Pathofisiologi Stroke

8/12/2019 Pathofisiologi Stroke

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PATHOPHYSIOLOGY OF STROKE

Adelina Y. Alfa

Bag/SMF Ilmu Panyakit Saraf

FK-Unpad / RS-Hasan Sadikin

Bandung 2002


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Stroke :Rapid onset of clinical signs of focal or globaldisturbance of cerebral function lasting more than

24 hours or leading to death with no apparent

cause other than a vascular lesion

TERM

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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Knowing to both types of stroke is a basis

in explaining the symptoms and signs,

technique of examination,

and treatment intervention


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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 requirementO2 500 mL

Glucose 75-100 mgEach minute !!


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BRAIN INFARCTION


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


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BRAIN INFARCTION


Cerebral Blood Flow (CBF) in 100mg/minute

If CBF decreases to 15-18electrical failure

Below 15change in somato-sensory evoked potential

Below 10ionic failure

Extracellular K+ , Intracellular Ca++ Free fatty acid releases, ATP breakdown,

intracellular acidosis

neuronal death


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BRAIN INFARCTION


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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BRAIN INFARCTION

Factors that determine CBF

Regional Cerebral Blood Flow (rCBF)

Auto-regulation

Microcirculation change Metabolic and neuro-chemical control


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BRAIN INFARCTION

Regional Cerebral Blood Flow (rCBF)Hagen Poisseuille Law

V=

V = velocity of blood flow to the brain

p = intravascular pressure

r4 = radius of the artery

n = blood viscosityl = arterial length

Changes of these factors can lead to ischemia

tissue necrosis

p . r4.

n . l . 8


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BRAIN INFARCTION

Auto-regulation

The capacity of cerebral circulation to maintain

relatively constant level of CBFdespite changing pressure

CBFrelatively 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

25

50

75

50 100 150 200

CBF

MABP


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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 stressblood 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 celldeath

Production of O2 free radicalsperoxidation fatty

acid in cell organelles and plasma membrane

damage cell functionAnerobic glycolysisaccumulation of lactic acid

and lowering pHacidosisimpaire 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 intocells

Water and Cl- follow Na+

cytotoxic edema


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Intracerebral Hemorrhage

Bleeding into the brain results from rupture of one ofthe cerebral vessels.

In many cases, derives from a ruptured arteriosclerotic

vessel.

Major cause -- rupture of microaneurysms. (end resultof 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 angiomaBlood dyscrasia

Aneurysm : found commonly in Willis circle and

its branchesAneurysm rupturesblood 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 capacitancearteries 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 theonset

Hyponatremia

Seizures


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Pathofisiologi Stroke

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