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Djadjang Suhana
!. Focal "rain dysfunction #$ % #ransient ischemic attac& ' Stro&e (. )ascular dementia *. +ypertensive encephalopathy
STROKE Definition , Stro&e is "rain dysfunction- sadden and very rapid development of symptoms- focal or glo"al- caused "y only primary cere"rovascular disease .hich persistence of the neurologic deficit for longer than !* hours or die. Primary cere"rovascular disease is refere to the ris& factors /lo"al "rain dysfunction is refere to unconsciousness status #$ if neurologic deficits last completelly less !* hours 3
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2orsening stro&e
Improving s ro!" 5omplete recovery of neurologic deficit "et.een !* hours to ( .ee&s #ors"nings ro!" Progresivity of nneurologic deficit- 6ualitative and 6uantitative- either anamnestic or follo. up 78 9 of cases in several minutes and hours Divided in , Smooth .orsening Stepli&e .orsening Fluctuating .orsening 5
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Based on pathologic appearance % type of stro&e ' $nfarction $% C&ini'(& '( "gor) : atherothrom"otic : cardioem"olic : lacunar *% M"'+(nism : #hrom"otic : em"olic : hemodinamic
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CLINICAL MANIFESTATION . 5arotid system Motor dysfunction 5ontralateral hemiparesis Motor crania nerves and e<trimities paresis ipsilateral dysarthria Sensory dysfunction 5ontralateral hemihypesthesia 5ranial nerves and e<trimities hypesthesia is ipsilateral 8
CLINICAL MANIFESTATION ( cont ) . 5arotid system )isual distur"ances 5ontralateral homonymous hemiamianopsia maurosis fuga< % #$ '
Motor cranial nerves and e<trimities paresis is contralateral Dysarthria Sensory dysfunction lternating hemihypesthesia
CLINICAL MANIFESTATION ( cont ) B. )erte"ro"asiler system )isual distur"ances +omonymous hemianopsia 5ortical "lindness % #$ , "lac&out ' =thers ;oss of "alance )ertigo Diplopia
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INFARCTION STROKE% MEC,ANISM OF ISC,EMIC INFARCTION 1. #hrom"otic #hrom"otic infarction occurs .hen a throm"us superimposed on an atherosclerotic pla6ue May "e precipitated "y an a"normality of "lood cloting !. 1m"olic =cclusion of an arteri "y an em"olus
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MEC,ANISMS OF ISC,EMIC INFARCTION ( CONT ) (. +emodynamic Severe stenosis or occlusion of the pro<imal arteries 5ollateral compensatory "lood flo. is inade6uate /lo"al cere"ral perfusion is critically decreased % e.g. cardiac output decreased '
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INFARCTION STROKE CLINICAL CATE-ORIES 1. therothrom"otic infarction Medical history one or more ris& factors +eadache and vomiting are unusual #he onset come rapily- may continue to .orse over hours or days
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INFARCTION STROKE ( cont ) CLINICAL CATE-ORIES 1. therothrom"otic infarction #he trom"us is superimposed on the atherosclerotic pla6ue therosclerotic pla6ue e<tracranial or intracranial arteries
INFARCTION STROKE ( cont ) CLINICAL CATE-ORIES !. 5ardioem"olic #he onset is rapid- focal deficit completely and may .orsening Usually at activity #he source of em"olus , 5ardiac conditions , trial fi"rillation- acute myocardial infarctioncongestive heart failure- mitral or aortic valve disease
#ranscardiac conditions % parado<ical em"olus ' 0ight to left cardiac shunt #he source of clot , peripheral venous throm"us 16
INFARCTION STROKE ( cont ) CLINICAL CATE-ORIES !. 5ardioem"olic Sometimes clinical finding> isolated homonymous hemianopsia or isolated aphasia Brain imaging , $nvolve the corte<- commonly in the distri"ution of "ranches of the M5 Possi"le haemmorhage infarction
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INFARCTION STROKE ( cont ) CLINICAL CATE-ORIES (. ;acunar infarction Small lesions- involvement of deep- smallpenetrating arteries #he arteries to "ranch at ?88 % e.g. lenticulostriate arteries and "rain stem ' #he causes are , Poor collateral connection Blood o"struction "y arterial disease #hrom"us 1m"olus 18
INFARCTION STROKE ( cont ) CLINICAL CATE-ORIES (. ;acunar infarction 5linical diagnosis usually rests on , Brain imaging Small lesions- < 1.7 cm in greatest diameter 5linical syndrome % anatomic location ' Pure motor hemiparesis Pure sensory stro&e ta<ic hemiparesis Dysarthria clumsy hand syndrome Prognosis is generally good ;arge lesions % giant lacunes ' are due to multiple 19 penetrating arteries
#he leading ris& factor is hypertension =ther ris& factors , aneurysm- )Mcavernous angioma- drug a"use % cocaineamphetamines- alcohol '- "lood dyscrasiaanticoagulant therapy- amyloid angiopathy"rain tumor Unli&ely to "e preceded "y #$ s
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CLINICAL MANIFESTATION ( cont ) Br(in +"morr+(g" #he onset is acute- severe headacheunconsciousness #he "lood pressure usually is elevated at onset #he most common locations of hypertensive "leeding are "asal gangliathalamus- lo"e of a hemispherecere"ellum- pons
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CLINICAL MANIFESTATION ( cont ) Br(in +"morr+(g" ;o"ar hemmorrhage % corte< or su"cortical ' is less fre6uently have a history of hypertension ;o"ar hemorrhage in elderly is commonly caused "y amyloid engiopathy #halamic hemorrhage oculomotor distur"ance such as forced do.nga@e or upga@e palsy- unreactive miotic pupilsconvergence paralysis
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CLINICAL MANIFESTATION ( cont ) Br(in +"morr+(g" 5ere"ellar hemorrhage % nucleus dentatus in cere"ellar hemisphere ' , Dise6uili"rium- lim" ata<ia- nauseavomiting- headache and di@@iness Usually a com"ination of signs indicative cere"eller and pontin dysfunction , peripheral facial palsynystagmus- miosis- decreased corneal refle<- a"ducens palsy
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CLINICAL MANIFESTATION ( cont ) Br(in +"morr+(g" Primary hemorrhage into the "rain stem , Usually has devastating effect Small hemorrhage can produce limited dysfunction #he common site is pons 5linical diagnosis 5# 3 Scan to compare a small hemorrhage .ith infarction
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CLINICAL MANIFESTATION ( cont ) S./(r('+noi0 +"morr+(g" ( SA, ) #he initial "leeding is into the su"arachnoid space 5linical finding , #he onset is suddenly Severe headache % usually dramatic- in seconds to minutes ' 0apid alteration of level of consciousness % recovery in a fe. minutes ' )omiting Aounger and less to have hypertension 25
CLINICAL MANIFESTATION ( cont ) S./(r('+noi0 +"morr+(g" ( SA, ) Usually no focal findings on e<aminationsometimes a partial oculomotor nerve palsy Meningeal irritation % stiffnec& ' BernigCs sign or Brud@ins&iCs sign Su"hyaloid hemorrhage Brain imaging sho. "lood in the su"arachnoid space on the day of the hemorrhage % diminishing after the onset '
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CLINICAL MANIFESTATION ( cont ) S./(r('+noi0 +"morr+(g" ( SA, ) ;um"ar puncture 5SF .ill "e "loodyand then <anthochromic .ithin a fe. hours after the hemorrhage Due to rupture of aneurysm % usually saccular aneurysm '- )M vie.ed on 5# or M0$ and arteriogram 4 angiogram. =ther cause is neoplasm- 18 3 17 9 cases the cause is un&no.n )asospasm % as a complication of S + ' may "e occur after *D hours follo.ing the 27 onset
RISK FACTORS A% M(1or ris! 2(' ors 1. +ypertension !. 5ardiac diseases (. Dia"etes mellitus A% Minor ris! 2(' ors 1. Dyslipidemia !. Smo&ing (. $ncrease hematocrit- hyperfi"rinogenemiadrug a"use- contraceptive pill- o"esity- etc
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COM3LICATIONS A% N".ro&ogi' 'omp&i'( ions Brain edema +emorrhage infarctin )asospasm +ydrocephalus +ygroma
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COM3LICATIONS ( cont ) B% Non 4 n".ro&ogi' 'omp&i'( ion $% D." o in r('r(ni(& pro'"ss $ncrease "lood presure +yperglicemia Pulmonary edema 5ardiac disorders *% D." o immo/i&i ( ion Bronchopneumonia #hrom"ophle"itis Bladder infection Decu"itus 5ontracture
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