Cerebrovascular Disease
Section 1 General
consideration

Cerebrovascular disease: any abnormality of
the brain resulting from a pathologic process
of the blood vessels.
 Cerebrovascular accident or stroke may be
defined as a sudden interruption of blood
supply or hemorrhage into apart of the brain.
 the third commonest cause of death
Classification

Ischemic
transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism
cerebral infarction
lacunar infarct
 Hemorrhagic
cerebral hemorrhage
subarachnoid hemorrhage (SAH)
Blood supply of brain

1. Internal carotid system
Branchiocephalic trunk→right common carotid artery
left common carotid artery
→internal carotid artery → carotid foramen →
 Ophthalmic artery
 Anterior choroidal artery
 Posterior communicating artery
 Anterior cerebral artery
 Middle cerebral artery
Supply eyes and anterior
3/5 of the brain: frontal,
parietal, part of temporal
lobe, basal ganglia.
Blood supply of brain

2. Vertebral-basilar system
 Subclavian artery → vertebral artery → C6-C1




transverse foramen → great occipital foramen →
basilar artery
posterior spinal arteries, anterior spinal artery
posterior inferior cerebellar artery
auditory artery
posterior cerebral arteries
supply cerebellum,
brain stem,
posterior 2/5 of
brain (occipital,
part of tempral lobe)
Blood supply of brain

3. Circle of Willis
Blood supply of brain

This forms a unique anastomotic system at
the base of the brain between the internal
carotid and vertebral-basilar systems.
internal carotid arteries
two anterior cerebral arteries anterior
communicating artery
two posterior cerebral arteries
two posterior communicating arteries
Risk factors of CVD

Age, family history, race
 Hypertension
 Heart disease
 Diabetes
 Hyperlipemia
 Smoking, excessive drinking
 Obesity, diet, contraceptive drugs
Section 2 TIA

A transient ischemic attack is a focal
disturbance of the cerebral circulation,
frequently repetitive, resulting in a period of
impaired function lasting for a short period
(anything from a few minutes to twentyfour hours). Attacks can occur in the carotid
and/or vertebral artery territories.
Etiology

Micro embolism
 Spasm of cerebral blood vessel
 Hemodynamic change
 Compression of vertebral artery, steal
syndrome
Clinical feature
1. 50-70, M>F
characteristics:
 Abrupt onset
 Transient
 Complete recovery
 Repetitive
Clinical feature
2. Transient carotid ischemic attacks
(1)Common symptoms:
 Weakness of the contralateral arm and/or leg.
(2) Characteristic symptoms:
 Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax).
 Horner sign
(3) Symptoms may present:
 Dysphasia
 Paraesthesia or numbness in the contralateral
limbs.
 hemianopia
Clinical feature
3. Transient vertebral –basilar ischemic attack
(1) Common symptoms
 Vertigo, nausea, vomiting
(2) Characteristic symptoms:
 Drop attack
 Transient global amnesia, TGA
 Cortical blindness
 Crossed paralysis or sensory disturbance
Clinical feature
(3) Symptoms may present:
 Dysphagia, dysarthria
 Ataxia
 Disturbance of consciousness
 diplopia
Diagnosis

clinical features
 No signs between attack
Differential diagnosis

Partial epilepsy
 Meniere disease
Treatment
1. Etiologic therapy
 Blood pressure, sugar, lipid
 Carotid endarterectomy, anastomosis of extraintra cranial vessels
2. Prophylactic treatment
 Anti-platelet aggregation drugs:
Aspirin 50-300mg Qd Po
Ticlopidine 250mg Qd Po
Treatment
2. Prophylactic treatment
 Anticoagulants: heparin
 Chinese herbs
Chuanxiong rhizome, Red sage root, Saf flower
 Others: vessodilator, volume expensor (Dextran40)
3. Brain protective agents
 Calcium antagonist: nimodipine 20-40mg tid po
flunarizine (Sibelium) 5mg Qn po
Prognosis
1/3 → repetitive attack
 1/3 → remission
 1/3 → cerebral infarction

Section 3 Cerebral Thrombosis

infarction of an area of the brain secondary
to arterial occlusion by thrombosis of a
major vessel with insufficient collateral
circulation.
Etiology

atherosclerosis
 Arteritis: such as leptospirosis, rheumatic
fever
 rare cause:
congenital vascular malformation,
polycythemia
blood hypercoagulability
Pathology

Vessel: carotid > middle > posterior >
anterior > vertebral-basilar
 Super-early stage: 1-6 hour
 Necrosis → cyst

White infarct
 Red infarct: hemorrhagic infarct
Pathophysiology

Neurons are sensitive to ischemia
 Central necrosis
 Ischemic penumbra
 Super early stage: < 6 hours
Clinical feature

onset is rapid
 usually occur in the rest and sleep
 premonitory symptoms such as weakness of
a limb, transient ischemic attack
 The headache, vomit, and loss of
consciousness may be absent or slight.
 Focal signs develop in several days
Clinical type

Complete stroke
 Progressive stroke
 Reversible ischemic neurological deficit,
RIND)
Clinical syndrome
1. Internal carotid artery
 May have no signs (if the collateral supply,
from the other side, is good )
 amaurosis fugax, uniocular blindness
 Horner's syndrome may present in the side
of the occlusion.
 contralateral hemiplegia and hemianesthesia.
Clinical syndrome
2. Middle cerebral artery
 contralateral hemiplegia, hemianesthesia,
hemianopia
 aphasia (if the dominant hemisphere is
affected)
 Disturbance of body image (non-dominant
hemisphere)
Clinical syndrome
3. Anterior cerebral artery
 contralateral hemiplegia, the leg frequently
being more affected than the arm.
 paracentral lobule: regulation of sphincter
function, retention or incontinence
 mental symptoms: apathy, euphoria
Clinical syndrome
4. Posterior cerebral artery
 contralateral hemianopia or quadrantanopia
 thalamic syndrome: contralateral hemianesthesia,
thalamic pain, ataxia, tremor, athetosis
Clinical syndrome
5. Vertebro-basilar artery
(1) Main trunk
 nausea, vomiting, tetraplegia, coma, death
(2) Weber syndrome
 Unilateral lesion of midbrain
 Ipsilateral oculomotor nerve paralysis, contra
lateral hemiplegia
Clinical syndrome

(3) locked-in syndrome
 Bilateral infarction in the basis pontis
 Tetraplegia, can not speak, can not swallow
 Conscious
 Can only respond by vertical gaze and
blinking
Clinical syndrome
6. posterior inferior cerebellar artery
Wallenberg's syndrome, Lateral medullary
syndrome
 Vertigo, vomiting, nystagmus
 Crossed sensory disturbance
 Ipsilateral Horner sign
 Dysphagia, dysarthria
 Ipsilateral ataxia
Investigation
1. CT
Low density
focus after 24-48
hours
Investigation

2. MRI
A right carotid
artery occlusion,
low signal of T1,
and high signal of
T2 weighted
image.
Investigation
3. Lumbar puncture
 Normal.
 Large infarct: pressure ↑
 Hemorrhagic infarction: RBC
4. DSA
5. TCD
Diagnosis

after middle or old age.
 rapid onset focal cerebral symptoms
 premonitory symptoms
 occurs in rest or sleep
 CT/MRI find cerebral infarction focus
Differential diagnosis

Cerebral hemorrhage
 Cerebral embolism
 Intracranial tumor
Treatment
1. Principle
2. Fibrinolytic therapy of super-early stage
 Within 6 hours
 Urokinase, rt-PA
3. Anticoagulant
 Heparin, low molecular heparin
4. Brain protect
 Calcium antagonist: nimodipine, flunarizine
 Mannitol
 Hypothermia
Treatment
5. Fibrinogen degradation
 Defibrase, Batroxobin
6. Anti platelet aggregation
 Aspirin, Ticlopidine
7. Others
 ? Vessel dilator
 ? Metabolic activator
Treatment
8. Surgical treatment
 Reduce intracranial pressure
9. General management
 Reduce intracranial pressure: mannitol
10. Stroke unit
11. Rehabilitation
12. Prophylactic treatment
 Aspirin, Ticlopidine
Lacunar infarct
Pathology

3-4mm, <15-20mm
 Small liquid cavity
 Basal ganglia, thalamus, brain stem
 Small artery: 100-200μm
 Atherosclerosis
Clinical feature

40-60 years of age
 Always combined with hypertension
Lacunar syndrome:
 1. Pure motor hemiparesis
 2. Pure sensory stroke
 3. Ataxic-hemiparesis
 4. Dysarthric-clumsy hand syndrome
 5. Sensorimotor stroke
 6. Lacunar state
Cerebral embolism
Occlusion of a major cerebral artery
by an embolus, with resultant
infarction of part of the brain.
Etiology

Cardiac cause:
Atrial fibrillation, rheumatic valve disease,
endocarditis, atrial myxoma, myocardial
infarction
 Non-cardiac:
Atherosclerosis plaque, pus embolus, fat
embolus, tumor embolus
 Embolus of unknown origin
Clinical feature

Left middle cerebral artery
 abrupt onset, maximum disability occurring
at once
 In some cases, there is rapid improvement
 The primary disease, such as rheumatic
heart disease
Treatment

Cerebrovasodilators
 Anticoagulant therapy
 Treatment of primary disease