PATHOPHYSIOLOGY AND

CLINICAL MANIFESTATION
OF STROKE

Dr Nurdjaman Nurimaba Sp.S(K)

Bag / UPF Ilmu Penyakit Saraf
FK-Unpad / RS-Hasan Sadikin
Bandung

I. PATHOPHYSIOLOGY
OF STROKE

CEREBROVASCULAR DISEASE :
1. Asymptomatic
2. Focal brain dysfunction
TIA ( Transient ischemic attack )

STROKE
3. Vascular dementia
4. Hypertensive encephalopathy

DEFINITION of STROKE
Focal / Global Neurological
Sudden - very rapid development of symptoms,
> 24 H or Leading to Death
No other Cause than primary CVD

 Primary CVD is referred to the risk factors

Global brain dysfunction is referred to
unconsciousness
TIA : Complete recovery < 24 H

Types of Vascular lesion

Occlusive

Hemorrhagic

Different Types of Stroke,

2000
Cerebral
Embolus
24%

Ischemic
Stroke
85%

TIA 3%

Cerebral
Thrombosis
61%

Intracerebral
Hemorrhage
Hemorrhagic
9%

Stroke
12%

Subarachnoid
Hemorrhage 3%

American Heart Association (AHA). Heart Disease and Stroke Statistics

2003 Update. 2003. Available at: http://www.americanheart.org/downloadable/heart/
10590179711482003HDSStatsBookREV7-03.pdf. Accessed October 13, 2003.

Ischemic Stroke ( ATHEROTROMBOTIK )

Embolic Source ( Cardio emboli )

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

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
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.

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

BRAIN INFARCTION
Micro-circulation change
Vessel occlusion result in
Low shear stress
blood aggregation
blood viscosity and resistency
Vasoconstriction caused by extracellular K

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

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

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

Hemorrhagic STROKE

Intracerebral Hemorrhage
Brain hematoma :
Compressive effect
Extend to ventricular system or subarachnoid space
Most common site - basal ganglia.

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.

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

II. CLINICAL
MANIFESTATION
OF STROKE

Improving stroke
Complete recovery : 24 Hours to 3 weeks

Worsening stroke
Progresivity of symptom ( qualitative- quantitative)
in anamnestic or follow up
50 % cases in several minutes and hours

Sub type : - Smooth

worsening
- Steplike
worsening
- Fluctuating worsening

II. Pathologic appearance ( type of stroke )

Infarction
1. Clinical category

2. Mechanism

- atherothrombotic

- Thrombotic

- cardioembolic
- lacunar

- embolic
- hemodinamic

Intracerebral hemmorhage

( ICH )

Subarachnoidal hemmorhage

( SAH )

III. Vascular location

Carotid system
Vertebro - Basilar ( VB ) system
Clinical manifestation Depend on :
Large of lesion
Site of Vascular lesion

CLINICAL MANIFESTATION

A. Carotid system
Motor dysfunction
Contralateral hemiparesis
Ipsilateral paresis : CN and extremities
dysarthria
Sensory dysfunction
Contralateral hemihypesthesia
ipsilateral hypesthesia : CN and extremities

CLINICAL MANIFESTATION ( cont )

A. Carotid system
Visual disturbances
Contralateral homonymous hemianopsia
Amaurosis fugax ( TIA )
Higher cortical dysfunction
Aphasia
Agnosia

CLINICAL MANIFESTATION ( cont )

B. VB system
Motor dysfunction
Alternating hemiparesis
( CN Paresis is contralateral to extrimities
paresis )
Dysarthria
Sensory dysfunction
Alternating hemihypesthesia
(CN Hypesthesia is contralateral to
extrimities hypesthesia)

CLINICAL MANIFESTATION ( cont )

B. VB system
Visual disturbances
Homonymous hemianopsia
Cortical blindness ( TIA : blackout )
Others
Loss of balance
Vertigo
Diplopia

INFARCTION STROKE.
MECHANISM OF ISCHEMIC INFARCTION

1. Thrombotic
Thrombus superimposed on an
atherosclerotic plaque
Precipitating by an abnormality of blood
clotting
2. Embolic
Arterial occlusion by an embolus

MECHANISMS OF ISCHEMIC INFARCTION ( CONT )

3. Hemodynamic
Severe stenosis or occlusion of the
proximal arteries
Inadequate Collateral compensatory
blood flow
Global cerebral perfusion is critically
decreased
( e.g. cardiac output
decreased )

CLINICAL MANIFESTATION
Brain hemorrhage
Approximately 10 % of all stroke
The leading risk factor is hypertension
Other risk factors : aneurysm, AVM,
cavernous angioma, drug abuse ( cocaine,
amphetamines, alcohol ), blood dyscrasia,
anticoagulant therapy, amyloid angiopathy,
brain tumor
Unlikely to be preceded by TIAs

CLINICAL MANIFESTATION ( cont )

Brain hemorrhage
The onset is acute, severe headache,
unconsciousness
The blood pressure usually is elevated at
onset
The most common locations of
hypertensive bleeding are basal ganglia,
thalamus, lobe of a hemisphere,
cerebellum, pons

CLINICAL MANIFESTATION ( cont )

Brain hemorrhage
Lobar hemmorrhage ( cortex or subcortical )
is less frequently have a history of
hypertension
Lobar hemorrhage in elderly is commonly
caused by amyloid engiopathy
Thalamic hemorrhage oculomotor
disturbance such as forced downgaze or
upgaze palsy, unreactive miotic pupils,
convergence paralysis

CLINICAL MANIFESTATION ( cont )

Brain hemorrhage
Cerebellar hemorrhage ( nucleus dentatus
in cerebellar hemisphere ) :
Disequilibrium, limb ataxia, nausea,
vomiting, headache and dizziness
Usually a combination of signs
indicative cerebeller and pontin
dysfunction : peripheral facial palsy,
nystagmus, miosis, decreased corneal
reflex, abducens palsy

CLINICAL MANIFESTATION ( cont )

Brain hemorrhage
Primary hemorrhage into the brain stem :
Usually has devastating effect
Small hemorrhage can produce limited
dysfunction
The common site is pons
Clinical diagnosis CT Scan to
compare a small hemorrhage with
infarction

CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH )
Bleeding into the subarachnoid space
Clinical finding :
Sudden Onset
Severe headache (dramatic, in seconds to
minutes )
Decreased level of consciousness
( recovery in a few minutes )
Vomiting
Younger and less to have hypertension

CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH )
Usually no focal findings on examination,
sometimes a partial oculomotor nerve
palsy
Meningeal irritation ( stiffneck )
Kernigs or Brudzinskis sign
Sub-hyaloid hemorrhage
Brain imaging Blood in the
subarachnoid space on the day of the
hemorrhage ( diminishing after the onset )

CLINICAL MANIFESTATION ( cont )

Subarachnoid hemorrhage ( SAH )
LP Bloody or xanthochromic CSF
Causes :
- Rupture of aneurysm (saccular aneurysm) or AVM
CT - MRI arteriogram - angiogram.
- Neoplasm
- Unknown : 10 15 % cases
Vasospasme complication may be occur after 48 H
following the onset

RISK FACTORS
A. Major
1. Hypertension
2. Cardiac diseases
3. Diabetes mellitus
B. Minor
1. Dyslipidemia
2. Smoking
3. Increase hematocrit, hyperfibrinogenemia,
drug abuse, contraceptive pill, obesity, etc

COMPLICATIONS

A. Neurologic complications
Brain edema
Hemorrhage infarction
Vasospasm
Hydrocephalus
Hygroma

COMPLICATIONS ( cont )

B. Non neurologic
1. Intracranial process
Increase BP
Hyperglicaemia
Pulmonary edema
Cardiac disorders

2. Immobilitation
Bronchopneumonia
Thrombophlebitis
Bladder infection
Decubitus
Contracture