Cerebrovascular Disease with clumsiness in using his right ... · PDF fileStroke Syndrome...
Transcript of 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
Acute Management - restorecirculation & stop necrosis
•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
Acute Management - restorecirculation & stop necrosis
•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
Acute Management - restorecirculation & stop necrosis
•Anticoagulant Drugs•Heparin, Coumadin•Prevent TIAs & impending stroke•Fluctuating basilar artery thrombosis•Impending carotid artery occlusion•Demonstrate w/Doppler
Acute Management - restorecirculation & stop necrosis
•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
Ruptured Saccular Aneurysm
•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
Ruptured Saccular Aneurysm
•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