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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
Blood supply of brain
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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
Blood supply of brain
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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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