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CERBROVASCULAR ACCIDENT

CERBROVASCULAR ACCIDENT. Case 1 : A 56 years old man diabetic and HT ; presents to EU with sudden onset right sided weakness and aphasia of one hour duration .no loss consciousness , mild headache .He is controlling sphincter

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CERBROVASCULAR ACCIDENT

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  1. CERBROVASCULAR ACCIDENT

  2. Case 1 : A 56 years old man diabetic and HT ; presents to EU with sudden onset right sided weakness and aphasia of one hour duration .no loss consciousness , mild headache .He is controlling sphincter • On exam: general: un remarkable apart of irregular pulse. BP= 160/100 • Medical : abnormal heart sound?? • Neurological : aphasic but conscious • Cranial R. facial upper motor palsy • No meningeal signs • Motor : Right sever hemi paresis grade 2 in UL and grade 3 in LL • Approach • Emergency ----------------?? See guideline in EU • Which system? most likely diagnosis • Where is lesion upper or lower ? Localization. • Ischemia or bleeding • Anterior circulation or posterior circulation • Causes of CVA?

  3. STROKE • It is third common cause of death after cancer and IHD in developed countries, the annual incidence of stroke above the age of 45 years in UK is about 350/100 000. • CVA: is a clinical syndrome characterized by acute onset *N. deficit resulting from disturbance in cerebral circulation*. • How we can understand CVA?

  4. anterior, posterior & middlecerebral arteries

  5. Circle of Willis

  6. Stroke in young • Stroke affecting old age ,common cause is atherosclerosis that progressed with aging, but if the CVA occurs under the age of 40 years you have to think about other causes and intensive investigation needed to know the causes: • Accelerated atherosclerosis. HT, DM---- • Embolic from cardiac origin or carotid dissection • Vasculitis like SLE ,APL syndrome------ • Others ,like thrombophilia ,congenital malformation :AVM, ------and idiopathic

  7. stroke • Pathological Classification of cerebral vascular accidents • focal cerebral ischemia (the most often) • (thrombosis & embolism) • 2.intracerebral hemorrhage • 3. Subarachnoid hemorrhage –neurosurg.

  8. CLASSIFICATION OF STROKE SYNDROME • Pathological classification 1-ischemic (80-85%) . can belarge V.D :80% of cases (thrombosis &embolic) which affect medium and large size aa . small VD: 20% of ischemic stroke called lacunar stroke which is due to lipohyalinotic degeneration of small penetrating aa seen mainly in HT. 2-hemorrhagic(15-20%) which is either hypertensive bleed due to high BP ,seen at 4 (now 5) common sites :basal ganglia ,thalamus, cerebellum and pons. Less commonly Sub cortical or lobar. non HT bleed: SAH, bleeding tendency, drug therapy, traumatic and amyloid angiopathy. Q: How you can differentiate between H. versus I. stroke? clinically • CLINICAL CLASSIFICATION of ischemia: in term of duration and residue of ND 1.Transient Ischemic Attack?----- it is a major risk factor for disabling stroke ,about 13 folds increase as a risk of having stroke in next year. 2-Reversible Ischemic ND(RIND)?---- 3-Completed Stroke?----- 4-Stroke in –evolution or progressing stroke?---

  9. Aetiology ( acute ischemic stroke) A- vascular • 1-atherosclerosis: common cause of ischemic stroke affecting extra-cranial aa in the neck and at the base of brain. The pathogenesis involving injury endothelium accumulation off cholesterol (LDLP) ------fatty streaks -----fibrous plague (lipid laden foam cell)+ platelets -----atheromatous lesion which carry risk of thrombus formation especially if ulcerated. What are the factors that accelerate the atherosclerosis? Quiz? • 2-fibromuscular dysplasia: traumatic or congenital segmental non-atherogenic thinning of tunica media with fragmentation of elastica lamina alternating with ring of muscle hyperplasia within media ,female > male ,ECBV>ICBV ,ICA>VA and usually bilateral . • 3-inflammatory disorder: giant cell arteritis SLE&APL syndrome PA nodosa granulomatous angiitis syphilis arteritis AIDS-direct OR by opportunistic infection or endocarditis

  10. 4-carotid or vertebral artery dissection: • can be spontaneous or traumatic-----pain in head and • neck+ND TIA or stroke • 5- lacunar stroke: pure sensory, motor ,ataxic H. ,and clumsy hand syndrome. • 6-drug abuse: cocaine and amphetamine mainly causing bleeding (may be within hours of intake from vasospasm rupture or vasculitis), stroke or SAH are less common .Heroin is causing embolic stroke from endocarditis. • 7-moya –moya disease:=progressive multiple IC arterial occlusion: • there is bilateral narrowing of ICA as primary (idiopathic-genetic) or secondary as may be seen in sickle cell A or basal meningitis. • Diagnosis : typical angiographic pattern of collateral circulation look like smoke. • 8-migraine : • rare cause of ischemic stroke seen in complicated migraine with genetic Aetiology (run in families) .also seen with use of contraceptive pile . • 9-venous sinus thrombosis: less frequently seen in comparism to A, stroke. We think about it in special clinical setup that predispose to cause venous occlusion. the patient is more toxic ,fever ,headache disturb consciousness ,PD, and seizure. • The feature depending on severity and onset of occlusion and site is very important factors. causes???? As any venous thrombosis it is important to think about Behcet's disease in male and post partum complication in female

  11. B-Cardiac causes: • Mural thrombosis; as complication of MI or cardiomyopathy. • rheumatic heart dis. as ms . • arrhythmias: AF ,sick sinus ,the others likely to cause pan cerebral hypoperfusion. • endocarditis: • infective (bacterial or fungal) :during active stage or few months after antibiotic cure. • Nonbacterial (marantic): in setup of systemic malignancy • MVP: • Paradoxical emboli: ASD &PFO • atrial myxoma: • prosthetic valve :artificial one. c.hematological disorder: • thrombocytosis polycythemia • sickle C .A. Leucocytosis • hypercoaguable state like APL syndrome ,LA, protein S or C deficiency.

  12. Pathophysiology of ischemic stroke • When there is occlusion of BV the brain tissue supplied by that BV got ischemia. the effect depending on severity of ischemia ,duration , and potency and patency of collateral circulation. • As a result ,the patient may develop on of the following: • no symptom • TIA: the flow is return before cellular death • stroke :the flow is not returned in which there will be area of dead tissue(<50ml/100gm BT) which is surrounded by an area of ischemia (viable but not functioning) called ischemic penumbra. • Our aim in approaching any case of stroke is to save or to make IP area viable and functioning by keeping balanced homeostasis (Bp, B.sugar and good oxygenation). • Histo: Cascade of cellular changes in ischemia: there is ATPase pump failure------influx of sodium and water------cytotoxic edema and release of excitatory aa mainly glutamate---further ca +2 influx----more damage. • The process fatherly worsened by anaerobic production of lactic A and fall in tissue PH .restoration of BF may cause hemorrhage in ischemic area (hemorrhagic transformation) especially in embolic stroke.

  13. Pathophysiology of Intracerebral bleedingThe damage here depending upon bleeding severity ,as the neurons structurally disrupted and WM fibers are splits apart (pushed) .the big hematoma can cause sever increase in ICP and conning.

  14. RISK FACTORS FOR ISCHEMIC STROKES ? How to prevent stroke • UNMODIFIABLE • MODIFIABLE

  15. Clinical features • Is it stroke? Sudden onset ND ?If it is ,Answer: is it---? • *Hemorrhagic? is it HT bleed or non HT? ----- high BP, meningeal S, sever H., and altered consciousness • *Ischemic? which clinical type ie :TIA ,RIND--------etc? large or small VD (lacunars) ?is it anterior or post circulation? How? • drop attack ,crossed hemiparesis, dysartheria, vertigo, ataxia, diplopia ,dysphagia, cranial nerve palsy and altered conscious goes with posterior. • cortical sensory loss ,aphasia goes with anterior C. : is this absolute? • We have to ask is it thrombotic or embolic? how? If onset is stepwise over minutes or hours, preceded by TIA is go with thrombosis. If it is sudden with max. deficit at the onset ,not preceded by TIA , presence of cardiac lesion and hemorrhagic transformation in CT scan are consistent with embolic. • Seizure? seen in 10-25% ,more with embolic , cortical lesion and permanent ND (up to 50%). • Headache? seen more with bleeding and in 15-25% of I. stroke

  16. Clinico-anatomic correlation to decide which V is involved

  17. anterior, posterior & middlecerebral arteries

  18. Clinico-anatomic correlation to decide which V is involved • ANTERIOR CIRCULATION 1.ACA : • Uncommon? • Contralateral hemiparesis affecting LL>UL with sensory defect affecting LL +affection of sphincter control resulting from loss of inhibitory control on bladder reflex. 2.MCA: • Main stem: contralateral hemiplegia (dense) +global aphasia if dominant H. is affected • Deep lenticulostriate a: contralateral dense sensory-motor H. with or with out capsular aphasia AND transcortical aphasia (repetition intact) if D. H is affected. • superior division: contralateral weakness affecting face ,arm (UL) &hand sparing leg, no VF defect, motor or expressive aphasia if dominant H. affected. • Inferior division: • -Weakness less prominent. • -VF defect contralateral ,sensory dysfunction include marked cortical sensory dysfunction (look to 2nd lecture) • -spatial thought disorder---lack of awareness that deficit is exist (anisoagnosia) , neglect or and failure to recognize contralateral limb • -in D.H affection----sensory aphasia & Gersmann syndrome • ((agraphia ---acalculia----left right disorient.----finger agnosia) • -non-D H affection----dressing apraxia, constructional apraxia and some times acute confusional like state.

  19. 3.ICA occlusion:20% of cases.-may be asymptomatic -ophthalmic a: range from Amurosis fugax (TIA) to permanent V. loss due to affection of retinal a. and ciliary a. (AION).-features of MCA&ACA occlusion*trans-cortical: motor or sensory or global*subcortical aphasias ( left thalamic and putamen)

  20. POSTERIOR CIRCULATION • PCA: depending on site of occlusion • Distal part------cortical dysfunction-----contra lateral H. H more dense superiorly • More proximal-----will affect subthalamus ,thalamus, midbrain and cranial nerves. • Clinical feature: vertical gaze palsy,3rd nerve palsy, inter N. ophthalmoplegia and vertical skew deviation of eye .Distal part features can be seen also. • Dominant H .--------anomic aphasia, alexia without agraphia, and V. agnosia =inability to identify object in seen in L side of V. field caused by lesion affecting corpus callosum which connect the R. V. cortex from language area in dominant H.

  21. bilateral ----Balint’s syndrome (bilateral parietal-occipital lesion)+ memory disturbance+ inability to recognize familiar faces (prospagoagnosia)+ variety of exotic V. and behavioral changes. • *visual inattention +optic ataxia =neither H. can represent location or spatially guided movement. (failure to send impulse to frontal area) • Balint's syndrome ?due to bilateral parietal-occipital infarction ,the pt. not moving the eyes voluntarily but reflexly (reflex EM).=psychic paralysis of gaze, the patient appear to have ataxia in reaching an object (optic ataxia) ,he is looking to detailed aspect of picture without looking for it’s meaning of picture (asimultagnosia) • Anton’s syndrome ?bilateral O . infarction ------cortical blindness with denial

  22. Basilar artery? Serious ?either thrombosis or embolic • Variety of clinical syndrome, some are incompatible with life ,can produce bilateral N. involvement with coma or disturbance of cons. Occlusion of both vertebral aa or lone congenital vertebral a can produce same CF. • *stenosis or occlusion of subclavian a. before it has given rise to VA Lead to subclavian steal syndrome? As the blood passes from VA into distal subclavian a. with physical exercise of ipsilateral limb . • Is it predictive of stroke in VB distribution? Pt usually asymptomatic . • 1-basilar thrombotic occlusion; • -it affect proximal portion which supply the pons (tegmentum) produces • unilateral or bilateral 6th nerve palsy & ataxia • horizontal gaze palsy • pupil is constricted ? • vertical N. and ocular bobbing. • Some time the infarction affecting basis pontis with sparing of tegmentum ,end result is locked in syndrome(pt is cons., tetraplegic, only moves eye vertically to command& EEG is normal to differentiate it from persistent vegetative state due diffuse cortical damage due any cause like diffuse cortical anoxia or ischemia ) =Hemiplegia or quadriplegia usually present with disturbed cons. May be coma ,which should differentiated from pontine bleed in which the patient is comatose ,hyperthermic with pinpoint pupil but reacting to light ,diagnosis by CT scan.

  23. 2-Basilar a. embolism? affecting distal seg. rarely proximal seg. • The origin of emboli either BA or VA. ascend up to be arrested at bifurcation of 2 PCA. Leading to: • --immediate loss of cons. (thalami and RAS) • --unilateral or bilateral 3rd nerve palsy (midbrain) &ataxia • --hemiplegia or quadriplegia (cerebral p.) • --features of one or both occipital lobe dysfunction? emboli may dislodge and ascend up to occlude one or both PCA . • posterior inferior cerebellara.?pica syndrome (Wallenberg’s) due to atheromatous lesion thrombosis, less likely embolic of pica or VA. ipsilaterally :ataxia, diplopia vertigo and nystagmus, Horner’s syndrome, deafness, facial sensory loss,dysphagia ,and hoarseness of voice, loss of taste. • controlateral there is sensory loss in UL &LL. (crossed sensory loss) • Balint’s Syndrome ?due to bilateral parietal-occipital infarction ,the pt. not moving the eyes voluntarily but reflexly (reflex EM).=psychicparalysis of gaze, the patient appear to have ataxia in reaching an object (optic ataxia) ,he is looking to detailed aspect of picture without looking for it’s meaning of picture (asimultagnosia) • Anton’s syndrome ?bilateral O . infarction ------cortical blindness with denial. • Alexia without agraphia • Visual agnosia • lacunar infarction?20%?cause?CF?

  24. What are the important points you have to look in physical examination? • General examination: look for the signs which are suggestive of underlying systemic disorder especially treatable one ex; polycythemia. • BP---HT is well risk factor for stroke • ---comparism of BP and pulse on 2 sides? • Examination of the neck? • Careful cardiac examination? • Palpation of temporal A? • Neurological examination: may be Normal as in TIA • N. deficit : you have to define anatomic site involved that may suggest the cause, if it is in ant. Circulation :angiographic evaluation may suggest surgically correctable cause, while in post. Circulation different action is taken. LOOK FOR • cognitive function assessment: is of significant in ACA disease specially in cortical lesion, speech is affected also. -Ophthalmoscopeexamination; - retina may provide a hint to an embolic phenomenon in RA -Optic disc for PD • v. field defect • ocular palsies, nystagmus, and INO ----in posterior circulation. • Hemiparesis • sensory defect including cortical one. • cerebellar signs.

  25. Investigations a-to confirm diagnosis b-to evaluate for the cause c-general assess. • CT scan • MRI specially for posterior circulation ischemia. • Conventional angiography (DSA ) when it is needed. • Ultrasonography: Doppler US . • cardiac assessment? • Lumbar puncture • Blood testsCBP&,ESR and screen for vasculitis in young • * biochemical assessment----- • *lipid profile------ • *serology specially in stroke in young.

  26. Management of acute stroke in EU? • Ensure ABCDE (vital signs, oxygen saturation, urine output) • Keep the patients in 30 degree position unless the patient had feature of impending herniation • IV line ----draw blood for blood sugar , urea and creatinine , HB. • ECG for any cardiac problem specially ischemia • History: onset in minutes and progression • If thrombolytic therapy is available ---send for all blood profile • Control high blood pressure (only if MAP> 120 mm Hg) and sugar before sending patient to CT scan • Control fit if present with 10 mg diazepam over 5min infusion ,can be repeated if fit persistent with monitoring RR • Send for CT brain to confirm diagnosis. • No mannitol or dexamethason should be given in 1st 3 days • Subsequent treatment: depending on type of stroke-physician decision.

  27. General measure: • Nursing measures –should be initiated with particular emphasis on reducing the risk of complication resulting from immobility such as pneumonia ,DVT, and UTI • Early physical, occupational and speech therapy. • Early assessment of swallowing ability reduce morbidity. • Prevention and treatment of hyperthermia. • Early observation of post stroke depression. • Primary stroke prevention • Identification & reduction of stroke risk factors are crucial to decrease the incidence of stroke ,including treatment of DM ,HT ,cardiac disease and Hyperlipedemia also stop smoking ,contraceptive pill ……….etc • Rehabilitation • The main cause of death among stroke patient are related to medical complication (MI, pneumonia ,sepsis and P. embolism • R. program should be started from the onset of stroke.

  28. management of cerebral edema?Only in cases of big cerebral ischemia there is edema enough to cause brain shift an d herniation that necessitate incubation and hyperventilation produce transient c. vasoconstriction and may reduce ICP. Manitol infusion acts by reducing the volume of surrounding unaffected brain but it’s effect is also transient. corticosteroid is of no help in cytotoxic edema. • Hypertensive encephalopathy • It is diffuse cerebral effect of sever hypertension that are not caused by ischemia or bleed and it is potentially reversible upon controlling of BP. • Patient presented with H. ,visual blurring , confusion and drowsiness. seizure may develop. • On exam.: the BP is very high (240/150) with papilledema and retinal bleed on fundoscopic examination. • CT &MRI is often revealed diffuse C. edema with predilection to occipital lobe. • Treatment : is a medical emergency ,you have to reduce BP urgently but smoothly to avoid hypotension by using sodium nitroprusside. • This condition clinically and pathophysiologically is similar to eclmapsia.

  29. Specific medical therapy • Thrombolytic Therapy. • Use of anticoagulation: heparin or nadroparin (enoxiparin) and warfarin. • INDICATION-although AP therapy remains the treatment of choice to prevent recurrent thrombo-embolism in majority of patient with stroke the AC is indicated in cases of stroke in set up of AF, cardiac ischemia ,progressing or stroke in evolution (propagated thrombus). • To use AC you need :CT scan to exclude IC bleed or SAH , baseline PT ,PTT &platelet count .Screening for hypercoaguable state may indicted in some cases. • ow we predict progression at onset and pt. may have TIA? Difficult • history of active PU or uncontrolled HT (systolic BP>200) preclude use of AC in stroke, unless the benefit out weight the risks.

  30. Atrial fibrillation& cardiac disease • In setting of valvular heart disease(17 fold risk/year) -------AC with warfarin to INR reaching 2-3 • In setting of non valvular AF with no other risk factors-----ASA 325mg/day is effective • Patient with prosthetic valve -----long term AC is important. • Patient with bacterial endocarditis-----AC should be avoided

  31. TIA: • -may indicate an impending stroke, so the treatment should include: • Prophylactic therapy with antiplatelet like aspirin, ticlopedine or clopidogrel has been shown to prevent secondary events. • Patient with evidence of thrombo-embolism(*cardiac or carotid) or *VB ischemia • *patient with V-B ischemia clinically-------MRI • No VB stenosis------ASA • VB stenosis-----angiography---- stenosis confirmed-----AC (INR=3) • *pt. with cardiac thrombo-embolic---do TEE------ • thrombus-------AC (INR 3) • NO thrombus---holter monitor for underlying episodic arrhythmia (AF) in this case give AC otherwise ASA or AP is quite enough • *carotid stenosis: • asymptomatic stenosis <60%-----ASA • >70 % with or without*symptom of ischemia in that vascular distribution---c. endarterectomy is indicated • 60-70% stenosis (moderate) asymptomatic-----medical versus surgery decided on individual case-by-case basis even If it is symptomatic? • Decision of surgery vs. medical therapy in C stenosis is not easy ?operative risk (medical condition, surgical morbidity and mortality, personal experience, &degree of stenosis) should weight against risk of future stroke. operative risk should be less than 6%. • Identification & reduction of stroke risk factors are crucial to decrease the incidence---------etc

  32. PROBLEMS WITH TRANSLATING NEUROPROTECTION TO THE CLINIC: THERAPEUTIC WINDOW THE LONDON HELICOPTER EMERGENCY MEDICAL SERVICE (HEMS) HEMS can reach anywhere inside the M25 motorway within 15 minutes

  33. Thrombolytic therapy • -patient presented within 3 hours of ischemic stroke should be evaluated for iv recombinant tissue plasminogen activators(rt-PA)? • Clinical Evaluations: to use it there should be NO---- • -surgery <14 d -stroke or head trauma in • 90 days • -H/O cerebral bleeding -BP > 185/110 (should be below 175/100 ) • -Rapidly improvement -hemorrhage <12 d • -seizure at onset -AC within 48 hr • lab . evaluations : no treatment if there is ---- • -sever anemia -platelet count<100000/cu.mm • -PT >15 sec. –glucose<50 or >400 mg/dl • radiological evaluation: no treatment if • *CT-scan is positive for blood or non-stroke disease. • Strategies for it’s use ----you have to explain to the patient or family that there is 6% risk of symptomatic IC bleeding and 50% chance of little or no disability compared to 38% chance without rt-PA. • -careful monitoring of BP and blood sugar • -no aspirin or AC use 24 hours after rt-PA administration. • -we give 0.9 mg/kg , max:90 mg • the results is promising ,but the use of intra-arterial thrombolytic therapy is under investigation( reteplase- - - ),or use it with neuroprotective agent (glutamate antagonist) may prolong therapeutic window >3 hr, or use it with aspirin or other new platelet glycoprotein 11b/111a antagonist is under evaluation .

  34. Antiplatelet: • Aspirin: is act through irreversible inhibition of cyclo-oxygenase enzyme ----inhibition of thromboxane A2 (a platelet aggregating and PG vasoconstriction properties). • Ticlopedine: block ADP receptor on P. preventing cascade activation of GP11b/111a complex on P. (clopidogrel have same effect) that lead to binding of fibrinogen to P. .It is given in dose of 25o twice .low incidence reversible neutropnia (BM suppression) should be followed, skin rash and diarrhea. • Is it more effective than aspirin? when indicated. • Dipyridamole: P. phosphodiesterase inhibition which inhibit breakdown of cAMP which inhibits P. aggregation . • Clopidogrel: 75 mg daily ,proved to be effective in some studies especially if combined with aspirin in patient at high risk of CVS events ,but risk of bleeding is high. It should be stopped few days before surgery. • Abciximb: monoclonal antibody to block GP111b/111a receptors complex activation . Neurotropic drugs : neuroaids ,citicholine • Surgical treatment: ? • SAH? Angio---------------surgery as early as possible • ICH??????????? • CEREBELLAR H.?

  35. Case 1 : • 56 years old man diabetic and HT ; presents with right sided weakness and aphasia of one hour duration .no loss consciousness , mild headache .he is controlling sphincter • On exam: general: un remarkable apart of irregular pulse. BP= 160/100 • Medical : abnormal heart sound?? • Neurological : aphasic but conscious • Cranial R. facial upper motor palsy • No meningeal signs • Motor : right sever hemi paresis grade 2 in UL and grade 3 in LL • Approach • Emergency ----------------?? • WHICH SYSTEM? MOST LIKELY diagnosis • Where is lesion upper or lower ? Where about. • Ischemia or bleeding • Anterior circulation or posterior circulation • Causes of CVA?

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