PATHOPHYSIOLOGY OF STROKE

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

Types of Vascular lesion Occlusive Hemorrhagic

Result in : Permanent lack of blood flow to a focal region of the brain Parenchymal changes

ALL lead to INFARCTION

HEMORRHAGIC Spontaneous rupture of the arterial in or outside the brain

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Perdarahan Subarahnoid; 5% Perdarahan Intraserebral; 10% Stroke Infark; 85%

Stroke Infark Perdarahan Intraserebral Perdarahan Subarahnoid

INRODUCTION
STROKE CLASSIFICATION STROKE

85 % Ischemic

15 % Hemorrhagic

80 % AT Stroke

20 %
Cardio embolic

50 % ICH

50 % SAB

BRAIN INFARCTION Normal metabolism and blood flow

Brain : A very metabolically active organ Glucose as a sole substrate Energy produced depends on oxygen presence ATP as energy for maintain neuronal integrity keep Ca++ outside and K+ within the cells Brain requirement O2 500 mL Each minute !! Glucose 75-100 mg

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

Metabolic and neuro-chemical changes

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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Brain hematoma : Compressive effect Extend to ventricular system or subarachnoid space

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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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