cerebrovascular disease (1)

7/28/2019 Cerebrovascular Disease (1)

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Cerebrovascular Disease


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Section 1 General

consideration Cerebrovascular disease: any abnormality of

the brain resulting from a pathologic process

of the blood vessels.

Cerebrovascular accident orstrokemay bedefined as a sudden interruption of blood

supply or hemorrhage into apart of the brain. the third commonest cause of death


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Classification

Ischemic transient ischemic attack (TIA)

cerebral thrombosis

cerebral embolism cerebral infarction

lacunar infarct

Hemorrhagic cerebral hemorrhage

subarachnoid hemorrhage (SAH)


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Blood supply of brain

1. Internal carotid system

Branchiocephalic trunkright 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


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Supply eyes and anterior

3/5 of the brain: frontal,

parietal, part of temporal

lobe, basal ganglia.


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Blood supply of brain 2. Vertebral-basilar system

Subclavian artery vertebral artery C6-C1transverse foramen great occipital foramen

basilar artery

posterior spinal arteries, anterior spinal artery

posterior inferior cerebellar artery

auditory artery

posterior cerebral arteries


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supply cerebellum,brain stem,posterior 2/5 of

brain (occipital,part of tempral lobe)


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3. Circle of Willis



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This forms a unique anastomotic system atthe base of the brain between the internal

carotid and vertebral-basilar systems.internal carotid arteries

two anterior cerebral arteriesanterior

communicating arterytwo posterior cerebral arteries

two posterior communicating arteries



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Age, family history, race

Hypertension

Heart disease Diabetes

Hyperlipemia

Smoking, excessive drinking

Obesity, diet, contraceptive drugs

Risk factors of CVD


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Section 2 TIA

A transient ischemic attack is a focaldisturbance of the cerebral circulation,

frequently repetitive, resulting in a period ofimpaired function lasting for a short period

(anything from a few minutes to twenty-

four hours). Attacks can occur in the carotidand/or vertebral artery territories.


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Etiology

Micro embolism

Spasm of cerebral blood vessel

Hemodynamic change

Compression of vertebral artery, steal

syndrome


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Clinical feature

1. 50-70, M>F

characteristics:

Abrupt onset

Transient

Complete recovery Repetitive


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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 tothe paresis (amaurosis fugax).

Horner sign

(3) Symptoms may present:

Dysphasia Paraesthesia or numbness in the contralateral

limbs.

hemianopia

Clinical feature


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3. Transient vertebralbasilar 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


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(3) Symptoms may present:

Dysphagia, dysarthria

Ataxia

Disturbance of consciousness

diplopia

Clinical feature


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Diagnosis

clinical features

No signs between attack


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Differential diagnosis

Partial epilepsy

Meniere disease


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Treatment1. Etiologic therapy

Blood pressure, sugar, lipid

Carotid endarterectomy, anastomosis of extra-

intra cranial vessels

2. Prophylactic treatment

Anti-platelet aggregation drugs:

Aspirin 50-300mg Qd PoTiclopidine 250mg Qd Po


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2. Prophylactic treatment

Anticoagulants: heparin

Chinese herbs

Chuanxiong rhizome, Red sage root, Saf flower

Others: vessodilator, volume expensor (Dextran-

40)

3. Brain protective agents

Calcium antagonist: nimodipine 20-40mg tid po

flunarizine (Sibelium) 5mg Qn po

Treatment


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Prognosis

1/3 repetitive attack

1/3 remission

1/3 cerebral infarction


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Section 3 Cerebral Thrombosis

infarction of an area of the brain secondary

to arterial occlusion by thrombosis of a

major vessel with insufficient collateralcirculation.


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Etiology

atherosclerosis

Arteritis: such as leptospirosis, rheumatic

fever rare cause:

congenital vascular malformation,

polycythemiablood hypercoagulability


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Pathology

Vessel: carotid > middle > posterior >

anterior > vertebral-basilar

Super-early stage: 1-6 hour

Necrosis cyst

White infarct

Red infarct: hemorrhagic infarct


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Pathophysiology

Neurons are sensitive to ischemia

Central necrosis

Ischemic penumbra

Super early stage: < 6 hours


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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


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Clinical type

Complete stroke

Progressive stroke

Reversible ischemic neurological deficit,

RIND)


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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.


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2. Middle cerebral artery

contralateral hemiplegia, hemianesthesia,

hemianopia

aphasia (if the dominant hemisphere is

affected)

Disturbance of body image (non-dominant

hemisphere)

Clinical syndrome


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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


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4. Posterior cerebral artery

contralateral hemianopia or quadrantanopia

thalamic syndrome: contralateral hemianesthesia,thalamic pain, ataxia, tremor, athetosis

Clinical syndrome


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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


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(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


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6. posterior inferior cerebellar artery

Wallenberg's syndrome, Lateral medullarysyndrome

Vertigo, vomiting, nystagmus

Crossed sensory disturbance

Ipsilateral Horner sign

Dysphagia, dysarthria

Ipsilateral ataxia

Clinical syndrome


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Investigation

1. CT

Low density

focus after 24-48

hours


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2. MRI

Investigation

A right carotid

artery occlusion,

low signal of T1,

and high signal of

T2 weighted

image.


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3. Lumbar puncture

Normal.

Large infarct: pressure

Hemorrhagic infarction: RBC

4. DSA

5. TCD

Investigation


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Diagnosis

after middle or old age.

rapid onset focal cerebral symptoms

premonitory symptoms

occurs in rest or sleep

CT/MRI find cerebral infarction focus


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Differential diagnosis

Cerebral hemorrhage

Cerebral embolism

Intracranial tumor


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Treatment

1. Principle2. 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


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5. Fibrinogen degradation

Defibrase, Batroxobin

6. Anti platelet aggregation

Aspirin, Ticlopidine

7. Others

? Vessel dilator ? Metabolic activator

Treatment


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8. Surgical treatment Reduce intracranial pressure

9. General management

Reduce intracranial pressure: mannitol10. Stroke unit

11. Rehabilitation

12. Prophylactic treatment Aspirin, Ticlopidine

Treatment


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Lacunar infarct


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Pathology

3-4mm,


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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


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Cerebral embolism

Occlusion of a major cerebral artery

by an embolus, with resultant

infarction of part of the brain.


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Etiology

Cardiac cause:

Atrial fibrillation, rheumatic valve disease,

endocarditis, atrial myxoma, myocardialinfarction

Non-cardiac:

Atherosclerosis plaque, pus embolus, fatembolus, tumor embolus

Embolus of unknown origin


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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


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Treatment

Cerebrovasodilators

Anticoagulant therapy

Treatment of primary disease


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cerebrovascular disease (1)

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