Transcript Cerebral Vascular Accidents

Brain Attacks
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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
– Females>Males over age 85
CVA
• Mortality by Race
– Age adjusted
• White
• Black
22.5 per 10,000
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
Neuron
glu Lactate
CO2
O2
CVA
• Decreasing order of vulnerability to
ischemia
– Neurons
– Support cells
– Astrocytes
– Endothelial cells
CVA
• Vulnerable regions
– Decreasing order of sensitivity
•
•
•
•
1.
2.
3.
4.
Hippocampus
Cerebellum
Stratum
Neocortex
CVA
• Vulnerable regions
– Hippocampal cells may live 24-72 hours
– CA1 > CA3 resistant to anoxia
– CA1 24-48 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