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Presentation on theme: "Brain Attacks CVA Add Corporate Logo Here To insert your company logo on this slide From the Insert Menu Select “Picture” Locate your logo file Click OK."— Presentation transcript:

1 Brain Attacks CVA Add Corporate Logo Here To insert your company logo on this slide From the Insert Menu Select “Picture” Locate your logo file Click OK To resize the logo Click anywhere inside the logo. The boxes that appear outside the logo are known as “resize handles.” Use these to resize the object. If you hold down the shift key before using the resize handles, you will maintain the proportions of the object you wish to resize.

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

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

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

5 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

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

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

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

9 Carotid Arteries

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

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

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

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

14 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

15 CVA Process –Induction –Amplification –Expression

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

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

18 Neurohistopathology

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

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

21 CVA Vulnerable regions –Hippocampal cells may live 24-72 hours –CA1 > CA3 resistant to anoxia –CA1 24-48 hours

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

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

24 Circle of Willis

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

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

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

28 CVA Types of CVA –Ischemic Thrombosis Embolism Systemic hypertension


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