Cerebral Vascular Accidents Pennsylvania State 脑血管意外宾夕法尼亚州.ppt

Brain Attacks CVA 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% Cancer 23.7% CVD 6.6% CVA Basic information Males have more strokes FemalesMales over age 85 CVA Mortality by Race Age adjusted White 22.5 per 10,000 Black 48.9 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 c