JROOZ REVIEW CENTER CVA/Stroke Defnition: sudden loss of neurological functions caused by an interruption of the blood ow to the brain SVN: -sudden neurologic decits -vascular cause -Non traumatic Epidemiology: old>young Male>female by !"#$ %lac&>white by "$ 'sian>'merican Rik !"#tor: Modiable()*+S,:)ypertension- -.$ lifestyle Smo&ing-"$ )ype )yperc rcho hole lest ster erol olem emia ia// hype hyperl rlip iped edem emia ia 0)1+ 0)1+-- good good cholesterol N- .2-"2/ greater than .2 (why good3 'dheres to +1+4 ta&es it to interstitial space to be absorbed preventing deposition in blood vessels +1+ 5 bad cholesterol N- 622 (low density4 oats in blood and becomes deposited in walls of blood vessels 5 causes atherosclerosis, 7riglycerides 7riglycerides- N- 6.# 6.# 7otal7otal- 6"22 (to-two,
*besity Non Non Modi Modia abl ble e (8'9 (8'9S, S,::
8ace 8ace44 'ge4 'ge4 9rev 9reviou ious s Stro Stro&e &e44 Se$ Se$
Medi Medica call (17) (17)", ",:: 1M1M- #$ 5 vis visco cosi sity ty of of bloo bloodd- set settl tles es// forms aggregate- ris& for development of thrombus 7;'- chance to develop stro&estro&e- #< with with in " days4 2< with in = mos4 =#< with in # years )ematocrit/ Serum ibrinogen- causes generali?ed reduction of cerebral blood ow@ chance of developing blood clot )eart disease (rheumatic heart valvular disease4 endocarditis4 cardiac surgery,- embolic stro&e 'trial ibrillation- #$ increased ris& Etiologi# Cl"if#"tion: ! ;schemia'rteriosclerosis'rteriosclerosis- hardening from loss of elasticity of of bld vessel@ inability to constrict and dilate A'therosclerosisA'therosclerosis- hardening "B to pla Cue formation with accumulation of lipids4 brin4 comple$ carbohydrates and calcium deposits in arterial walls that leads to progressive narrowing of blood vessels
Dommon sites of lesion: (bifurcation4 constrictions4dilations4 angulations of arteries, *rigin of Dommon carotid 'rtery4 MD' (transition from Dommon Darotid or its main bifurcation,4 Eunction of vertebral arteries with the basilar artery a! 7hrombosis(2<,- clot of coagulated blood attached at the site of its formation onset: gradual 7;': #2< undergo 7;' +arger arteries aFtected Severe decits- larger parts *ccurs G night- decrease bld pressure- stasis- thrombus 'therosclerosis'therosclerosis- conducive G night 5slow circadian rhythm b! Hmbolus- "2< Hmbolus- (not refer only to dislodged thrombus, any foreign obIect4 Cuantity of air or gas4 bit of tissue or tumor4 or piece of a thrombus that circulate in the bloodstream until it becomes lodged in a vessel (intra arterial4 cerebral4 fat4 air4 septic, *nset gradual 7;'- (-, 'rteries- smaller- MD aFected- MD' MD origin- heart MD Dardiac Dause: 'trial ibrillation Jstasis (slow or stopped blood ow, Jhypercoagulability Jthrombus formation Jheart valves open Jthrombus e$its Jbloc&s arteries in the brain Manifestations- milder than thrombotic but more severe than lacunar c! +acunar- thrombosis of smallest arteries lacunes- small part of brain supplied by small arteries 'rteries aFected: deep perforating arteries 5 reticulo striatal arteries Dauses: 'therosclerosis " to )tn *nset: gradual but faster than thrombosis7;': thrombosis7;': =#
+"ter"l "! subarachnoid 5 occurs from !ront"l MD' bleeding into sub arachnoid space &"riet"l MD' usually from a saccular or berry Tempor"l MD' aneurysm aFecting usually large O##ipit"l MD' blood vessel@ -closely lin&ed to chronic hypertensionL2/2 chance for rupture =! 'VM 'triovenous Mlaformatio- abN connection bet arteries and vein with no capilliaries in between4 'bnormal vessel undergo progressive dilatation with age and eventually bleed in #2< of the cases!
Monroe elly )ypothesis- if one area of the brain 4 the other contents 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 5 reversible4 complete recovery@ may develop stro&e- #< with in " days4 2< with in = mos4 =#< with in # years Maybe caused by occlusive episodes4 emboli4 reduced cerebral perfusion (" to arrhythmias4 decreased D*4hypotension4 overmedication with hypertensive drugs, -subclavian steal syndrome- caused by occlusion of the subclavian artery pro$imal to the origin of the vertebral artery@ results in reversal of normal blood pressure gradient in the vertebral artery and decreased bld ow distal to the occlusion@ S$ include: (=9Qs, paralysis of the arm (accid,4 pain in mastoid and occipital areas4 pulse (radial, dimished or absent on involved side
"! 8;N1- 8eversible ;schemic Neurologic 1ecits- >" hours but less than 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 present symptoms gets worse, Areview Neuroana !ront"l
Tempor"l
&"riet"l
O##ipit"l
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-edi"l Voluntary Motor 'D' $n 'D' ;ntelligence/ 9D' Dognitive 9D' function Speech Hmotion personality center RSeat of personality Eudgment T conscience +ong term memory
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perception and recognition of auditory stimuli (hearing, Memory (short term, +earning,
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AbrodmanQs area !ront"l primary Motor . pre motor or motor association U- frontal eye eld 424 Eudgment4 insight4 personality 4#- %roccaQs
Tempor"l
4"- 9rimary auditory ""- ernic&eQs
Rig't (r"in in)*ry ;mpulsive4 Cuic& Visual perceptual decits 1iWculty sustaining a movement
Xnaware of impairments (anosognosia,
Sensory lobe 9QarayQtal- all body sensation e$cept for visual and hearing touch4 pressure4 temperature T pain! awareness of the body in space T spatial relation analy?es and relays sensory info to other parts of the brain Kustatory corte$
&"riet"l
=44" 9rimary Sensory #4L Sensory assoc! = Kustatory area = angular
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Visual corte$ perception 4 processin g
O##ipit"l
L- primary visual area U4secondary visual
+e,t (r"in in)*ry Dautious b$4 slow Speech T language (aphasia, 1iWculty planning seCuencing movQt (apra$ia, Very aware of impairments
9oor Iudgment@ inability to self correct 1iWculty processing visual cues 1iWculty with e$pression of emotions4 perception of emotions (aFective agnosia, WERNIC>E
3ROCA
89S
%HHM'N
non-uent H$pressive Motor 'nterior H$ecutive
'n$ious about poor performance
"p'"i"
1iWculty processing verbal cues4 commands 1iWculty with e$pression of positive emotions
8808=7 3ro#"< "re" Synt"#ti# Ap'"i"
Ne*ro"n"tomi#"l Cl"if#"tion / Clini#"l Syndrome AMX+'- MD' X99H84 +ower 'D' ! MD' SYN18*MH- Most common 4.- Dontra )emiplegia XH>+H 9re motor or parietal corte$-limb &inetic apra$ia =44"- contra )emi anesthesia
XH>+H U- loss of conIugate eye movement to opposite side (loo&s towards side 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 enory mod"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 movQt4 cant formulate reCuired motor p rograms 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 567 $"ng*l"r% 897 Apr"i"
+E!T $DO-INANT% Kerstmann syndrome ;deomotor ;deational
&"riet"l lo(e At"i"
;deational
;;7 Werni#ke< "re" Sem"nti#
ernic&eQs 'phasia (uent4 receptive4 sensory4 posterior,
RI42T
1ressing Donstructional Keographic 9erceptual decits- Neglect syndrome4 'nosognosiadenial of neurological decits Spatial disorgani?ation 'Fective agnosia 'musia
%roccaQs 'phasia (non-uent4 e$pressive4 motor4 anterior4 e$ecutive,
'prosodia- monotonous speech 'melodosia- no melody with songs
7ypes of aphasia (Name co u8e 7y4 'D7 %7 ;K, ernic&eQs VS %rocas
Syntactic aphasia- telegraphic speech4 no conIunctions (broccas, Semantic 'phasia- word substitution (wernic&eQs, Neologism- new words 9araphasia- half right words 9honemic- sound li&e Dircumlocution- spea&ing around +ogorrhea-inability to stop spea&ing R)" sa taas (hemiplegia 4 hemianesthesia4 upper e$ more aFected, ang maid (med! mca,4 inaapisia (aphasia,4 inapraa$ia (apra$ia,4 naaagnosia &asi neglected (neglect syndrome, ng amo na Kerman (gerstmann, "! 'D' Dontra h" (hemiplegia4 hemianesthesia, +H> XH Xrinary incontinence 'pra$ia- 1isconnection apra$ia 9roblems with imitation and bimanual tas& lesion to corpus callosum '&inetic mutism (abulia,5 Rcoma vigil alert but totally unresponsive4 no movement4 no sound 9erseveration- same answer on diF! Cuestions or doing the same thing [ Krasping (gegenhalten, and suc&ing ree$ R)" (hemiplegia hemianesthesia, si 'D' na model sa baba (+H more aFected,4 umihi &asi din a napigilan (incontinence,! Nahuli ng pulis4
grasp at suc& nya ang pulis (grasp T suc&ing ree$,! )indi na gustuhan ng pulis4 tinanong siya pabali& bali& ang sagot (perseveration, &aya tinutu&an na sya ng baril- biglang nanigas di na gumalaw di na nagsalita ( a&inetic mutism, =! 9D' =pQs 9hotodecits- visual decits 9ain syndrome- thalamic pain syndrome / 1eIerine 8ousy1eIerine 'raysy 9ast memory decits- inferomedial temporal aFectation 9hoto/visual decits (2A &VD, )omonymous hemianopsia- contralateral-primary visual corte$/ optic radiation (of interna+ D'9SX+H,-MD' %ilateral (calcarine corte$, 'le$ia without agraphia- canQt read but can write 9rosopagnosia- inability to recogni?e familiar faces/ name people Visual agnosia- inability to recogni?e familiar obIects 1yschromatopsia- problems with color identication ! +acunar -"ni,et"tion &*re enory &*re -otor Dy"rt'ri" .it' #l*my '"nd Dy"rt'ri" .it' ,"#i"l .e"kne At"i" .it' 'emip"rei Song- Rlacunar bridge is falling down Anote correction
Verte(r"l Artery Synd1 We(er<
3enedikt<
+o#k in -illi"rd 4*(ler AICA S?CA
Medial basal midbrain 7egmentum of midbrain
%ilateral basal pons +ateral pons Derebellum4 brainstem Derebellum4 brainstem
syndrome4 pain and 7emp of face DN ;;;
)emiplegia
DN ;;;
9ain and 7emp )ypesthesia hyper&inesia (7remor4 Dhorea4 ata$ia4 athetosis, 9roprioception *nly upward ga?e is spared (opposite of parinaud\s, DN V;4V;; hemiplegia
DN V4 V;4 V;; 'ta$ia )ornerQs syndrome
9ain and 7emp of body 9ain and 7emp of body and face
ASong Rtele cranial nerve V9+ nucleus of 7halamus 9ost! +imb of internal Dapsule &?S2ER S@NDRO-E- 9osterolateral thalamus aFected @ active A'nt! limb of internal Dapsule pushing of stronger e$tremity towards hemiparetic side A1orsal 9ons +eads to lat! 9ost! ;mbalance@ Ventral 9ons Daused by severe misperception of body orientation in rel! to gravity@ perceives body as vertical when in fact tilted Udeg! Visual and vestibular intact- able to correct with feedbac& 9oorer rehab outcomes with longer hospital stay@ use of cane incr! pushing@ problems with ambulation4 transfers4 standing and gait #! %rainste m syndromes- a e %e +o Mi- alm em %et +ob Mil D*N78'+'7H8'+ )HM;9+HK;' NE?RO+O4ICA+ RE2A3I+ITATION ;9S;+'7H8'+ D8'N;'+ NH8VH 9'+SY %obath: Neuromuscular 1evelopmental 7reatment4 ma&es use of ALSO KNOWN AS ALTERNATING /CROSSED HEMIPLEGIA normal movement patterns4 discourage use of synergies 8;94 facilitation4 inhibition4&ey points of control RS' %8';NS7HM S78*H ipsinerve4 ipsicerebellar4 ipsi horner contra %runnstrom: movement therapy in hemiplegia@ use of synergy4 then hemi sa body movement sout of synergy and movement combinations H$cept benedi&t contra cerebellar 'ssociated r$n4 homolateral limb syn&inesis4 Syndrome Str*#t*re ipi #ontr" limb synergies4 W"llen(erg< +ateral DN V4;Z4Z 9ain and 7emp raimisteQs phenomenon +"t medillry medulla ata$ia of body SoCueQs phenomenon Syn1/ nystagmus4 Stages of recovery &ICA Synd/ )ornerQ abat4 nott T Voss:9N4 mass movement paterns4 overow
Sherrington:theories of motor control 8oodQs(based on Sherrington and ree$ stimulus model, all motor out put was result of past and present sensory input4 t$ based on sensorimotor learning acilitatoty inhibitory techniCues
Sh! le$ed above 2 9ron sup with elbows e$tended Stage .- isolated It movQts@ ne motor s&ills
-"ni,et"tion
Stage - hand behind bac& Sup /pron with Hlbow e$ 2 Sh! le$ed to 2 Stage #'rm abducted to 2
;nitial accidity@ no voluntary movement
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Hmergence of spasticity4 hyperree$ia4 synergies (mass movement patterns,
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9ea& spasticity@ Voluntary movement possible but only in synergies
1ecline of spasticity and synergie@ voluntary control in isolated Ioint movQts emerging
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;ncreasing voluntary control with out of synergy movQts4 ([,coordination decits
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Dontrol and coordination near normal
