cerebrovascular disease with clumsiness in using his right ... · pdf filestroke syndrome...

CerebrovascularDisease

Ian A. Cook, M.D.

Case for Discussion•58 yo WM, former smoker, develops

sudden onset of dysarthria•Two weeks previously, had awakened

with clumsiness in using his right(dominant) hand; this persisted for afew hours, then resolved•What thoughts are you considering?

Source: Murray CJL, Lopez AD, eds. The Global Burden of Disease. Boston:Harvard School of Public Health, World Health Organization, World Bank, 1996.

Global Burden of Disease

2.6HIV102.7Diarrheal diseases93.0War injuries83.0Tuberculosis73.1Lower respiratory infections64.2Chronic obstructive pulmonary disease54.4Cerebrovascular disease45.1Road traffic accidents35.7Unipolar major depression25.9Ischemic heart disease1

% Total CauseRank

Projection 2020Terms

•Cerebrovascular disease - anybrain abnormality arising frompathologic processes in the vessels•occlusion via embolism or thrombosis•vessel rupture•viscosity problems•small vessel disease, developmental

•The brain depends on a continuoussupply of oxygenated blood,maintained by a series ofbaroreceptors & vasomotor reflexescontrolled by the brain stem•LOC in 10 sec•irreversible damage in 4-5 min

•Infarction, ischemic necrosis,encephalomalacia•arterial obstruction is the usual cause of focal ischemic

damage• focal + diffuse ischemia with circulatory collapse or

hypotension•pale infarction - devoid of blood•hemorrhagic infarction - w/blood (seen w/embolisms)

Infarction

Incidence•Stroke•500,000 strokes in US per year•400k infarctions, 100k hemorrhages•175,000 fatalities per year

Stroke Syndrome

•Sudden appearance of anonconvulsive neurologic deficit•apoplexy•cerebrovascular accident (CVA)•brain attack

Stroke Syndrome•embolic - very sudden onset•frequently regression of deficit within a

few hours to days•thrombotic - abrupt + evolution•improvement occurs over weeks to months•multiple simultaneous vascular

occlusions are an exception

Stroke Syndrome•Deficit reflects location & size•hemiplegia•confusion•sensory deficits•aphasia•visual deficits•Sometimes “silent”

Stroke Syndrome•Risk Factors•hypertension•heart disease•atrial fibrillation•diabetes•smoking•hyperlipidemia•hypercoagulable states

Ischemic Stroke

•Global - no collateral flow soirreversible destruction begins in4-8 min at normal body temp.•Focal - collaterals mean that there

may be some oxygen & glucoseavailable

Ischemia-modifying Factors•Effects depend upon location•Circle of Willis•ophthalmic artery•Depend upon speed of occlusion•gradual narrowing allows collateral

channels to open•Viscosity, hypotension

Pathophysiology I

•Loss of oxygen and glucose•Changes in cellular metabolism

and collapse of energy-producingprocesses and cell membranedisintegration

Pathophysiology II•ATP depletion, incr extracelluar K, incr in

intracellular Ca, cellular acidosis•Free fatty acids are activated and destroy

phospholids of membranes•Prostaglandins, leukotrienes, free radicals

accumulate•Lactic acid from anerobic conditions is

neurotoxic

Pathophysiology III•Excitatory neurotransmitters•Glutamate, aspartate

•Excite neurons leading to influx of Na and Ca•A glutamate receptor, the NMDA (N-methy-D-

aspartate) channel, may be a therapeutic target,though trial results are less dramatic thananticipated.•Other neuroprotective strategies (hypothermia,

magnesium sulfate, citicoline [a Phosphatidyl-choline precursor], albumin, and erythropoietin)may be of benefit.

Ovbiagele Curr Treat Options Neurol 2003

Punctate WMH Lesions (blue) exhibited a scattered distribution,while Confluent Lesions (red) localized in watershed regions,suggesting different etiologies

Enzinger J Neurosci 2006

Clinical Diagnosis•Nature of defict(s)•Time course•Lab tests•Doppler ultrasound•CT scan immediately•MRI a few days later shows softened tissue

changes•MR angiography•LP (rarely), EEG

Prognosis

•94% survived 5 days•84% at one month•54% at 3 years•40% at 7 years•Of survivors, ~65% were capable

of independent existence

Acute Management - restorecirculation & stop necrosis

•Thrombolytic agents•tisue plasminogen activator t-PA•streptokinase•IV within 3 hrs of onset - benefit•IV within 6 hrs - much less benefit•NO hemorrhage by CT


•Surgical revascularization•within first 12 hrs•remove clot•difficult unless already in hospital

because of time frame•newer devices (Merci Retriever) may

show promise

Mechanical Devices for Retrieval

Leary Ann Emerg Med 2003


•Edema & Raised ICP•Mannitol•Not steroids (no benefit)•Hemicraniotomy•“Strokectomy” of infarcted tissue

Delays to Treatment•Despite available treatments, most

patients arrive late (2 hrs to seek care,4 to hospital)•Decreased delay - perceiving as

severe, advice of others, contacting anambulance•Increased delay - perceived control of

symptoms, female genderMandelzweig Stroke 2006


•Anticoagulant Drugs•Heparin, Coumadin•Prevent TIAs & impending stroke•Fluctuating basilar artery thrombosis•Impending carotid artery occlusion•Demonstrate w/Doppler


•Antiplatelet Drugs•Aspirin (325mg/d) - inhibits platelet

cyclooxygenase•Ticlopidine, clopidogrel, dipyridamole -

maybe•Hemodilution - reduce viscosity

Physical Therapy & Rehab

•Begin within a few days of strokein all but most ill patients•Passive ROM to avoid contracture•Regain strength, teach new

strategies for movement•Neuroplasticity ....

Prevention

•ASA•control HTN, atrial fibrillation•avoid oversedation with deep sleep•treat anemia, polycythemia•avoid rapid diuresis•obsess during surgical procedures

Primary Intracranial Hemorrhage•Chronic hypertension•Bleeding into tissue, rarely into

subarachnoid space except withaneurysms•CT scans - blood shows as white

acutely; less dense 2-3 after wks•Skip the LP

Intracranial Hemorrhage•Apoplexy•“obese, plethoric hypertensive male who,

while sane and sound, falls senseless tothe ground, breathes stertorously, anddies in a few hours”•30-35% die in 1-30 days•In survivors, surprising degree of

recovery

Intracranial Hemorrhage•ICU care - hyperventilate to keep pCO2 to

25-30mmHg•Control hypertension (beta blockers, ACE

inhibitors)•Surgical evacuation of the clot - not too

helpful in hemispheral clots, better withcerebellar hematomas

Ruptured Saccular Aneurysm

•“Berry aneurysm” at branch pts•26,000 per year•90-95% in anterior Circle of Willis


•Excruciating headache•maybe also with emesis•sometimes sudden loss of

consciousness•not often, there may be small leaks

before the “big one” with neuro sx


•CT Scan•LP•Angiography

Ruptured Saccular Aneurysm•Surgical obliteration of sac•bedrest, fluids, keep SBP < 150mm

prevent DVT, pain control•Ca channel blockers (nimodipine) may

reduce vasospasm•watch for hyponatremia•Risk of rerupture is elevated

AV Malformation•Functionally, an AV fistula•Thin walls, at risk for hemorrhage•90% survive the first bleed•chronic recurrent headache may

precede a bleed•CT with contrast, arteriography•Surgical excision

cerebrovascular disease with clumsiness in using his right ... · pdf filestroke syndrome...

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