Cerebrovascular Disease

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Presentation transcript:

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 twenty-four 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 extra-intra 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 (Dextran-40) 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