CHAPTER ONE

INTRODUCTION

A. BRIEF DESCRIPTION OF THE DISEASE CONDITION

Cerebrovascular accident (CVA) is the medical term for what is commonly termed

as stroke. It refers to the injury to the brain that occurs when flow of blood to brain tissue is

interrupted by a clogged or ruptured artery, causing brain tissue to die because of lack of

nutrients and oxygen.

The severity associated with cerebrovascular accident can best be demonstrated by

many facts. It has been noted that CVA is the leading cause of adult disability in the world.

Worldwide, one-quarter of all strokes are fatal. Two-thirds of strokes occur in people over the

age of 65. Strokes affect men more often than women, although women are more likely to die

from a stroke. The incidence of strokes among people ages 30 to 60 is less than 1%. This

figure triples by the age of 80.

The quote says that everything occurring in our lives are the result of our previous

choices- choices that may lead to a good present status or the opposite, especially in health

were most of the conditions met by patients are results of their chosen lifestyle and other

health practices.

Some choices made by certain people may have detrimental health effects that may

progress to a clinical condition. A person’s diet, activity of daily living, health beliefs and others

can result to health illness. Like the case of this study, a person’s way of life, along with other

non-modifiable factors resulted to the occurrence of weakness and slurred speech that lead to a

condition called Cerebrovascular Accident (CVA).

1
 A stroke (sometimes called a cerebrovascular accident (CVA)) is the rapidly

developing loss of brain function(s) due to disturbance in the blood supply to the brain, caused

by a blocked or burst blood vessel. This can be due to ischemia (lack of glucose and oxygen

supply) caused by thrombosis or embolism or due to a hemorrhage. As a result, the affected

area of the brain is unable to function, leading to inability to move one or more limbs on one

side of the body, inability to understand or formulate speech, or inability to see one side of the

visual field. A stroke is a medical emergency and can cause permanent neurological damage,

complications, and death. It is the leading cause of adult disability in the United States and

Europe. It is the number two cause of death worldwide and may soon become the leading

cause of death worldwide. Risk factors for stroke include advanced age, hypertension (high

blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high

cholesterol, cigarette smoking and atrial fibrillation. High blood pressure is the most important

modifiable risk factor of stroke.

A stroke is occasionally treated with thrombolysis ("clot buster"), but usually with

supportive care (speech and language therapy, physiotherapy and occupational therapy) in a

"stroke unit" and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole),

blood pressure control, statins, and in selected patients with carotid

endarterectomy and anticoagulation.

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases

do not progress further. The symptoms depend on the area of the brain affected. The more

extensive the area of brain affected, the more functions that are likely to be lost. Some forms of

stroke can cause additional symptoms: in intracranial hemorrhage, the affected area may

compress other structures. Most forms of stroke are not associated with headache, apart from

2
subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral

hemorrhage.

Disability affects 75% of stroke survivors enough to decrease their employability. Stroke

can affect patients physically, mentally, emotionally, or a combination of the three. The results

of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to

areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include paralysis,

numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned

movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss,

and pain. If the stroke is severe enough, or in a certain location such as parts of the

brainstem, coma or death can result.

Emotional problems resulting from stroke can result from direct damage to emotional

centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke

emotional difficulties include anxiety, panic attacks, flat affect (failure to express

emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy,

irritability, sleep disturbances, lowered self esteem, and withdrawal. Depression can reduce

motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the patient to switch quickly

between emotional highs and lows and to express emotions inappropriately, for instance with

an excess of laughing or crying with little or no provocation. While these expressions of emotion

usually correspond to the patient's actual emotions, a more severe form of emotional lability

causes patients to laugh and cry pathologically, without regard to context or emotion. Some

3
patients show the opposite of what they feel, for example crying when they are happy.

Emotional lability occurs in about 20% of stroke patients.

Cognitive deficits resulting from stroke include perceptual disorders, speech

problems, dementia, and problems with attention and memory. A stroke sufferer may be

unaware of his or her own disabilities, a condition called anosognosia. In a condition

called hemispatial neglect, a patient is unable to attend to anything on the side of space

opposite to the damaged hemisphere.

Up to 10% of all stroke patients develop seizures, most commonly in the week

subsequent to the event; the severity of the stroke increases the likelihood of a seizure.

Hippocrates (460 to 370 BC) was first to describe the phenomenon of

sudden paralysis that is often associated with ischemia. Apoplexy, from the Greek word

meaning "struck down with violence,” first appeared in Hippocratic writings to describe this

phenomenon.

The word stroke was used as a synonym for apoplectic seizure as early as 1599, and is a

fairly literal translation of the Greek term.

In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause

of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding

in their brains. Wepfer also identified the main arteries supplying the brain,

the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known

as cerebral infarction] when he suggested that apoplexy might be caused by a blockage to

those vessels. Rudolf Virchow first described the mechanism of thromboembolism as a major

factor.

4
B. STATISTICS

Global Statistics

According to the World Health Organization, 15 million people suffer stroke worldwide

each year. Of these, 5 million die and another 5 million are permanently disabled.

High blood pressure contributes to over 12.7 million strokes worldwide.

Europe averages approximately 650,000 stroke deaths each year.

In developed countries, the incidence of stroke is declining - largely due to efforts to

lower blood pressure and reduce smoking. However, the overall rate of stroke remains

high due to the aging of the population.

Sources: World Health Report - 2007, from the World Health Organization; International

Cardiovascular Disease Statistics (2007 Update), a publication from the American Heart

Association.

UK

Stroke is a major cause of mortality in the UK, accounting for around 53,000 deaths

every year (around 9% of all deaths). As a single cause of death, stroke is second only to

coronary heart disease as the biggest killer in the UK. Stroke is also a major cause of premature

mortality, responsible for over 9,500 deaths every year in people under the age of 75, about

one in twenty of all deaths in this age group.

There are a number of different forms of stroke, including subarachnoid haemorrhage,

haemorrhagic stroke and ischaemic stroke. It is often difficult for medical practitioners to

identify the particular stroke subtype without access to evidence from autopsy or a brain scan.

5
 Therefore a large number of stroke mortalities are recorded as either ‘unspecified stroke’

or ‘other cerebrovascular disease’. Because of this, it is not possible to know exactly how many

deaths are caused each year by the individual stroke subtypes.

(http://www.heartstats.org/datapage.asp?id=8164)

May 2007

The burden of stroke

 Each year 16 million people experience a stroke and 5·7 million die.1

 87% of global stroke mortality occurs in low- and middle-income countries.1

 Unless there are population-wide interventions, by 2030 there will be 23 million strokes

and 7·8 million deaths each year.1

 Over the next two decades stroke mortality will triple in Latin America, the Middle East,

and sub-Saharan Africa.2

 Globally, stroke is the second leading cause of death above the age of 60 years, and the

fifth leading cause in people aged 15 to 59 years old.3

 Stroke is the third most common cause of death in developed countries, behind coronary

heart disease (CHD) and cancer.3

 Stroke is uncommon in people under 40 years.3

 In many developed countries the incidence of stroke is declining but the actual number

is increasing because of ageing populations.3

(http://www.worldheart.org/press/facts-figuresstroke/)

CURRENT TRENDS-Imaging Modalities Used for Diagnosis

6
Breakthrough for fast 3D stroke imaging

Cerebrovascular diseases (for example, ischemic stroke) are the second leading cause of

death worldwide and this trend is expected to continue and even grow until 2030 [1].

Unfortunately, most people with stroke symptoms still do not get to the hospital in time. This

hinders them from being considered for time-dependent treatments that can reduce disability or

death. Such incidents show that the system of care for stroke victims can be improved. In the

first 3 hours after a suspected cerebrovascular accident (CVA), non-contrast head computed

tomography (CT) is the primary imaging modality for the differential diagnosis of acute stroke.

However, the latest research shows significantly improved clinical outcomes in patients with

acute stroke after lysis therapy with Alteplase even in the range of three to four and a half

hours after the first stroke symptoms [2]. Based on these results we expect that using perfusion

CT in addition could be even more beneficial in order to reduce serious adverse events and

predict a beneficial outcome for these patients by looking at the relation between core infarct

and tissue at risk. This has been not performed in this study and has to be proven in future

studies.

7
Faster stroke diagnosis

CT perfusion imaging with syngo® Volume Perfusion CT Neuro can be used to diagnose

acute ischemic stroke in the emergency department quicker than with magnetic resonance

imaging (MRI), according to results of a large single-center study [2]. The study shows that CT

perfusion had 100 percent accuracy for detecting the acute ischemic stroke (AIS). If adopted,

the researchers say that this advancement in stroke detection will mean dramatically faster

diagnosis times - less than half the time of MRI screening - and enable physicians to provide

more accurate and targeted care, thereby avoiding potentially life-threatening complications

that can occur when thrombolytic drug therapy is used inappropriately. The study also reveals

that within five minutes of the patient getting on the CT scanner table, results can be achieved,

as opposed to MRI, which takes half an hour. The study also reveals that the widespread use of

CT perfusion is a practical way to help busy emergency departments to significantly save time

in acute stroke diagnosis, target treatment, and reduce the risks of inappropriate thrombolytic

use. According to the researchers, it is remarkable that the average time between an

emergency room neurological exam and CT scan was only 35 minutes. They confirmed that CT

perfusion imaging is very effective for diagnosing acute stroke and concluded that their result

could change national stroke triage protocols.

8
Precise information

Apart from the speed advantage, dynamic perfusion CT has become an increasingly

accepted examination for the differential diagnosis of acute stroke patients. Multislice CT, with a

continuously increasing number of detector rows, has quickly made high-resolution CTA of the

cerebral vasculature a clinical routine examination. It has, however, not really overcome the

limitations with respect to traditional CT perfusion imaging, which is restricted to the detector

width. Innovative technology such as the unique Adaptive 4D Spiral mode of the Siemens

SOMATOM® Definition family overcomes the limitations of static detector designs and now

allows volume perfusion imaging of the whole brain in clinical routine.

Key Benefits of syngo Volume Perfusion CT Neuro

 Whole brain and 3D tissue at risk evaluation with dynamic information*

 All perfusion parameters at hand: cerebral blood flow (CBF), cerebral blood volume (CBV),

time to peak (TTP) and mean transit time (MTT)

 Auto Stroke: therapeutic decision without complex user interaction ready for 24/7 use.

9
 Increased confidence: integrated automated motion corrections compensates for patient

movement

 * Requires Adaptive 4D Spiral

___________

[1] World Health Statistics 2008

[2] The Role of CT Perfusion Imaging in Acute Stroke Diagnosis: A Large Single-Center

Experience, Rai et al., The Journal of Emergency Medicine, Volume 35, Issue 3, Pages 237-354,

October 2008)

The antidepressant Lexapro may help protect key thinking functions if taken soon after a

stroke, U.S. researchers said. People who took Forest Laboratories Inc's (FRX.N) Lexapro, or

escitalopram, after a stroke recovered more of their thinking, learning and memory skills than

others who had counseling-type therapy normally used to treat depression or who were given a

placebo. It is not clear why Lexapro helped, but they said there is increasing evidence that

antidepressants cause changes in key brain structures needed for memory and thinking --

including the visual cortex, hippocampus and cerebral cortex -- that may help explain the

memory improvements.

New research finds that one out of 12 people who have a stroke will likely soon have

another stroke, and one out of four will likely die within one year. Researchers say the findings

highlight the vital need for better secondary stroke prevention. These findings suggest that

South Carolina and possibly other parts of the United States may have a long way to go in

preventing and reducing the risk factors for recurrent strokes.

10
 Eating chocolate may lower your risk of having a stroke, according to an analysis of

available research that will be presented at the American Academy of Neurology's 62nd Annual

Meeting in Toronto April 10 to April 17, 2010. Another study found that eating chocolate may

lower the risk of death after suffering a stroke. Chocolate is rich in antioxidants called

flavonoids, which may have a protective effect against stroke, but more research is needed.

The first study found that 44,489 people who ate one serving of chocolate per week were 22

percent less likely to have a stroke than people who ate no chocolate. The second study found

that 1,169 people who ate 50 grams of chocolate once a week were 46 percent less likely to die

following a stroke than people who did not eat chocolate.

11
 CHAPTER TWO

CASE STUDY PROPER

PATIENT PROFILE

Patient Name: CVA

Age: 66 years old

Status: Married

Birthday: April 26, 1947

Sex: Male

Location: San Pedro, Mexico, Pampanga

Diagnosis: Cerebrovascular Accident

Chief Complaint: slurred speech and right sided weakness

Date of Diagnosis: December 20,2013

Imaging Modalities: X-ray and Computed Tomography Scan

Personal History

Mr. CVA is 62 years old and is married. He was born on April 26, 1947 at San Pedro,

Mexico, Pampanga. He resides with his family at Mexico, Pampanga. He was admitted last

December 20, 2013. Mr. CVA lives with his wife and children.

His children are responsible for the welfare of their parents since both of their parents

are not working anymore. Their family is a Baptist Christian. They don’t necessarily believe in

the so-called manghihilot. They rely much on doctors when it comes with their health status.

The family of Mr. CVA lives at Sapang Makulangut. The place where they live is known for many

“tambays”. Mrs. CVA Verbalized description of their community as “Ay! Nuko, ding tao Karin

12
pagalduk da ing emperador…”. It is also seen to have many street vendors who sell street foods

such as barbeque, quail eggs and fried chicken skin.

Mr. CVA eats his meal on a regular basis (breakfast, lunch and dinner). He even has

snacks in between his meals approximately three times a day. They usually eat pork, rice and

vegetables. He often buys street foods such as isaw, chicken skin, chicken feet, fish ball, halo

halo, turon and quail eggs. Mr. CVA is fond of drinking coffee and softdrinks. According to his

wife he can consume a liter of softdrinks in one sitting. This persists even after he was

diagnosed with diabetes.

He is also an occasional alcohol drinker and a smoker. Whenever he is engaged with

situations wherein he is forced to drink he can consume an average of 4 bottles of Red Horse.

He smokes for like 2-3 sticks per day since his mid-20 (with a pack years of 6.3 pack years). His

sleep cycle goes from around 7pm-4am.

He takes his breakfast around 8am while reading his daily newspaper. He usually eats

pandesal and coffee for breakfast. After eating, he takes a 30 minute nap. Upon awakening, he

eats a meryenda such as turon where he buys at a store in front of their house accompanied by

another cup of coffee. For lunch, he often eats meat and rarely eat vegetables as his ulam with

an average of 2-3 cups of rice as his meal. For his afternoon meryenda, he eats street foods

available nearby their house accompanied with softdrinks. And for his dinner, it is usually the

same with his lunch preference. He doesn’t have any forms of exercise. His forms of usual

activities for the day are watching tv, reading newspaper and sleeping. His wife even said,

“Sarapngbuhayniyan, kain at tuloglang”

Computation for Pack Years: (# of sticks per day (3 sticks)/ 20) X 42 years

13
Family Health Illness History

Mr. CVA

14
 It is very evident that Mr. CVA is at high risk of developing Cerebrovascular Accident

(CVA). One of his grandparents experienced of having CVA and the other two grandparents

have the factors that contribute to occurrence of CVA such as Diabetes Mellitus (DM) and

Hypertension. His mother inherited DM for his grandfather while his father had a history of CVA

and hypertension. His Aunts and Uncles in both sides had hypertension. Two of his siblings died

from CVA, and the other one had a hypertension. Based from his family history, it is very

apparent on how Mr. CVA developed hypertension and DM that made him at risk for CVA.

History of Past Illness

Mr. CVA was never hospitalized and had no history of chickenpox, mumps and measles.

Usually, according to his wife, Mr. CVA only experience common coughs, fever and colds due to

weather changes. He self-medicates with Paracetamol for fever, Robitussin for common coughs

and Neozep for colds. There was an instance wherein he was brought to a clinic for severe

stomach ache due to hyperacidity last 2007. The doctor who checked him told Mr. CVA that his

fondness of drinking softdrinks contributed to his hyperacidity. He was asked to take antacids

as his medications.

History of Present Illness

It was around 2006 when Mr. CVA was diagnosed by the doctor with DM Type II. And

around mid-2008, Mr. CVA was first hospitalized for his first attack of stroke. According to Mr.

CVA’s wife, he was brought to the hospital that time because the patient was complaining of

slurred speech and dizziness while he was watching tv. From then on he was taking

15
maintenance drugs for his DM which is Metformin (taken every evening) and Insulin (25 units

during morning and another 15 units during evening). According to his wife, oftentimes it is Mr.

CVA who injects insulin to himself. Another maintenance drug for his hypertension is Bascorten

which he takes 10mg of it every day. Whenever he experiences hypertension his BP is around

140-200 for the systole and 90-110 for the diastole.

Few days before his symptoms occurred, he complained to his wife a feeling of being

nervous when he found out that their neighbor died because of DM and having the same

disease condition this triggered him to be anxious, this feeling manifested the day before he

was admitted to the hospital (December 20, 2013). According to Mr. CVA’s wife, it was around

3:00pm of February 23, 2015 when her husband felt something uncommon. Around 9:00 am

of December 19, 2013 he was feeling slight light-headedness while he was taking his breakfast.

He just lay down thinking that he would feel okay after doing so. This feeling persisted for

about 2 hours as verbalized by the patient’s wife. And around 2:00pm, while he was taking his

lunch, the patient was asking for a glass of water to his wife but he could not speak clearly. All

they could hear were a bit of groaning and slurd speech. Some of the words the patient tries to

say weren’t that clear. The wife of Mr. CVA immediately got worried thinking that these

symptoms were the same as with his first episode of stroke. Mr. CVA’s wife also noticed that

when they asked him to walk he was having difficulty because of his dizziness and that he is

also complaining that he can’t move properly the right side of his body especially his arms and

legs. Immediately after that, they rushed him to the hospital and around 3:00pm later that day

Mr. CVA was admitted. His chief complaint was slurred speech and right sided weakness.

16
DIAGNOSTIC RESULT

Diagnostic/Laboratory Date Indication or Results Normal Values Analysis and

Procedures ordered/Date Purpose Interpretation

result in of the result

Chest X-ray Ordered Mr. CVA undergone There are no A normal chest x ray will The results

December 20, chest x-ray to check pulmonary show normal structures show that Mr.

2013 if there are infiltrates, cardiac for the age and medical CVA’s heart is

pulmonary infiltrates, size and history of the patient. not enlarged.

Result check the cardiac configuration are Findings, whether

February 24, size and normal. normal or abnormal, will

2015 configuration The diaphragm, be provided to the

dynamic precordium sulci and ribs are referring physician in

was noted upon intact. the form of a written

admission which is report.

an indicator of

enlarged heart.

17
Diagnostic/ Date Indication or Purpose Results Normal Analysis and

Laboratory ordered/Dat Values Interpretation

Procedures e result in of the result

CT scan December 20, Mr. CVA undergone CT Plain multiple axial views of N.A. The test indicates

2013 scan to have multiple axial the head using incremental CT that there is

views of the head to reveals a small hypodense Foci presence of an

Distinguish the cause of on the anterior limb on the left infarct at left lobe

the signs and symptoms internal capsule and the left of the brain

present. putamen. explaining right

There is also a hypodense sided weakness

focus on the left parietal

cortex.

The ventricles and cistern are

not dilated The middle line

structures are not displaced.

The sellafurica posterior fossal

18
and basal skull structures are

intact.

Impression: Acute infarct,

anterior limb or left internal

capsule left putamen and left

parietal cortex.

19
 CHAPTER THREE

Anatomy and Physiology

Nervous System

The nervous system is the body's information gatherer, storage center and control

system. Its overall functions are to collect information about the body's external/internal states

and transfer this information to the brain (afferent system), to analyze this information, and to

send impulses out (efferent system) to initiate appropriate motor responses to meet the body's

needs.

The system is composed of specialized cells, termed nerve cells or neurons that

communicate with each other and with other cells in the body. A neuron has three parts:

20
 1. the cell body, containing the nucleus

2. dendrites, hair-like structures surrounding the cell body, which conduct incoming

signals.

3. The axon (or nerve fiber), varying in length from a millimeter to a meter, which conduct

outgoing signals emitted by the neuron. Axons are encased in a fat-like sheath, called

myelin, which acts like an insulator and, along with the Nodes of Ranvier, speeds

impulse transmission.

Typically a given neuron is connected to many thousands of neurons. The specific point of

contact between the axon of one cell and a dendrite of another is called a synapse. Messages

passed to and from the brain take the form of electrical impulses, or action potentials, produced

by a chemical change that progresses along the axon. At the synapse, the impulse causes the

release of neurotransmitters (like acetylcholine or dopamine) and this, in turn, drives the

impulse to the next neuron. These impulses travel very fast along these chain of neurons -- up

to 250 miles per hour. This contrasts with other systems, such as the endocrine system, which

may take many hours to respond with hormones.

The nerve cell bodies are generally located in groups. Within the brain and spinal cord, the

collections of neurons are called nuclei and constitute the gray matter, so-called because of

their color. Outside the brain and spinal cord the groups are called ganglia. The remaining

areas of the nervous system are tracts of axons, the white matter, so-called because of white

myelin sheath. Tracts carrying information of a specific type, such as pain or vision, generally

have specific names. .

Major Divisions of the Nervous System

The nerves of the body are organized into two major systems:

 the central nervous system (CNS), consisting of of the brain and spinal cord,

21
  the peripheral nervous system (PNS), the vast network of spinal and cranial nerves

linking the body to the brain and spinal cord. The PNS is subdivided into:

1. the autonomic nervous system (involuntary control of internal organs, blood

vessels, smooth and cardiac muscles), consisting of the sympathetic NS and

parasympathetic NS

2. the somatic nervous system (voluntary control of skin, bones, joints, and

skeletal muscle).

The two systems function together, with nerves from the periphery entering and becoming part

of the central nervous system, and vice versa.

Brain Structures

The brain, the body's "control central," is one of the largest of adult organs, consisting

of over 100 billion neurons and weighing about 3 pounds. It is typically divided into four parts:

the cerebrum, the cerebellum, the diencephalon (thalamus, hypothalamus, sometimes

22
classed as cerebral structures) and the brain stem(medulla oblongata, pons, midbrain), which

is an extension of the spinal cord.

Cerebrum

The largest division of the brain, the cerebrum, consists of two sides, the right and left

cerebral hemispheres, which are interconnected by the corpus callosum. The two

hemispheres are "twins," each with centers for receiving sensory (afferent) information and for

intiating motor (efferent) responses. The left side sends and receives information to/from the

right side of the body, and vice versa. Various intellectual functions are concentrated in either

the left or right hemispheres.

The hemispheres are covered by a thin layer of gray matter known as the cerebral

cortex. The interior portion consists of white matter, tracts, and nuclei (gray matter) where

synapses occur. Each hemisphere of the cerebral cortex is divided into four "lobes" by various

sulci and gyri: The sulci (or fissures) are the grooves and the gyri are the "bumps" on the

brain's surface.

23
The four lobes perform specific functions:

a) Frontal - controls fine movements (Betz cells)/ upper motor neuron) and smell. Also,

center for abstract thinking, judgment, and language (left hemisphere)

b) Parietal - coordinates afferent information dealing with pain, temperature, form, shape,

texture, pressure, and position. Some memory functions are also found here.

c) Temporal - handles dreams, memory, and emotions. Center for auditory function.

d) Occipital - governs vision

In addition to the four lobes, is the basal ganglia. The basal ganglia aggregates of

neurons (gray matter), constitute the extrapyramidal system. The extrapyramidal system

governs postural adjustment and gross voluntary movements, as opposed to fine movements,

controlled by the frontal lobe. The basal ganglia receive afferent input from the cerebral cortex

and thalamus. Their axons synapse in the brain stem and the spinal cord.

Cerebellum

The cerebellum, the second largest brain structure, sits below the cerebrum. Like the

cerebrum, the cerebellum has an outer cortex of gray matter and two hemispheres. It

receives/relays information via the brain stem. The cerebellum performs 3 major functions, all

of which have to do with skeletal-muscle control:

Function summary:

 Balance/ Equilibrium of the trunk (See also: Vestibular System)

 Muscle tension, spinal nerve reflexes, posture and balance of the limbs

 Fine motor control, eye movement. (Incoming information is transferred from the

cerebral cortex via the pons. Outgoing information goes back to the cortex via the

thalamus.)

24
Cerebellar disease (abscess, hemorrhage, tumors, and trauma) results in ataxia (muscle

incoordination), tremors, and disturbances of gait and equilibrium. This can also interfere with a

person's ability to talk, eat, and perform other self care tasks. Paralysis does not result from

loss of cerebellar function.

Diencephalon

The diencephalon, located between the cerebrum and the midbrain, consists of several

important structures, two of which are the:

 Thalamus: large, bilateral (right thalamus/left thalamus) egg-shaped mass of gray

matter serving as the main synaptic relay center. Receives/relays sensory information

to/from the cerebral cortex, including pain/pleasure centers.

 Hypothalamus: a collection of ganglia located below the thalamus and associated with

the pituitary gland. It has a variety of functions: senses changes in body temperature;

controls autonomic activities and hence regulates the sympathetic and parasympathetic

nervous systems; links to the endocrine system/controls the pituitary gland; regulates

appetite; functions as part of the arousal or alerting mechanism; and links the mind

(emotions) to the body -- sometimes, unfortunately, to the degree of producing

"psychosomatic disease."

Brain-Stem

The medulla oblongata, pons, and midbrain (mesencephalon or cerebral

peduncles) -- often referred to collectively as the brain stem -- control the most basic life

functions. Of these three, the medulla is the most important. In fact, so vital is the medulla to

survival that diseases or injuries affecting it often prove fatal. All functions of the brain stem are

associated with cranial nerves III-XII.

25
Function summary:

 Breathing/respiration (pons, medulla)

 Heart rate/ action (medulla)

 Blood pressure (vasoconstriction)/ blood vessel diameter (medulla)

 Reflex centers for pupillary reflexes and eye movements (midbrain, pons); and for

vomiting, coughing, sneezing, swallowing, and hiccupping (medulla).

Blood supply

An intricate arterial structure supplies the brain with oxygen-rich blood. At the brain

stem, two vertebral arteries, entering through the first cervical vertebrae, join to form the

basilar artery. The basilar artery along with two internal carotid arteries, entering through holes

at the base of the skull, interconnect at the Circle of Willis. From there, the anterior and middle

cerebral arteries arise; the posterior cerebral artery arises from the basilar system.

Cranial Nerves

There are 12 pairs of cranial nerves. Some bring information from the sense organs to

the brain; some control muscles; others are connected to glands or internal organs.

26
 Cranial Nerves Major Function

I. Olfactory Smell

II. Optic Vision

III. Occulomotor Eyelid and eyeball movement

IV. Trochlear Innervates superior oblique turns eye

downward and laterally

V. Trigeminal Chewing face & mouth touch & pain

VI. Abducens Turns eye laterally

VII. Facial Controls most facial expressions secretion

of tears & saliva taste

VIII. Vestibulocochlear Hearing equilibrium sensation

IX. Glossopharyngeal Taste senses carotid blood pressure

X. Vagus Senses aortic blood pressure slows heart

rate stimulates digestive organs taste

XI. Spinal Accessory Controls trapezius & sternocleidomastoid,

controls swallowing movements

XII. Hypoglossal Controls tongue movements

The pancreas is a glandular organ that secretes digestive enzymes (internal secretions)

and hormones (external secretions). In humans, the pancreas is a yellowish organ about 7

inches (17.8 cm) long and 1.5 inches. (3.8 cm) wide.

27
The Pancreas

The pancreas (Figs. 1097, 1098) is a compound racemose gland, analogous in its

structures to the salivary glands, though softer and less compactly arranged than those

organs. Its secretion, the pancreatic juice, carried by the pancreatic duct to the

duodenum, is an important digestive fluid. In addition the pancreas has an important

internal secretion, probably elaborated by the cells of Langerhans, which is taken up by

the blood stream and is concerned with sugar metabolism. It is long and irregularly

prismatic in shape; its right extremity, being broad, is called the head, and is connected to

the main portion of the organ, orbody, by a slight constriction, the neck; while its left

extremity gradually tapers to form the tail. It is situated transversely across the posterior

wall of the abdomen, at the back of the epigastric and left hypochondriac regions. Its

length varies from 12.5 to 15 cm., and its weight from 60 to 100 gm.

28
FIG. 1097– Transverse section through the middle of the first lumbar vertebra, showing

the relations of the pancreas. (Braune.)

FIG. 1098– The duodenum and pancreas

29
 FIG. 1099– The pancreas and duodenum from behind. (From model by His.)

Relations.—The Head (caput pancreatis) is flattened from before backward, and is

lodged within the curve of the duodenum. Its upper border is overlapped by the superior

part of the duodenum and its lower overlaps the horizontal part; its right and left borders

overlap in front, and insinuate themselves behind, the descending and ascending parts of

the duodenum respectively. The angle of junction of the lower and left lateral borders

forms a prolongation, termed the uncinate process. In the groove between the

duodenum and the right lateral and lower borders in front are the anastomosing superior

and inferior pancreaticoduodenal arteries; the common bile duct descends behind, close to

the right border, to its termination in the descending part of the duodenum.

Anterior Surface.—The greater part of the right half of this surface is in contact with the

transverse colon, only areolar tissue intervening. From its upper part the neck springs, its

right limit being marked by a groove for the gastroduodenal artery. The lower part of the

right half, below the transverse colon, is covered by peritoneum continuous with the

inferior layer of the transverse mesocolon, and is in contact with the coils of the small

30
intestine. The superior mesenteric artery passes down in front of the left half across the

uncinate process; the superior mesenteric vein runs upward on the right side of the artery

and, behind the neck, joins with the lienal vein to form the portal vein.

Posterior Surface.—The posterior surface is in relation with the inferior vena cava, the

common bile duct, the renal veins, the right crus of the diaphragm, and the aorta.

The Neck springs from the right upper portion of the front of the head. It is about

2.5 cm. long, and is directed at first upward and forward, and then upward and to the left

to join the body; it is somewhat flattened from above downward and backward. Its antero-

superior surface supports the pylorus; its postero-inferior surface is in relation with the

commencement of the portal vein; on the right it is grooved by the gastroduodenal artery.

The Body (corpus pancreatis) is somewhat prismatic in shape, and has three

surfaces: anterior, posterior, and inferior.

The anterior surface (facies anterior) is somewhat concave; and is directed

forward and upward: it is covered by the postero-inferior surface of the stomach which

rests upon it, the two organs being separated by the omental bursa. Where it joins the

neck there is a well-marked prominence, the tuber omentale, which abuts against the

posterior surface of the lesser omentum.

The posterior surface (facies posterior) is devoid of peritoneum, and is in contact

with the aorta, the lienal vein, the left kidney and its vessels, the left suprarenal gland, the

origin of the superior mesenteric artery, and the crura of the diaphragm.

The inferior surface (facies inferior) is narrow on the right but broader on the

left, and is covered by peritoneum; it lies upon the duodenojejunal flexure and on some

31
coils of the jejunum; its left extremity rests on the left colic flexure.

The superior border (margo superior) is blunt and flat to the right; narrow and

sharp to the left, near the tail. It commences on the right in the omental tuberosity, and is

in relation with the celiac artery, from which the hepatic artery courses to the right just

above the gland, while the lienal artery runs toward the left in a groove along this border.

The anterior border (margo anterior) separates the anterior from the inferior

surface, and along this border the two layers of the transverse mesocolon diverge from

one another; one passing upward over the anterior surface, the other backward over the

inferior surface.

The inferior border (margo inferior) separates the posterior from the inferior

surface; the superior mesenteric vessels emerge under its right extremity.

The Tail (caudapancreatis) is narrow; it extends to the left as far as the lower part

of the gastric surface of the spleen, lying in the phrenicolienal ligament, and it is in contact

with the left colic flexure.

Birmingham described the body of the pancreas as projecting forward as a

prominent ridge into the abdominal cavity and forming part of a shelf on which the

stomach lies. “The portion of the pancreas to the left of the middle line has a very

considerable antero-posterior thickness; as a result the anterior surface is of considerable

extent; it looks strongly upward, and forms a large and important part of the shelf. As the

pancreas extends to the left toward the spleen it crosses the upper part of the kidney, and

is so moulded on to it that the top of the kidney forms an extension inward and backward

of the upper surface of the pancreas and extends the bed in this direction. On the other

hand, the extremity of the pancreas comes in contact with the spleen in such a way that

32
the plane of its upper surface runs with little interruption upward and backward into the

concave gastric surface of the spleen, which completes the bed behind and to the left,

and, running upward, forms a partial cap for the wide end of the stomach.

FIG. 1100– The pancreatic duct.

The Pancreatic Duct (ductuspancreaticus [Wirsungi]; duct of Wirsung) extends 1

transversely from left to right through the substance of the pancreas (Fig. 1100). It 5

commences by the junction of the small ducts of the lobules situated in the tail of the

pancreas, and, running from left to right through the body, it receives the ducts of the

various lobules composing the gland. Considerably augmented in size, it reaches the neck,

and turning downward, backward, and to the right, it comes into relation with the common

bile duct, which lies to its right side; leaving the head of the gland, it passes very obliquely

through the mucous and muscular coats of the duodenum, and ends by an orifice common

to it and the common bile duct upon the summit of the duodenal papilla, situated at the

33
medial side of the descending portion of the duodenum, 7.5 to 10 cm. below the pylorus.

The pancreatic duct, near the duodenum, is about the size of an ordinary quill. Sometimes

the pancreatic duct and the common bile duct open separately into the duodenum.

Frequently there is an additional duct, which is given off from the pancreatic duct in the

neck of the pancreas and opens into the duodenum about 2.5 cm. above the duodenal

papilla. It receives the ducts from the lower part of the head, and is known as

the accessory pancreatic duct (duct of Santorini).

Development (Figs. 1101, 1102).—The pancreas is developed in two parts, a dorsal 1

and a ventral. The former arises as a diverticulum from the dorsal aspect of the duodenum 6

a short distance above the hepatic diverticulum, and, growing upward and backward into

the dorsal mesogastrium, forms a part of the head and uncinate process and the whole of

the body and tail of the pancreas. The ventral part appears in the form of a diverticulum

from the primitive bile-duct and forms the remainder of the head and uncinate process of

the pancreas. The duct of the dorsal part (accessory pancreatic duct) therefore opens

independently into the duodenum, while that of the ventral part (pancreatic duct) opens

with the common bile-duct. About the sixth week the two parts of the pancreas meet and

fuse and a communication is established between their ducts. After this has occurred the

terminal part of the accessory duct, i. e., the part between the duodenum and the point of

meeting of the two ducts, undergoes little or no enlargement, while the pancreatic duct

increases in size and forms the main duct of the gland. The opening of the accessory duct

into the duodenum is sometimes obliterated, and even when it remains patent it is

probable that the whole of the pancreatic secretion is conveyed through the pancreatic

duct.

34
 CHAPTER FOUR
BOOKBASED PATHOPHYSIOLOGY
Precipitating Factor

Overweight/ Stress
Obesity Smoking

↑Serum
Vaso- ↑Carbon
Cholesterol ↑Fat on the Eat Smoke Stimulati ↑RBC
↑LDL ↓Oxygen constrict monoxide
level abdomen more more on of carry in blood
and hips catechol
↑LDL capacity
amines ↑vascular
of blood resistance
↓HDL ↑blood
↑Serum
↑Workload thickness
Cholesterol
of the heart ↑blood ↓Tissue
Accumulate ↓Tissue? perfusion
of LDL sugar ↑clot
perfusion
formation

↑blood ↑BP
viscosity ↑risk of injury
to intimal
Diet high in Fats, Sodium arterial wall
and Cholesterol
Cocaine use/ Sedentary Lifestyle
abuse

Accumulation of fatty Increase attraction

streaks in the arterial wall of water in the blood Deposits of fatty materials in
the arterial walls of arteries

Induce Enhance Increases

↑BP Increase in blood
vasospa of tablet cardiovascular
volume Vascular changes
sm activity
Poor disorder
circulation Increase blood 35
cholesterol level and
blood pressure
 Diabetes

Previous
heart ↑blood
disease sugar
Predisposing Factor
Inc workload of the heart
Hypertension Age Gender Altered
arterial wall ↑blood
integrity viscosity
Male hormones
Uncontrolled cardiomegaly Degenerative
↑BP
changes in the
function of the
heart ↓HDL Accumulation
Inc. vascular resistance of LDL in the ↑workload
arterial wall of the heart
Heart weakens Dec.
Inc pressure in cerebral blood over time
↓elastin
vessels vessel ↑lipid/platelet
flexibility Atheroma/ clot adherence to
formation vessel walls
↓elasticity of
Loss of Dec. cardiac output the blood
elaticity Impaired
vessels Hardening
cerebral ↑size of heart
autoregul of arterial Thrombus
ation wall formation
Rupture of Microvascular
cerebral blood Atherosclerosis changes
vessel Familial
History
Increased risk Weaker heart
for vessel
injury
↑risk for DM , heart ↓cardiac output
diseases,
hypercoagualable state,
Increased hypercholesterolemia
Increased ↓tissue perfusion
lipid/platelet risk for
adherence to rupture
vessel walls Altered
macrovascular
integrity

36
Thrombotic stroke

Development of
atherosclerosis
of the blood
vessel wall

Plsgues develop
on the inner wall
of the affected
blood vessel

First step Accumulation of LDL within the arterial wall

Stimulate methodical cells to adhere to monocytes and feels

Second step

Undegoes chemical changes

Maturation of monocytes into macrophages

Ingest LDL particle

Macrophage ingest a critical mass of LDL

Becomes foam cells

37

Constitutes fatty streaks on the inner arterial wall

(earliest manifestation of arterial plague)
 Third step
Form a fibrous cover over the liquid core

Fourth step Separates it from blood flow through the vessel

Fifth step Plaque rupture

Exposes foam cells to clot-promoting elements in the blood

Clot formation

Dislodgement

If at sufficient size

ISCHEMIC CASCADE May interrupt blood flow Embolic stroke

to the brain tissue implies

Ischemia

Neutroxins
(oxygen free radical nitric
oxide glutamate) released
Stroke area or core
38
 Ischemia develop
neurologic damage

Embolus dislodgement

Travels to the cerebral arteries via carotid artery or vertebrobasilar system

Lodge in smaller cerebral arteries blood vessel at point of bifurcation or where the lumen narrow

Emboli occlude the vessel

Ischemia develop Ischemic Cascade

Enters small blood vessels If damage to vessel wall is significant

Hemorrhagic
Vessel integrity interrupted
If embolus breaks off into fragments Stroke

Embolus is Vasospasm Cerebral hemorrhage

absorbed

Remission of Nuchal rigidity

s/sx Headache
Increase in blood pressure
39
 Decrease cerebral Entry of blood to
Inflammatory
perfusion meningeal space
process

Ischemic
cascade HYPOXIA Release
Increase
leukocytes in
intracranial
interstitial space
neurologic damage Altered level of pressure
and neutrophils
consciousness for phagocytosis
CEREBRAL
COMPRESSION
HYPOXIA AND INJURY

coma

BRAIN TISSUE INFARCT

death
NEUROLOGICAL DEFICITS

 Middle cerebral artery (MCA) most commonly affected

 Internal carotid artery second most frequently affected

Massive infarction of most lateral hemisphere and

deeper structure of the frontal, parietal and temporal
lobes

Sensory Dysphagia
Hemiplegia hemipharesis apraxia Aphasia/
Deficits
Dysarthia
40
 In a healthy, anatomical structure of the body, the carotid arteries form the main blood

supply to the brain. Following a stroke, voluntary control of the muscles may be lost, depending

on the type of stroke the victim is encountering. Strokes can also result from embolism or due

to a ruptured blood vessel. Embolism blocks small arteries within the brain, causing dysfunction

to occur. Spontaneous rupture of a blood vessel in the brain causes a hemorrhagic stroke.

Another form of cerebrovascular disease includes aneurysms. In females with defective

collagen, the weak branching points of arteries give rise to protrusions with a very thin covering

of endothelium that can tear to bleed easily with minimal rise of blood pressure. This can also

occur with defective capillaries caused by tissue cholesterol deposition especially in hypertensive

subjects with or without dyslipidemia. If bleeding occurs in this process, the resulting effect is a

hemorrhagic stroke in the form of subarachnoid hemorrhage, intracerebral hemorrhage or both.

Ischemia is the loss of blood flow to the focal region of the brain. The beginning process

of this is quite rapid. The duration of a stroke is usually two to fifteen minutes. One side of the

face, hand, or arm may swell up. During this time, the person may lose conscious control and

faint. Brain deficits may improve over a maximum of 72 hrs. Deficits do not resolve in all cases.

The neurological recovery period includes stable, to improving, brain function. Stable is the

period by which neither nutrient supply is regained, nor is it lost. Improving, depending on a

hospital code, generally means that the arteries gain control and blood flow functions

consistently within the brain. The cartoid arteries connect to the vertebral arteries. These

branch off into the cerebellar and posterior meningenial arteries, which supply the back of the

brain.

Also, during ischemia, interneurons weaken, causing an insufficient amount to perform vital

functions to be present. The neuroglis become congested or maintain loss during a

41
cerebrovascular accident. If impulse amount ceases, then life itself will cease and the victim

may enter the stage of clinical death. Neural pathways weaken, therefore decreasing action

potential. The neural arc, which in general consists of sensory and motor neurons, weaken as

well. The muscles become paralyzed, in some cases for life. Paralysis also includes the

weakening of the receptors in the body, unless improvement is made. Cerebrovascular damage

to the brain is what makes it difficult for receptors to receive the impulse and transmit it of a

neuron. This chemical reaction is then transmitted creating a poor reflex to the body. The

meninges that also protect the brain and spinal cord are deeply weakened, allowing the victim

to suffer vast transmission of diseases or unstable growth or maintenance if the victim is not in

resting position.

During the stage of paralysis, the spinal tracts do not have much to do with the

enduring condition of cerebrovascular disease, either, in time may shorten the life of a victim

who is suffering because the nutrient supply is weakened in transmission during

cerebrovascular disease. Descending and ascending tracts will generally be cut off during

cerebrovascular disease, which conducts impulses down from the cord of the brain. This is

known as anesthesia in a minor case.

PREDISPOSING FACTORS:

Age (above 60 years old) — the chance of having a stroke about doubles for each decade of

life after age 55. While stroke is common among the elderly, over 25 percent of people who

have strokes are under age 65. Increasing age causes degenerative changes to the blood

vessels thus increasing the risk for arterial wall injury.

Gender -- Stroke is more common in men than in women. In most age groups, more men

than women will have a stroke in a given year. At older ages, the incidence is higher in women

42
than in men. Overall, more women than men die of stroke. Female hormones decrease LDL

levels and Increase HDL level while male hormones does otherwise.

Familial disposition-chance of stroke is greater in people who have a family history of stroke

Previous heart disease-- A diseased heart increases the risk of stroke. The percentage of

people with a first myocardial infarction who will have a stroke within five years at ages 40–69

is 4 percent of men and 12 percent of women. At age 70 and older, 6 percent of men and 11

percent of women will have a stroke after having a heart attack. Atrial fibrillation (the rapid,

uncoordinated quivering of the heart’s upper chambers), in particular, raises the risk for stroke.

Heart attack is also the major cause of death among stroke survivors

PRECIPITATING FACTORS:

Diet

Cigarette smoking — Cigarette smoking is an important risk factor for stroke. The nicotine

and carbon monoxide in cigarette smoke damage the cardiovascular system in many ways.

Physical inactivity — An inactive lifestyle is a risk factor for coronary heart disease. Regular,

moderate-to-vigorous physical activity is important in preventing heart and blood vessel

disease. Even moderate-intensity physical activities are beneficial if done regularly and long-

term. More vigorous activities are associated with more benefits. Physical activity can help

control blood cholesterol, diabetes and obesity, as well as help lower blood pressure.

High blood pressure — High blood pressure increases the heart’s workload, causing the heart

to enlarge and weaken over time. It also increases the risk of stroke, heart attack, kidney

failure and heart failure. When high blood pressure exists with obesity, smoking, high blood

cholesterol levels or diabetes, the risk of heart attack or stroke increases several times.

Obesity and overweight — People who have excess body fat — especially if a lot of it is in

the waist area — are more likely to develop heart disease and stroke even if they have no other

43
risk factors. Excess weight increases the strain on the heart, raises blood pressure and blood

cholesterol and triglyceride levels, and lowers HDL (good) cholesterol levels. It can also make

diabetes more likely to develop. Many obese and overweight people have difficulty losing

weight. If you can lose as little as 10 to 20 pounds, you can help lower your heart disease risk.

Stress — Individual response to stress may be a contributing factor. Some scientists have

noted a relationship between coronary heart disease risk and stress in a person’s life, their

health behaviors and socioeconomic status. These factors may affect established risk factors.

For example, people under stress may overeat, start smoking or smoke more than they

otherwise would.

Sickle cell anemia — This genetic disorder mainly affects African-American and Hispanic

children. "Sickled" red blood cells are less able to carry oxygen to the body’s tissues and organs.

These cells also tend to stick to blood vessel walls, which can block arteries to the brain and

cause a stroke.

Certain kinds of drug abuse — Intravenous drug abuse carries a high risk of stroke from a

cerebral embolism (blood clot in the brain). Cocaine use has been closely related to strokes,

heart attacks and a variety of other cardiovascular complications. Some of them have been fatal

even in first-time cocaine users.

Diabetes is an independent risk factor for stroke and is strongly correlated with high blood

pressure. While diabetes is treatable, having it still increases a person’s risk of stroke. People

with diabetes often also have high cholesterol and are overweight, increasing their risk even

more.

44
CLIENT CENTERED PATHOPHYSIOLOGY

Precipitating Factor Smoking

Sedentary Diet high in Fats, Sodium

Lifestyle and Cholesterol
↑LDL Vasoconstriction ↑RBC
↓Oxygen
Accumulation carry
↑Carbon
of fatty Poor capacity
Deposits of fatty monoxide
streaks in the circulation Increase of blood
materials in the ↑vascular in blood
arterial wall attraction of water ↑blood
in the blood arterial walls of resistance
arteries thickness

↓Tissue
Increases Increase in blood ↓Tissue perfusion
cardiovascular volume Vascular changes perfusion
disorder
↑clot
Increase blood cholesterol level and ↑BP formation
blood pressure
↑risk of injury
to intimal
arterial wall

45
 Hypertension
Dynamic precordium
140/100mmHg Predisposing Factor
Inc workload of the
heart
Age Gender Previous CVA Diabetes
37
cardiomegaly
Male hormones ↑blood
Uncontrolled Altered sugar
Degenerative
arterial wall
Heart weakens changes in the
integrity
over time function of the ↓HDL
↑ vascular resistance heart ↑blood
viscosity

↓ cardiac output
Inc pressure in cerebral Dec. Accumulation ↑lipid/platelet
blood vessels ↓elastin vessel of LDL in the adherence to ↑BP
flexibility arterial wall vessel walls

↓elasticity of ↑workload
Hardening
Impaired the blood Atheroma/ clot of the heart
Loss of of arterial
elaticity cerebral vessels wall formation
autoregulation

Thrombus ↑size of heart

Atherosclerosis formation
Rupture of cerebral
blood vessel Weaker heart
Familial
Increased risk History
for vessel ↓cardiac output
injury
↑risk for DM ,
heart diseases ↓tissue perfusion

Increased risk
Increased
for rupture
lipid/platelet
adherence to 46
vessel walls
 Microvascular
changes

Thrombotic stroke

Chronic inc.
blood glucose
Development of
atherosclerosis
of the blood
vessel wall Altered
macrovascular
integrity
Plaques develop
on the inner wall
of the affected
blood vessel

First step Accumulation of LDL within the arterial wall

Undergoes chemical changes

47
 Stimulate methodical cells to adhere to monocytes and feels

Second step Maturation of monocytes into macrophages

Ingest LDL particle

Macrophage ingest a critical mass of LDL

Becomes foam cells

Constitutes fatty streaks on the inner arterial wall

(earliest manifestation of arterial plague)

Additional growth of the lesion through

influence of inflammatory molecules

Third step Form a fibrous cover over the

liquid core

Fourth step Separates it from blood flow through the vessel

Plaque rupture 48
Fifth step
 Exposes foam cells to clot-promoting elements in the blood
ISCHEMIC CASCADE

Clot formation

May interrupt blood flow

to the brain tissue implies

Ischemia

Neutroxins
(oxygen free radical nitric
oxide glutamate) released

Local acidosis develop

Membrane depolarization occur

Influx of calcium sodium

Cytoxic edema and Cell death Stroke area or core

Zone of hypoperfusion
neurologic damage
(penumbra) becomes prone to
death if circulation is not
restored
49
 Cerebral Hypoxia

Presence of an infarct at left lobe of the brain

explaining right sided weakness ( CT scan Feb.
23, 2010)

Dysphagia Sensory Deficits Dizziness

Hemiparesis of Apraxia Dysarthria
the right side of Pt exhibited @ lunch
the body as S.O. slurring of time, prior to
observed by assists pt speech admission Lack of
S.O. in am of in ADLs Mrs. CVA balance
Feb 23 post Described when
stroke this as walking
‘NAuutal’
↓ muscle strength
Limited
right rm:3/5; ROM
right leg:2/5;
left arm: 4/5;
left leg:4/5

50
 CHAPTER FIVE

RADIOLOGIC PROCEDURES

Inroduction to the procedure

A cranial CT scan is a diagnostic tool used to create detailed pictures of features inside

your head, such as your skull, brain, paranasal sinuses, ventricles, and eye sockets. CT stands

for computed tomography, and this type of scan is also referred to as a CAT scan. A cranial CT

scan is known by a variety of names as well, including brain scan, head scan, skull scan, and

sinus scan.

This procedure is noninvasive, meaning it doesn’t require surgery. It’s usually suggested to

investigate various symptoms involving the nervous system before turning to invasive

procedures.

A. PATIENT PREPARATION

1. Internal Preparation

The patient do not need to fast (have nothing to eat or drink prior to the examination. There

is no other internal preparation needed.

2. External Preparation

The patient should wear comfortable, loose-fitting clothes for the examination. The

patient is also asked to wear a gown during the procedure. The patient must remove metallic

objects, jewelry’s, safety pin and bra. The procedure must be well explained to the patient or

relative respectively.

Women should always inform their physician and the CT technologist if there is any possibility

that they may be pregnant.

51
 B. HOW IS THE PROCEDURE PERFORMED?

The technologist begins by positioning you on the CT examination table, usually lying

flat on your back. Straps and pillows may be used to help you maintain the correct position and

to help you remain still during the exam.

Many scanners are fast enough that children can be scanned without sedation. In special

cases, sedation may be needed for children who cannot hold still. Motion will cause blurring of

the images and degrade the quality of the examination the same way that it affects

photographs.

If contrast material is used, depending on the type of exam, it will be swallowed, injected

through an intravenous line (IV) or, rarely, administered by enema.

Next, the table will move quickly through the scanner to determine the correct starting

position for the scans. Then, the table will move slowly through the machine as the actual CT

scanning is performed. Depending on the type of CT scan, the machine may make several

passes.

You may be asked to hold your breath during the scanning. Any motion, whether breathing

or body movements, can lead to artifacts on the images. This loss of image quality can

resemble the blurring seen on a photograph taken of a moving object.

When the examination is completed, you will be asked to wait until the technologist verifies that

the images are of high enough quality for accurate interpretation.

A CT scan of the head is usually completed within 10 minutes.

52
 C. HOW DOES THE PROCEDURE WORK?

In many ways CT scanning works very much like other x-ray examinations. Different

body parts absorb the x-rays in varying degrees. It is this crucial difference in absorption that

allows the body parts to be distinguished from one another on an x-ray film or CT electronic

image.

In a conventional x-ray exam, a small amount of radiation is aimed at and passes

through the part of the body being examined, recording an image on a special electronic image

recording plate. Bones appear white on the x-ray; soft tissue, such as organs like the heart or

liver, shows up in shades of gray, and air appears black.

With CT scanning, numerous x-ray beams and a set of electronic x-ray detectors rotate

around you, measuring the amount of radiation being absorbed throughout your body.

Sometimes, the examination table will move during the scan, so that the x-ray beam follows a

spiral path. A special computer program processes this large volume of data to create two-

dimensional cross-sectional images of your body, which are then displayed on a monitor. CT

imaging is sometimes compared to looking into a loaf of bread by cutting the loaf into thin

slices. When the image slices are reassembled by computer software, the result is a very

detailed multidimensional view of the body's interior.

Refinements in detector technology allow nearly all CT scanners to obtain multiple slices

in a single rotation. These scanners, called multislice CT or multidetector CT, allow thinner slices

to be obtained in a shorter period of time, resulting in more detail and additional view

capabilities.

Modern CT scanners are so fast that they can scan through large sections of the body in

just a few seconds, and even faster in small children. Such speed is beneficial for all patients

53
but especially children, the elderly and critically ill, all of whom may have difficulty in remaining

still, even for the brief time necessary to obtain images.

D. MACHINE USED (GE LIGHTSPEED 16)

Computed tomography, more commonly known as a CT or CAT scan, is a diagnostic medical

test that, like traditional x-rays, produces multiple images or pictures of the inside of the body.

The cross-sectional images generated during a CT scan can be reformatted in multiple planes,

and can even generate three-dimensional images. These images can be viewed on a computer

monitor, printed on film or by a 3D printer, or transferred to a CD or DVD.

CT images of internal organs, bones, soft tissue and blood vessels provide greater detail than

traditional x-rays, particularly of soft tissues and blood vessels.

CT scanning provides more detailed information on head injuries,stroke, brain tumors and other

brain diseases than regular radiographs (x-rays).

E. SCANNING TECHNIQUE

Patient should be supine, head first into the gantry, with the head in the head-holder

whenever possible. Center the table height such that the external auditory meatus (EAM) is at

the center of the gantry. To reduce or avoid ocular lens exposure, the scan angle should be

parallel to a line created by the supraorbital ridge and the inner table of the posterior margin of

the foramen magnum. This may be accomplished by either tilting the patient’s chin toward the

chest (“tucked” position) or tilting the gantry. Scan range should top of C1 lamina through top

of calvarium.

54
 GE LIGHTSPEED 16 / OPTIMA CT580 PROTOCOL

(Cranial scan)

Position/Landmark Supine head first or feet first.

Zero at outer canthus of eye.

Topogram Direction Craniocaudal

Respiratory Phase

Scan Type Axial

KV / mA / Rotation time (sec) Pitch / 120kv / 480 mA / .5 sec

Speed (mm/rotation) Noise Index 2i

Detector width x Rows = Beam 0.625mm x 16 = 10mm

Collimation

Average Tube Output ctdi – 51.1 mGy

dlp – 872 mGy.cm

Axial Set body thickness/ recon

Slice Thickness/ Spacing Recon part spacing algorithm destination

Algorithm 1. Brain 5mmx5mm standard pacs

Recon Destination 2. Bone 5mmx5mm bone pacs

Scan Start / End Locations Skull base

DFOV Skull vertex

25 cm decrease appropriately

15 degrees cephlad to the OML

55
CT SCAN RESULT DONE: 12/20/2013

CHEST X-RAY RESULT DONE 12/20/2013

CHAPTER SIX

CONCLUSIONS AND RECOMMENDATIONS

56
 CHAPTER SIX

Conclusions

Based from the research and the discussion of the patient’s case which is

Cerebrovascular Accident, the following conclusions were drawn:

1.Cerebrovascular Accident is a sudden loss of function resulting from disruption of the blood

supply to a part of the brain. Stroke, also called brain attack or ischemic stroke, happens when

the arteries leading to the brain are blocked or ruptured. When the brain does not receive the

needed oxygen supply, the brain cells begin to die, a stroke can cause paralysis, inability to

talk, inability to understand, and other conditions brought on by brain damage.

2.In addition to a complete medical history and a full physical examination, the procedures for

diagnosing CVA may include: X-ray, Computed Tomography Scan and Magnetic Resonance

Imaging.

3. Stroke is a medical emergency and can cause permanent neurological damage,

complications, and death. It is the leading cause of adult disability in the United States and

Europe. It is the number two cause of death worldwide and may soon become the leading

cause of death worldwide. Risk factors for stroke include advanced age, hypertension (high

blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high

cholesterol, cigarette smoking and atrial fibrillation. High blood pressure is the most important

modifiable risk factor of stroke.

57
 Recommendations

Based from the conclusions of this case study, the researchers arrived to the following

recommendations which may be supplemental to the patient, its relatives, healthcare workers

and other people who encounter this type of disease:

1. Since CVA is a medical emergency, family history and signs and symptoms should

be known so that early diagnosis may be done and interventions may follow as soon as

possible.

2. Any early signs and symptoms should be consulted to a doctor and should not be

taken for granted.

3. Diagnosis may require the use of imaging modalities that uses radiation. Patient that

is considered to undergo such diagnosis should not worry about the dose of radiation

because there is an allowable dosage of radiation that could be received by a person.

58
 REFERENCES

Chew, F (2013). Skeletal Radiology.Third Edition. Philadelphia: Wolters Kluwer/Lippincott

Williams & Wilkins.

Hospital of Philadelphia. (2014). What is Cerebrovascular Accident?.Retrieved November 10,

2015, from www.chop.edu/conditions-disease/cerebrovascularaccident#VkG0uNIrKUk

Dickey, I. (2015).Cerebrovascular Accidenta Treatment & Management. Retrieved on November

7, 2015, from http://emedicine.medscape.com/article/1256477-treatment#d14

Hacking, C. & Gaillard, F. (2015).Cerebrovascular Accident. Retrieved on November 7, 2015,

from http://radiopaedia.org/articles/ Cerebrovascular Accident

John Hopkins University. (2015). Cerebrovascular Accident Retrieved November 5, 2015, from

http://www.hopkinsmedicine.org/healthlibrary/conditions/bone_disorders/Cerebrovascul

ar Accident _85,P00125/

Jones, J. & Gaillard, F. (2015).Salter-Harris Fracture. Retrieved November 6, 2015, from

http://radiopaedia.org/articles/salter-harris-fractures

59
Kushner, B.H., Roberts, S.S., Friedman, D.N., Kuk, D., Ostrovnaya, I., Modak, S., Kramer, K.,

Basu, E.M. & Cheung, N.K. (2015).Cerebrovascular Accident in long-term survivors of

high-risk,Retrieved on November 7, 2015, from

http://www.ncbi.nlm.nih.gov/pubmed/25728463

North Shore-LIJ.(2014 Cerebrovascular Accident, causes, symptoms. Retrieved on November 8,

2015 from http://ortho.northshorelij.com/conditions-treatments/cerebrovascular

accident

Pediatric Surgery Center (2014).Cerebrovascular Accident Retrieved November 6, 2015, from

http://pedsurgerycenter.com/patient-

education/index.dot?id=96746&lang=English&db=hlt&ebscoType=static&widgetTitle=

Premkumar, K. (2012). Anatomy & physiology: the massage connection. Philadelphia: Wolters

Kluwer/Lippincott Williams & Wilkins.

Taylor, T. (2015). Joints.Retrieved November 10, 2015, from

www.innerbody.com/image/skel07.html

American Academy of Orthopaedic Surgeons (2012).Osteochondroma. Retrieved Novemver 5,

2015 from: http://orthoinfo.aaos.org/topic.cfm?topic=A00079

Therapeutic Research Faculty.(2009). Calcium. Retrieved November 06, 2015, from

http://www.m.webmd.com/vitamins/ai/ingredientmono-781/calcium/source-3

University of Leeds.(n.d.).Bone.Retrieved November 10, 2015, from

www.histology.leeds.ac.uk/bone/cartilage_types.php

University of Maryland Medical Center.(2015). Phosphorus. Retrieved November 06, 2015, from

https://emm.edu/health/medical/altmed/supplement/phosphorus

VanPutte, C., Regan, J. & Russo, A.(2013). Seeley’s essentials of anatomy & physiology.Eight

edition. Singapore: Mc-Graw Hill.

60
Vigorita,V.J. (2008). Orthopaedic pathology.Second edition. China: Lippincott Williams &

Wilkins.

(http://www.heartstats.org/datapage.asp?id=8164)

(http://www.worldheart.org/press/facts-figures/stroke/)

61