Download Cerebral Vascular Accidents

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Brain Attacks
Add
Corporate
Logo
Here
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