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CEREBRAL INFARCTION The Oxford Community Stroke Project Classification (OCSP, known the Bamford or Oxford Classification) relies primarily on the initial symptoms. Based on extent of the symptoms, the stroke episode is classified as total anterior cerebral infarction (TACI), partial anterior cerebral infarction (PACI), lacunar infarction (LACI), and posterior circulation infarction (POCI). These four entities predict the extent of stroke, the area of the brain affected, the underlying cause, and the prognosis. The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations. On this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation). Brainstem localization of infarction will result in brainstem syndromes, typical: Wallenberg’s syndrome, Weber’s syndrome, Millard-Gubler syndrome, Benedikt syndrome or others. Infarction on the left side of brain, speech will be slurred. Reflexes may also be aggravated as well. Risk factors are the same for atherosclerosis: high blood pressure, diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. In thrombotic ischemic stroke, a thrombus forms and block blood flow. A thrombus forms when the endothelium is activated by a variety of signals to result in platelet aggregation in the artery. This clump of platelets interacts with fibrin to form a platelet

Cerebral Infarctio1

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CEREBRAL INFARCTIONThe Oxford Community Stroke Project Cl!!i"ction #OCSP$ kno%n the Bmford or Oxford Cl!!i"ction& relie! 'rimrily on the initil !ym'tom!( B!ed on extentof the !ym'tom!$ the !troke e'i!ode i! cl!!i"ed ! totl nterior cere)rl infrction #TACI&$ 'rtil nterior cere)rl infrction #PACI&$ lcunr infrction #LACI&$ nd 'o!terior circultion infrction #POCI&( The!e four entitie! 'redict the extent of !troke$ the re of the )rin *ected$ the underlyin+ cu!e$ nd the 'ro+no!i!(The TOAST #Tril of Or+ ,-,./ in Acute Stroke Tretment& cl!!i"ction i! )!ed on clinicl !ym'tom! ! %ell ! re!ult! of further in0e!ti+tion!( On thi! )!i!$!troke i! cl!!i"ed ! )ein+ due to #,& throm)o!i! or em)oli!m due to thero!clero!i! oflr+e rtery$ #/& em)oli!m of crdic ori+in$ #1& occlu!ion of !mll )lood 0e!!el$ #2& other determined cu!e$ #3& undetermined cu!e #t%o 'o!!i)le cu!e!$ no cu!e identi"ed$ or incom'lete in0e!ti+tion&(Brin!tem locli4tion of infrction %ill re!ult in )rin!tem !yndrome!$ ty'icl5 6llen)er+7! !yndrome$ 6e)er7! !yndrome$ 8illrd9:u)ler !yndrome$ Benedikt !yndrome or other!(Infrction on the left !ide of )rin$ !'eech %ill )e !lurred( Re;exe! my l!o )e ++r0ted ! %ell(Ri!k fctor! re the !me for thero!clero!i!5 hi+h )lood 're!!ure$ di)ete! mellitu!$ to)cco !mokin+$ o)e!ity$ nd dy!li'idemi(In throm)otic i!chemic !troke$throm)u! form! nd )lock )lood ;o%( A throm)u! form! %hen the endothelium i! cti0ted )y0riety of !i+nl! to re!ult in 'ltelet ++re+tion in the rtery( Thi! clum' of 'ltelet! interct! %ith ")rin to form'ltelet 'lu+( Thi! 'ltelet 'lu+ +ro%! intothrom)u!$ re!ultin+ in!tenotic rtery( Throm)otic i!chemi cn occur in lr+e or !mll )lood 0e!!el!( In lr+e 0e!!el!$ the mo!t common cu!e! of throm)i re thero!clero!i!nd 0!ocon!triction( In !mll 0e!!el!$ the mo!t common cu!e i! li'ohylino!i!( Li'ohylino!i! i! %hen hi+h )lood 're!!ure nd +in+ cu!e!)uild9u' of ftty hyline mtter in )lood 0e!!el!( Atherom formtion cn l!o cu!e !mll 0e!!el throm)otic i!chemic !troke(An em)olic !troke refer! to the )lock+e of n rtery )y em)olu!$tr0elin+ 'rticle or de)ri! in the rteril )lood!trem ori+intin+ el!e%here( An em)olu! i! mo!t freOR& i!re;ex eye mo0ement tht elicit! eye mo0ement )y !timultin+ the 0e!ti)ulr !y!tem( Thi! re;ex function! to !t)ili4e im+e! on the retin! #in yoked 0i!ion& durin+ hed mo0ement )y 'roducin+ eye mo0ement! in the direction o''o!ite to hed mo0ement$ thu! 're!er0in+ the im+e on the center of the 0i!ul "eld!( 6hen the hed mo0e! to the ri+ht$ the eye! mo0e to the left$ nd 0ice 0er!( Since !li+ht hed mo0ement i! 're!ent ll the time$ the >OR i! 0ery im'ortnt for !t)ili4in+ 0i!ion5 'tient! %ho!e >OR i! im'ired "nd it di@cult to red u!in+ 'rint$ )ecu!e they cnnot !t)ili4e the eye! durin+ !mll hed tremor!$ nd l!o )ecu!e dm+e to the >OR cn cu!e 0e!ti)ulr ny!t+mu!(A/B The >OR doe! not de'end on 0i!ul in'ut( It cn )e elicited )y cloric #hot or cold& !timultion of the inner er$ nd %ork! e0en in totl drkne!! or %hen the eye! re clo!ed( Co%e0er$ in the 're!ence of li+ht$ the "xtion re;ex i! l!o dded to the mo0ement(A1BIn other niml!$ the +r0ity or+n! nd eye! re !trictly connected( A "!h$ forin!tnce$ mo0e! it! eye! )y re;ex %hen it! til i! mo0ed( Cumn! h0e !emicirculr cnl!$ neck mu!cle D!tretchD rece'tor!$ nd theutricle #+r0ity or+n&( Thou+h the !emicirculr cnl! cu!e mo!t of the re;exe! %hich re re!'on!i0e to ccelertion$ the mintinin+ of )lnce i! medited )y the !tretch of neck mu!cle! nd the 'ull of +r0ity on the utricle #otolith or+n& of the inner er(A1BThe >OR h! )oth rottionl nd trn!ltionl !'ect!( 6hen the hed rotte! )out ny xi! #hori4ontl$ 0erticl$ or tor!ionl& di!tnt 0i!ul im+e! re !t)ili4ed )y rottin+ the eye! )out the !me xi!$ )ut in the o''o!ite direction(A2B 6hen the hed trn!lte!$ for exm'le durin+ %lkin+$ the 0i!ul "xtion 'oint i! mintined )y rottin+ +4e direction in the o''o!ite direction$ )y n mount tht de'end! on di!tnce(A3Circuit[edit]The VOR is ultimately driven by signals from the vestibular apparatus in the inner ear. The semicircular canals detect head rotation and drive the rotational VOR, whereas the otoliths detect head translation and drive the translational VOR. The main "direct path" neuralcircuit for the horiontal rotational VOR is fairly simple. !t starts in the vestibular system, where semicircular canals get activated by head rotation and send their impulses via the vestibular nerve "cranial nerve V!!!# through $carpa%s ganglion and end in thevestibular nuclei in the brainstem. &rom these nuclei, fibers cross to the contralateral cranial nerve V! nucleus "abducens nucleus#. There they synapse with ' additional pathways. One pathway pro(ects directly to the lateral rectus of eye via the abducens nerve. )nother nerve tract pro(ects from the abducens nucleus by the medial longitudinal fasciculus to the contralateral oculomotor nucleus, which containsmotorneurons that drive eye muscle activity, specifically activating the medial rectus muscle of the eye through the oculomotor nerve.)nother pathway "not in picture# directly pro(ects from the vestibular nucleus through the ascending tract of *ieters to the ipsilateral medial rectus motoneuron. !n addition there are inhibitory vestibular pathways to the ipsilateral abducens nucleus. +owever no direct vestibular neuron to medial rectus motoneuron pathway e,ists.[-]$imilar pathways e,ist for the vertical and torsional components of the VOR.!n addition to these direct pathways, which drive the velocity of eye rotation, there is an indirect pathway that builds up the position signal needed to prevent the eye from rolling bac. to center when the head stops moving. This pathway is particularly important when the head is moving slowly, because here position signals dominate over velocity signals. *avid ). Robinson discovered that the eye muscles re/uire this dual velocity0position drive, and also proposed that it must arise in the brain by mathematically integrating the velocity signal and then sending the resulting position signal to the motoneurons. Robinson was correct1 the %neural integrator% for horiontal eye position was found in the nucleus prepositus hypoglossi[2] in the medulla, and the neural integrator for vertical and torsional eye positions was found in the interstitial nucleus of 3a(al[4] in the midbrain. The same neural integrators also generate eye position for other con(ugate eye movements such as saccades and smooth pursuit.Excitatory example[edit]&or instance, if the head is turned cloc.wise as seen from above, then e,citatory impulses are sent from the semicircular canal on the right side via thevestibular nerve "cranial nerve V!!!# through $carpa%s ganglion and end in the right vestibular nuclei in the brainstem. &rom this nucleie,citatory fibers cross to the left abducens nucleus. There they pro(ect and stimulate the lateral rectus of the left eye via the abducens nerve. !n addition, by the medial longitudinal fasciculus and oculomotor nuclei, they activate the medial rectus muscles on the right eye. )s a result, both eyes will turn countercloc.wise.&urthermore, some neurons from the right vestibular nucleus directly stimulate the right medial rectus motoneurons, and inhibits the right abducens nucleus.Speed[edit]The vestibulo0ocular refle, needs to be fast1 for clear vision, head movement must be compensated almost immediately5 otherwise, vision corresponds to a photograph ta.en with a sha.y hand. To achieve clear vision, signals from the semicircular canals are sent as directly as possible to the eye muscles1 the connection involves only three neurons, and is correspondingly called the three neuron arc. 6sing these direct connections, eye movements lag the head movements by less than 78 ms,[9] and thus the vestibulo0ocular refle, is one of the fastest refle,es in the human body.Gain[edit]The "gain" of the VOR is defined as the change in the eye angle divided by the change in the head angle during the head turn. !deally the gain of the rotational VOR is 7.8. The gain of the horiontal and vertical VOR is usually close to 7.8, but the gain of the torsional VOR "rotation around the line of sight# is generally low.[:] The gain of the translational VOR has to be ad(usted for distance, because of the geometry of motion paralla,. ;hen the head translates, the angular direction of near targets changes faster than the angular direction of far targets.[