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STROKE

CLINICAL MANIFESTATION

Djadjang Suhana

Department of Neurology

Medical Faculty Padjadjaran University

Bandung

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CEREBROVASCULAR DISEASE :

1. Asymptomatic

2. Focal brain dysfunction

TIA ( Transient ischemic attack )

Stroke

3. Vascular dementia

4. Hypertensive encephalopathy

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STROKE

Definition :

Stroke is brain dysfunction, sadden and very rapid

development of symptoms, focal or global, caused

by only primary cerebrovascular disease which

persistence of the neurologic deficit for longer

than 24 hours or die.

Primary cerebrovascular disease is refere to the

risk factors

Global brain dysfunction is refere tounconsciousness status

TIA if neurologic deficits last completelly less 24

hours

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CLASSIFICATION

I. Based on clinical appearance and temporalprofile

FORMERLY RECENTLY ( CVD III )

TIA

RIND Improving stroke

( Reversible ischemic

neurological deficit )

S.I.E. Worsening stroke

( Strokeinevolution /Progressing stroke )

Completed stroke Stable stroke

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Improving stroke

Complete recovery of neurologic deficit between

24 hours to 3 weeks

Worseningstroke

Progresivity of nneurologic deficit, qualitative and

quantitative, either anamnestic or follow up

50 % of cases in several minutes and hours

Divided in :

Smooth worsening

Steplike worsening

Fluctuating worsening

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II. Based on pathologic appearance ( type of stroke )

Infarction

1. Clinical category 2. Mechanism

- atherothrombotic - Thrombotic

- cardioembolic - embolic

- lacunar - hemodinamic

Intracerebral hemmorhage

Subarachnoidal hemmorhage

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II. Based on vascular location

Carotid system

Vertebrobasilar system

Clinical manifestation

Depend on :

Large of lesion

Vascular lesion

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CLINICAL MANIFESTATION

A. Carotid system

Motor dysfunction

Contralateral hemiparesis

Motor crania nerves and extrimities paresis

ipsilateral

dysarthria

Sensory dysfunction

Contralateral hemihypesthesia

Cranial nerves and extrimities hypesthesia is

ipsilateral

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CLINICAL MANIFESTATION ( cont )

A. Carotid system

Visual disturbances

Contralateral homonymous hemiamianopsia

Amaurosis fugax ( TIA )

Higher cortical dysfunction

Aphasia

Agnosia

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CLINICAL MANIFESTATION ( cont )

B. Vertebrobasiler system Motor dysfunction

Alternating hemiparesis

Motor cranial nerves and extrimities paresis iscontralateral

Dysarthria

Sensory dysfunction

Alternating hemihypesthesia

Cranial nerves and extremities hypesthesia is

contralateral

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CLINICAL MANIFESTATION ( cont )

B. Vertebrobasiler system Visual disturbances

Homonymous hemianopsia

Cortical blindness ( TIA : blackout )

Others

Loss of balance

Vertigo

Diplopia

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INFARCTION STROKE.

MECHANISM OF ISCHEMIC INFARCTION1. Thrombotic

Thrombotic infarction occurs when a thrombus

superimposed on an atherosclerotic plaque

May be precipitated by an abnormality of blood

cloting

2. Embolic

Occlusion of an arteri by an embolus

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MECHANISMS OF ISCHEMIC INFARCTION ( CONT )

3. Hemodynamic

Severe stenosis or occlusion of the proximal

arteries

Collateral compensatory blood flow is inadequate

Global cerebral perfusion is critically decreased

( e.g. cardiac output decreased )

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INFARCTION STROKECLINICAL CATEGORIES

1. Atherothrombotic infarction

Medical historyone or more risk factors

Headache and vomiting are unusual

The onset come rapily, may continue to worse

over hours or days

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INFARCTION STROKE ( cont )

CLINICAL CATEGORIES

1. Atherothrombotic infarction

The trombus is superimposed on the

atherosclerotic plaque

Atherosclerotic plaqueextracranial orintracranial arteries

There are 2 mechanisms :

a. Atherosclerotic plaque enlargestenotic /occlusion

b. Embolism or plaque fragmentsocclusion

( arterytoartery embolus )

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INFARCTION STROKE ( cont )

CLINICAL CATEGORIES

2. Cardioembolic

The onset is rapid, focal deficit completely and mayworsening

Usually at activity

The source of embolus :

Cardiac conditions :

Atrial fibrillation, acute myocardial infarction,congestive heart failure, mitral or aortic valvedisease

Transcardiac conditions ( paradoxical embolus )

Right to left cardiac shunt

The source of clot : peripheral venous

thrombus

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INFARCTION STROKE ( cont )

CLINICAL CATEGORIES2. Cardioembolic

Sometimes clinical finding; isolated

homonymous hemianopsia or isolated aphasia

Brain imaging :

Involve the cortex, commonly in the

distribution of branches of the MCA

Possible haemmorhage infarction

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INFARCTION STROKE ( cont )

CLINICAL CATEGORIES

3. Lacunar infarction

Small lesions, involvement of deep, small,

penetrating arteries

The arteries to branch at 900( e.g.lenticulostriate arteries and brain stem )

The causes are :

Poor collateral connection

Blood obstruction by arterial disease

Thrombus

Embolus

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INFARCTION STROKE ( cont )

CLINICAL CATEGORIES

3. Lacunar infarction

Clinical diagnosis usually rests on :

Brain imaging

Small lesions, 1.5 cm in greatest diameter

Clinical syndrome ( anatomic location )

Pure motor hemiparesis

Pure sensory stroke

Ataxic hemiparesis

Dysarthria clumsy hand syndrome

Prognosis is generally good

Large lesions ( giant lacunes ) are due to multiple

penetrating arteries

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CLINICAL MANIFESTATION

Brain hemorrhage

Approximately 10 % of all stroke

The leading risk factor is hypertension

Other risk factors : aneurysm, AVM,

cavernous angioma, drug abuse ( cocaine,

amphetamines, alcohol ), blood dyscrasia,

anticoagulant therapy, amyloid angiopathy,brain tumor

Unlikely to be preceded by TIAs

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CLINICAL MANIFESTATION ( cont )

Brain hemorrhage

The onset is acute, severe headache,

unconsciousness

The blood pressure usually is elevated atonset

The most common locations of

hypertensive bleeding are basal ganglia,thalamus, lobe of a hemisphere,

cerebellum, pons

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CLINICAL MANIFESTATION ( cont )

Brain hemorrhage

Lobar hemmorrhage ( cortex or subcortical )

is less frequently have a history of

hypertension Lobar hemorrhage in elderly is commonly

caused by amyloid engiopathy

Thalamic hemorrhage oculomotordisturbance such as forced downgaze or

upgaze palsy, unreactive miotic pupils,

convergence paralysis

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CLINICAL MANIFESTATION ( cont )

Brain hemorrhage

Cerebellar hemorrhage ( nucleus dentatus

in cerebellar hemisphere ) :

Disequilibrium, limb ataxia, nausea,vomiting, headache and dizziness

Usually a combination of signs

indicative cerebeller and pontindysfunction : peripheral facial palsy,

nystagmus, miosis, decreased corneal

reflex, abducens palsy

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CLINICAL MANIFESTATION ( cont )

Brain hemorrhage

Primary hemorrhage into the brain stem :

Usually has devastating effect

Small hemorrhage can produce limited

dysfunction

The common site is pons

Clinical diagnosis CTScan to

compare a small hemorrhage with

infarction

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CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH )

The initial bleeding is into the subarachnoidspace

Clinical finding :

The onset is suddenly

Severe headache ( usually dramatic, inseconds to minutes )

Rapid alteration of level of consciousness( recovery in a few minutes )

Vomiting

Younger and less to have hypertension

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CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH ) Usually no focal findings on examination,

sometimes a partial oculomotor nerve

palsy

Meningeal irritation ( stiffneck ) Kernigs

sign or Brudzinskis sign

Subhyaloid hemorrhage

Brain imaging show blood in the

subarachnoid space on the day of the

hemorrhage ( diminishing after the onset )

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CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH )

Lumbar punctureCSF will be bloody,and then xanthochromic within a few

hours after the hemorrhage

Due to rupture of aneurysm ( usuallysaccular aneurysm ), AVMviewed on

CT or MRI and arteriogram / angiogram.

Other cause is neoplasm, 1015 %

cases the cause is unknown

Vasospasm ( as a complication of SAH )

may be occur after 48 hours following the

onset

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RISK FACTORS

A. Major risk factors

1. Hypertension

2. Cardiac diseases

3. Diabetes mellitus

B. Minor risk factors

1. Dyslipidemia

2. Smoking

3. Increase hematocrit, hyperfibrinogenemia,

drug abuse, contraceptive pill, obesity, etc

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COMPLICATIONS

A. Neurologic complications

Brain edema

Hemorrhage infarctin

Vasospasm

Hydrocephalus

Hygroma

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COMPLICATIONS ( cont )

B. Non neurologic complication

1. Due to intracranial process

Increase blood presure

Hyperglicemia

Pulmonary edema

Cardiac disorders

2. Due to immobilitation

Bronchopneumonia

Thrombophlebitis

Bladder infection

Decubitus

Contracture

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