1. Cerebrovascular Disease

2. 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

3. Classification Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)

4. 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

5. Supply eyes and anterior 3/5 of the brain: frontal, parietal, part of temporal lobe, basal ganglia.

6. 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

7. supply cerebellum, brain stem, posterior 2/5 of brain (occipital, part of tempral lobe)

8. Blood supply of brain
3. Circle of Willis

9. 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

10. Risk factors of CVD Age, family history, race Hypertension
Heart disease
Diabetes
Hyperlipemia
Smoking, excessive drinking
Obesity, diet, contraceptive drugs

11. 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.

12. Etiology Micro embolism Spasm of cerebral blood vessel
Hemodynamic change
Compression of vertebral artery, steal syndrome

13. Clinical feature 1. 50-70, M>F characteristics: Abrupt onset
Transient
Complete recovery
Repetitive

14. 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

15. 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

16. Clinical feature (3) Symptoms may present: Dysphagia, dysarthria
Ataxia
Disturbance of consciousness
diplopia

17. Diagnosis
clinical features
No signs between attack

18. Differential diagnosis
Partial epilepsy
Meniere disease

19. Treatment 1. Etiologic therapy Blood pressure, sugar, lipid
Carotid endarterectomy, anastomosis of extra-intra cranial vessels
2. Prophylactic treatment
Anti-platelet aggregation drugs:
Aspirin mg Qd Po
Ticlopidine 250mg Qd Po

20. 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

21. Prognosis 1/3 → repetitive attack 1/3 → remission
1/3 → cerebral infarction

22. 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.

23. Etiology atherosclerosis
Arteritis: such as leptospirosis, rheumatic fever
rare cause:
congenital vascular malformation, polycythemia
blood hypercoagulability

24. Pathology
Vessel: carotid > middle > posterior > anterior > vertebral-basilar
Super-early stage: 1-6 hour
Necrosis → cyst
White infarct
Red infarct: hemorrhagic infarct

25. Pathophysiology Neurons are sensitive to ischemia Central necrosis
Ischemic penumbra
Super early stage: < 6 hours

26. 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

27. Clinical type Complete stroke Progressive stroke
Reversible ischemic neurological deficit, RIND)

28. 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.

29. Clinical syndrome 2. Middle cerebral artery
contralateral hemiplegia, hemianesthesia, hemianopia
aphasia (if the dominant hemisphere is affected)
Disturbance of body image (non-dominant hemisphere)

30. 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

31. Clinical syndrome 4. Posterior cerebral artery
contralateral hemianopia or quadrantanopia
thalamic syndrome: contralateral hemianesthesia, thalamic pain, ataxia, tremor, athetosis

32. 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

33. 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

34. 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

35. Investigation
1. CT
Low density focus after hours

36. Investigation
2. MRI
A right carotid artery occlusion, low signal of T1, and high signal of T2 weighted image.

37. Investigation 3. Lumbar puncture Normal. Large infarct: pressure ↑
Hemorrhagic infarction: RBC
4. DSA
5. TCD

38. Diagnosis after middle or old age. rapid onset focal cerebral symptoms
premonitory symptoms
occurs in rest or sleep
CT/MRI find cerebral infarction focus

39. Differential diagnosis
Cerebral hemorrhage
Cerebral embolism
Intracranial tumor

40. 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

41. Treatment 5. Fibrinogen degradation Defibrase, Batroxobin
6. Anti platelet aggregation
Aspirin, Ticlopidine
7. Others
? Vessel dilator
? Metabolic activator

42. Treatment 8. Surgical treatment Reduce intracranial pressure
9. General management
Reduce intracranial pressure: mannitol
10. Stroke unit
11. Rehabilitation
12. Prophylactic treatment
Aspirin, Ticlopidine

43. Lacunar infarct

44. Pathology 3-4mm, <15-20mm Small liquid cavity
Basal ganglia, thalamus, brain stem
Small artery: μm
Atherosclerosis

45. 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

46. Cerebral embolism
Occlusion of a major cerebral artery by an embolus, with resultant infarction of part of the brain.

47. 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

48. 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

49. Treatment Cerebrovasodilators Anticoagulant therapy
Treatment of primary disease