs
5. An electrical sensation elicited by neck flexion and
radiating down the spine from neck (Lhermite’s
syndrome or symptoms) usually indicates cervical or
upper, thoracic (T1-T2) spinal cord involvement
6. When little or no neck pain accompanies the cord
compression, the diagnosis may be confused with
amyotrophic lateral sclerosis, multiple sclerosis, spinal
cord tumors or syringomyelia.
7. Lumbar radiculopathy or polyneuropathy may mask an
associated cervical myelopathy.
Other Causes of Neck Pain
• Rheumatoid arthritis of cervical apophyseal joints result
in neck pain, stiffness and limitation of motion.
• In advanced RA, synovitis of atlantoaxial joints (C1-C2)
may damage the transverse ligament of atlas, producing
forward displacement of atlas on axis atlantoaxial
subluxation.
• When subluxation is present, careful neurological
assessment is important to identify early sign of
myelopathy.
• Occasional patients develop high spinal cord
compression leading to quadriparesis, respiratory
insufficiency and death.
• Ankylosing spondylitis can cause neck pain and on
occasion atlantoaxial subluxation. When spinal cord
compression is present or threaten, surgical intervention
is indicated.
• Herpes zoster produces neck and postoccipital pain in
C2-C3 distribution prior to outbreak of vesicles.
• Neoplasms metastatic to cervical spine, infection
(osteomyelitis and epidural abscess) and metabolic bone
disease may also cause neck pain.
• Neck pain may be referred from heart in setting of
coronary artery ischemia (cervical angina syndrome).
• The injury to thoracic outlet (first rib, subclavian a. and
v., branchial plexus, the clavicle and lung apex), may
result in posture or taste-related pain around shoulder
and supraclavicular region.
Lymphatic Gland and Salivary Glands
• In inflammation of tonsils, the lymph glands at angle of
jaw are enlarged. Those below the jaw are enlarged in
patients with metastasis from cancer in mouth.
• Enlarged TB glands may occur in groups or in long
chains behind sternocleidomastoid. Scar shows past
suppuration in untreated cases.
• In HIV, Hodgkin’s, other reticuloses and secon-dary
neoplasms, the glands are enlarged and discrete.
• In lymphatic leukemia there may be great enlargement
of gland on both sides.
• In secondary syphilis, glands under upper parts of
trapezium are often palpable.
• If glands are swollen and tender, their opening of ducts
into mouth should be inspected with the tip of patients
tongue rolled upwards this may reveal a salivary calculus.
• In young babies the sternocleidomastoid muscle should
be checked for thickened area known as SCM tumor.
Lump in Neck
1. Less than 20 years of age
a. Inflammatory
b. Congenital—thyroglossal and brachial cyst, midline
dermoid, cystic hygroma
c. Lymphoma.
2. Between 20 and 40 years
a. Salivary gland pathology—calculus, inflam-mation
and tumor
b. Thyroid pathology—goiter, inflammatory thyroiditis
lymophoma, tumor.
c. Chronic infection—HIV, TB, actinomycosis.
3. More than 40 years
a. Secondary malignancy.
b. Primary malignancy—lymphoma.
Features that suggest malignancy are—progressive
enlargement, hardness, lack of tenderness, fixation to deep
structures and size (as node >2 cm is likely to be malignant.)
• Neck pain may radiate through the occiput to the vertex
or to shoulder and down to arms with paresthesiae if
there is nerve root impingement
• The most common cause of local discomfort and
tenderness in neck is infammatory lymphadenopathy,
severe tenderness of thyroid itself, especially when
accompanied by fever and sign of thyrotoxic suggest a

diagnosis of viral subacute thyroiditis (de Quervain’s
thyroiditis)
• Occasionally, autoimume thyroiditis may give rise to pain
and tenderness, which mimics a viral thyroiditis but is
less severe.
• A sudden onset of localized pain and swelling in thyroid
is indicative of bleeding into pre-existing thyroid nodule
and is a recognized complication of multinodular goiter.
The symptoms are self-limiting.
• In addition to meningeal irritation, neck rigidity is also
caused by disease of cervical spine and by increased
ICT especially due to posterior fossa tumor with rostral
-caudal displacement of vermis in foramen magnum
leading to local dural irritation
• Head retraction—now rare, represents an extreme degree
of neck rigidity. It was formally a feature of untreated
TB meningitis.
Meningitis
1. Meningitis may be recognized by rapid onset of
drowsiness, lethargy or stupor with fever and signs of
meningeal irritation.
2. The pulse may be unexpectedly low in relation to fever
in pyogenic meningitis although the respiration is usually
rapid.
3. Seizure and focal neurological sign may develop and
there is H/o of headache and neck stiffness perhaps
vomiting.
4. In meningococcal septicemia, there may be characteristic
rash.
5. A primary site of infection such as otitis media or
sinusitis may be apparent in other forms of purulent
meningitis or brain abscess.
6. The ocular fundi is examined with ophthalmoscopy for
papilloedema, retinal hemorrhages or exudates or intra-
arterial emboli which appear as luminescent highly
refractive yellow or white plaque-like material occluding
vessels.
7. Causes of neck stiffness with coma:
a. SAH
b. Meningitis—bacterial and viral (aseptic)
c. Encephalitis
d. Intracerebral hemorrhage
e. Cerebral malaria
Torticollis
1. May be of a continues or of spasmodic variety
2. Acute torticollis causing deviation of head on one side,
associated with pain is usually due to inflammation of
sternocleidomastoid or trapezius.
Examination of the Spine 277
3. Spasmodic torticollis results in chronic jerking of head
with rotation. This is also seen in cranio - cervical
spasms due to extrapyramidal lesions.
Acute Lymphadenitis
1. The glands are swollen, painful and tender.
2. Fixed and skin overlying them is red in color and warm
to touch.
3. As acute lymphadenitis is secondary to septic focus in
mouth, head and neck or scalp, the examination of these
areas should be carried out to find it. Common infection
in scalp is lice infestation.
Chronic Lymphadenitis
It is seen in TB and syphilis is generally painless.
Lymphosarcoma
1. Massive enlargement of affected glands.
2. Glands are tender and invade the surrounding structure
and they can ulcerate through skin.
3. Mediastinal lymphadenopathy is usually associated with
this cervical enlargement and precedes it.
Thyroid
1. Diffuse tenderness usually implies thyroiditis.
2. Localized tenderness may occur following bleeding into
a cyst.
Others
1. Degenerative arthrosis of cervical spine is common in
middle age and elderly such patients may develop neck
pain, long tract features or radicular symptoms.
2. Flexion of neck sometimes evokes electric shock-like
sensation which shoot into limbs, when the cervical spinal
cord sensory tracts are diseased (Lhermitte’s sign). The
phenomenon is particularly common in multiple sclerosis
but is also seen in syringomyelia, cervical cord tumors
and spondylotic myelopathy.
3. Neck movements are restricted by meningeal irritation.
4. When a node is found, it should be assessed properly.
Nodes which are >0.5 cm in diameter, firm in
consistency and round in shape, usually pathological, a
common cause being metastases from a bronchial
carcinoma.
5. Large fixed masses are present in some cases. Hard,
craggy nodes may, however, be caused by healed and
calcified TB. Other pathological processes include
lymphoma and sarcoidosis.
6. Nerve roots particularly in lower cervical spine may be
compressed or irritated by lateral disk prolapse or
osteophytes causing from facet of neurocentral joints.
7. A central disk prolapse may produce pressure on cord
itself.
278 Essentials of Clinical Medicine

Common Abnormal Findings 2. Disk lesions are rare but may be accompanied by girdle
1. Local cervical tenderness may help to identify the site pain radiating around chest, mimicking cardiac or pleural
of pathology. disease.
2. Regional and paraspinal muscle tenderness, is commonly 3. Pain arising from joints at thoracolumbar junctions may
associated with neck pathology. occur in ankylosing spondylosis and again may be
3. Widespread muscle tenderness may be a feature of confused with pulmonary, renal, or cardiac problems.
psychological disorders. 4. Patients with osteoporosis may complain of becoming
4. Loss of movement. progressively stooped (Dowager hump) with loss of
5. Torticollis associated with acute neck pain. height but without neurological features.
6. Loss of cervical lordosis associated with chronic neck 5. Acute osteoporosis and malignant vertebral collapse are
pain. common causes of acute thoracic pain and the latter is
7. Loss of sensation in upper limb, dermatomes, associated not infrequently associated with spinal cord com-
with n. root irritation. pression.
6. With acute pain, infection should be suspected.
Disorders (Causes of Abnormal Neck Postures) 7. When thoracic pain is poorly localized and no satisfactory
1. Loss of lordosis or flexion deformity—acute lesions, explanation could be found, intrathoracic causes such
RA. as aortic aneurysm should be thought of.
2. Increased lordosis—ankylosing spondylitis
Causes of Pain in Thoracic Spine
3. Torticollis (wryneck)—sternocleidomastoid contracture
4. Lateral flexion (Cock-Robin position)—erosion of lateral 1. Adolescent and young adults:
mass of atlas in RA. • Scheuermann’s disease.
• Ankylosing spondylosis
Cervical Spine • Disk protrusion (rare)
1. The patient may report paresthesia in arm due to nerve 2. Middle age and elderly:
root irritation, or less commonly when spinal cord is • Degenerative change.
involved, symptoms of lower limb weakness, difficulty – Osteoporotic, fracture.
in walking, loss of sensation and sphincter control. 3. Any age:
2. Disease of upper cervical spine affecting the atlantoaxial • Tumor
joints produce pain radiating into occiput in distribution • Infection.
of C2 nerve root.
3. Disease of middle and lower cervical spine tends to Lumbar Spine
cause pain radiating into upper border of trapezius,
interscapular region or into arms, often associated with Causes
local tenderness. 1. Acute disk protrusion
4. Irritation of C6 and C2 nerve root can give rise to widely 2. Spinal stenosis
referred pain in the interscapular region or into radial 3. Ankylosing spondylosis
fingers and thumbs. 4. Osteoporotic fracture
5. Irritation of C8 can produce pain on ulnar side of forearm 5. Infection
and into ring and little finger. 6. Tumors—weight loss and fever
6. Neck pathology should also be considered in any patient 7. Abdominal or retroperitoneal pathology
complaining of diffuse pain in arm, head, upper trunk 8. Age-related degenerative changes in disk or facet joints
or interscapular region if associated with sensory or (spondylosis)
other neurological disturbances. 9. Psychological distress
10. Low back pain due to standing too long, sitting in
BACKACHE poor posture.
11. Poor posture: pain worsens as day passes on and
Thoracic Spine relieved after rest or awakening.
Description of pain 12. Mood disturbances.
1. May present as pain radiating around chest wall or as 13. Inflammatory disease pain such as ankylosing
symptom of paresis, sensory loss, leg weakness and spondylosis worsens in morning or after inactivity
loss of bladder or bowel control. and ease with movement.

14. Morning stiffness in osteoarthritis lasting 30-60 min.
15. Other clues—peri.joints, non-articular features such
as iritis or family H/o spondylarthritis
16. Acute onset with bending or lifting is a feature of
acute disk protrusion. Coughing exacerbates this pain.
17. Poor posture.
18. Loss of sensory sensation, loss of bowel, sphincter
control and perianal sensation.
19. Long steroid therapy may cause osteoporosis. Pain
of this type is eased by lying, exacerbated by spinal
flexion and is not associated with neurological
symptoms.
20. Acute onset of progrssively Increasingly pain with
malaise, weight loss, night sweat—pyogenic or TB
of lumbar spine—may spread to psoas muscle causing
painful flexed hip or as a swelling in groin.
21. Unremitting spinal pain of recent onset with sleep
disturbances, malignant disease involving a vertebral
body should be considered. H/o carcinomas, sys-temic
symptoms or weight loss is present. Tumors rarely
affect intervertebral disk.
22. Diffuse pain in buttock or thighs brought on by
standing too long or walking is the presenting
complaint of lumbosacral spinal stenosis which can
be difficult to distinguish from intermittent clau-
dication. Relieved by rest or flexion of spine.
23. Narrowing of spinal canal or neural exit foraminae, is
usually caused by degenerative changes in inter-
vertebral disk and facet joint. There is long H/o
discomfort typical of degenerative joint disease.
TYPES OF BACK PAIN
1. Local pain: Stretching of pain sensitive structures.
2. Pain referred to back: from abdominal viscera
– Pelvis viscera
– Unaffected by posture.
3. Pain of spinal injury
– May be localized
– May be reffered to buttocks, posterior thighs, calves,
feet
– Sclerotomal pain.
4. Radicular back pain
– Sharp and radiates from spine to legs within the
territory of nerve root
– Coughing, sneezing, voluntary control of abdominal
muscles (stool, lifting object) may elicit radiating
pain.
a. Sitting stretches the sciatic nerve (L5-S1)
b. Femoral nerve (L2, L3, L4) passes anterior to hip
and not stretched on sitting
Examination of the Spine 279
5. Pain associated with muscle spasm:
– Spine disorders
– With abnormal posture
– Taut paraspinal muscles and dull pain
Congenital Anomalies of Lumbar Spine
Spondylolysis
Bony defects in pars interarticularis (a segment near the
junction of pedicle with the lamina) of vertebra.
Spondylolisthesis
• Anterior slippage of vertebral body pedicles and superior
articular facets
• Associated with spondylolysis and degeneration
• Occurs frequently in women
• The slippage may be asymptomic but may cause low
back pain, nerve root injury (L5 mainly) or symptomatic
spinal stenosis
• The trunk may be shortened and abdominal protruberant
as a result of extreme forward displacement of L4 on
L5 in severe degree
• In these cases cauda equina syndrome may occur.
Trauma
• Back pain.
• Inability to move legs—may be due spinal fracture or
dislocation.
• Fracture above L11—spinal cord compression.
Sprains and Strains
• Confined to lower back.
• No radiation to buttocks or legs.
• Patients with low back pain and para spinal muscle spasm
often assume unusual postures.
Vertebral Fractures
• Pars interarticularis fractures of L5 vertebrae is common
• Neurological impairment is commonly associated with
these injuries.
• Bones may be weakened by osteomalacia, hyper-
parathyroidism, hyperthyroidism, multiple myeloma,
metastatic carcinoma, glucocorticoid therapy.
Lumbar Disk Disease
• Most likely at L4-L5 and L5-S1 levels
• Risk in overweight persons
• Sneeze, cough or trivial movement may cause nucleus
palposus to prolapse, pushing the frayed and weakened
280 Essentials of Clinical Medicine
annulus posteriorly. In severe disk disease, the nucleus
may protrude the annulus (herniation) or become
extruded to lie as a free fragment in spinal canal.
• The inner annulus fibrosus and nucleus palposus are
normally devoid of innervation but inflammation and
production of proinflammatory cytokines within the
protruding or ruptured disk may trigger or perpetuate
back pain.
• Ingrowth of nociceptive (pain) nerve fiber into inner
portion of diseased intervertebral disk may be responsible
for chronic “diskogenic pain”.
• Symptoms of intervertebral disk include back pain,
abnormal posture, limitation of spine motion (particularly
flexion) or radicular pain.
• A dermatomal pattern of sensory loss or a reduction in
or loss of a deep tendon reflex is more suggestive of a
specific root lesion than pattern of pain.
• Motor findings—(focal weakness, muscle atrophy or
fasciculations) occurs less frequently than sensory reflex
changes but a myotomal pattern of involvement can
suggest specific root injury
• Degeneration of intervertebral disk without frank
extrusion of disk tissue may cause low back pain.
• There may be referred pain in leg, buttock or hip with
little or no disk comfort in back and no sign of nerve
root involvement.
• Lumbar disk syndromes are usually unilateral but large
central disk herniation can cause bilateral symtomps/
signs and may cause cauda equina syndrome.
Differential Diagnosis(D/D) of
Lumbar Disk Disease
• Epidural abscess
• Hematoma
• Tumors
• Fever, constant pain, uninfluenced by position sphinc-
teric abnormalities or signs of spinal cord disease suggest
etiology other than lumbar disk disease
• Bilateral absence of ankle reflexes can be normal finding
in old age or a sign of bilateral S1 radiculopathy.
• An absent deep tendon reflex or focal sensory loss may
show injury to a nerve root and other sites of nerve root
injury.
• Absent knee reflex may be due to femoral neuropathy
rather than L4 nerve root injury.
• A focal decrease in sensation over foot and distal lateral
calf muscle may result from peroneal or lateral sciatic
neuropathy rather than L5 nerve root injury.
• Focal muscle atrophy may reflect loss of motor axons
from a nerve root or peripheral nerve injury, an anterior
horn cell injury or disease.
Spinal Stenosis
• Narrowed lumbar or cervical spinal canal.
• Neurogenic claudication consists of back and buttock
or leg pain induced by walking or standing relieved by
sitting.
• Symptoms in legs are usually bilateral.
• Focal weakness, sensory loss or reflex changes may
occur when associated with radiculopathy.
• Unlike vascular claudication, standing often provokes
the symptoms without walking.
• Unlike lumbar disk disease, sitting relieves the symptoms.
• Severe neurogenic deficit includes paralysis, urinary
incontinence (rare)
• Congenital spinal stenosis are characterized by short,
thick pedicles that produce both spinal canal and lateral
recess stenosis.
• Acquired stenosis result from degenerative disease
(spondylosis, spondylolisthesis, scoliosis), trauma, spinal
surgery (postlaminectomy, fusion) metabolic or
endrocrine (epidural lipomatosis, osteoporosis, acro-
megaly, renal osteodystrophy, hyperpara-thyroidism) and
Paget’s disease.
Facet Joint Hypertrophy
• Unilateral radicular symptoms due to bony com-pression.
• The patient shows stress signs, focal motor weakness,
hyporeflexia or sensory loss.
Lumbar Adhesive Arachidonitis
• Back and legs pain with motor sensory and reflex changes
• Multiple lumbar operations
• Chronic spinal infections
• Spinal chord injury
• Intrathecal hemorrhage
• Intrathecal injection of steroids and anesthetics
• Foreign body.
Arthritis
Spondylosis
• Later in life
• Cervical and lumbosacral spine
• Back pain, which is incresed by motion and associated
with stiffness or limitation of motion.
Ankylosing Spondylolitis
Description of pain:
• Present with insidious onset of low back and buttock
pain

• Onset males >40 years.
• Associated with
– Morning back stiffness
– Nocturnal pain
– Unrelieved by rest
– Increased sedimentation rate
• HLA-B-27.
Differential Diagnosis (D/D) of
Ankylosing Spondylolitis
1. Tumor
2. Infection.
– Onset at young and back pain improving with exercise
suggests ankylosing spondylolitis
– Loss of normal lumbar lordosis and exaggeration of
thoracic kyphosis are seen as the disesase progresses.
– Bamboo spine
– Similar restricted movements may accompany
Reiter’s syndrome, psoriatic arthritis, chronic bowel
disease.
– Stress fracture through spontaneously ankylosed
posterior bony elements of the rigid, osteoporotic
spine may result in focal spinal pain, spinal cord
compression and cauda equina syndrome
– Sometimes atlantoaxial subluxation with compression
occurs.
– Bilateral ankylosis of ribs to spine and a decrease in
height of axial thoracic structures may cause marked
impairment of respiratory function.
Neoplasms
Description of pain
1. Back pain is the most common neurologic symptom
among patients with systemic cancer.
2. Metastatic ca. (breast, lung, prostrate, thyroid, kidney,
GIT) multiple myeloma, non-Hodgkin’s and Hodgkin’s
lymphoma frequently involve spine.
3. Pain is dull, constant, unrelieved by rest and worse by
night (in contrast mechanical low back pain is usually
improved with rest).
Infection
1. Verbal osteomyelitis
• Caused by Staphylococcus. But other bacteria or
tubercle bacilli (Pott’s disease) may be the causative
microorganisms.
• Primary source of infection most often is from
urinary tract infection, skin or lungs in 40 percent.
Intravenous drug abuse is a well-recognized risk
factor.
Examination of the Spine 281
• Back pain exacerbated by motion and unrelieved by
rest, spine tenderness over the involved spine
segment and an elevated ESR.
• Fever with elevated WBC count in some patients.
2. Spinal epidural abscess
• Back pain (aggravated by palpation or movement)
and fever.
• The patient may exihibit nerve root injury or spinal
cord compression with sensory level, inconti-nence,
or paraplagia.
Osteoporosis and Osteosclerosis
• Loss of bone with hyperparathyroidism, chronic
glucocorticoid use, or immobilization.
• Compression fractures occur in up to half of patients
with severe osteoporosis.
• The sole manifestation of a compression fracture may
be focal lumbar or thoracic aching (often after a trivial
injury), i.e. exacerbated by movement.
• Other patients experience thoracic upper lumbar radicular
pain.
• Focal spine tenderness is common.
• Compression fractures above the midthoracic region
suggest malignancy.
• Osteosclerosis may or may not produce back pain.
Referred Pain from Visceral Diseases
• Occasionally, back pain may be the first and only sign
of a referred pain from diseases of pelvis, abdomen and
thorax.
• Local signs (pain with spinal palpation, paraspinal muscle
spasm) are absent and minimal or no pain accompanies
normal spine movements.
Low Thoracic and Upper Lumbar Pain in
Abdominal Diseases
• Paraspinal pain or midline back pain due to peptic ulcer
or tumor of post. stomach or duodenum. (if the
retroperitoneal extension is present).
• Back pain due to peptic ulcer may be precipitated by
ingestion of an orange, alcohol, coffee, and relieved by
food and antacids.
• Fatty foods are more likely to induce back pain
associated with biliary disease.
• Disease of pancreas may produce back pain to right of
spine (head of pancreas involved) or to left (body or tail
involved).
• Pathology in retroperitoneal structures (hemorrhage,
tumors, pyelonephritis) may produce paraspinal pain
with radiation to lower abdomen, groin, or anterior
thighs.
282 Essentials of Clinical Medicine
• Mass in iliopsoas region often produces unilateral lumbar
pain with radiation towards groin, labia, or testicles.
• The sudden appearance of lumbar pain in a patient
receiving anticoagulant therapy suggests retroperitoneal
hemorr-hage.
• Isolated low back pain occurs in 15 to 20 percent of
patients with rupture of an abdominal aortic aneurysm.
• Classic triad of abdominal pain, shock, back pain in
elderly men occurs in fewer than 20 percent of patients.
• Two of these features are present in 2/3rd of patients.
And hypotension is present in ½. Ruptured abdominal
aortic aneurysm (AAA) is typically the elderly patient
male with back pain.
• Common misdiagnosis include nonspecific back pain,
diverticulitis, renal colic, sepsis, and myocardial
infarction. A careful abdominal examination revealing a
pulsatile mass (in 50-75 percent patients) is an important
finding.
Lumbar Pain with Lower Abdominal Disease
• Inflammatory bowel disease (colitis, diverticulitis) or
colonic neoplasms may produce lower abdominal pain,
midlumbar back pain or both.
• Pain may have belt like distribution around the body.
• Lesions in transverse or initial descending colon may
refer pain to upper sacral or midline suprapubic regions
or left lower quadrant of the abdomen.
Sacral Pain in Gynecological and
Urological Diseases
• Endometriosis or uterine carcinoma may invade the
uterosacral ligaments, malposition of uterus may cause
uterosacral ligament traction.
• Pain associated with endometriosis begins during the
premenstrual phase and often continues until it merges
with menstrual pain.
• Malposition of uterus (retroversion, descensus, and
prolapse) may lead to sacral pain after standing for several
hours.
• Other pelvic sources of low back pain include neoplastic
invasion of pelvic nerve, radiation, necrosis and
pregnancy.
• Menstrual pain may be felt in sacral region. The poorly
located cramping pain can radiate down to legs.
• Pain due to neoplastic infiltration of nerves is typically
continuous, progressive in severity and unrelieved by
rest at night.
• Radiation therapy of pelvic tumors may produce sacral
pain from late radiation necrosis of tissues or nerves.
• Low back pain with radiation into one or both thighs is
common in last week of pregnancy.
• Urologic sources of lumbosacral pain:
– chronic prostatitis
– prostatic carcinoma with spinal metastasis
– diseases of kidney and ureter.
• Lesions of bladder and testis usually do not cause back
pain.
• Infections, inflammatory, or neoplastic renal disease may
result in ipsilateral lumbosacral pain as can renal artery
or vein thrombosis.
• Ureteral obstructions due to renal stone causes paraspinal
lumbar pain.
Postural Back Pain
1. Chronic non-specific low back pain with no anatomic
or pathologic lesion can be found despite exhaustive
investigation.
2. The patient complains of vague diffuse, backpain with
prolonged sitting or standing that is relieved by rest
3. Physical exam is unrevealing except for “poor posture”.
Psychiatric Diseases
1. Chronic low back pain (CLBP) may be encountered in
patients with compensation hysteria, maligering,
substance abuse, chronic anxiety states or depression.
2. Many patients with CLBP have a history of psychiatric
illness (depression, anxiety and substance abuse) or
childhood trauma (physical or sexual abuse).
Unidentified
1. Cause is unclear.
2. No definite neurological sign or a minor disk bulge noted
on CT or MRI.
3. Some patient have had multiple operation for disk disease
but have persistent pain and disability.
Physiological
1. Faulty posture
2. Asthenic individual.
3. Pregnancy.
Trauma
1. Prolapsed intervertebral disk.
2. Lumbosacral strain.
Infection
1. Osteomyelitis.
2. TB of spine (Pott’s disease).

Neoplastic
1. Primary tumor.
2. Secondaries.
3. Multiple myeloma.
Metabolic
1. Osteoporosis.
2. Osteomalacia.
3. Hyperparathyroidism.
Congenital
1. Spina bifida.
Arthiritis
1. RA (rheumatoid arthritis).
Examination of the Spine 283
2. Osteoarthritis.
3. Ankylosing spondylolysis.
Referred
1. Pancreatitis.
2. Retroperitoneal tumor.
3. Cholecystitis.
4. Diverticulitis.
5. Retroverted uterus.
6. Uterine prolapse.
Spinal Abnormalities
1. Kyphosis.
2. Scoliosis.
3. Lordosis.
 10
Common Cases Encountered in
Clinical Medicine: Hypothyroidism,
Myxoedema and Thyrotoxicosis

HYPOTHYROIDISM Table 10.2: Differences between primary and

secondary hypothyroidism
Causes of Hypothyroidism
Features Primary Secondary
Primary: Autoimmine, Hashimoto’s thyroiditis, defect in
Skin changes Thick, without wrinkles Thin, with wrinkles
hormone synthesis—iodine deficiency, dyshormono- Hair changes Coarse Fine
genesis, thyroid carcinoma, thyroid infiltrates, tissue Menstrual Menorrhagia Amenorrhea
resistance to T4 and T3. irregularities
Secondary sexual Normal Poor
Secondary: Due to hypopituitarism. character
Heart size May be enlarged Small
Goiter May be present Absent
Signs of Hypothyroidism in Adults
Soft tissue edema Present Absent
Puffy face, pallor, bradycardia, dry skin, brittle hair, anemia, BP Normal or high Low
Cholesterol High Normal
lung up reflexes, stock and glove type of anesthesia, carpal TSH Elevated Low
tunnel syndrome, obesity, hoarse voice. Plasma cortisol Normal Low
Thyroid antibodies May be present Absent
Causes of Hypothyroidism with Enlarged TRH stimulation Exaggerated response No response
test
Goiter (Goitrous Hypothyroidism)

• Iodine deficiency MYXOEDEMA

• Dyshormogenesis History
• Malignancy
• Chief complaints
• Thyroiditis. – Constipation since birth
– Delayed milestones
Table 10.1: Clinical manifestation of hypothyroidism
– Stunted growth
Neurological manifestations Cardiovascular – Poor feeding in newborn
manifestations
– Prolonged jaundice in newborn.
• Psychosis • Bradycardia • Associated history/history of complications
• Nerve deafness • Cardiomegaly due CCF or – H/o lethargy
• Aeroparesthesia cardiomyopathy – H/o excessive somnolence
• Cerebellar ataxia • Pericardial effusion – H/o temperature instability—hypothermia, dry skin
• Epilepsy • ECG changes – low voltage, – H/o stridor—hoarse cry/voice
• Drop attacks sinus bradycardia, PR – H/o repeated LRTI (cough, cold, fever, breath-
prolong lessness)
• Peripheral neuropathy. ST segment depression – H/o swelling in anterior region of neck—goiter
– H/o edema over body—myxoedema
 Common Cases Encountered in Clinical Medicine: Hypothyroidism, Myxoedema and Thyrotoxicosis 285

– H/o hearing loss-Pendrade syndrome (defect in iodine • Weight loss

uptake/iodination) • Sweating
– Conductive deafness (myxoedema/repeated LRTI • Tremors
and otitis media). • Increased appetite
• Etiological history • Heat intolerance
– H/o endemicity—endemic goiter (iodine deficiency). • Irritability and nervousness
• Palpitation
Neurological Manifestations • Oligomenorrhea
• Diarrhea
• Aeroparesthesia • Prominence of eyes
• Cerebellar ataxia • Fever
• Drop attacks • Pain as of thyroid gland.
• Peripheral neuropathy
Symptoms
Cardiovascular Manifestations of Myxoedema
• Insomnia
Bradycardia, cardiomegaly due to CCF or cardiomyopathy, • Nervousness
pericardial effusion, ECG changes—low voltage, sinus • Emotional liability
bradycardia, PR prolongation and ST segment depression. • Perspiration.
• Hyper irritability
Differential Diagnosis of Myxoedema • Hyperkinesia.
• Depression monia
• Aging • Psychosis.
• Nephrotic syndrome. • Difficulty in raising from squatting position.
• Angioneurotic edema.
• Mongolism, pernicious anemia. Signs of Thyrotoxicosis
• Postmenopausal syndrome.
• Exophthalmos, lid lag
Table 10.3: Differences between cretinism and mongolism • Tremors
Features Cretinism Mongolism
• Sinus tachycardia
• Atrial fibrillation
Alertness Lethargic Active
Skin Dry coarse Normal
• Moist warm hands
Bone age Retarded Normal • Systolic murmur
Special feature All features of Obliquity of eye, epicanthal • Hyperdynamic apex beat
cretinism folds, palmar and plantar • Systolic hypertension
creases abnormal • Proximal myopathy
• Increased bowel sounds
Myxoedema Coma or Myxoedema Madness • Diarrhea
Bizarre psychiatric symptoms in hypothyroidism is called • Osteoporoses
myxoedema madness. It is a stage of severe and acute • Hyperglycemia
thyroid hormone deficiency marked by hypotension, • Leukopenia with lymphocytosis.
hypothermia, hypoventilation, hyponatremia and occa-
Differential Diagnosis of Thyrotoxicosis
sionally seizures. Treat with 0.3 to 0.4 mgm T4 IV 12 hourly,
hydrocortisone, assisted ventilation, antibiotics, treat CCF • Anxiety neurosis.
and arrhythmia. Saline infusion, treat infection. • T3 and T4 thyrotoxicosis.
• Chronic wasting disease—malignancy.
THYROTOXICOSIS • Addison’s disease.
• Diabetes mellitus.
History Taking
• Nutritional deficiency.
• History of thyroid medication, iodine therapy, family • Chronic cor pulmonale.
history of thyroid disease, goiter • Chronic alcoholism.
286 Essentials of Clinical Medicine

Differential Diagnosis for Proptosis Complications of Thyrotoxicosis

• Dysthyroid exophthalmos. • CVS—CCF, atrial fibrillation.
• Retro-orbital neoplasm. • Thyroid crisis—thyroid storm.
• Capillary hemangioma. • Muscle—proximal muscle weakness.
• Orbital cellulitis.
• Cavernous sinus aneurysm. HYPERTHYROIDISM
• Sarcoidosis. Manifestations of Hyperthyroidism
• Histiocytosis.
• Warm and moist skin, palmar erythema
Table 10.4: Differences between • Fine, silky and friable hair
thyrotoxicosis and anxiety state • Plummer’s nails—separation of distal margin of nail from
Findings Thyrotoxicosis Anxiety state nailbed. Best seen in fourth finger.
1. Sleeping pulse Raised Normal • Pretibial myxoedema—occurs over the shin of tibia in
2. Pulse pressure Wide Normal graces, diseases wither during toxicosis stage or after
3. Palms Warm and moist Cold and moist the treatment is started. Hyperpigmented, pruritic with
4. Thyroid function test Abnormal Normal peau de orange appearance, lesions are discrete or plaque
like or nodular.
Table 10.5: Differences between primary and secondary • Thyroid acropathy—clubbing of digits with bony
thyrotoxicosis changes resembling pulmonary osteoarthropathy, occurs
Features Primary thyrotoxicosis Toxic nodular in hyperthyroidism
or Grave’s disease goiter or secondary • Rarely spider nevi.
thyrotoxicosis
Age Less than 35 years More than 30 years Causes of Hyperthyroidism
Thyroid gland Diffuse and smooth Nodular
Onset With thyroid enlargement After thyroid
• Grave’s disease.
enlargement • Solitary toxic adenoma.
Exophthalmos Severe Slight • Toxic multinodular goiter.
CNS symptoms Prominent Slight • Autoimmine thyroiditis.
CVS symptoms Slight Severe • TSH and hCG producing tumors.
Pressure symptoms Rare Common
Thyroid scan Uniform uptake Localized increased ECG Changes in Hyperthyroidism
uptake
Recurrence after More Less • Sinus tachycardia.
thyroidectomy • Atrial fibrillation.
Response to anti- Good Not good • Supraventicular tachycardia.
thyroid drug • Non-specific T wave changes.
 Diabetes Mellitus

HISTORY TAKING Table 10.8: Signs and symptoms of

diabetic ketoacidosis
• While taking history, the following points should be
considered: Symptoms Signs
– Family H/o DM—means mostly NIDDM Polyuria Hypothermia
– H/o dimness of vision—cataract, retinopathy Polydipsia Kussmaul’s breathing
– H/o tingling and numbness—peripheral neuropathy Weakness Acetone breath
– H/o swelling over whole body—diabetic nephropathy Lethargy Dehydration
– Leukoderma with DM—autoimmune Myalgia Hyporeflexia
– Alcohol intake history Headache Acute abdomen
– Past H/o pancreatitis or pancreatic surgery Anorexia Stupor-coma
– Secondary DM Nausea Hypotonia
– Nocturia, diarrhea, orthostatic hypertension, auto- Vomiting Incoordinated movements
nomic neuropathy of eye
Abdominal pain Fixed dilated pupil
• On examination
Dyspnea
– Check BP for postural changes
– Skin—increased pigmentation, bronze diabetes,
vitiligo present, autoimmune association. Table 10.9: Differences between hypoglycemia
– Fundus—retinopathy, eye-stye, cataract and diabetic ketoacidosis
– CVS—hypertension, CCF, LVF, angina MI, diabetic Hypoglycemia Diabetic ketoacidosis
cardiomyopathy
History of skipping meal History of skipping insulin
– CNS—polyneuritis, cranial neuritis, ptosis—third
nerve palsy, seventh nerve palsy, autonomic Rapid onset Insidious onset
neuropathy, CVA Moist skin Dry skin and mucous membrane
– Respiratory—secondary infection, PTB at typical Tachycardia, good volume Tachycardia, low volume
sites Respiration normal Respiration deep and hurried
– Weight, height BMI waist-hip ratio to find out obesity Urine normal Glycosuria and ketonuria
– GIT—hepatomegaly in uncontrolled DM Blood glucose decreased below Blood glucose increased
– Joints—periarthritis shoulder. 50 mgm

Table 10.6: Etiological factors

Table 10.10: Differences between diabetic ketoacidosis
IDDM NIDDM and hyperosmolar nonketotic coma
Viral infection Obesity Factors Diabetic ketoacidosis Hyperosmolar
HLA antigen DR3 DR4, B8,15 Hereditary nonketotic coma
Autoimmune process Drugs
Genetic Pancreatic factors Age Young Old
Use of refined carbohydrate Respiration Hyperventilation Normal or shallow
Urbanization Dehydration Moderate Severe
Receptor defects Consciousness Diminished Comatose
Temperature Normal Raised
Table 10.7: Diagnosis criteria of Blood glucose More than 300 More than 600
DM during pregnancy
Acetone Severe Mild to nil
Fasting 2 hours 3 hours Urea 42-70 mg 60-180 mg
Normal Less than 90 Less than 145 Less than 90 Sodium, potassium Decreased Normal
GDM If any two of the values above the normal, indicates Bicarbonate Decreased Normal
gestational diabetes Osmolarity 300-380 mmol/1 50 mmol/1
288 Essentials of Clinical Medicine

DIFFERENTIAL DIAGNOSIS OF • Tachycardia—absence of sinus arrhythmia

DIABETIC KETOACIDOSIS • Postural hypotension
• Cerebrovascular accident • Sleep apnea
• Brainstem hemorrhage • Gustatory sweating
• Hypoglycemia • Gastroparesis
• Uremia • Nocturnal diarrhea
• Metabolic acidosis • Loss of sweating
• Acylates, methanol poisoning
• Importance and absence of testicular sensation
• Gastroenteritis with peripheral circulatory failure
• Pneumonia (hyperventilation). • Retrograde ejaculation
• Charcot joint
SIGNS AND SYMPTOMS OF HYPOGLYCEMIA • Pseudo-Argyll-Robertson pupil.
Autonomic Symptoms
RENAL INVOLVEMENT IN DIABETES
• Hunger
It clinically manifests as:
• Tachycardia
• Tremor • Pedaledema
• Sweating • Diabetic nephropathy
• Anxiety/nervousness • Arterionephrosclerosis
• Weakness • Chronic interstitial nephritis
• Nausea and vomiting • Pyelonephritis
• Papillary necrosis
Neuroglycopenic Symptoms • Commonest lesion is diabetic nephropathy with KW
• Perioral anesthesia lesion
• Headache and visual disturbance
• Mental confusion GI MANIFESTATIONS OF DIABETES
– Inability to speak • Gastric atony
• Speech slurred and gait ataxic
• Motility disturbance of esophagus, stomach and colon
• Diplopia
• Diabetic enteropathy
• Bizarre mood
• Semicoma, coma • Chronic pancreatitis
• Chronic fibrocalculus pancreatitis—in MRDM
CLINICAL FEATURES SUGGESTIVE OF • Fatty liver
AUTONOMIC NEUROPATHY • Acalculous cholecystitis
• Hypoglycemic unresponsiveness—lack of warning signs • Increased incidence of carcinoma gallbladder and Ca
absent pancreas.
 Lymphadenopathy

HISTORY TAKING Table 10.11: Differences between Hodgkin’s and

non-Hodgkin’s lymphoma
• Fever—Pel-Ebstein type of fever—intermittent type of
Hodgkin’s Non-Hodgkin’s
remittent fever—Hodgkin’s disease
Frequency Commoner Less common
• Evening rise of fever—TB Age Two peaks seen Any age, more with
• Itching after alcohol drink—Hodgkin’s lymphoma younger and elderly increasing age
• Anemia, lymphadenopathy, generalized in elderly male Constitutional symptoms Late Early
Anemia Late Early
with splenomegaly, leukemia Lymph node
• Fever with generalized lymphadenopathy, hepatomegaly, – Presentation 90% nodal, 60% nodal,
palatal rash in a boy aged 15 years—infectious mono- 10% extra nodal 40% extra nodal
nucleosis – Size Small Large
– Rate of growth Slow Fast
• Lymphadenopathy after prolonged drug therapy— – Consistency Rubbery Variegated
phenytoin – Matting Rare Often early
• Genital and inguinal lymphadenopathy—chancre, – Temperature Normal May be raised
– Tenderness No +
chancroid – Epitrochlear – +
• Foot and leg swelling, nonpitting edema with inguinal gland
lymphadenopathy, filariasis – Waldeyer’s ring – +
• Axillary lymphadenopathy with hard lump in breast— – Mediastinal ++ –
Pruritis +++ +
carcinoma breast. Splenomegaly +++ +
GIT involvement Uncommon Common
CNS involvement Uncommon Common
Alcohol test Common Uncommon
Pathogenesis Functional T B cell defect
lymphocyte defect
Involvement and Unicentric and orderly Multicentric
progression progression
Invasive staging Needed Not needed
procedure
 Arthritis

It is very important to first of all know the difference – Lumbar vertebrae—osteoarthritis

between arthritis and arthralgia. – Temporomandibular joint—rheumatoid
– Small joint rheumatoid
Table 10.12: Differences between arthritis and arthralgia – Distal IP joint—osteoarthritis, psoriasis
Arthritis Arthralgia – First metasophalangeal joint—gout
1. Subjective and objective Only subjective – First carpometacarpal joint—osteoarthritis
2. Signs of inflammation present No signs of inflammation – Metasophalangeal—rheumatoid arthritis. Serone
3. May be because of a disease Signs of generalized disease Gative Arthritis
• Tenderness
HISTORY TAKING • Synovial effusion, Heberden’s node—osteroarthritis
• Age • Joint movement and crepitus
– Young—SLE, Reiter’s disease • Deformities, muscle wasting
– Old—osteoarthritis • Spine and gait
• Pain—location, nature, progression • On systemic examination, look for:
• Number of joints involved – Eyes—Reiter ’s syndrome, Behçet’s disease,
• Fever, weight loss sacoidoisis
• Morning stiffness – Skin—subcutaneous nodules
• Inactivity stiffness – Scalp—psoriasis.
• Past history of medications EXAMINE A JOINT
• Associated disorder like peptic ulcer
• Family history of rheumatoid, gout • Inspection of joint—fullness, redness, for tophi, muscle
• Male—gout, spondyloarthritis; female—rheumatoid wasting, muscle swelling
arthritis • Palpation—crepitus, synovial effusion, pitting edema,
• Presence of nail, scalp, oral, skin, genital lesions tenderness, painless joint swelling (Charcot joint).
• Bowel involvement—postdysentery, ulcerative colitis, • Movements—passive/active.
Crohn’s disease
• Urinary problem like urethritis DIFFERENTIAL DIAGNOSIS OF ARTHRITIS
• Venereal disease and AIDS Inflammation of tissues around the joint may mimic arthritis.
• Onset • Disease of skin:
– Acute—gout, septic – Cellulitis.
– Chronic—osteoarthritis • Diseases of muscles:
• Symmetrical, rheumatoid arthritis is symmetric – Myalgia
• Extremely affected—upper rheumatoid, lower—gout, – Trichinosis
Reiter’s syndrome – Muscle abscess
• Migratory arthritis—rheumatic arthritis • Diseases of bones:
• Joints affected – Scurvy
– Big toe—gout – Osteomyelitis.
– Cervical spine—rheumatoid – Multiple mycloma.
– Lower cervical vertebrae—osteoarthritis – Leukemias.
 Common Cases Encountered in Clinical Medicine 291

Table 10.13: Causes of mono articular arthritis and Contd...

poly articular arthritis Features Gout Pseudogout
Monoarticular arthritis Polyarticular arthritis 5. Effect of uricase Crystals dissapear Crystals do not disappear
• Gonococcal infection • Rheumatic fever on synovial fluid
• TB • Rheumatoid arthritis crystals
• Gout • Viral infection 6. Serum uric acid Raised Normal
• Post-traumatic inflammation • Postdysenteric levels
• Pyogenic infection within the joint • Syphilis in secondary stage. 7. Radiological Punched out areas Evidence of chodrocalci-
• Infective endocarditis findings nosis in the form of linear
• Osteoarthritis • Erythema nodosum calcification
leprosum
• Neuropathic • SLE
• Rheumatoid arthritis • Seronegative spondy-
SYNOVIAL FLUID EXAMINATION IN THE
loarthritis DIAGNOSIS OF JOINT DISEASE
– Juvenile RA
– Ank. spondylitis Table 10.16: Gross examination
– Psoriatic arthritis
– Reiter’s syndrome Condition Color Clarity Viscosity
– Beçhet’s syndrome Normal Yellow Translucent High
Rheumatoid Yellow or Translucent or Low
Table 10.14: Diagnostic approach in monoarthritis arthritis purulent opaque
Osteoarthritis Yellow Transparent High
Features Investigations Diagnosis Tuberculosis Yellow Opaque Low
Trophic change Uric acid, X-ray Gout Septic arthritis Purulent Turbid High
cartilage calcification
and meniscal calci- Table 10.17: Microscopy
fication
Skin pustule Gram stain Gonococcal arthritis Condition WBC/cu.mm Polymorphs
Tenosynovitis
Normal Less than 200 Less than25
Urethritis
Rheumatoid 3,000-5,000 50-70
Erythema nodosum X-ray chest, MT, biopsy TB sarcoid
Heberden’s node X-ray Osteoarthritis arthritis
Bleeding tendency Coagulation profile Hemophilia Osteoarthritis Less than 2,000 Less than 25
Warm hot joint Synovial fluid Gram Pyogenic arthritis Septic arthritis More than 50,000 More than 60
stain, culture positive
Extra-articular TB AFB of synovial fluid TB Table 10.18: Biochemical examination
Steroid therapy X-ray Avascular necrosis
Condition Serum glucose Complement Smear and
in mg% culture
Causes of Intermittent Arthritis
Normal Same Normal Negative
• Gout, pseudogout. Rheumatoid 70-100 Normal or low Negative
• Palindromic rheumatism. arthritis
• Episodic rheumatoid arthritis. Osteoarthritis Same Normal Negative
• Relapsing polychoridritis. Tuberculosis 50-70 Normal or low Positive
Septic arthritis Less than 50% of Normal Positive
• Hyperlipidemia related to arthritis.
blood sugar
Table 10.15: Difference between gout and pseudogout

Features Gout Pseudogout

CLINICAL FEATURES OF
RHEUMATOID ARTHRITIS
1. Age. Adult Over 50 years
2. Joints involved Great toe Knee, wrist, elbow, hip, and • It is a chronic nonsuppurative inflammation of diarthodial
glenohumeral joint
3. Synovial fluid Uric acid deposits Calcium pyrophosphate joints frequently associated with extra-carricular
4. Crystals Negative biref- Needle-like crystals, manifestations. Etiology—genetic predisposition—
ringence under pola- positive birefringence association with HLA-D locus Haplo type, frequency of
rized beam of light under polarized beam
HLA DR 4 and DW4 is twice as compared to general
of light
population.
Contd...
292 Essentials of Clinical Medicine

• Following agents are known to produce RA in genetically Neurological Diseases Encountered in RA

predisposed persons—Mycoplasma, Clostridium • Myopathy—steroid induced
perfringens, Ebstein-Barr virus, hepatitis ‘B’ virus, • Entrapment neuropathy—carpal tunnel syndrome
rubella virus. • Rheumatoid neuropathies:
• Clinical features – Sensory, mixed type
– Polyarthritis affects small as well as large joints – Vasculitis mononeuritis multiplex
– Joints involved: – Cervical myclopathy at atlantoaxial joint
 Common—proximal interphalangeal joints of – Antimalarial induced neuropathy
hands, metacarpophalangeal joints, wrists, knees, • Drug-induced myasthenia—penicillamine
elbows, ankles, less common joints include hip • Lumbert-Eaton myasthenic syndrome
and temporomandibular joints • Neurasthenia
 Rare—cricoarytenoid joint of larynx, cervical • Hyperthyroidism
spine, atlantoaxial joint, sternoclavicular joint • Botulism
• Arthritis, fever, hepatosplenomegaly with lymphade- • Progressive extrinsic ophthalmoplegia.
nopathy
Table 10.19: Conditions in which RA factor is positive
• Carpal tunnel syndrome
• Palmar erythema Old age Rheumatoid arthritis
• Skin atrophy with pigmentation Cirrhosis of liver Infective hepatitis
• Vasculitis, subcutaneous nodules SLE SABE
Tuberculosis Leprosy
• Anemia. Syphilis Polymyositis
Sarcoidosis Sicca syndrome
Diagnostic Features of Acute Trypnosomiasis Cryoglobulinemia
Waldenström’s macroglobulinemia Chronic interstitial pulmonary
Rheumatic Arthritis
fibrosis
• Occurs following streptococcal throat infection.
• Acute onset. DIFFERENTIAL DIAGNOSIS OF
• Characterized by migratory fleeting polyarthritis, large RHEUMATIC FEVER
joints are involved, residual joint deformity does not • Polyarthritis is due to infective endocarditis in patients
occur. with pre-existing rheumatic heart disease.
• Valvular heart disease may be a sequela. • Gonococcal arthritis—responds dramatically to
therapeutic trial of penicillin.
American Rheumatic Association (ARA)
Criteria for Diagnosis of RA Table 10.20: Differences among rhematic arthritis,
rheumatoid arthritis and osteoarthritis
1. Morning stiffness (of at least one hour duration). Factors Rheumatic Rheumatoid Osteoarthritis
2. Arthritis of 3 or more joints areas. arthritis arthritis
3. Arthritis of hand joints. Age Young Middle aged Old
4. Symmetrical arthritis. Sex Female Female Male
5. Rheumatoid modules. Joint affected large Small-hand
temporomandi-
6. Presence of rheumatoid factors. bular, upper
7. Radiological changes (hand and wrist). cervical spine
Rheumatoid arthritis is said to be present, if the patient H/o sore throat Yes No No
Season – Winter –
has at least 4 of the above 7 criteria. Criteria 1-4 frame to
Trauma – – Aggravates
be present for at least 6 weeks. ESR Increased Increased Normal
Transient Yes No No
Neuro Sites of Subcutaneous Nodules in RA Systemic No Yes No
symptoms
Common sites: Olecranon bursa, tendo-Achilles, extensor Response to Good Variable Variable
surface of forearm, ischial tuberosity. therapy
Joint damage Nil Residual Residual
Uncommon sites: Synovial membrane, periarticular tissue, Effect on heart Yes Sometimes
dura mater, intestine, lungs and pleura. aortic valve No
 Renal System Presentation

CHRONIC RENAL FAILURE • Hemotological changes:

– Anemia due to decreased erythropoietin.
History of Chronic Renal Failure
– Bone marrow depression.
• Infancy enuresis – Hemolysis—hemorrhage
• Nephritis – Due to frequent blood sampling investigations.
• Nephritic • Coagulation disorders like decreased platelet factor,
• Urinary tract infection prothrombin consumption, decreased platelet aggre-
• Loin pain gation.
• Drug intake—NSAID, aminoglycosides • GIT complications—vomiting, anorexia, diarrhea or
• Hematuria constipation.
• Renal calculi • Musculoskeletal changes—myopathy, renal osteo-
• Hypertension dystrophy.
• Pregnancy—toxemia
• Systemic diseases like diabetes, SLE Table 10.21: Differences between acute and
• Gout chronic renal failure
• Familial. Acute renal failure Chronic renal failure
1. Onset acute Chronic
Classical Presentation of a Case of 2. No anemia Anemia present
Chronic Renal Failure 3. Normal BP except in acute High BP
• Anemia glomerulonephritis
• Pigmentation 4. Urine scanty 150 ml Urine has low fixed specific
gravity, polyuria,
• Brown nail
5. Etiology-AGN, crush injury, Chronic pyelonephritis, collagen
• Skin excoriation
mismatched blood transfusion, disorder, diabetic nephropathy
• Hypertension septicemia, poisoning with
• Polycystic kidney mercury, after sulfa and
• Hydronephrosis aminoglycosides therapy,
• Senile enlarged prostate multiple myeloma, obstructive
• Neurogenic bladder. uropathy
6. Treatment—treat the cause, Correct anemia, hypertension,
Complications of Chronic Renal Failure treat hyperkalemia with insulin infection, aluminum hydroxide
and diuretics, dialysis if needed, to bind phosphate, Diet—restrict
• Hypertension is normally seen. If the patient is restrict protein water, sodium, potassium
normotensive, think of dehydration, hyponatremia, salt
loosing nephropathy, drug therapy with diuretic, beta Effects of Renal Failure on Other
blockers and ACE inhibitors. Organ Systems
• Pulmonary edema or CCF is due to volume overload,
sodium retention, anemia, hypoproteinemia and 1. Disturbances of water and electrolyte balance:
associated IHD. • Breathless due to salt and water overload
• Pericarditis is due to high area chemically mediated. • Deep sighing breathing (Kussmaul’s breathing) due
There is pericardial rub. This is an indication for dialysis. to acidosis.
If tapped, the fluid is hemorrhagic. • Weakness and nocturnal fainting due to hyponatremia
• Skin changes like pigmentation, itching and decreased caused by salt and water depletion.
• Lethargy and weakness from hypokalemia.
sebum production are seen.
294 Essentials of Clinical Medicine

2. Disturbances of hematological systems: (It should not be confused with corneal arcus senilis
• Lethargy and breathlessness associated with anemia this in a broader band at edge of cornea and merges
of impaired production of erythropoietin by kidneys. with sclera).
• Defective coagulation and excessive bruising – Arcus senilis — superior and inferior.
(advance renal failure) – Coneal calcification — medially and laterally
• Hemorrhage from GIT tract or lungs. • Retinal hemorrhages and exudates thrombosis of central
3. Disturbances of CVS: retinal artery or its branches and of central retinal vein
• Cardiac failure or angina associated with fluid and its branches
overload, hypertension, anemia and impaired ventri-
cular function (uremic cardiomyopathy) NEPHROTIC SYNDROME
• Pericardial chest pain due to pericarditis
Clinical Presentation of Nephrotic Syndrome
• Cardiac arrhythmias associated with hyperkalemia/
hypokalemia. • Pale, BP normal except in membranoproliferative
4. Disturbances of respiratory system: nephritis
• Breathlessness and hemoptysis from fluid overload. • Edema foot, sacral edema
• Chest pain due to pleurisy. • Ascites, pleural effusion, bilateral
5. Disturbances of musculoskeletal system: • Oliguria
• Muscular weakness and bone pain due to impairment • Ultrasound—enlarged kidneys.
of vit. D activation and to exclusive parathyroid gland
activity. Table 10.22: Common causes of nephrotic syndrome
• Acute pain due to gout. Causes Children Adults
6. Disturbances of nervous system: 1. Minimal leision 70% 15%
• Hypertensive stroke and encephalopathy. 2. Mesangio proliferative 15% 5%
• Clouding of consciousness, fits, coma in advanced 3. Focal glomerulosclerosis 10% 10%
renal failure. 4. Secondary 5% 30%
• Impaired sensations of parethesiae in the feet, due 5. Membranous 35%
6. Membranoproliferative Rare 5%
to peripheral neuropathy in longstanding uremia.
• Impaired higher/mental/intellectual functions.
7. Disturbances of eye: Complications of Nephrotic Syndrome
• Pain from conjunctivitis caused by local deposits of • Protein catabolism.
calcium. • Impaired resistance.
• Visual blurring from hypertensive retinal damage or • Thromboembolism due to loss of antithrombin III in
retinal vascular disease. urine.
• Hypovolemia.
Eye of Uremia
• Renal failure.
• Corneal calcification (limbus calcification): Hyper- • Accelerated sclerosis.
porathyroidism • Fluid retention, hydrothorax, pericardial effusion.
 Skin Lesion

ENNUMERATE SKIN LESION Table 10.23: Various skin tests in the diagnosis of
lymphadenopathy and other diseases
• Skin nodules—rheumatic fever, rheumatoid arthritis,
gout, hyperlipidemia Name of the test From which disease When to read
• Rash—SLE, rheumatic fever, juvenile chronic arthritis, 1. Montoux test TB 48-72 hours
psoriasis, Reiter’s disease, dermatomyositis, cutaneous 2. Kveim’s test Sarcoidosis 6 weeks
vasculitis, drugs, Lyme arthritis, viral infection, Kaposi’s 3. Frie’s test Lymphogranuloma 48-72 hours
venerum
sarcoma 4. Casoni’s test Hydatid disease (40- 25 mm diameter at 20-
• Erythema nodosum—TB drugs, streptococcal sore (15% false) 90% positive) 30 minutes
throat, Behçet’s syndrome, sarcoidosis 5. Dick’s test Scarlet fever Tells susceptibility to
• Pancreaculitis—Crohn’s disease, SLE toxin
• Raynaud’s phenomenon—progressive systemic 6. Schick test Diphtheria Tells susceptibility to
sclerosis, polymyositis, dermatomyositis, SLE toxin
• Sclerodactyly—psoriasis, CREST
• Leg loss—SLE, polyarteritis nodosa Table 10.24: Campbell de Morgan spots and vascular stars
• Hair loss—SLE, cytotoxic drugs, hypothyroidism Campbell de Morgan spots Vascular stars
• Skin pustules—Behçet’s syndrome, gonococcal 1. Site—over anterior abdominal 1. Site
• Heberden’s node—osteoarthritis wall, chest on back
• Bouchard’s nodules—osteoarthritis 2. Seen in elderly, very commonly 2. Seen more clearly in fair skin
• Oral cavity in chronic venous congestion people
– Aphthous ulcer—Behçet’s syndrome 3. Size—usually large in size 3. They are also usually large in
– Superficial painless ulcer—reactive arthritis 4. Disappearance—do not size
– Palatal excoriation—SLE disappear on applying pressure 4. They also do not disappear on
– Dry mouth—Sjögren’s syndrome applying pressure.
5. Diagnosis—We rub ice-cubes
• Occular—conjuctivitis—reactive arthritis
over this area, and when the area
– Anterior uveitis—juvenile chronic arthritis becomes white (blenched), then
– Iritis—spondyloarthritis vascular stars are confirmed.
– Dry eye—Sjögren’s syndrome.
 Case of Anemia
Pallor suggests anemia. But pallor can be there without
anemia also.
So best way to confirm anemia is by hemoglobin
estimation, which is reduced in anemia.
HISTORY IN ANEMIA
a. History to find the effect of anemia on the body and to
find from history the cause of anemia. Effect of anemia
are as follows:
Palpitation LVF,CCF, breathlessness, edema feet,
giddiness—due to reduced cerebral flow. Syncope—
blackouts in front of eyes. GIT symptoms like epigastric
burning due to duodenitis in hookworm infestation.
b. Iron deficiency—nutritional history, bleeding from any
site, multiple pregnancy, chronic dysentery, worm
infestation, drug intake like aspirin, lactation, chronic
blood loss, upper GI hemorrhage as seen in cirrhosis
of liver from esophageal varices, piles.
History of drugs: History of intake of primaquine,
nitrofurantion in hemolytic anemia, history of intake of
DBITD-B 12 deficiency, 6 mecraptopurine- folate
deficiency, pregnancy, hemolytic anemia, phenytoin
therapy, chronic hemodialysis. In aplastic aneamia, ask
history of intake of heavy metals, e.g. gold, arsenic and
use of chloramphenicol, and anticancer drugs.
History of nocturia, polyuria with hypertension and
anemia suggest chronic renal failure. Here erythropoietin
deficiency causes anemia.
Chronic infections like PTB, rheumatoid arthritis are
associated with anemia. History of passing black urine-
black water fever, nocturnal paroxysmal hemoglobinuria.
History of recent jaundice-hemolytic anemia. History of
malabsorption-chronic diarrhea. History of “PICA” that
is craving for:
• Starch - Amylophagia
• Ice - Pagophaiga
• Clay - Geophagia
Children with iron defiency and PICA have risk of lead
poisoning.
SIGNS OF ANEMIA
• Pallor, spoon-shaped nails—koilonychias, edema,
glositis, angular stomatitis, breathlessness and tachy-
cardia
• GIT signs—liver enlarged in hemolytic jaundice,
retracted in cirrhosis, massive splenomegaly in chronic
CML, small spleen in sickle cell anemia, epigastric
renderness, glossitis, gastric atrophy.
• SVS signs—hemic murmur, venous hum over jugular
vein, third heart sound present. Water hammer pulse,
cardiomegaly.
• Respiratory signs—basal crepts if LVF is there.
• CNS (a) peripheral neutritis- deep tendon reflexes poor,
stock and glove anesthesia present, (b) subacute
combined degeneration—deep tendon reflexes lost with
stock and glove anesthesia present, plantar extensor.
• Skin changes—xerosis, perifollicular hyperkeratosis,
angular stomatitis, cheilosis (fissuring of angle of lips),
scrotal dermatitis, niacin deficiency causes dermatitis
of exposed surface of skin, glossitis.
NEUROLOGICAL SIGNS OF ANEMIA
• Peripheral neuritis—nutritional deficiency
• Subacute combined degeneration—pyramidal, posterior
column, and lateral column are affected.
• Korsakoff’s pshychosis
• Dementia in pellagra.
ABDOMINAL FINDINGS OF ANEMIA
• Splenomegaly—chronic malaria, chronic myeloid
leukemia, lymphatic leukemia
• Hepatomegaly—soft tender in CCF with anemia
• Hard or firm—cirrhosis, malignancy of liver
• Ascites
• Abdominal glands, lump in right illac fossa (ileocecal
TB)
• Epigastric veins prominent.
Causes of Anemia with Generalized
Lymphadenopathy
• Acute leukemia
• Chronic lymphatic leukemia
• Lymphoma non-Hodgkin’s
• Hodgkin’s lymphoma
• TB lymphadenitis with anemia.
 Common Cases Encountered in Clinical Medicine 297

Causes of Anemia with Jaundice Marrow Disease

• Hemolytic anemia Metastatic, multiple mycloma, aleukemic leukemia, myelo-
• Carcinoma stomach with gland at porta hepatis. fibrosis, aplastic anemia, megaloblastic anemia, paroxysmal
nocturnal hemoglobinuria.
Anemia with Sternal Tenderness
Causes of Anemia of Chronic Infection
• Chronic myeloid leukemia, marrow infiltrated with • Chronic infection like TB.
leukemic cells.
• Connective tissue disorders.
• Hemolytic anemia.
• Uremia.
• Hypercellular bone marrow.
• Endocrine failure.
Table 10.25: Causes of anemia • Liver disease.
Micocytic hypochromic Normocytic normo- Macrocytic anemia
Characteristic Features
chromic
Iron deficiency Chronic infection B12 deficiency • Reduced hemoglobin
Sideroblastic anemia Chronic renal failure Pernicious • Myeloid hyperplasia
Pyridoxine deficiency Aplastic anemia gastrectomy • Increased plasma cell
Thalassemia trait Hemolytic Malabsorption
After acute blood Blind loop syndrome
• Reduced serum iron
loss Ileal resection • Reduced TIBC
Folate deficiency– • Reduced transferritin
Tropical sprue • Increased serum feritin.
Coclinc disease
Pregnancy Symptoms of Anemia
Phenytoin therapy
Alcoholism Weakness, fatigue, lightheadedness, giddiness, palpitation,
breathlessness, angina, tingling of extremities.
Cardiovascular Signs of Anemia
• Tachycardia. Common Causes of Severe Anemia
• High volume pulse. • Nutritional
• Bruit over carotid. • Hookworms
• Hyperdynamic apex best. • Hematemesis—variceal bleeding
• Hemic murmur. • Hemorrhoids (piles)
• Loud first sound.
• Aplastic anemia
Causes of Pancytopenia • Acute leukemia
Hypersplenism, congestive splenomegaly, malignancy • Thalassemia
lymphoma, histiocytosis, TB, sarcoidosis, kala-azar, primary • Menorrhagia
splenic pancytopenia. • Carcinoma of stomach, colon or lung.
 11
Pelvic Pain
PAIN
May originate in pelvic or may be referred from another
region from body.
Physiological Pelvic Pain (Pain Associated with
Ovulation) (Mittelschemerz)
• Typically, a dull aching pain at midnight in one lower
quadrant lasting from minutes to hours.
• Rarely severe or incapacitating.
• Pain may result from peritoneal irritation by follicular
fluid released into peritoneal cavity at ovulation. The
onset of pain at midcycle and short duration suggests
this diagnosis.
Premenstrual or Menstrual Pain
• Somatic symptoms during the few days prior to menses
may be insignificant or disabling.
• Symptoms include edema, breast engorgement and
abdominal bloating or discomfort.
• Symptom complex of cyclic irritability depression, and
lethargy — premenstrual syndrome (PMS).
• Severe or incapacitating uterine cramping during
ovulatory menses and in absence of demonstrable
disordes of pelvis is termed primary dysmenorrhea,
caused by prostaglandin-induced ischemia.
Pelvic Pain due to Organic Causes
Severe dysmenorrhea associated with disease of pelvis is
termed secondary dysmenorrhea.
Uterine Pain
• Often chronic and continous and increases in intensity
during menstruation and intercourse.
• Causes are leiomyomas (particularly submucous and
degenerating leiomyomas), adenomyosis, cervical
stenosis.
• Infection of uterus with intrauterine manipulation
following dilatation and curettage or with the insertion
of IUD can also cause pelvic pain.
• Pelvic pain due to endometrial or cervical carcinoma is
usually a late manifestation.
Adnexal Pain
Adnexae: (Fallopian Tube and Ovaries)
• Most common cause is infection.
• Acute salpingo-ophoritis presents as low abdominal pain,
fever and chills, begins a few days after a menstrual
period and is usually due to chlamydial or gonoccocal
disease or without a superimposed pyogenic infection.
• Chronic PID presents as infertitity associated with
chronic pelvic pain that increase in intensity with menses
or intercourse.
• Cervical motion tenderness, adnexal tenderness, and
adnexal thickening and /or masses may be present.
• PID may be a surgical emergency if peritonitis results
from rupture of tubo-ovarian abscess.
• Ovarian cyst or neoplasm may cause pelvic pain that
becomes more severe with torsion or rupture of mass
and ectopic pregnancy must be considered in differential
diagnosis.
• Endometriosis involving fallopian tubes, ovaries or
peritoneum may cause both chronic low abdominal pain
and infertility.
• Endometriosis pain typically increase with menstru-ation
and if the post. ligament of the uterus are involved, with
intercourse.
Vulvar or Vaginal Pain
• Most often due to infectious vaginitis caused by Monilia,
Trichomonas or bacteria
• Characterized by vaginal discharge and pruritis
• Herpetic vulvitis, other dermatologic conditions of vulva,
condyloma accuminatum and cysts or abscesses of
Bartholin’s glands may be causing vulvar pain.
 Pelvic Pain 299

Pregnancy-Associated Disorders • Multiple sclerosis

• Threatened abortion and incomplete abortion causes— • Vaginitis
uterine cramping, bleeding or passage of tissue following • Endometriosis
a period of amenorrhea. • Salpingo-ophoritis
• Ectopic pregnancy may be insidious in presentation or • Carcinoma
result in abrupt intraperitoneal hemorrhage and maternal • CVS diseases
death. • Psychological factors
• Vaginismus—painful involuntary contraction of
Sexual Dysfunction
musculature surrounding entrance to vagina is a rare
Normal sexual response is interrupted by: cause of dyspareunia.
• DM
 Appendix-I
Weights and Measurements of
Normal Organs
Adrenal Gland
Weight ..................................................................... +5 gm
Brain
Weight (in males) ................................................. 1400 gm
Weight (in females) .............................................. 1250 gm
Measurements (sagittal x vertical) (in males) ....................
.................................................................... 16.5×12.5 cm
Volume of cerebrospinal fluid (in males) ......... 120-150 ml
Heart
Weight (in males) ........................................... 300-350 gm
Weight (in females) ........................................ 250-300 gm
Thickness of right ventricular wall .................. 0.3-0.5 cm
Thickness of right ventricular wall .................. 1.3-1.5 cm
Circumference of mitral valve ................................. 10 cm
Circumference of pulmonary valve ......................... 12 cm
Volume of pericardial fluid ...................................10-30 ml
Intestines
Length of duodenum ................................................ 30 cm
Total length of small intestine ........................ 150-170 cm
Kidneys
Weight each (in males) ........................................... 150 gm
Weight each (in females) ....................................... 135 gm
Measurements .................................... 3.5 × 5.5 × 11.5 cm
Liver
Weight (in males) ............................. 1400-166 (1500) gm
Weight each (in females) ................ 1200-1400 (1330) gm
Measurements ........................................... 27 × 8 × 20 cm
Lungs
Weight ( right lung) .............................. 375-500 (450) gm
Weight (left lung) ................................. 325-450 (400) gm
Volume of pleural fluid ...........................................< 15 ml
Esophagus
Length (cricoid cartilage of cardia) ......................... 25 cm
Distance from incisors to gastro-esophageal junction
................................................................................. 40 cm
Ovaries
Weight (each) ................................................... 4-8 (6) gm
Measurements .......................................... 1 × 25 × 4.5 cm
Pancreas
Total weight ............................................. 60-100 (80) gm
Weight of endocrine pancreas ............................. 1-1.5 gm
Measurements ....................................... 3.8 × 4.5 × 18 cm
Parotid glands
Weight (each) ........................................................... 30 gm
Pituitary gland (hypophysis)
Weight .................................................................... 500 mg
Placenta
Weight at term ................................................ 400-600 gm
Prostate
Weight ...................................................................... 20 gm
 Appendix-II

Clinical Chemistry of Blood

Reference value Contd...

Component Fluid Conventional SI Units Reference value
Alcohol ethyl Serum/whole Negative Negative Component Fluid Conventional SI Units
Mild-to-moderate blood 80-200 mg/dl High <130 mg/dl
intoxication 250-400 mg/dl LDL-cholesterol, >40 mg/dl
Marked intoxi- >400 mg/dl desirable range
cation HDL- cholesterol, <160 mg/dl
Severe intoxi- protective range
cation triglycerides
Aminotrans-
ferases Copper Serum 70-140 mg/dl 11-22 mmol/dl
(transferases) Creatine kinase Serum
Aspartate (CK)
(AST, SGOT) Males 55-170 IU/L 55-170 IU/L
Alanine Females 30-135 IU/L 30-135 IU/L
(ALT, SGPT) Serum 8.33 karmen units 8.33 IU/L Creatinine Serum 0.5-1.5 mg/dl 9-15 mmol/L
Serum 4-36 karmen units 4-36 IU/L Electrophoresis, Serum
Ammonia Plasma 80-110 pg/dl 47-65 mmol/L protein
Amylase Serum 16-120 somogyi 60-180 IU/L Fatty acids
units/dl Total
Bicarbonate Plasma 21-28 mmol/L 21-28 mmol/L Non-etherified
Bilirubin (free)
Total Serum 0.3-1.0 mg/dl 5.1/17 mmol/L Gamma-glutamyl Serum 4-60 IU/L 0.07-1.00 µmol/
Direct Serum 0.1-0.3 mg/dl 1.7-5.1 mmol/L transpeptidase dl
(conjugated) (transferase
Blood volume 60-80 ml/kg body (γ-GT)
weight Gases
Total 30 ml/kg body weight PH Whole blood 7.38-7.44 7.38-7.44
Red cell volume, 25 ml/kg body weight (arterial) arterial
Males 39 ml/kg body weight 35-40 mm Hg 7.36-7.41
Females 40 ml/kg body weight (arterial) venous
Plasma volume, pCO2 Whole blood 40-45 mm Hg 4.7-5.3 kPa
Males (arterial)
Females 95-100 mm hg 5.3-6.0 kPa
Bromsulfalein (venous)
(BSP) test pO2 Whole blood 95-100 mm hg 12.7-13-3 kPa
5 mg/kg body Serum <5% retention in (arterial)
weight serum after 45 min. Gastrin Serum 40-200 ng/dl
Calcium, ionized Serum 4-0-4.8 mg/dl 1.0-1.2 mmol/L Glucose (fasting) Plasma/serum
Calcium, total Plasma 9.2-11.0 mg/dl 2.3-2.7 mmol/L Normal 75-115 mg/dl 3.9-6.1 mmol/L
CO2 content Whole blood 19-24 mmol/L 19-24 mmol/L Diabetes mellitus >140 mg/dl
(arterial) (arterial) Glucose (2 hr Plasma
Chloride (CI–) Serum 98-106 mEq/L 98-106 mmol/L postprandial)
Cholestrol Serum Normal <140 mg /dl 3.9-6.1 mmol/L
Total desirable 200-3\239 140-200 mg/dl 3.88-6.47 Impaired glucose 140-200 mg/dl
for adults mg/dl mmol/L tolerance (IGT)
Borderline high >240 mg/dl Diabetes mellitus >200 mg/dl

Contd... Contd...
 Appendix-II 303

Contd... Contd...
Reference value Reference value
Component Fluid Conventional SI Units Component Fluid Conventional SI Units
Glucose tolerance Whole troponin 1 (cTnl) Serum 0-0.1 mg/L 0-0.1 mg/L
test (GIT) blood/plasma Urea Blood 15-40 mg/dl
Immunoglobulins Serum Urea nitrogen
IgA 90-325 mg/dl (BUN) Blood 10-20 mg/dl
IgD 0.8 mg/dl Uric acid Serum 0.24-0.51
IgE <0.025 mg/dl Males 2.5-8.0 mg/dl mmol/L
IgG 800-1500 mg/dl Females 1.5-6.0 mg/dl 0.16-0.43
IgM 45-150 mg/dl mmol/L
Lactate Serum 80-120 units 38-62 U/L OTHER BODY FLUIDS
dehydrogenase Body volume,
(LDH) water
Lactate/pyruvate Total 50-70% (60%)
ratio 10/1 Intracellular 33%
Lipids Serum Extracellular 27%
Interstitial fluid 12%
Non-protein Serum <35 mg/dl including
nitrogen (NPN) lymph fluid
Oxygen Intravascular 5%
(% saturation) fluid or blood
Arterial blood Whole blood 94-100 % plasma
Venous blood Whole blood 60-85 % Fluid in mesenchymal tissues 9%
pH Blood 7.38-7.44 Transcellular fluid 1%
Phosphatases Serum Catecholamines 24 hr urinary excretion
Acid phosphatase 1.0-3.0 king- 2.2-10.5 U/L Epinephrine <10 ng/day
armstrong units Free
Alkaline 4.0-13.0 king- 20-130 U/L catecholamines <100 mg/day
Phosphates armstrong units alkaline Free
Phosphates, Serum 3-4.5 mg/dl 1.0-1.4 mmol/L catecholamines <100 mg/day
inorganic Metanephrine <13 mg/day
Potassium Serum 3.8-5.0 mEq/L 3.8-5.0 mmol/L Vanillyl mandelic
Proteins Serum acid (VMA) <8 mg/day
Total 5.5-8 g/dl Cerebrospinal
Albumin 3.5-5.5 g/dl (50-60%) fluid (CSF) CFC
Globulin 2.0-3.5 g/dl (40-50%) CFC volume 120-150 ml
αl globulin 0.2-0.4 g/dl CFC pressure 60-150 mm water
α2 globulin 0.2-0.4 g/dl Leukocytes 0-4 lymohocytes/ml
β globulin 0.5-0.9 g/dl pH 7.31-7.34
γ globulin 0.7-1.7 g/dl Glucose 50-80 mg/dl
A/G ratio 1.5-3:1 Proteins 15-45 mg/dl
Renal blood flow 1200 ml/min FIGLU 24-hr urine <3 mg/day <17.2 mmol/day
Sodium Serum 136-145 mEq/L 136-145 mmol/L Gastric analysis Gastric juice
pH 2-3 L
Thyroid function Basal acid
tests output (BAO) 1.6-1.8 1.6-1.8
Radioactive iodine Maximal acid
uptake output (MAO) 1-5 mEq/hr 1.5 mmol/hr
(RAIU) 24 hr 5-30% after injection
thyroxine (T4) Serum 4-12 mg/dl of stimulant
thyroidothyro- BAO/MAO ratio <0.6
nine (T3) Serum 80-100 ng/dl Glomerular
thyroid stimula- filtration rate Urine 180 L/day
ting hormone Serum 0.4-5 m /ml (GFR) (about 125 ml/min)
(TSH) 5-HIAA 24 hr urinary 2-8 mg/day
Troponins, erection
cardian (cTn) Females 4-15 mg/day
Troponin 1 (cTn) Seminal fluid Semen
troponin 1 (cTnl) Serum 0-0.6 mg/ml 0-0.6 mg/L Liquefaction within 20 min.

Contd... Contd...
304 Essentials of Clinical Medicine

Contd... Contd...
Reference value Reference value
Component Fluid Conventional SI Units Component Fluid Conventional SI Units

Sperm morphology >70% normal, (MCV) 77-93 fl

mature Mean corpuscular
spermatozoa hemoglobin
Sperm mortality >60% Concentration
pH > 7.0 (average 7.7) (MCHC)
Sperm count 60-150 million/ml 60-159 ×106/ml Erythrocyte
Volume 1.5-5.0 ml life-span Blood 120 days
Stool Erythrocyte
examination Stool life-span Blood
Coproporphyrin 400-1000 mg/day Westergren’s
Fecal fat Males 0-15 mm
excreation <6.0 g/day Females 0-20 mm
Occult blood Negative (<2 ml blood/day) Ferritin Serum
Urobilinogen 40-280 mg/day Males 15-200 ng/ml 15-200 mg/L
Schilling’s test 24 hr volume 600-1800 ml Females 12-150 ng/ml 15-150 mg/L
(variable) Folate
Specific gravity Urine 1.003-1.030 Body stores 2-3 mg
(random) (average 1.018) Daily requirement 100-200 mg
Protein excretion 24 hr urine <150 mg/day Red cell level Red cells 150-450 ng/ml
Protein, Serum level Serum 6-12 ng/ml 11-57 nmol/L
qualitative Urine Negative Free erythrocyte
(random) protop- Red cells 20mg/dl
Glucose excretion 24 hr urine 50-300 mg/day orphyrin (FEP)
Glucose qualitative Urine Negative Hematocrit
(random) (PCV) Blood
Porphobilinogen urine(random) Negative Males 40-54% 0.47±0.07 L/L
Urobilinogen 24 hr urine 1.0-3.5 mg/day Females 37-47% 0.42±0.05 L/L
Urobilinogen urine(random) Present in Haptoglobin Serum 60-270 mg/dl 0.6-2.7 g/L
1:20 edition Haemoglobin
D-xylose (Hb)
extraction Stool 5-8 g within 5 hr Adult haemo-
after oral dose of 25 g globin (HbA) Whole blood
HEMATOLOGIC VALUES Males 13.0-18.0 g/dl 130-180 g/L
Myelogram Females 11.5-16.5 g/dl 115-165 g/L
Erythrocytes and Plasma Hb
Hemoglobin (quantative) 0.5-5 mg/dl 5.50 mg/L
Erythrocyte Hemoglobin
count Blood A2 (Hb A2) 1.5-3.5%
Males 4.5-6.5 × 1012/L Hemoglobin,
(mean 5.5 × 1012/L) fetal (HbF)
Females 3.8-5.8 × 1012/L in adults <1%
(mean 4.8 × 1012/L) HbF, children
Erythrocyte under 6 months <5%
diameter 6.7-7.7 mm Iron, total Serum 80-180 mg/dl 10.7-26.9
(mean 7.2 mm) mmol/L
Erythrocyte Total iron
thickness binding capacity Serum 250-4600 mg/dl 44.8-7.16
Peripheral 2.4 mm (TIBC) mmol/L
Central 1.0 mm Iron saturation Serum 20-45% mean 33%
Iron intake 10-15 mg/day
Erythrocyte
Iron loss
indices (absolute
Males 0.5-1.0 mg /day
values) Blood
Females 1-2 mg/day
Mean corpuscular
Iron, total
hemoglobin (MCH) 27-32 pg
body content
Mean corpu- Males 50 mg/kg
scular volume body weight
Contd... Contd...
 Appendix-II 305

Contd... Contd...
Reference value Reference value
Component Fluid Conventional SI Units Component Fluid Conventional SI Units
Adults
Females 35 mg/kg
Infants
body weight
Transferrin Serum 200-900 pg/ml 200-900 pmol/L
Iron storage form
Vitamin B12 Serum
(ferritin and
Baby stores 10-12 mg
hemosiderin) 30% of body iron
Daily requirement 2-4 mg
Osmotic fragility Blood
Serum level 200-900 pg/ml 200-900 pmol/L
Slight hemolysis at 0.45 to 0.39 g/dl NaCl
Leukocytes in Blood
Complete at 0.33 to 0.36 g/dl NaCl
Health
hemolysis 0.4-0.45 g/dl NaCl
Total leukocyte 4000-11000/ml
Mean corpus-
count (TLC)
cular fragility
Adults 10000-25000/ml
Reticulocytes Blood
Infants (full term, at birth) 6000-16000/ml
Contd... Infants (1 year)
 Index

A Anemia 15, 296 clinical features 215 adventitious sounds 90

abdominal findings 296 differential diagnosis 216 bronchial 89
Abdominal distention 12, 120
approach 120 causes 296 pregnancies 216 bronchovesicular 89
liver pathology 120 history 296 tarsal tunnel syndrome 216 types 89
neurological signs 296 vesicular 89
Abnormal movements 242, 249
ataxia 251 signs 296 B Breathing 83
cerebellar function 251 Anorexia 25 types 83
Backache 278
components 249 Anuria 55 arthritis 280
superficial reflexes 244 Aortic regurgitation 162 congenital anomalies 279 C
interpretation 243 causes 162 facet joint hypertrophy 280 Campbell de Morgan spots 295
observation 243 clinical features 163 infection 281 Cardiac cycle 147
parkinsonism 244 Aortic stenosis 162 lumbar adhesive atrial diastole 148
Parkinson’s disease 249 causes 162 arachidonitis 280 atrial systole 147
Parkinson’s tremors 250 clinical features 162 lumbar disk disease 279 ventricular diastole 148
Acid regurgitation 50 Appetite 10, 25 lumbar spine 278 ventricular systole 147
Alcohol-related disorders 6 excessive 25 neoplasms 281 Cardiovascular system 7, 13, 133
Alimentary system 103 perverted 25 osteoporosis 281 anemia 15
auscultation 114 Arthritis 280, 290 osteosclerosis 281 arrhythmias 16
arterial bruits 115 causes 291 postural back pain 282 auscultation 145
cirrhosis 116 differential diagnosis 290 referred pain 281 principles 146
hepatic facies 118 history taking 290 sacral pain 282 purpose 146
peristaltic sounds 115 rheumatic fever 292 spinal stenosis 280 cardiovascular disorder 16
portal hypertension 117 rheumatoid arthritis 291 sprains and strains 279 chest pain 13
principles 114 Ascites 119 thoracic spine 278 approach 13
skin manifestations 118 causes 119 trauma 279 cough 14
splenic bruit 115 clinical features 119 types 279 cyanosis 15
succussion splash 115 diagnosis 120 vertebral fractures 279 dizziness 15
venous hum 115 distention 119 visceral diseases 281 dyspnea 13
examination 103 jaundice 119 Bad breath 49 edema 14
inspection 104 signs 119 Basic sounds 149 examination 133
abdomen 105 symptoms 119 heart sound 149 fatigue 15
skin and surface 108 Ataxia 251 first 149 hemoptysis 14
surgical incisions 109 Auscultation 88, 114, 145 fourth 157 infective endocarditis 16
umbilicus 106 aims 88 second 149 inspection 139
palpation 109 general principles 88 third 151 apex beat 140
abnormal findings 110 Auscultatory vocal resonance 92 Bell’s palsy 201 distended veins 142
gallbladder 112 Autonomic nervous system 264 Blood 2, 302 precordium 140
kidneys 112 clinical features 264 clinical chemistry 302 retraction 141
liver 110 disorders 264 hematologic values 304 scars 142
methods 109 Autonomic neuropathy 215 other body fluids 303 sinuses 142
sequence 109 alcoholic 216 Bowel disease 129 visible pulsations 141
spleen 111 ataxic 216 inflammatory 129 orthopnea 13
urinary bladder 113 causes 215 Breath sounds 89 palpation 142
308 Essentials of Clinical Medicine

apex beat 143 postural cough 52 Dyspepsia 12 types 233

golden rules 142 respiratory causes 51 Dysphagia 55 Gastrointestinal tract 103
palpitation 14 sputum production 52 causes 55 disorders 103
percussion 144 Cranial nerves 190 esophageal causes 56 General examination 61
principles 145 abnormalities 195 pre-esophageal causes General symptoms 7
pyrexia 15 accessory nerve 203 55 cardiovascular system 7
syncope 15 acuity of vision 193 pressure 56 central nervous system 8
ulceration 17 additional tests 202 Dyspnea 46 endocrine system 8
Central nervous system 8, 172 clinical application 193 grades 47 gastrointestinal system 7
common symptoms 172 clinical examination 190 pulmonary edema 47 general health 7
disorders 172 extraocular eye muscles 195 locomotor and joint system
Chest pain 13, 34 facial nerve 199 E 8
cardiac causes 34 glossopharyngeal nerve 203 respiratory system 7
Eaton-Lambert syndrome 257
aneurysm 35 hypoglossal nerve 204 urogenital system 8
angina pectoris 34 Ebstein’s anomaly 163
nystagmus 197, 202 Edema 66 Genitourinary system 18
cardiomyopathy 35 urinary incontinence 19
olfactory nerve 191 anasarca 66
infective endocarditis 35 Goiter 284
optic disk 194 lymphatic 67
myocardial infarction 34
optic nerve 191 pedal 66
pericarditis 35
valvular heart disease 35
pupils 193 venous 67 H
trigeminal nerve 198 Emphysema 96 Hair 67
Coma 263, 285
vagus nerve 203 Cheyne-Stokes breathing 97 body 68
causes 263
vestibular gait 202 clinical features 96 facial 68
history taking 263
investigation 264 vestibulocochlear nerve 201 complications 97 scalp 67
Common symptoms 9 Cyanosis 62, 164 diagnosis 96 secondary sexual 68
abdominal distention 12 approach 64 findings 96 Halitosis 49
appetite 10 causes 63 Epistaxis 58 Head 72
constipation 11 central 63 general causes 58 buccal mucosa 77
diarrhea 11 differential diagnosis 63 Examination ears 76
dysgeusia 13 heart diseases 164 hospital wards 70 eyes 73
dysphagia 10 pathology 63 appearance 70 facies 73
flatulence 10 peripheral 63 decubitus 70 forehead 73
halitosis 13 posture 70 gums 77
heartburn 10 D Extra sounds 152 lips 76
hematemesis 13 click 152 lymph glands 78
Descending tracts 177
hiccups 12 ejection sound 152 nose 76
Diabetes mellitus 287
indigestion 12 gallop rhythm 152 palate 78
diabetic ketoacidosis 288
jaundice 11 murmur 153 pharyngeal wall 78
differential diagnosis 288
melena 13 opening SNAP 153 salivary glands 78
etiological factors 287 skull 72
pain 9 venous hum 159
GI manifestations 288 teeth 76
rectal bleeding 12
history taking 287 tongue 77
vomiting 10 F
hypoglycemia 288 tonsils 78
water brash 10
renal involvement 288 Facial nerve palsy 200 Headache 37, 174
weight gain 12
Diarrhea 58, 123 Fever 25 aggravating factors 175
weight loss 12
acute 58, 124 benefits 27 associated features 175
xerostomia 13
chronic 58, 125 bradycardia 26 causes 174
Complexion 62
dysentery 125 causes 25 characteristics 174
plethoric 63
amebic 125 drug fever 27
Constipation 11, 57 complaints 174
bacillary 125 grading 27
causes 57 duration 174
history taking 123 harmful effect 27
types 57 frequency 175
malabsorption 125 types 25
Constrictive pericarditis 164 hemorrhage 41
clinical features 164 mechanism 124 intraparenchymal 41
pathophysiology 124 G
Coordination 230 inquiry 174
testing 230 physical signs 125 Gait 61, 233 intracranial causes 37
Cough 51 Dwarfism 71 abnormalities 235 migraine 37
nocturnal cough 52 Dysautonomia 215 disorders 235 meningitis 40
 Index 309

bacterial 40 neuroses 187 Involuntary movements 65 pulmonary hypertension

intracranial 41 obsession 187 161
recurrent 41 phobia 187 J X-ray findings 160
spinal 41 psychoses 187 Motor pathways 177
Jandressik’s maneuver 224
viral 40 schizophrenia 188 corticospinal and corticobul-
Jaundice 64, 125
occurrence 175 spatial 184 bar tracts 177
alcohol 127
periodicity 175 vegetative symptoms 182 extrapyramidal tracts 178
causes 127
relieving factors 175 visual and body perceptions functions 178
cholestatic conditions 127
severity 174 184 levels 179
differential diagnosis 126
sites 174 History taking 1 pyramidal tracts 177
fulminant hepatic failure 128
subarachnoid 42 direct questions 2 signs 180
hard liver 128
symptoms 175 general scene 1 Motor system 176, 204
hemolytic 128
Heartburn 60 interview 3 examination 204
hepatocellular 128
Height and weight 65 medical history 6 frontal eye field 177
hepatocellular conditions 127
hydration 66 non-verbal clues 2 interpretation 230
history taking 125
obesity 65 personal history 6 maneuvers 230
hyperbilirubinemia 128
types 65 proforma 3 motor area 176
intermittent 128
Hematemesis 52 social history 5 motor cortex 176
obstructive 128
causes 52 surgical history 6 premotor cortex 176
viral hepatitis 128
general 53 treatment history 6 reflexes 230
Joint pain 46
local 52 Hoarseness 59 Muscle pain 251
Jones criteria 16
Hematochezia 12, 60 Hyperbilirubinemia 64 causes 253
Jugular venous pulse 138
Hematuria 55 Hypertension 165 patterns 252
“a” wave 138
disease 55 antihypertensive agents 166 Muscle spindle 223
“C” wave 139
drugs 55 signs 165 neural connections 223
“V” wave 139
general causes 55 symptoms 165 reinforcement 224
“X” wave 139
lesion 55 Hyperthermia syndrome 26 Muscle strength and movements
“Y” wave 139
Hemiplegia 245 Hyperthyroidism 286 205
localization 246 causes 286 grading 205
paraplegia 249 ECG changes 286
L testing 206
past history 245 manifestations 286 Locomotor system 22 weakness 211
pronation drift 246 Hypertonia 255 general assessment 22 abdominal 210
Hemoptysis 52 definition 255 localization 23 approach 211
differential diagnosis 52 types 256 pain 22 functional 211
primary vascular source 52 physical examination 23 Muscle wasting 219
Hypertrophy 219
pulmonary parenchymal Lymphadenopathy 289 Muscular dystrophy 254
Hyperventilation syndrome 48
source 52 conditions 255
symptoms 48 history 289
tracheobronchial source 52 generalized wasting 254
Hypothermia 27 Hodgkin’s lymphoma 289
Herniation 259 lower limbs 255
Hypothyroidism 284 non-Hodgkin’s lymphoma types 254
central 260 causes 284 289 upper limbs 254
uncal 259 clinical manifestation 284 Myasthenia gravis 257
Hiccups 50 goiter 284 M Myotonia 257
Higher functions 181 signs 284 Melanin 64 causes 257
abstract thought 184 Hypotonia 256 Myxoedema 284
apraxia 185 hypercarotenemia 64
causes 256 Micturition 54 cardiovascular manifesta-
attention and orientation 183 tions 285
calculation 183 Mitral regurgitation 162
I coma 285
delirium 186 causes 162
differential diagnosis 285
delusion 186 Inspection 80 clinical features 162
history 284
examination 181 abnormalities 81 Mitral stenosis 159
madness 285
hallucination 186 chest 81 atrial fibrillation 160 neurological manifestations
illusion 187 size and shape 81 clinical features 159 285
impulse 187 chest wall 82 complications 160
memory 183 movements 83 differential diagnosis 160
embolic manifestations 161
N
mental state 182 respiratory rate 82
minimental state test 182 retraction 82 mitral facies 161 Nails 68
mood 182 rhythm 83 non-rheumatic causes 161 clubbing 69
310 Essentials of Clinical Medicine

causes 69 small bowel obstruction subacute axonal polyneur- fine crackles 90

grades 69 29 opathy 215 types 91
theories 69 nature 29 Peritonism 29 Reflexes 221
Schammroth’s maneuver 70 paralyticus ileus 30 Physical examination 67 ankle reflex alternative 229
Schammroth’s sign 70 psychogenic abdominal pain vitals 67 Bell-Magendie law 222
signs 68 32 blood pressure 67 classification 222
Nausea and vomiting 50 referred pain 31 jugular venous pressure monosynaptic 222
vomitus 50 Occupational diseases 4 67 clinical significance 228
character 50 chemical agents 4 pulse 67 polysynaptic reflexes 225
Neck pain 275 physical agents 4 temperature 67 reflex testing 225
other causes 276 Odors 65 Plantar 229 special points 226
trauma 275 abdominal reflex 229 stretch 223
Neonatal cholestasis 129 alternative stimuli 229 supinator reflex 229
P
Nerve injury 217 Babinski’s sign 229 tendon 222, 226
Pack years 7 testing 221
median 217 methods 229
Pain 27, 268, 298 types 225
radial 217 primitive reflexes 229
abdominal pain 27 Wartenberg’s sign 229
ulnar 218 testing 229
peritonitis 27 Renal system presentation 293
lesion 218 Pleural effusion 94
arm 268 chronic renal failure 293
Nervous system 19, 176 causes 94
menstrual pain 298 nephrotic syndrome 294
basic components 176 characteristics 94
organic causes 298 Respiratory system 17, 79
guidelines 19 complication 96
perforation 29 approach 79
headache 19 differential diagnosis 95
physiological pelvic pain 298 progressive dyspnea 80
neurological assessment 19 Pleural rub 91
Neurological deficit 43 sexual dysfunction 299 Rhonchi 90
POEMS syndrome 216
extracranial causes 44 thoracic spine 268 causes 90
Polyuria 54
hydrocephalus 43 Pallor 62 classification 90
Posture 61
hyponatremia 43 causes 62 Rupture spleen 129
Pulmonary tuberculosis 97
re-rupture 43 Palpation 54, 84 general signs 129
differential diagnosis 97
vascular anomalies 43 aims 84 local signs 129
hydropneumothorax 99
vasospasm 43 respiratory movements 84
pneumonia 98
Neurological history taking 173 tactile vocal fremitus 85 pneumothorax 99 S
Nocturia 54 thoracic wall 84 Pulse 133 Salivation 50
Normal organs 301 outer 84 abnormalities 137 disorders 50
weights and measurements posterior 85 mechanism 137 Sensory system 238
301 Percussion 85 character 136 additional tests 242
Nutrition 72, 219 aims 86 definition 133 approach 241
state 72 hydropneumothorax 88 examination 133 examination 239
mechanism 86 force 135 joint position 240
O pleural effusion 88 pulse rate 134 light touch 241
pneumothorax 88 pulsus alternans 136 other modalities 241
Obstruction 29
principles 86 pulsus bigeminus 135 pin prick test 241
acid peptic disease 32
tidal 87 pulsus bisferience 136 sensory deficits 242
duodenal 32
Traube’s semilunar space 87 rhythm 134 sensory inattention test 241
gastric 32
Peripheral arterial disease 167 tension 136 sensory loss 242
acute intussusception 30
acute limb ischemia 168 volume 136 temperature sensation 241
causes 30
chronic lower limb ischemia Pulsus paradoxus 138 vibration sense 239
colics 31
168 causes 138 Skin lesions 68, 295
appendicular 31
lower limb symptoms 167 definition 138 conditions 68
biliary 31
Peripheral neuropathy 212 mechanism 138 extremities 68
common features 31
acute demyelinating poly- Pyrexia 26 Smoking index 7
intestinal 31
neuropathy 215 Pyrosis 10, 60 Sore mouth 49
renal 31
ureteric 31 assessment 213 causes 49
distention 33 carpal tunnel syndrome 215 R Sore tongue 49
hepatic pain 33 clinical features 212 Rales 90 Special inquiries 7
mechanical obstruction 29 definition 212 coarse 90 menstrual history 7
colonic obstruction 29 peripheral neuritis 214 common causes 91 obstetric history 7
 Index 311

Speech 188 pathophysiological basis 122 proptosis 286 carotid artery 168
aphasia 189 Spot diagnosis 61 secondary 286 subclavian artery 169
assessment 189 Stridor 91 signs 285 vasospastic conditions
dysarthria 189 classification 91 symptoms 285 169
dysphonia 189 Succussion splash 91 Tobacco-related disorders 6 venous disorders 169
Spinal cord 168 Symptomatology 24 Tonus 220 vertebrobasilar artery
clinical applications 273 Syncope 59 clonus 220 169
Brown-Sequard ankle 221 visceral ischemia 169
syndrome 273 T knee 221 Vertebral column 266
corticospinal tracts 273 Temperature 26 lengthening reaction 220 cervical spine 266
medulla oblongata 274 physiological variation 26 tone 221 inspection 266
midbrain 274 Tests 268 Tracheal signs 85 lumbar spine 267
motor neurons 273 bowstring sign 268 Tricuspid regurgitation 163 neck posture 267
pons 274 femoral nerve stretch test 268 causes 163 palpation 266
sensory tracts 273 flip test 268 sacroiliac joints 267
signs and symptoms 274 nerve root compression 268
U sacrum 267
complications 273 straight leg raising test 268 thoracic spine 267
functions 269 Thrills 143 Ulcer pain 32 Vertigo or giddiness 59
hemisection 272 golden rules 144 Urine 54 central 59
lesions 268 mechanism 143 retention 54 functional 59
site 275 murmurs 144 causes 54 non-pathological 59
pathways 269 pathology 144
peripheral 59
tracts 269 pericardial rub 144
ascending 269 tracheal tug 144
V Voice and speech 65
descending 269 Thyrotoxicosis 285 Valvular heart disease 159
transaction 270 complications 286 Vascular diseases 168 W
Spine 266 differential diagnosis 285 neurological presentation 168 Weight gain 12, 24
Splenomegaly 121 history taking 285 abdominal aortic Weight loss 12, 24
mechanism 121 primary 286 aneurysm 169 Wheeze 90