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JROOZ REVIEW CENTERCVA/Stroke

Defnition:sudden loss of neurological functions caused by aninterruption of the blood ow to the brainSVN: -sudden neurologic decits -vascular cause -Nontraumatic

Epidemiology: old>youngMale>female by !"#$%lac&>white by "$'sian>'merican

Rik !"#tor:Modiable()*+S,:)ypertension- -.$

lifestyleSmo&ing-"$)ypercholesterolemia/ hyperlipedemia 0)1+- good

cholesterol N- .2-"2/ greater than .2 (why good3 'dheres to +1+4ta&es it to interstitial space to be absorbed preventing deposition inblood vessels

+1+ 5 bad cholesterol N- 622 (low density4 oats in blood andbecomes deposited in walls of blood vessels 5 causesatherosclerosis,

7riglycerides- N- 6.# 7otal- 6"22 (to-two,

*besity

Non Modiable (8'9S,: 8ace4 'ge4 9revious Stro&e4 Se$

Medical (17)",: 1M- #$ 5 viscosity of blood- settles/forms aggregate- ris& for development of thrombus7;'- chance to develop stro&e- #< with in " days4 2< within = mos4 =#< with in # years)ematocrit/ Serum ibrinogen- causes generali?ed reductionof cerebral blood ow@ chance of developing blood clot)eart disease (rheumatic heart valvular disease4 endocarditis4cardiac surgery,- embolic stro&e

'trial ibrillation- #$ increased ris&

Etiologi# Cl"if#"tion:! ;schemia-'rteriosclerosis- hardening from loss of elasticity of of bld vessel@

inability to constrict and dilate

A'therosclerosis- hardening "B to plaCue formation with accumulationof lipids4 brin4 comple$ carbohydrates and calcium deposits in arterialwalls that leads to progressive narrowing of blood vessels

Dommon sites of lesion: (bifurcation4 constrictions4dilations4angulations of arteries,

*rigin of Dommon carotid 'rtery4 MD' (transition fromDommon Darotid or its main bifurcation,4 Eunction of vertebralarteries with the basilar artery

a! 7hrombosis(2

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"! subarachnoid 5 occurs frombleeding into sub arachnoid spaceusually from a saccular or berryaneurysm aFecting usually largeblood vessel@-closely lin&ed to chronic hypertensionL2/2 chance for rupture=! 'VM 'triovenous Mlaformatio- abN connection bet arteries andvein with no capilliaries in between4 'bnormal vessel undergoprogressive dilatation with age and eventually bleed in #2< of the

cases!Monroe elly )ypothesis- if one area of the brain 4 the othercontents should O to give way for the in pressure!in ;D9- Ocerebral perfusion J altered level of consciousness

Tempor"l Cl"if#"tion: $time% TRCS! 7;'-7ransient ;schemic 'ttac&sP S$ are less than " hours 5reversible4 complete recovery@ may develop stro&e- #< with in " days42< with in = mos4 =#< with in # yearsMaybe caused by occlusive episodes4 emboli4 reduced cerebralperfusion (" to arrhythmias4 decreased D*4hypotension4overmedication with hypertensive drugs,

-subclavian steal syndrome- caused by occlusion of the subclavianartery pro$imal to the origin of the vertebral artery@ results inreversal of normal blood pressure gradient in the vertebral arteryand decreased bld ow distal to the occlusion@S$ include: (=9Qs,paralysis of the arm (accid,4 pain in mastoid and occipital areas4pulse (radial, dimished or absent on involved side

"! 8;N1- 8eversible ;schemic Neurologic 1ecits- >" hours but lessthan L days4 temporary decits with longer recovery time than& 7;'=! Domplete stro&e- stable4 symptoms does not get worse over time! Stro&e in Hvolution- unstable4 progressive S$ (Anew S$ or presentsymptoms gets worse,

Areview Neuroana!ront"l Tempor"l &"riet"l O##ipit"l

Voluntary Motor$n

;ntelligence/Dognitivefunction

Speech

Hmotion

personality

center RSeat ofpersonality Eudgment T

conscience +ong term

memory

perception andrecognitionof auditorystimuli(hearing,

Memory (shortterm,

+earning,

Sensory lobe 9QarayQtal- all

body sensatione$cept for visualand hearing

touch4 pressure4temperature Tpain!

awareness of the

body in space Tspatial relation

analy?es andrelays sensoryinfo to otherparts of the brain

Kustatory corte$

Visualcorte$

perception4processing

AbrodmanQs area!ront"l Tempor"l &"riet"l O##ipit"l

primaryMotor. pre motor ormotorassociationU- frontal eyeeld

424Eudgment4insight4personality4#- %roccaQs

4"- 9rimaryauditory""- ernic&eQs

=44" 9rimarySensory#4L Sensoryassoc!= Kustatoryarea= angular

L- primaryvisual areaU4-secondaryvisual

Rig't (r"in in)*ry +e,t (r"in in)*ry

;mpulsive4 Cuic& Dautious b$4 slow

Visual perceptual decits Speech T language (aphasia,

1iWculty sustaining a movement 1iWculty planning seCuencingmovQt (apra$ia,

Xnaware of impairments(anosognosia, Very aware of impairments

"

+"ter"l -edi"l

!ront"l MD' 'D'&"riet"l MD' 'D'Tempor"l MD' 9D'O##ipit"l MD' 9D'

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9oor Iudgment@ inability to selfcorrect

'n$ious about poor performance

1iWculty processing visual cues 1iWculty processing verbal cues4commands

1iWculty with e$pression ofemotions4 perception of emotions(aFective agnosia,

1iWculty with e$pression ofpositive emotions

Ne*ro"n"tomi#"l Cl"if#"tion /Clini#"l Syndrome

AMX+'- MD' X99H84 +ower'D'! MD' SYN18*MH- Most common4.- Dontra )emiplegia XH>+H9re motor or parietal corte$-limb&inetic apra$ia=44"- contra )emi anesthesia

XH>+HU- loss of conIugate eye movement to opposite side (loo&s towardsside of lesion4 away from hemi side,'9)'S;'- ;mpairment of language comprehension4 formulation and use'KN*S;'- inability to recogni?e a familiar obIect .it' one enorymod"lity $i*"l0 t"#tile0 "*ditory0 et#1%'98'Z;'- inability to perform learned movements@ (-,tas&conceptuali?ation@ (-,tas& seCuencing@ no idea how to do the movQt4cant formulate reCuired motor programs Ide"tion"l- (-,movQts on command@ (-, automatic movements@

Ideomotor- (-,movtQs on command4 ([, automatic movQts@habitual tas&s @ ([,perseveration=424 9'87 * H8N;DHQS

AREAS O! T2E

3RAIN

+E!T

$DO-INANT%

RI42T

567 $"ng*l"r% Kerstmannsyndrome

897 Apr"i" ;deomotor;deational

1ressingDonstructionalKeographic

&"riet"l lo(eAt"i"

;deational 9erceptual decits- Neglectsyndrome4 'nosognosia-denial of neurologicaldecits Spatialdisorgani?ation

;;7 Werni#ke

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grasp at suc& nya ang pulis (grasp T suc&ing ree$,! )indi nagustuhan ng pulis4 tinanong siya pabali& bali& ang sagot(perseveration, &aya tinutu&an na sya ng baril- biglang nanigas di nagumalaw di na nagsalita (a&inetic mutism,

=! 9D'=pQs 9hotodecits- visual decits

9ain syndrome- thalamic pain syndrome / 1eIerine 8ousy-1eIerine 'raysy

9ast memory decits- inferomedial temporal aFectation

9hoto/visual decits (2A &VD,)omonymous hemianopsia- contralateral-primary visual corte$/

optic radiation (of interna+ D'9SX+H,-MD'%ilateral (calcarine corte$,

'le$ia without agraphia- canQt read but can write9rosopagnosia- inability to recogni?e familiar faces/ name

peopleVisual agnosia- inability to recogni?e familiar obIects1yschromatopsia- problems with color identication

! +acunar-"ni,et"tion

&*re enory V9+ nucleus of 7halamus&*re -otor 9ost! +imb of internal DapsuleDy"rt'ri" .it' #l*my '"nd A'nt! limb of internal DapsuleDy"rt'ri" .it' ,"#i"l .e"kne A1orsal 9onsAt"i" .it' 'emip"rei Ventral 9onsSong- Rlacunar bridge is falling down Anote correction

#! %rainstem syndromes- a e %e +o Mi- alm em %et +ob Mil D*N78'+'7H8'+ )HM;9+HK;' ;9S;+'7H8'+ D8'N;'+ NH8VH 9'+SY ALSO KNOWN AS ALTERNATING /CROSSED HEMIPLEGIA

RS' %8';NS7HM S78*H ipsinerve4 ipsicerebellar4 ipsi horner contrahemi sa bodyH$cept benedi&t contra cerebellar

Syndrome Str*#t*re ipi #ontr"

W"llen(erg

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Sherrington:theories of motor control8oodQs(based on Sherrington and ree$ stimulus model, all motor output was result of past and present sensory input4 t$ based onsensorimotor learning

acilitatoty inhibitory techniCues

Stage - hand behind bac&Sup /pron with Hlbow e$ 2

Sh! le$ed to 2Stage #- 'rm abducted to 2

Sh! le$ed above 29ron sup with elbows e$tended

Stage .- isolated It movQts@ ne motor s&ills

#

-"ni,et"tion

;nitial accidity@ no voluntary movement

" Hmergence of spasticity4 hyperree$ia4 synergies (massmovement patterns,

= 9ea& spasticity@ Voluntary movement possible but only insynergies

1ecline of spasticity and synergie@ voluntary control in isolatedIoint movQts emerging

# ;ncreasing voluntary control with out of synergy movQts4([,coordination decits

. Dontrol and coordination near normal