PATHOPHYSIOLOGY OF STROKE

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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

Types of Vascular lesion

Occlusive
Hemorrhagic

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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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 INRODUCTION
STROKE CLASSIFICATION

STROKE

85 % 15 %
Ischemic Hemorrhagic

80 % 20 % 50 % 50 %
AT Stroke Cardio ICH SAB
embolic
 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

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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

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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

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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 !!.

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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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