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TERM
Stroke : Rapid onset of clinical signs of focal or global disturbance of cerebral function lasting more than 24 hours or leading to death with no apparent cause other than a vascular lesion
Result in : Permanent lack of blood flow to a focal region of the brain Parenchymal changes
INRODUCTION
STROKE CLASSIFICATION STROKE
85 % Ischemic
15 % Hemorrhagic
80 % AT Stroke
20 %
Cardio embolic
50 % ICH
50 % SAB
Cerebral Blood Flow (CBF) 53 ml/100 gm brain/minute (range 50-60) Cerebral Metabolism Rate for Oxygen (CMRO2) Cerebral O2 Consumption 3.5 ml/mg/minute
Cerebral Blood Flow (CBF) in 100mg/minute If CBF decreases to 15-18 electrical failure Below 15 change in somato-sensory evoked potential
Below 10 ionic failure Extracellular K+ , Intracellular Ca++ Free fatty acid releases, ATP breakdown, intracellular acidosis neuronal death
Cerebral Blood Flow (CBF) in 100mg/minute In 10-15 ml (between electrical and ionic failure) Neuron not functioning, but still viable These neuron appear in the periphery, around infarcted area (perifocal area). Their existence is determined by collateral system. The area is called PENUMBRA. It is a target of intervention !!.
The Ischemic Cascade and Secondary Injury Clot Area of core infarction Cells die quickly without reperfusion
Ischemic penumbra Cells at risk but not permanently 20-50% of perfusion from collateral circulation
K+ moves across the cell membrane into the extracellular space potentiate and enhance cell death Production of O2 free radicals peroxidation fatty acid in cell organelles and plasma membrane damage cell function Anerobic glycolysis accumulation of lactic acid and lowering pH acidosis impaire cell metabolic function
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Production of excitatory neurotransmitter (glutamate, aspartate, kainic acid) Na+ and Ca++ influx into cells Water and Cl- follow Na+ cytotoxic edema
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Intracerebral Hemorrhage
Bleeding into the brain results from rupture of one of the cerebral vessels. In many cases, derives from a ruptured arteriosclerotic vessel. Major cause -- rupture of microaneurysms. (end result of longstanding arterial hypertension) at penetrating arteries. Atherosclerosis (in aging or chronic HTN) microaneurysms at penetrating arteries + 1mm : Charcot-Bouchard aneurysm Most common site - basal ganglia.
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Subarachnoid Bleeding
The causes : Ruptured aneurysm Ruptured AVM Ruptured angioma Blood dyscrasia Aneurysm : found commonly in Willis circle and its branches Aneurysm ruptures blood fills in subarachnoid space and brain parenchym close to it.
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Complications of Subarachnoid Hemorrhage Vasospasm : Delayed narrowing of large capacitance arteries at the base of the brain after SAH Often occurs at day 2 to 12 after the onset. Hydrocephalus Rebleeding : occurs in a few weeks after the onset Hyponatremia Seizures
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