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Cerebral Vascular Accidents Now referred to as strokes or brain attacks Acute and treatable condition Third leading cause of death Leading cause of disability

CVA Mortality –1. Heart disease 33.2% –Cancer23.7% –CVD 6.6%

CVA Basic information –Males have more strokes –Females>Males over age 85

CVA Mortality by Race –Age adjusted White 22.5 per 10,000 Black48.9 per 10,000 Morbidity –Prevalence 2.9 million in 1991 –Cost $30 billion per year

CVA Mechanisms –Anoxia –CA+ influx –Excitatory amino acids –Free radicals

CVA Morphology –Penumbra develops –Region of encapsulated cells, alive but not well

CVA Some treatment methods –Surgical clinical trials - carotid ectomy –Woman’s Estrogen Trials (WEST) –Prevention by aspirin –Neuron salvage agent

Carotid Arteries

CVA Long term results –Revascularization local factors increase blood levels –Neural plasticity and regeneration –Recurrent strokes

CVA Ischemic cell damage (Choi) –Cells are stimulated to death –Glutamate neurotoxicity –Cycle of hypoxia, hypoglycemia, ischemia

CVA Glutamate neurotoxicity –Energy depletion –Glu increase –Uptake of glu –Toxic glu exposure –Cell death –Glu release

CVA Glutamate cell death –Cellular swelling –Cell death in under 5 minutes

CVA Other Mechanism –High rates of Ca+ entry into cell –AMPA yields Na+ –MMDA yields Ca+, Na+ –AMPA toxicity after 3+ hours –Yields 70% cell death –24 hours yields 100% cell death

CVA Process –Induction –Amplification –Expression

CVA Hypoxic injury to brain –Bulbous swelling of the dendrites –Swelling of the cell body –MK801 (Ca+ blocker) greatly slows cell death –MMDA antagonistic

CVA Cardiac Arrest Victims –“Window of Opportunity” –Histopathology –Heart attack - the entire brain becomes ischemic

Neurohistopathology

CVA Decreasing order of vulnerability to ischemia –Neurons –Support cells –Astrocytes –Endothelial cells

CVA Vulnerable regions –Decreasing order of sensitivity 1. Hippocampus 2. Cerebellum 3. Stratum 4. Neocortex

CVA Vulnerable regions –Hippocampal cells may live hours –CA1 > CA3 resistant to anoxia –CA hours

CVA Syndromes –Transitant Ischemic Attack (TIA) –Resolving Ischemic Neurological Deficits (RIND) –Stroke

CVA Common patterns –1. Middle cerebral artery occlusion –Redundancy in the neurovascular system –Circle of Willis

Circle of Willis

CVA Some principles –“Time is brain” –Focal symptoms “Fit” Migraine “Swoon”

CVA Some principles –Non-Focal symptoms syncope hypoglycemic “Toxic”

CVA Types of CVA –Hemorrhage Subarachnoid (vomiting, back of head, blood in CSF) Intracerebral (focal onset, gradual increase in signs)

CVA Types of CVA –Ischemic Thrombosis Embolism Systemic hypertension