STROKE CLINICAL MANIFESTATION

Djadjang Suhana

Department of Neurology Medical Faculty Padjadjaran University Bandung

CEREBROVASCULAR DISEASE : 1. Asymptomatic

2. Focal brain dysfunction

TIA ( Transient ischemic attack ) Stroke 3. Vascular dementia 4. Hypertensive encephalopathy

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 to unconsciousness status TIA if neurologic deficits last completelly less 24 hours
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CLASSIFICATION I. Based on clinical appearance and temporal profile

FORMERLY

RECENTLY ( CVD III )

TIA RIND Improving stroke

( Reversible ischemic neurological deficit )

S.I.E. ( Stroke in evolution / Progressing stroke )

Worsening stroke

Completed stroke

Stable stroke

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 - atherothrombotic - cardioembolic 2. Mechanism - Thrombotic - embolic

- lacunar
Intracerebral hemmorhage Subarachnoidal hemmorhage

- hemodinamic

II.

Based on vascular location Carotid system Vertebrobasilar system

Clinical manifestation

Depend on :
Large of lesion Vascular lesion

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

CLINICAL MANIFESTATION ( cont ) B. Vertebrobasiler system Motor dysfunction Alternating hemiparesis Motor cranial nerves and extrimities paresis is contralateral 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 INFARCTION 1. 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 STROKE CLINICAL CATEGORIES 1. Atherothrombotic infarction Medical history one 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 plaque extracranial or intracranial arteries There are 2 mechanisms : a. Atherosclerotic plaque enlarge stenotic / occlusion b. Embolism or plaque fragments occlusion ( artery to artery embolus )
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INFARCTION STROKE ( cont )

CLINICAL CATEGORIES
2. Cardioembolic The onset is rapid, focal deficit completely and may worsening Usually at activity The source of embolus : Cardiac conditions : Atrial fibrillation, acute myocardial infarction, congestive heart failure, mitral or aortic valve disease Transcardiac conditions ( paradoxical embolus ) Right to left cardiac shunt The source of clot : peripheral venous thrombus
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INFARCTION STROKE ( cont ) CLINICAL CATEGORIES 2. 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 at onset 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 oculomotor disturbance 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 pontin dysfunction : 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 CT Scan to compare a small hemorrhage with infarction

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CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH )

The initial bleeding is into the subarachnoid space Clinical finding : The onset is suddenly

Severe headache ( usually dramatic, in seconds 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 puncture CSF will be bloody, and then xanthochromic within a few hours after the hemorrhage Due to rupture of aneurysm ( usually saccular aneurysm ), AVM viewed on CT or MRI and arteriogram / angiogram. Other cause is neoplasm, 10 15 % 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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