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 3 .

10% Stroke Infark. 85% Stroke Infark Perdarahan Intraserebral Perdarahan Subarahnoid 4 .Perdarahan Subarahnoid. 5% Perdarahan Intraserebral.

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 6 .

5 ml/mg/minute 7 .Cerebral Blood Flow (CBF) 53 ml/100 gm brain/minute (range 50-60) Cerebral Metabolism Rate for Oxygen (CMRO2)  Cerebral O2 Consumption 3.

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 acidosis  neuronal death 8 . ATP breakdown. Intracellular Ca++  Free fatty acid releases.

Cerebral Blood Flow (CBF) in 100mg/minute In 10-15 ml (between electrical and ionic failure) Neuron not functioning. Their existence is determined by collateral system. 9 . It is a target of intervention !!. around infarcted area (perifocal area). but still viable These neuron appear in the periphery. The area is called PENUMBRA.

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 12 .

aspartate.Production of excitatory neurotransmitter (glutamate.follow Na+  cytotoxic edema 13 . kainic acid)   Na+ and Ca++ influx into cells Water and Cl.

basal ganglia. Major cause -. derives from a ruptured arteriosclerotic vessel. Atherosclerosis (in  aging or chronic HTN)  microaneurysms at penetrating arteries  + 1mm : Charcot-Bouchard aneurysm Most common site .rupture of microaneurysms.Intracerebral Hemorrhage Bleeding into the brain results from rupture of one of the cerebral vessels. In many cases. 14 . (end result of longstanding arterial hypertension) at penetrating arteries.

Brain hematoma : Compressive effect Extend to ventricular system or subarachnoid space 15 .

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18 .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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Hydrocephalus Rebleeding : occurs in a few weeks after the onset Hyponatremia Seizures 20 .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.