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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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