Department of Neurology and Psychiatry, Faculty of Medicine

Udayana University
‘The Founding Father’
 CEREBROVASCULAR DISEASE
(CVD)

CHRONIC CVD
- VASCULAR DEMENTIA
ACUTE CVD
* MULTI INFARCT DEMENTIA
- ACUTE STROKE
* BINSWANGER’S DISEASE
 A Global public Health Problem.
 Generic name of Brain attack.
 Death rate are rising in some countries.
 A Community Health Problem and at times stroke cases are of
acute medical emergency problem  needs early & accurate
diagnosis  prompt treatment.
Stroke or CVA is an acute disorder or syndrome
of the blood vessel of the brain.
The term stroke refers to the sudden death of
brain tissue caused by a lack of oxygen
resulting from an interupted blood supply.

There are two ways that brain tissue death can

occur, (ischemic stroke)
or (hemorrhagic stroke).
 leading cause of death in USA was
, following disease of the and
(1997).
Stroke death rate rise steeply with age.
Stroke was also a leading major cause of
in USA.
Ischemic stroke mortality rate 20 – 40%, and
hemorrhagic stroke mortality rate 40 – 80%.
20% of stroke patients die within 1 month and
about 30% within 1 year.
65 – 85% of first stroke were due to
supplying the brain (ischemic stroke /
non hemorrhagic stroke: cerebral thrombosis or
embolism, and infarction).
15 – 35% were cause by
(hemorrhagic stroke), mostly caused by
.
The risk of recurrent stroke within five years of a
first stroke is between 30% and 43%.
Hypertension is the major cause of stroke.
In hypertension, severely elevated blood
pressure damages the blood vessels. If blood
vessels are subjected to high blood pressure for
an extended period of time, their response is
the thicken, making them less flexible. This
condition is called .
Also, if excessive amounts of fat are found in
the blood, the arteries can accumulate fatty
deposits called . This build up, called
MOTOR ACTIVITY SENSORY ACTIVITY

MOTOR HOMONCULUS
SENSORY HOMONCULUS
PYRAMIDAL SYSTEM

Normal functional
area of brain.
Lateral surface

Median surface
Inferior surface

Coronal section
Coronal section

Horizontal section
 is a blockage or reduction of
blood flow in an artery that feeds that area of the
brain. This blockage may result from
and .
It is the most common cause of an infarct. An
infarct is the area of the brain that has ‘died’
because of this lack of oxygen.
 result from bleeding
within and ground the brain causing
compression and tissue injury, the most
common presentations are
and
.
Diagram of circle of Willis showing common sites of artherosclerosis
Diagram showing aortic arch with great vessels of the neck indicating the common
sites of artherosclerosis
 Atheroma and occlusion of the
internal carotid artery. The lumen of
the left artery (right of picture) is
reduced to a pinhole by atheroma.
The right artery ia occluded by a
thrombus. There is severe atheroma
of the posterior communicating and
basilar arteries with irregularity of
their walls (X 2.75).

Carotid angiogram showing the common

carotid and its bifurcation into the
internal and external with a block of the
internal carotid artery.
The most common sites of carotid artery stenosis (A) and occlusion (B).
Values are percent. (from Imprato and Riles; with permission)
Autopsy case of cerebral infarction due to thrombosis.
Necrosis is seen in the territory of middle cerebral artery.
Sagital section through the brain showing a large intracerebral hematoma.
Large intrapenchymal hemorrhage originating from the basal ganglia in
a hypertensive patient (Courtesy of Dr. M. Ambler)
BASAL GANGLIA HEMORRHAGE
A, B: Operative photo of subarachnoid
hemorrhage.
C: Photo at autopsy, showing blood clot at the
basal cistems.
Anterior communcating cerebral artery Middle cerebral artery
Anterior cerebral artery Basilar artery
Rupture of an arteriovenous
malformation (AVM)
DEFINITION:
Clinical symptoms of acute developing focal (or global)
cerebral dysfunction lasting 24 hours or longer, or lasting to
death, without any apparent cause other than vascular origin
(WHO, 1986)

TIA (Transient Ischemic Attack) has the same definition but

last s less than 24 hours, often just for a few minute.

SAH (Subarachnoid hemorrage) is the exeption to this

definition and usually present without focal neurological
deficit.
 STROKE
15% Primary
85% Hemorrhage
 Intraparenchymal.
 subarachnoid.
Ischemic stroke

20% 25% 20% 30% 5%

Atherosclerotic Penetrating Cardiogenic Cryptogenic Other, unsual

Cerebrovascular Artery Embolism Stroke Causes
disease Disease Atrial fibrillation Prothrombic states
(“lacunae”) Valve disease Dissections
Ventricular thrombi Arteritis
Many others Migraine/vasospasm
Drug abuse
Many more

hypoperfusion Arteriogenic emboli

Classification of stroke by mechanism, with frequency estimates of the abnormalities.

Note that about 30% of stroke is cryptogenic (From Albers GW. Et al: Chest 2001; 119:3005, with permission)
CLINICAL CLASIFICATION:
OXFORDSHIR E CSP CLINICAL
I. ISCHEMIC/NON-HEMORRHAGIC CLASIFICATION/BAMFORD
STROKE 1. Partial Anterior
1. RIND (Reversible Circulation Infarction (PACI)
Ischemic Neurological VARIABLE
2. Total Anterior Circulation
Deficit)
Infarction
2. Stroke in (TACI) POOR
evolution/progressing 2. Lacunar Infarction
stroke. (LACI) GOOD
3. Completed stroke. 4. Posterior Circulation Infarction
(POCI) VARIABLE
I. HEMORRHAGIC STROKE

A.A.B.N. Nuartha, 2007

I. Ischemic/non hemorrhagic stroke:
1. Reversible ischemic neurological deficit
(RIND):
The sudden or rapid onset of a focal neurological
deficit that is caused by a cerebrovascular
disease, but the deficit lasts over 24 hours and
regression completely to normal within about
1 – 3 weeks.
2. Stroke in evolution (progressing stroke):
Refer to the progression of a focal
neurological deficit over 24 hours secondary
to a stroke in the carotid artery distribution,
or 72 hours in the vertebral basilar artery
distribution.
3. Completed stroke:
Refer to a stable neurological deficit for more
than 24 hours with infarcts in the carotid
artery distribution, or 72 hours with infarcts in
the vertebral basilar artery distribution.
II. Hemorrhagic stroke:
Usually presents with a sudden onset of focal
neurologic deficit that may be accompanied by
alteration in mental status, headache, and
vomiting.
1. Intra cerebral hemorrhage:
Present as a rapidly expanding mass lesion
(hematoma) with sign of increased intracranial
pressure.
2. Subarachnoid hemorrhage:
A hemorrhage from cerebral blood pressure,
aneurysm or vascular malformation (arterio
venous malformation) in to the subarachnoid
space, ie the space surroundings the brain where
blood vessles lie between the arachnoid and pial
layers.
Clinical syndromes
Lacunar infarcts (LACI).
Total anterior circulation
infarcts (TACI).
Partial anterior circulation
infarcts (PACI).
Posterior circulation infarcts
(POCI).
Sympton and signs
Pure motor stroke.
Pure sensory stroke.
Sensory-motor stroke.
Ataxic hemiparesis (faciobrachial and brachiocrural involvement
were included).
Combination of new higher cerebral dysfunction (dysphasia,
dyscalculia, visuospatial disorders).
Homonymous visual field defects.
Ipsilateral motor and / or sensory deficit of at least two areas of
the face, arm, or leg.
Only two of the three components of the TACI syndrome (higher
cerebral dysfunction alone, or with motor / sensory deficit more
restricted than those classified as LACI).
Ifsilateral cranial nerve palsy with contralateral motor and / or
sensory deficit.
Bilateral motor and / or sensory deficit.
Disorder of conjugate eye movement.
Cerebellar dysfunction without ipsilateral long-tract deficit.
Isolated homonymous visual field defect.
The sudden or rapid onset of a focal neurological
deficit that is caused by a cerebrovascular disease,
but the deficit lasts less than 24 hours, reverting
completely to normal.

TIA is a minor stroke or mini stroke and a risk factor

for ischemic stroke.
Lacunar infarcts are small infarcts (0,5 – 1,5 cm) that
are usually multiple and associated with a history
of hypertension, characterized by hyaline
thickening of the small penetrating artery of the
brain (lipohyalinosis).
Ischemic penumbra is the area between
ischemic core and normal brain tissues
(cerebral blood flow / CBF : 8 or 10 – 20
ml/100 gram brain tissue / minute)
 60
%
Maintained by autoregulation;
Higher CBF in bray matter.
45
Increase O2 extraction
may maintain normal CMRO2
35

? ↑ Glycolysis
I ? ↓ Protein synthesis
S
20 C Threshold of electrical failure
H
E The “PENUMBRA”
M
I
10 A Threshold of ionic failure
Anoxic depolarization
(↑ ECF K+ & ↓ ECF Ca++)

Unmodifiable risk factors
Age
Sex
Race
Family history
Previous stroke
Major modifiable risk factors
Atrial fibrillation
Hypertension
Isolated systolic hypertension
Myocardial infarction
Other heart disease
Diabetes mellitus
Transient ischemic attacks
smoking
Questionable, rare, or weak
modifiable risk factors Risk factors predominant in the young
AIDS Mitral velve leaflet prolapse
Alcohol Sicle cell disease and other
Fibrinogen and platelets hemoglobinophathies
Lipids Migraine
Exercise Cocaine abuse
Obesity Obstructive sleep apnea
Hematocrit Intercurrent infection and
Water supply inflammation
Anticardiolipin antibodies Patent foramen ovale
Oral contraceptives Atrial septal aneurysm
Pregnancy Systemic lupus erythematosus
Homocystinuria
Diet
Socioeconomic status
Season
claudication
Etiology of intracerebral hemorrhage
Hypertension (50% - Cerebral amyloid
60%). angiopathy .
Arteriovenous Coagulopathy
Malformation, (deficiency of factors VII,
aneurysm. VIII, IX, XIII, von
Willebrand’s factors,
Bleeding into a tumor. afibrinogenemia,
Anticoagulant use. idiopathic
thrombocytopenic
Fibrinolytic agents. purpura, thrombotic
thrombocytopenic
Sympathomimetic purpura, disseminated
drugs. intravascullar
coagulation, uremia)
Vasculitis.
Myeloproliferative
disorders (multiple
myeloma, acute and
chronic myelogenous
leukemia, essential
thrombocythemia).
Eclampsia.
Moyamoya syndrome.
Acute elevation of blood
pressure or reperfusion of
ischemic area (prolonged
migraine, exposure to cold,
dental pain,
postendarterectomy).
LEFT- SIDE STROKE
 Right-sided hemiparesis/paralysis.
 Right-side hemihypesthesia/anesthesia.
 Hoonymous hemianopsia of right visual field.
 Right sided dysarthria.
 Motor and/or sensory aphasia.

RIGHT-SIDE STROKE
 Left-sided hemiparesis/paralysis.
 Left-sided hemihypesthesia/anethesia.
 Hemianopsia of left visual field.
 Left-side dysarthria.
 OCCLUSION
 Monocular blindness (ipsilateral)
 Aphasia (motor and/or sensory in
dominant hemisphere)
 Hemiparesis/paralysis (contralateral) ICA
 Hemihypesthesia/anesthesia (contralateral) MCA

 Homonymous hemianopsia (contralateral)

 Motor paresis and/or sensory loss of face and
upper limb (contralateral)
 Motor paresis and sensory loss of lower
ACA
limb (contralateral)
 Transient hemiparesis (contralateral)
 Transient hemihypesthesia (contralateral)
PCA
 Homonymous hemianopsia (contralateral)
 Sensory aphasia (in dominant hemisphere)
 Bilateral visual disturbance.
 Double vision (diplopia).
 Nistagmus.
 Tinnitus, Vertigo, Hearing disturbance.
 Circumoral paresthesia.
 Motor/sensory disturbance (bilateral, alternating, crossed).
 Ipsilateral cerebellar ataxia.
 Nausea, vomitus.
 Dysphasia.
 Dysarthria.
 Amnesia, confusion.
 Intermitten loss of consciousness.
 Drowsy tendency.
 Drop attacks (drop spells).
 Ipsilateral Horner syndrome.
 Internuclear opthalmoplegia.
Anatomic area of Clinical findings
imvolvement
Lobar 15%
Frontal Frontal headache, motor weakness arm> leg behavioral
abnormalities.
Parietal Unilateral headache, hemisensory deficit, spatial neglect
(nondominant), visual field deficits.
Temporal Unilateral headache, aphasia (dominat), visual field
defect.
Occipital Ipsilateral periorbital headache, visual field loss or
blurring.
Deep
Putaminal 55% Unilateral motor, sensory and visual field loss, aphasia
(dominant), neglect (nondominat), coma.
Thalamic 10% Hemisensory deficit > hemiparesis. Gaze deviation, pupil
asymetry.
Cerebellum 10% Nausea, vomiting, ataxia, depressed level of
consciousness.
Pontine 10% Coma, quadriplegia, decerebrate posturing, pinpoint
pupils.
Possible causes of deterioration in acute stroke patients

Hemorrhagic conversion of infarction.

Cerebral edema formation.

Concurrent seizures.

Intercurrent infection (pneumonia, urosepsis, and so forth)

Metabolic abnormalities (hypoglycemia, hyponatremia, and so forth)

Hypotension (including iatrogenic).

MEDICAL HISTORY GENERAL EXAMINATION MULTIDICIPLINARY
(ANAMNESIS) NEUROLOGICAL EXAMINATION TEAM

INVESTIGATIONS
CLINICAL LABORATORY TEST.
DIAGNOSTIC RADIOLOGIC/IMAGING EXAMINATION:
 CHEST X-RAY.
 CT, CTA,MRI, MRA, MRS.
 DSA, CATHETER ANGIOGRAPHY
 PET, SPECT, CT-PET.
 TRANSCRANIAL DOPPLER AND DUPLEX
CAROTID ULTRASONOGRAPHY.
 EEG.
ECHOCARDIOGRAPHY (TTE, TEE).
 LUMBAR PUNCTURE.

ISCHEMIC STROKE HEMORRHAGIC STROKE

MANAGEMENT
 Digital subtraction
angiogram showing
significant stricture due to
atheroma in the left internal
carotid.

Carotid arteriogram
showing a large
carotid aneurysm.
MRA in the cervical area (AP
view) shows stenosis of right
internal carotid artery. The
artery appears occluded, which
is a typical finding of marked
stenosis in MRA.
Extensive right sided posterior inferior Extensive right middle cerebral infarct.
cerebellar infarct with right vertebral
occlusion.
Extensive infarct in the territory of the left anterior cerebral artery. This infarct was
due to extensive vasospasm after a subarachnoid hemorrhage (see operative defect)
a. Extensive recent territorial infarct in the distribution of the right posterior crebral artery, with
demonstration of a hipodense lesion in the left thalamic region, presumably the expression of
involvement of the posterior thalamoperforating arteries (arrow).
b. Territorial infarction in the distribution of both posterior cerebral arteries.
Extensive borderzone infarct in the anterior cerebral/middle cerebral borderzone
area, right. The lesion reaches the cortex (arrow).
Cerebral angiogram in case with
occlusion of middle cerebral
artery (lateral view).
Contrasct medium from the
anterior cerebral artery and
partly posterior cerebral artery is
filled in retrograde into the
territory of the middle cerebral
artery (B,C).
CT scans of hypertensive intracerebral hemorrhage.
A: left putaminal hemorrhage. The verticles are compressed to the right side.
B: left thalamic hemorrhage. Hematoma ruptured into the lateral ventricle.
C: hemorrhage in the right cerebellar hemisphere. Inferior horns of the lateral
ventricle are observed, indicating ventricullar enlargement.
D: hemorrhage in the brain stem.
A, C, E,: Plain CT showing high density sres s long the basal cistems.
B, D, F, : Enhanced CT showing rather homogeneous enhancement in each high
density area.
A: Plain CT slightly high density area in a round shape is observed at the left
temporal tip.
B: Enhanced CT marked round enhancement is observed.
AP view of cerebral angiography demonstrates an anterior communicating artery
aneurysm.
CT scan of cerebral arteriovenous malformation in the left frontal lobe.
A part of slight high density area can be seen. Enhanced CT shows circular, rod-like,
or serpentine uniform high density area, which corresponds to thick draining veins.
Large AVM occupying right cerebellar hemisphere: pre-(upper row) and post-embolization (low row).
Lateral view of right vertebral angiography was shown in the left, plain CT scan in the center and CT
scans after contrast enhancement in the right. Numerous embolic material were found in the nidus,
which markedly reduced AVM flow.
TWO PHASE OF STROKE
Reversible release of functional
0h activity
THERAPEUTIC
WINDOWS 3h
Stage of potential functional
6h inactivity
.
Therapeutic
Window End stage of functional
.
12h restoration
ISCHEMIA
.

Appearance of cell necroses

. 24h

.
Appearance
THERAPEUTIC WINDOW: < 6 h
of infarct .
(with Thrombolytics: < 3h )

48h CT-Scan appearance of infarct

MANAGEMENT
I. General medical management.
II. Ischemic stroke.
1. Therapeutic reperfusion/revascularization.
1.1. Thrombolytic agents
1.2. Anticoagulants
1.3. Anti platelets.
1.4. Endovascular intervention (cerebral neurovascular
angioplasty with stenting).
2. Cerebral neuroprotection
III. Hemorrhagic stroke
1. Critical care management.
2. Elevated blood pressure management.
3. Increased ICP or seizure prophylaxis and therapy.
4. Body temperature management.
5. Rebleading prophylaxis and therapy.
6. Vasospasm prophylaxis and therapy.
7. Cerebral neuroprotection.
8. Surgical intervention.
9. Endovascular intervention/strereotaxic
radiosurgery.
ICH location Clinical/CT features Treatment
Putamen. Alert, small ICH (<30ml). Nonsurgical.
Comatose, large ICH (>60ml). Nonsurgical.
Drowsy, intermediate ICH (30 – 60 ml). Consider evacuation.
Caudate. Alert or Drowsy with intraventricular Consider ventriculostomy.
hemorrhage and hydrocephalus.
Thalamus. Drowsy or lethargic, with blood in the Consider ventriculostomy.
third ventricle and hydrocephalus.
Lobar white Drowsy or lethargic, with intermediate Consider evacuation.
matter. ICH (20 – 60 ml), progressive decline in
level of consciousness.
Pons, midbrain, - Nonsurgical.
medula.
Cerebellum. Noncomatose, with ICH > 3 cm in Evacuation recommended,
diameter, and / or hydrocephalus, and / or preceded by
effacement of quadrigeminal cistem. ventriculostomy if patient is
actively deteriorating.
ISCHEMIC STROKE (ANTERIOR CIRCULATION):
PROGNOSTICATOR OF POOR OUTCOME

 ↓Level of conciousness after ictus.

 ↓Gaze palsy, gaze preference, pupillary
asymmetry.
 Hypodensity > 50% of arterial territory, brain
swelling, or early midline shift on CT scan.
 Need for reintubation and mechanical
ventilation.

(Wijdicks, Scott, 1997).

ISCHEMIC STROKE (POSTERIOR CIRCULATION):
PROGNOSTICATOR OF POOR OUTCOME

 Basilar artery occlusion causing locked-in

syndrome or coma.
 Cerebellar infarction with brain stem
compression and hydrocephalus.
 Bilateral thalamic infarcts.

(Nadeau, et al, 1992).

HEMORRHAGIC STROKE (ICH):
PROGNOSTICATOR OF POOR OUTCOME

 > 70 years.
 ↓Level of conciousness after ictus (each grade).
 Limb paresis (each grade).
 Hyperglicemia after ictus.
 ICH : Blood volume > 60 cc.
 IVH : blood volume > 20 cc.
 Midline shift of septum pellucidum/pineal gland (6 – 10
mm) on CT scan.
 Acute hydrocephalus (putaminal hemorrhage)
(Daverat et al, 1991; Fieschi et al, 1988; Phan et al, 2000)

A.A.B.N. Nuartha, 2007

 Secondary Disease are more often the cause of death than stroke
Complication of Acute Stroke
%

70%

40%

20%

13% 13%
9% 10% 8% 9%

3% 4%
<1% <1% <1%

Ischemic Infarct
Cerebral Hemorrhage
No treatment of stroke can be as
successful as of the even
from occuring.
Prevention is the most effective way to
avoid or suffering from stroke:
I. Promotion.
II. Primary prevention.
III. Secondary prevention.
 STROKE CONTROL STRATEGY

HEALTHY RISK FACTOR STROKE/TIA

PROMOTION PRIMARY PREVENTION SECONDARY REVENTION

- MODIFY LIFE-STYLE - MODIFY LIFE-STYLE - MODIFY LIFE-STYLE

- CONTROL OF RISK FACTOR - CONTROL OF RISK FACTOR
- ANTI THROMBOTIC.
- THROMBECTOMY/CAROTID
ENDARTERECTOMY.
- ANGIOPLASTY AND
STENTING
 MODIFY LIFE- CONTROL OF ANTI THROMBECTOMY/ ANGIOPLASTY
STYLE RISK FACTORS THROMBOTIC CAROTID AND STENTING
ENDARTERECTOMY

1. Diet 1. Inmodifiable. 1. Anti platelet. 1. Symptomatic stenosis 1. Patient with high

2. Physical exercise. 2. Modifiable. 2. Anti coagulant. (>70%). risk symptomatic
3. Cessation of 2. Asymptomatic stenosis caroted stenosis
smoking. (<90%). or inoperable
cases.
4. Alcohol reduction.
 Reducing body weight.
 Restricting dietary salt.
 Increasing fibers and decreasing fat in
your diet.
 Not smoking.
 Avoiding exess alcohol.
 Exercising regularly.
 Practicing relaxation techniques.
1. Modify life style.
2. Control of risk factor.
3. Anti platelet agent:
 Asetosal/ASA tab: 75 – 325 mg/day, 1 X I.
 ASA 25 mg/Dipyridamole 200 mg cap: 2 X I.
 Clopidogrel 75 mg tab: 1 X I.
 Ticlopidine 250 mg tab: 2 X I.
 Aspirin 75 mg tab + Clopidogrel 75 mg tab: 1 X I.
 Triflusal 300ml mg tab: 1 X 2.
4. Oral anti coagulant:
 Warfarin  with AF, prosthetic heart valves and other cardio emboli
5. Surgery-microsurgery/radiosurgery-intervention
(gamma-knife, angioplasty with stent, coils, glue, or
ballons embolization).
 A. B.

A. Marked stenosis of the cervical ICA.

B. The stenosis was cleared after carotid
endarterectomy.