PATHOPHYSIOLOGY OF STROKE

Adelina Y. Alfa

Bag/SMF Ilmu Panyakit Saraf FK-Unpad / RS-Hasan Sadikin Bandung 2002

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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

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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Knowing to both types of stroke is a basis in explaining the symptoms and signs, technique of examination, and treatment intervention

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

BRAIN INFARCTION Normal metabolism and blood flow

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 Maximum compensation to maintain CMRO2 at CBF 20-25 ml/100 gm/min

BRAIN INFARCTION Normal metabolism and blood flow

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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BRAIN INFARCTION Normal metabolism and blood flow

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 !!.

BRAIN INFARCTION Factors that determine CBF Regional Cerebral Blood Flow (rCBF) Auto-regulation Microcirculation change Metabolic and neuro-chemical control

BRAIN INFARCTION Regional Cerebral Blood Flow (rCBF)

Hagen Poisseuille Law V= V p r4 n l p . r4 . n.l.8 = velocity of blood flow to the brain = intravascular pressure = radius of the artery = blood viscosity = arterial length

Changes of these factors can lead to ischemia tissue necrosis

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BRAIN INFARCTION Auto-regulation

The capacity of cerebral circulation to maintain relatively constant level of CBF despite changing pressure
CBF relatively constant in MABP 50-150 mmHg Chronic hypertension : Upper and lower levels of auto-regulation are raised.
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BRAIN INFARCTION Auto-regulation

CBF
75

50

25

MABP
50 100 150 200
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BRAIN INFARCTION Auto-regulation

The ability of auto-regulation and collateral system have a role in stroke attack. If blood pressure increases, the vessels will constrict and if blood pressure decreases, they will dilate.
Damage of auto-regulation and collateral system decreased regional CBF ischemic-infarction
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BRAIN INFARCTION Micro-circulation change

Vessel occlusion result in Low shear stress blood aggregation blood viscosity and resistency Vasoconstriction caused by extracellular K

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BRAIN INFARCTION 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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BRAIN INFARCTION Metabolic and neuro-chemical changes

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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Intracerebral Hemorrhage
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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Subarachnoid Bleeding
Complications Associated With 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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