Anamnesis, Topikal Diagnosis, Istilah Neurologi-2

ANAMNESIS,
Blok 11. Neuropsikiatri

Semester Genap TA. 2022/2023
TOPIKAL DIAGNOSIS,
Periode 20 Maret sd 5 Mei 2023
ISTILAH NEUROLOGI
Fitriah Handayani
Fakultas Kedokteran Universitas Tadulako

Fitriah Handayani
1. INTRODUCTION (WIIPP)
Wash your hands
Introduce yourself: give your name and your job (e.g. Dr. Louise Gooch,
ward doctor)
Identity: confirm you’re speaking to the correct patient (name and date of
birth)
Permission: confirm the reason for seeing the patient (“I’m going to ask
you some questions about your chief complaint/headache,etc, is that OK?”)
Positioning: patient sitting in chair approximately a metre away from you.

Ensure you are sitting at the same level as them and ideally not behind a
desk.
Anamnesis, Topikal Diagnosis, Istilah Neurologi

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2. HISTORY OF PRESENTING COMPLAINT
P
Q
R
S
T
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2. HISTORY OF PRESENTING COMPLAINT
Site
Onset
Character
Radiation
Alleviating factors
SOCRATES
Timing
Exacerbating factors
Severity (1-10)

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SITE
Ask about the location of the headache:
“Where is the headache?”
“Can you point to where you experience the headache?”

•Migraines typically present as a unilateral headache
•bilateral headache is most commonly associated with
a tension headache.

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ONSET
Clarify how and when the headache developed:
“Did the headache come on suddenly or gradually?”

“When did the headache first start?”
“How long have you been experiencing the headache?”
•Headaches that have a very sudden onset, reaching their
maximum intensity within seconds are typically associated
with subarachnoid haemorrhage (often described as
‘thunderclap’ in nature).
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CHARACTER
Ask about the specific characteristics of the symptom:
“How would you describe the headache?”

“Is the headache constant or does it come and go?”
•Common descriptors of headaches may include: ‘aching’, ‘throbbing’,
‘pounding’, ‘pulsating’, ‘pressure’, ‘pins and needles’ and ‘stabbing’.
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RADIATION
Ask if the headache moves anywhere else:

“Does the headache spread elsewhere?”
The radiation of a headache to another anatomical

location may help to narrow the differential diagnosis:
•Radiation to the neck is associated with meningitis.
•Radiation to the face may suggest a diagnosis
of trigeminal neuralgia.
•Radiation to the eye occurs in acute closed-angle glaucoma.

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ASSOCIATED SYMPTOMPS
Ask if there are other symptoms which

are associated with the headache:
“Are there any other symptoms that seem associated

with the headache?”
See the key symptoms section below for examples.

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KEY SYMPTOMPS-headache
•Nausea and vomiting: may indicate raised intracranial pressure (e.g. space-occupying
lesion).
•Visual disturbance: may be migraine aura related or secondary to local neural
compression by a space-occupying lesion or haemorrhage.
•Photophobia: most commonly associated with migraine, but also a typical finding in
meningitis which may be chemical (e.g. subarachnoid haemorrhage) or infective (e.g.
bacterial meningitis).
•Neck stiffness: commonly associated with meningitis but may also be due to
musculoskeletal issues of the neck which can also cause headaches (cervicogenic
headache).
•Fever: indicative of an infective process which may be viral (e.g. HSV encephalitis),
bacterial (e.g. cerebral abscess) or fungal (e.g. fungal meningitis).
•Rash: a non-blanching purpuric rash may indicate meningococcal sepsis.
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KEY SYMPTOMPS-headache
•Weight loss: may indicate underlying malignancy (e.g. primary intracranial
tumour or brain metastases).
•Sleep disturbance: headaches which disturb sleep are concerning for serious
underlying pathology (e.g. raised intracranial pressure).
•Temporal region tenderness: associated with temporal arteritis. Patients may
report tenderness when brushing their hair.
•Neurological deficits: these may include motor or sensory deficits, cognitive
symptoms or a reduced level of consciousness. Different patterns of these
symptoms may be present in a wide range of pathology (e.g. migraine, space-
occupying lesions, intracranial infection and intracranial haemorrhage).

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RED FLAG HEADACHE SYMPTOMPS

Headache that :
•wakes them at night
•present on awakening in the morning
•progressively worsens headache triggered or aggravated by coughing, sneezing or
bending down
•with fever and features of meningism
•associated with vomiting
•associated with ataxia (disorders that affect co-ordination, balance and speech)
•associated with change in conscious level or pervasive lethargy
•associated with squint or failure of upward gaze ('sunsetting')
•occurring within 5 days of a head injury

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TIME COURSE
Clarify how the headache has changed over time:
“How has the headache changed over time?”

“Is the headache worse at a particular time of day?”
“In a 30 day period, how many of those days would you experience
the headache on average?”
•Headaches that are worse in the mornings are suggestive

of raised intracranial pressure (e.g. space-occupying lesion).

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Exacerbating or relieving factors

Ask if anything makes the headaches worse or better:
“Does anything seem to trigger or make the headaches worse?”

“Does anything make the headaches better?”
•Triggers for headaches may include caffeine,

excessive codeine use, stress, coughing (suggestive of raised ICP), lying
flat (suggestive of raised ICP) and standing up (suggestive of low ICP).
•Relieving factors for headaches may include hydration, standing
up (suggestive of raised ICP) and lying down (suggestive of low ICP).

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SEVERITY
Assess the severity of the headaches by asking the patient

to grade it on a scale of 0-10:
“On a scale of 0-10, how severe is the headache, if 0 is no pain

and 10 is the worst pain you’ve ever experienced?”
•Ask the patient how the headaches are affecting their daily life. Regular
migraines may make it difficult for the patient to function.

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3. PAST MEDICAL HISTORY

•Medical Conditions • Allergies
Myocardiac infarction • Ask if the patient has
Jaundice any allergies
Tuberculosis • clarify what kind of reaction they
Hypertension had to the substance (e.g. mild
Rheumatic fever rash vs anaphylaxis
Epilepsy • Risk Factors
Asthma
Diabetes
Stroke
Cancer (and treatment if so)
MJ THREADS Ca

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Relevan medical conditions relevant to headache
•Recent head trauma (last three months) • Cancer (any site due to potential of
•Migraine brain metastases)
•Benign intracranial hypertension • Hypertension (risk of malignant
hypertension and haemorrhagic
•Cerebrospinal fluid shunt devices (blocked
or overdraining shunts present with stroke)
headache) • Infectious disease (risk of cerebral
abscess)
•Subarachnoid haemorrhage
• Thrombophilia (increased risk of
•Acute angle-closure glaucoma venous sinus thrombosis)
•Polymyalgia rheumatica (increased risk of • Bleeding disorders (increased risk of
temporal arteritis) intracranial bleeding)

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4. DRUG HISTORY
•Ask if the patient is currently taking any prescribed medications or over-the-
counter remedies:
•“Are you currently taking any prescribed medications or over-the-counter treatments?”
•If the patient is taking prescribed or over the counter
medications, document the medication name, dose, frequency, form and route. Specifically ask
about blood-thinning medications such as aspirin, warfarin and NOACs (e.g. apixaban).
•Ask the patient if they’re currently experiencing any side effects from their
medication:
•“Have you noticed any side effects from the medication you currently take?”
•Ask the patient if they are using any medication to treat their headaches and gather details of
how frequently they are using these medications:
•“Are you currently taking anything to treat the headaches?”
•“How many days in a month are you using the medications?”

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Medication-overuse headache
Medication overuse headache is counterintuitively associated with

medications used for the treatment of headache. Overuse of these
medications is defined as use on more than 15 days of a month.
Medications which are associated with medication-overuse headaches
include:
•Opiates (e.g. codeine and co-codamol)

•Triptans
•NSAIDs (e.g. ibuprofen, aspirin)
•Paracetamol

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5. FAMILY HISTORY
•Ask the patient if there is any family history of headaches, cancer, bleeds on the brain, clotting
disorders or bleeding disorders:
•“Do any of your parents or siblings have problems with headaches such as migraines?”
•“Have your parents or siblings ever been told they have a bleeding or clotting disorder?”
•“Have your parents or siblings ever suffered from bleeds on the brain or cancer?”
•Clarify at what age these diseases developed (disease developing at a younger age is more
likely to be associated with genetic factors):
•“At what age did your father develop the subarachnoid haemorrhage?”
•“When was your mother first diagnosed with lung cancer”
•If one of the patient’s close relatives are deceased, sensitively determine the age at which they
died and the cause of death:
•“I’m really sorry to hear that, do you mind me asking how old your dad was when he died?”
•“Do you remember what medical condition was felt to have caused his death?”

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6. SOCIAL HISTORY
•General social context

•Smoking
•Alcohol
•Recreational drug use
•Occupation

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General Social Context

Explore the patient’s general social context including:
•the type of accommodation they currently reside in (e.g. house, bungalow)
and if there are any adaptations to assist them (e.g. stairlift)
•whether there is a gas fire or boiler and if they have a carbon monoxide
detector (carbon monoxide poisoning can present with headache and
drowsiness)
•who else the patient lives with and their personal support network
•what tasks they are able to carry out independently and what they require
assistance with (e.g. self-hygiene, housework, food shopping)
•if they have any carer input (e.g. twice daily carer visits)

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Smooking
•Record the patient’s smoking history, including the type and amount of
tobacco used.
•Calculate the number of ‘pack-years‘ the patient has smoked for to
determine their risk profile:
•pack-years = [number of years smoked] x [average number of packs
smoked per day]
•one pack is equal to 20 cigarettes
•Smoking is an important risk factor for
both malignancy and thrombotic disease.

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Alcohol
•Record the frequency, type and volume of alcohol consumed on a
weekly basis.
•Alcohol can cause headaches, particularly when used excessively.
Patients may also experience alcohol withdrawal headaches.

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Recreational Drug Use
•Ask the patient if they use recreational drugs and if so determine the
type of drugs used and their frequency of use.
• Headaches can be associated with the use
of cocaine, amfetamine and cannabis.

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Occupation
Ask about the patient’s current occupation:
•Assess the impact of their symptoms on their ability to work.

•Ask about their responsibilities and identify potential exposure to
agents such as carbon monoxide which can cause headaches.

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7. SUMMARY
•Provide a short summary of the history including:

• Name and age of the patient, presenting complaint, relevant
medical history
•Give a differential diagnosis
•Explain a brief investigation and management plan

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SYSTEMS REVIEW
•Cardiovascular: chest pain, palpitations, peripheral oedema, paroxysmal nocturnal
dyspnoea (PND), orthopnoea
•Respiratory: Cough, shortness of breath (and exercise tolerance), haemoptysis,
sputum production, wheeze
•Gastrointestinal: Abdominal pain, dysphagia, heartburn, vomiting, haematemesis,
diarrohea, constipation, rectal bleeding
•Genitourinary: Dysuria, discharge, lower urinary tract symptoms
•Neurological: motor or sensory disturbances, blackouts, visual change, seizure
•Psychiatric: Depression, anxiety
•General review: Weight loss, appetite change, lumps/bumps (nodes), fevers
•Musculoskeletal: chest wall pain, trauma
•Dermatological: rashes, ulcers

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NEUROLOGICAL DISEASES
CLUE-SYMPTOMS

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KEY SYMPTOMPS-stroke
Weakness
•Ask the patient if they have noticed any weakness:
•“Have you noticed any new weakness?”
•Gather more details about the weakness:
•Distribution of the weakness (e.g. right arm, leg and face)
•Severity of the weakness (e.g. subtle, struggling with holding a cup, completely
flaccid)
•Onset and duration of the weakness
•Course of the weakness (i.e. improving, fluctuating, worsening)

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Sensory disturbance
•Ask the patient if they have noticed any changes in sensation:
•“Have you noticed any changes in the sensation of your arms, legs or face?”
•Gather more details about the sensory disturbance:
•Distribution of the sensory disturbance
•Severity of the sensory disturbance (e.g. completely numb, tingling, feeling
slightly different)
•Onset and duration of the sensory disturbance

Visual disturbance
•Ask the patient if they have noticed any changes to their vision:
•“Have you noticed any recent changes to your vision?”
•Gather more details about the visual disturbance:
•Type of visual disturbance (e.g. vertigo, hemianopia, quadrantanopia,
amaurosis fugax)
•Severity of the visual disturbance (e.g. blurred vision, complete loss of vision)
•Onset and duration of the visual disturbance
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Ataxia
Ask the patient if they have noticed any problems with
their balance or coordination:
•“Have you noticed any difficulties with balancing or problems with coordinating
the movement of your arms or legs?”
•Gather more details about the ataxia including:
•Impact on the patient’s ability to walk and use their limbs to carry out tasks.
•Presence of associated symptoms suggestive of a posterior circulation stroke
(e.g. vertigo, nausea).

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Speech disturbance
Ask the patient if they have noticed any changes to their speech:
•“Have you noticed any changes to your speech, such as slurring, problems
getting your words out or issues understanding others?”
•Clarify the type of speech disturbance:
•Expressive dysphasia: “I knew what I wanted to say, but I couldn’t get it out”
•Receptive dysphasia: “I wasn’t able to understand anyone, they were speaking
gibberish”
•Dysarthria: “My speech was really slurred, it sounded like I was drunk”
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Dysphagia
•Ask the patient if they have noticed any dysphagia:
•“Have you experienced any difficulties when trying to swallow food or liquids?”
•Gather more details about the dysphagia including:
•Solid foods: “Are you able to manage solid foods?” “Does it feel like they get
stuck in your gullet?”
•Liquids: “Do you struggle to drink liquids?” “Do you find yourself coughing after
drinking liquids?”
•Dysphagia is common in stroke and if not recognised early it can lead to
aspiration pneumonia and choking episodes.
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Reduced level of consciousness
If a collateral history is possible ask about the patient’s reduced level of

consciousness:
•“When did the patient begin to become more drowsy?”
•Gather more details about the reduced level of consciousness including:
•History of head trauma
•Associated symptoms such as headache, nausea, vomiting and jerking
movements.

NERVOUS SYSTEM
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Central nervous system (CNS)

1. Brain
2. Spinal cord
Peripheral nervous system (PNS)
1. Cranial n. （12 pairs)
2. Spinal n. (31 pairs)
3. Visceral n.
Visceral sensory n.
Visceral motor n.
Sympathetic part
Parasympathetic part
PEMERIKSAAN FISIK
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Status vitalis : Nn.Craniales : Pupil bundar, isokor Ø 2,5 mm

TD = 140/90 mmHg RCL +/+, RCTL +/+ (reaktif)
N = 78 x/mnt (reguler, kuat angkat) Nn. Craniales yang lain : parese N.VII dextra tipe
P = 24 x/mnt (thoracoabdominal) sentral
S = 36,5ºC Motorik :
NPS =0
Status Interna :
Kepala : Anemia (-)/(-), ikterus (-)/(-)
Leher : dalam batas normal
Thoraks : Cor : BJ I/II (N), bising (-), murmur(-)
Pulmo : BP : Vesikuler, ronkhi -/-, wheezing -/-
Abdomen : Hepar dan Lien : tidak teraba membesar
Status Neurologis :
GCS : E4 M6 V5
Fungsi kortikal luhur : fluent(+) comprehensive(+) Sensibilitas : Raba Kasar : Hemihipestesi dextra
repetitive (+) SSO : BAK : Dalam batas normal
Rangsang menings : KK (-), Kernig´s sign (-)/(-) BAB : Dalam batas normal

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WEAKNESS / FOCAL MOTOR DEFICIT

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Medical Research Council (MRC) Grading Power

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WEAKNESS → muscle strenght
Motorik :

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WEAKNESS terminology
•Paresis is the partial / incomplete paralysis (strength 1-5<)

•Paralysis (or –plegia) is complete paralysis (strength 0)

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WEAKNESS-terminology
•Mono-plegia/parese = paralysis of a single limb, usually an arm
•Hemi-plegia/parese = paralysis of the arm, leg, and trunk on the same side
of the body / half body
•Para-plegia/parese = an impairment in motor or sensory function of the
lower extremities
•Tri-plegia/parese = paralysis of three limbs.
•Quadri-plegia/parese = paralysis of all limbs.

•Monoparese
• Monoplegia
Affects one limb,

usually an arm
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•Hemiparese
• Hemiplegia
Affects one side of the

body, including arm, leg, Anamnesis, Topikal Diagnosis, Istilah Neurologi
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•Paraparese
• Paraplegia
Affects simetrical parts of

the body (arms or legs) Anamnesis, Topikal Diagnosis, Istilah Neurologi
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•Tetraparese/
Quadriparese
• Hemiparese duplex
• Tetraplegia/
Quadriplegia
Affects all four limbs Anamnesis, Topikal Diagnosis, Istilah Neurologi

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CNS PNS
UMN symptoms LMN symptoms
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Fasciculations are irregular contractions of a group of muscle fibers

innervated by one axon. Clinically this appears as a small muscle
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• UMN weakness symptoms → topical diagnosis in CNS (brain / spinal

cord)
1. The anterior (ventral) horn cell

2. The peripheral nerve, (ventral and
• LMN weakness symptoms → dorsal nerve roots i.e., radiculopathy
or nerve i.e., neuropathy)
3. The neuromuscular junction
4. The muscle (i.e. myopathy)

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Neurological Diagnosis
1. Clinical Diagnosis
2. Topical Diagnosis
3. Ethiological Diagnosis NEUROANATOMY
FUNCTIONAL NEUROANATOMY
Clinical Diagnosis : Hemiparese dextra
typica
Topical Diagnosis : MCA
Ethiological Diagnosis : NHS
Pathological Diagnosis : Ischemic / Infark Anamnesis, Topikal Diagnosis, Istilah Neurologi
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Know where the clinically important tract cross:
• Tractus corticospinalis (motoris): it crosses in the pyramidal decussation

(medulla)
Lesion below the medulla will cause ipsilateral weakness
Lesion above the medulla will cause contralateral weakness
• Tractus spinothalamicus (pain and temperature) :crosses 2-3 spinal segments

above the entry point into the spine
Lesion will cause loss of sensation contralaterally,starting 2-3
dermatomal segments below the level of the lesion
• Fasciculus gracilis and cuneatus (proprioceptive) : crosses in the medulla

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Traktus kortikospinalis
= mempersarafi ekstremitas superior & inferior
(motoric)
Traktus menyilang di medulla oblongata
Traktus kortikonuklearis
= mempersarafi nervus kranialis (motoric
volunter) → N.V, N.VII, N.IX, N.X, N.XI, N.XII
Traktus ini menyilang di tingkat PONS
• Semua lesi di atas tingkat Medulla →

kelemahan kontralateral
• CONTOH : jika lesi di hemisfer kiri → akan
menyebabkan hemiparese dextra;
sebaliknya jika lesi di hemisfer kanan →
menyebabkan hemiparese sinistra

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Keluhan : lemah separuh badan sebelah kiri, mata kiri
berbayang, mulut
mencong kanan, lidah mencong kiri (jika dijulurkan)
Pemfis : parese N.III dextra, parese N.VII sisnistra, parese N.XII
sinistra
CT Scan kepala : Infark
cerebri
Clinical Diagnosis : Hemiparese sinistra

alternans
Topical Diagnosis : Mesencephalon
Pathological Diagnosis : Ischemic / Infark

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Keluhan : lemah separuh badan sebelah kiri, mulut
mencong kiri
Pemfis : parese N.VII dextra

cerebri

alternans
Topical Diagnosis : Pons

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Keluhan : lemah separuh badan sebelah kiri, lida mencong
kanan (jika
dijulurkan
Pemfis : parese N.XII dextra
cerebri

alternans
Topical Diagnosis : Medulla Oblongata

HEMIPARESE TYPICA
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TONE
Tone is defined as the tension in a muscle at rest. It is the muscle’s response to an outside force,
such as a stretch or change in direction.
•Normal: slight resistance through whole range of movements. Heel will lift minimally off the bed.
•Flaccid / cecreased tone: loss of resistance through movement. Heel does not lift off the bed
when the knee is lifted quickly.
•Increased tone:
•Spasticity : resistance increases suddenly (‘the catch’); the heel easily leaves the bed when the knee is lifted heel
easily leaves the bed when the knee is lifted quickly.
•Lead pipe rigidity : increased through whole range, as if bending a lead pipe
•Cogwheel rigidity : regular intermittent break in tone through whole range
•Gegenhalten or paratonia : patient apparently opposes your attempts to move his limb. In frontal lobe damage
•Special situations
•Myotonia: slow relaxation following action. Demonstrated by asking the patient to make a fist and then release it
suddenly. In myotonia the hand will only unfold slowly.
•Dystonia: maintains posture at extreme of movement with contraction of agonist and antagonist

REFLEXES
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Localizing to the Medulla Oblongata

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Localizing to the Medulla Oblongata

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Localizing to the Pons

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Localizing to the Pons

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Localizing to the Midbrain (Mesencephalon)

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Localizing to the Midbrain (Mesencephalon)

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Cross-sectional spinal cord and vascular anatomy.

Letters denote somatotopic arrangement of fibers
within tracts.
A = arm; L = lumbar area; N = neck; S = sacral area; T =
thoracic area.

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• The spinothalamic tract : drawn on the

opposite side of the cord, to represent
that those nerve fibres crossover in the
cord, → providing contralateral pain
and temperature sensation.
• Dorsal column carries ipsilateral

proprioception/vibration
• Corticospinal tract contains ipsilateral

motor function.

ANTERIOR CORD SYNDROME
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ETIOLOGY
• flexion injury, injury to the anterior spinal
artery. vascular or atherosclerotic disease (elderly),
iatrogenic secondary to cross clamping of the aorta.
SYMPTOMS
• preserved function of their posterior column, →
proprioception and vibration sense is intact / normal
• the anterior portion of their cord is affected → have
bilateral loss of motor function, light touch, pain and
temperature below the level of the lesion.

CENTRAL CORD SYNDROME
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Remember MUD-E
Motor > Sensory
Upper extremity > Lower
extremity
Distal > Proximal
Extension injury

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Cross-sectional spinal cord and vascular anatomy. Letters denote

somatotopic arrangement of fibers within tracts.
A = arm; L = lumbar area; N = neck; S = sacral area; T = thoracic area.

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Ascendens medulare → ruang vertebra naik dan berhenti pd

vertebra L1 dan medulla spinalis lebih pendek dari corpus
vertebra → tinggi segmen tempat keluar saraf spinalis
berbeda dgn corpus vertebra.

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CONTOH
Pria, lemah kedua tungkai, riw. TB (+).
Refleks 3+, refleks patologis babinsky +
Sensoris : hipoestesi dari akral sd. Dermatom Th.10
Kemungkinan Lesi corpus vertebra di area V.Th8

Sentrasi foto :
Foto V. Th.5 – V.L1 AP/Lat, Oblique
Diagnosis : Paraparese UMN / paraprese spastik ec
spondylitis Tb

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Dermatome system
T4 – papilla mammae
T6 – processus xiphoideus
T10 – umbilicus
L1 – inguinal ligament

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• Plexus brachialis = C5-T1

• Plexus lumbalis = T12-L4

TETRAparese
Ekstremitas sup. UMN
Ekstremitas inf. UMN
TETRAparese
Ekstremitas sup. LMN
TETRA
Ekstremitas inf. UMN
PARAparese
UMN
PARAparese LMN
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-opathy
suffix indicating abnormality at the level of the nervous system indicated in the
prefix
•Encephalopathy: abnormality of the brain, refined by adjectives such as focal or diffuse, or metabolic
or toxic.
•Myelopathy: abnormality of the spinal cord, refined by terms indicating aetiology, e.g. radiation,
compressive.
•Plexopathy: abnormality of nerve plexus (brachial or lumbar).
•Peripheral neuropathy: abnormality of peripheral nerves, refined using adjectives such as
diffuse/multifocal, sensory/sensorimotor/motor and acute/chronic.
•Polyradiculopathy: abnormality of many nerve roots, reserved for proximal nerve damage and to
contrast this with length-dependent nerve damage.
•Polyneuropathy: similar term to peripheral neuropathy, but may be used to contrast with
polyradiculopathy.
•Mononeuropathy: abnormality of a single nerve.
•Myopathy: abnormality of muscle.

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• Mononeuropathy → 1 nerve lesion

• Mononeuropathy multiplex → several nerve lessions
• Polyneuropathy → symmetrically nerve lessions on both
side

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-itis
suffix indicating inflammation of the level of the nervous system indicated in the prefix
•Encephalitis: inflammation of the brain. May be refined by adjectives such as focal or

diffuse. May be combined with other terms to indicate associated disease, e.g.
meningo-encephalitis = meningitis and encephalitis.
•Meningitis: inflammation of the meninges.
•Myelitis: inflammation of the spinal cord.
•Myositis: inflammatory disorder of muscle.

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MOTOR, SENSORY, REFLEX FUNCTION OF

LUMBOSACRAL NERVE ROOTS

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The Language Centre
Lesion on the dominant hemisphere
Right-handed Left-handed
95 % (left) 60 % (left)
5 % (right) 30 % (right)
10 % (Bilateral)
Language centre always on the dominant hemisphere

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SPEECH DISORDERS
Dysphonia
a disorder of voice production of sound as air goes through the vocal cords. It results in inability to
produce a normal volume of speech or sound. It is usually recognized during the history taking,
because the sound the voice generates is low, hollow or hoarse.
Dysarthria
an inability to coordinate the movements of tongue, lips and pharynx to articulate or produce
understandable sounds. This makes words sound slow and slurred and leads to difficult to
understand.
Dysphasia / aphasia
a disorder of language production resulting in either a loss of understanding or expression of words
or both. It arises because of damage to the speech areas in the brain in the dominant hemisphere.

Fitriah Handayani
APHASIA
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

APHASIA
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
Fitriah Handayani
•Aphasia: lesion in the dominant (usually left) hemisphere. LOCALIZING APHASIA

•Global aphasia: lesion in the dominant hemisphere affecting
both Wernicke’s and Broca’s areas
•Wernicke’s aphasia: lesion in Wernicke’s area (supramarginal
gyrus of the parietal lobe and upper part of the temporal lobe).
May be associated with FIeld defect.
•Broca’s aphasia: lesion in Broca’s area (inferior frontal gyrus).
May be associated with a hemiplegia.
•Conductive aphasia: lesion in arcuate fasciculus.
•Transcortical sensory aphasia: lesion in the posterior
•Transcortical sensory aphasia: lesion in the posterior parieto-
occipital region.
•Transcortical motor aphasia: incomplete lesion in Broca’s area.
•Nominal aphasia: lesion in the angular gyrus.

Fitriah Handayani
Language disturbance (Aphasia)
Motoric Aphasia
(Broca) Global Aphasia
39
181
9
Conductive Aphasia
Sensoric Aphasia
(Wernicke)
99
Fitriah Handayani
DYSARTHRIA
NORMAL RHYTM
Lower motor neurone:

ABNORMAL RHYTM • Palatal: nasal speech, as with a bad cold
• Tongue: distorted speech, especially letters
•Spastic: slurred, the patient hardly opens the t, s and d
mouth, as if trying to speak from the back of the • Facial: diffculty with b, p, m and w, the
mouth sounds avoided by ventriloquists.
Myasthenic:
•Extrapyramidal: monotonous, without rhythm,
• Muscle fatiguability is demonstrated by
sentences suddenly start and stop
making the patient count.
•Cerebellar: slurred as if drunk, disjointed rhythm • Observe for the development of dysphonia
sometimes with scanning speech (equal emphasis or a lower motor neurone pattern of
on each syllable). dysarthria. (N.B. Myasthenia gravis is a
failure of neuromuscular transmission)

Fitriah Handayani

Fitriah Handayani
ABNORMALITIES OF GAIT

Fitriah Handayani
ETIOLOGI
• Parkinsonian: Parkinson’s disease, major tranquillisers.
• Marche à petits pas: bilateral diffuse cortical dysfunction.
• Scissoring: cerebral palsy, multiple sclerosis, cord
• compression.
• Sensory ataxia: loss of joint position sense (Romberg’s positive).
Causes: peripheral neuropathy, posterior column loss
• Cerebellar ataxia: veers towards side of lesion. cause: drugs (e.g.
phenytoin), alcohol,multiple sclerosis, cerebrovascular disease.
• Waddling gait: proximal myopathies, bilateral congenital
dislocation of the hip.
• Apraxic gait: frontal lobe pathology.causes: normal pressure
hydrocephalus, cerebrovascular disease.
• Hemiplegic: unilateral UMN lesion. Common causes: stroke,
multiple sclerosis.
• Foot drop: Common causes: unilateral—common peroneal palsy,
pyramidal lesion, L5 radiculopathy;bilateral—peripheral
neuropathy.

Fitriah Handayani

Fitriah Handayani
Loss of consciousness
• Ascending reticular activating system
(ARAS) : midbrain, upper pons
• Descending reticular activating system:
lower pons, medulla
• Coma: diencephalic, bihemispheric
◼ Cardiovascular center and respiratory
center
A
B
Consciousness has two easily assessable components: arousal and awareness. Most simply put, arousal implies the appearance of being awake.
• Wakefulness and alertness are maintained by a system of upper brain stem and thalamic neurons, the reticular activating system (RAS), with its
connections to the cerebral hemispheres.
• For this reason, reduced consciousness results from depression of either the RAS or of neuronal activity in both cerebral hemispheres. An intact brain
stem is necessary for arousal to occur, and a patient who looks awake generally has an intact brain stem.

Fitriah Handayani
STATE OF ALTERED CONSIOUSSNESS

Fitriah Handayani
DIFFERENTIATING BRAIN STEM AND HEMISPHERIC COMA

Fitriah Handayani
PHYSICAL SIGNS OF COMA BY LEVEL

Fitriah Handayani
NYSTAGMUS
Nystagmus : is a slow drift in one direction with a fast correction in the

opposite direction. Nystagmus can be :
•Physiological : oculokinetic nystagmus (as seen in people looking out of

the windows of trains)
•Peripheral : due to abnormalities of the vestibular system in the ear, the
eighth nerve nucleus or the nerve itself
•Central : due to abnormalities of the central vestibular connections or
cerebellum
•Retinal : due to the inability to fixate.
Fitriah Handayani
NYSTAGMUS
• Rotatory (or rotary) nystagmus = Pure rotatory nystagmus : central;
peripheral horizontal nystagmus usually has a rotatory horizontal nystagmus
usually has a rotatory component.
• Unusual and rare eye movement abnormalities:
• Opsoclonus: rapid oscillations of the eyes in the horizontal rotatory or vertical direction—
indicates brainstem disease, site uncertain, often a paraneoplastic syndrome
paraneoplastic syndrome
• Ocular bobbing: eyes drifting up and down in the vertical plane—associated with pontine
lesions.
• Vertical nystagmus(rare): indicates brainstem disease.
•Upbeat: indicates upper brainstem. Common causes: demyelination, stroke, Wernicke’s
encephalopathy.
•Downbeat: indicates medullary–cervical junction lesion. Common causes: Arnold–Chiari
malformation, syringobulbia, demyelination.

Fitriah Handayani
NYSTAGMUS
• Horizontal nystagmus (common):
✓Ataxic nystagmus: nystagmus of abducting eye >> adducting eye, associated with internuclear
ophthalmoplegia. Common causes: multiple sclerosis, cerebrovascular disease.
✓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 degeneration, cerebellar tumours.
✓Central vestibular syndromes. Common causes: younger patients-multiple sclerosis); older patients-
vascular disease.
✓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 cerebellar syndrome. Common causes: as central vestibular syndromes.Rarer causes:
tumour or abscess
▪unilateral central vestibular syndrome. Common causes: as central vestibular syndromes.

NEUROMUSCULAR JUNCTION
Fitriah Handayani
•No atrophy
•Normal or reduced tone
•Weakness: patchy i.e. doesn’t conform to an
anatomic structure, fluctuation with time &
exercise i.e. fatigability
•Normal or depressed reflexes
•No sensory changes
•Fatigability of weakness or facilitation of power.
Weakness that gets worse or better with muscle
exertion.
• Look for fluctuating weakness and muscle wasting

• Mysthenia gravis: produces worsening double vision,
ptosis and weakness with exercise
• Lambert-Eaton Syndrome: p roduces improving weakness
with exercise
Muscle
• Look for weakness without
sensory changes
• Proximal weakness without
sensory changes
• Pain in the muscles may be
present
• Myositis is often associated
with skin rash, alopecia, joint
pain and swelling
• Hereditary myopathies are
associated with exercise
intolerance and progrssive
weakness
Fitriah Handayani
MYOPATHY
•Muscle may be normal, wasted or pseudohypertrophied, depending on the disease & time
of presentation
•Weakness, usually more proximal than distal
•Usually proximal rather than distal weakness, but there are distal myopathies. Also, some
myopathies are restricted to certain muscle groups e.g. ocular and pharygeal muscles
•Usually symmetric weakness
•Pure motor weakness without sensory signs
•Tendon reflexes are usually preseved until late in the disease. They may be depressed later
on in the disease. Normal abdominal & plantar reflexes
•Make an attempt to characterize which muscle groups are affected: upper limb shoulders
girdle (deltoids, rotator cuff), lower limb girdle (gluteal, quadreceps), distal muscles (finger
flexors, peroneal muscles), occular muscles, pharyngeal muscles, diaphgram or heart.
•Bowel and bladder sphincters are usually spared.

Fitriah Handayani

Fitriah Handayani
DIFFERENCE BETWEEN BULBAR and PSEUDOBULBAR PALSY

Fitriah Handayani

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ANAMNESIS,

Blok 11. Neuropsikiatri

Fakultas Kedokteran Universitas Tadulako

Positioning: patient sitting in chair approximately a metre away from you.

Anamnesis, Topikal Diagnosis, Istilah Neurologi

2. HISTORY OF PRESENTING COMPLAINT

2. HISTORY OF PRESENTING COMPLAINT

Anamnesis, Topikal Diagnosis, Istilah Neurologi

“Can you point to where you experience the headache?”

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Clarify how and when the headache developed:

“Did the headache come on suddenly or gradually?”

Ask about the specific characteristics of the symptom:

“How would you describe the headache?”

Ask if the headache moves anywhere else:

The radiation of a headache to another anatomical

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Ask if there are other symptoms which

“Are there any other symptoms that seem associated

See the key symptoms section below for examples.

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

RED FLAG HEADACHE SYMPTOMPS

Anamnesis, Topikal Diagnosis, Istilah Neurologi

“How has the headache changed over time?”

•Headaches that are worse in the mornings are suggestive

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Exacerbating or relieving factors

“Does anything seem to trigger or make the headaches worse?”

•Triggers for headaches may include caffeine,

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Assess the severity of the headaches by asking the patient

“On a scale of 0-10, how severe is the headache, if 0 is no pain

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

3. PAST MEDICAL HISTORY

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Relevan medical conditions relevant to headache

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Medication overuse headache is counterintuitively associated with

•Opiates (e.g. codeine and co-codamol)

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

•General social context

Anamnesis, Topikal Diagnosis, Istilah Neurologi

General Social Context

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Recreational Drug Use

Anamnesis, Topikal Diagnosis, Istilah Neurologi

Ask about the patient’s current occupation:

•Assess the impact of their symptoms on their ability to work.

Anamnesis, Topikal Diagnosis, Istilah Neurologi

•Provide a short summary of the history including: