Cerebral Vascular Disease

1. Cerebral Vascular Disease

2. Risk factors for stroke • Systolic or diastolic hypertension • Diabetics • Hypercholesterolemia • Heart disease (afib) • Cigarette smoking • Heavy alcohol consumption • High homocystine • Oral contraceptive use

3. The major types of cerebrovascular disease • Cerebral ischemia and infarction • Transient Ischemic Attacks • Atherosclerotic thrombosis • Lacunes • Embolism • Hemorrhage • Hypertensive hemorrhage • Ruptured aneurysms and vascular malformations • Other

4. Cerebral ischemia and infarction Anatomy and pathology • The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it.

9. Anatomy and pathology • Occlusion leads to sudden severe ischemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise to the clinical picture of a transient ischemic attack.

10. Anatomy and pathology • When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischemic neurological deficit ( RIND ) if it recovers completely in a few days,or a completed stroke if there is a persistent deficit.Sometimes recovery is very slow and incomplete.

11. Neurological symptoms and signs • The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischemic process.

12. Neurological symptoms and signs • The following suggest middle cerebral territory: • Dysphasia;Dyslexia, dysgraphia, dyscalculia;Loss of use of contralateral face and arm;Loss of feeling in contralateral face and arm.

13. Neurological symptoms and signs • The following suggests anterior cerebral territory:Loss of use and/ or feeling in the contralateral leg. • The following suggests posterior cerebral territory:Development of a contralateral homonymous hemianopia.

14. Neurological symptoms and signs • The following suggests a deep-seated lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins:Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia.

15. Neurological symptoms and signs • The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis):Monocular loss of vision.

16. Neurological symptoms and signs The following suggest vertebro-basilar territory: • double vision • facial numbness • facial weakness • vertigo • dysphagia • dysarthria • ataxia • drop attacks;motor or sensory loss in both arms or legs.

17. Transient Ischemic Attacks(TIA) • Definition of term • Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischemic neurologic disturbance, Consensus has been that their duration should be less than 24 h.

18. Clinical picture • Transient Ischemic Attacks can reflect the involvement of any cerebral artery. The loss of function entirely depends on the influenced artery.It may last a few seconds or up to 12 to 24 h, Most of them last 2 to 15 min.There are only a few attacks or several hundred.Between attacks, the neurologic examination may disclose no abnormalities.A stroke may occur after numerous attacks have occurred over a period of weeks or months.

19. Differential diagnosis of TIAs • Transient episodes, indistinguishable from TIAs, are known to occur in patients with Seizure,Migraine,Transient global amnesia,and occasionally in patients with multiple sclerosis, meningioma, glioblastoma ,metastatic brain tumors situated in or near the cortex ,and even with subdural hematoma.

20. Cerebral thrombosis • Most cerebrovascular disease can be attributed to atheroscleroses and chronic hypertension; until ways are found to prevent or control them, vascular disease of the brain will continue to be a major cause of morbidity.

21. Pathogenesis • Pathogenesis of Ischemic neuronal death Ischemia ↓ Excitatory amino acid receptors ↓ Borderzone or penumbra↓ Programmed cell death

22. Clinical picture • In general, evolution of the clinical phenomena in relation to cerebral thrombosis is more variable than that of embolism and hemorrhage. The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischemic process.(above)

23. Clinical picture • In more than half of patients, the main part of the stroke is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction. The final stroke may be preceded by one or two attacks or a hundred or more brief TIAs, and stroke may follow the onset of the attacks by hours, weeks, or, rarely, months. • The most occurrence of the thrombotic stroke is during sleep. The patient awakens paralyzed. Either during the night or in the morning. • Unaware of any difficulty, he may arise and fall helplessly to the floor with the first step.

25. Clinical picture • Associated symptoms • Seizures accompany the onset of stroke in a small number of cases (10-50%); in other instances, they follow the stroke by weeks to years. The presence of seizures does not definitively distinguish embolic from thrombotic strokes, but seizure at the onset of stroke may be more common with embolus.

26. Clinical picture • Associated symptoms • Headache occurs in about 25% of patients with ischemic stroke, possibly because of the acute dilation of collateral vessels.

27. Laboratory Findings • CT Scan or MRI: A CT scan or MRI should be obtained routinely to distinguish between infarction and hemorrhage as the cause of stroke, to exclude other lesions (eg, tumor, abscess) that can mimic stroke, and to localize the lesion. CT is usually preferred for initial diagnosis because it is widely available and rapid and can readily make the critical distinction between ischemia and hemorrhage. • Lumbar Puncture: This should be performed in selected cases to exclude subarachnoid hemorrhage.

28. Laboratory Findings • Cerebral Angiography: Intra-arterial angiography is used to identify operable extracranial carotid lesions in patients with anterior circulation TIAs who are good surgical candidates. It also can be used for intra-arterial thrombolysis ( r-tPA) • Magnetic resonance angiography (MRA) may detect stenosis of large cerebral arteries, aneurysms, and other vascular lesion, but its sensitivity is generally inferior to that of conventional angiography.

29. Differential Diagnosis • Vascular disorders are mistaken for ischaemic stroke include intracerebral hemorrhage, subdural or epidural hematoma , and subarachnoid hemorrhage from rupture of an aneurysm or vascular malformation. These condition can often be distinguished by a history of trauma or of excruciating headache at onset, a more marked depression of consciousness, or by the presence of neck stiffness on examination. They can be excluded by CT scan or MRI.

30. Differential Diagnosis • Differential Diagnosis: Other structural brain lesion such as tumor or abscess can also produce focal cerebral symptoms of acute onset. Brain abscess is suggested by concurrent fever, and both abscess and tumor can usually be diagnosed by CT scan or MRI. Metabolic disturbances, particularly hypoglycemia and hyperosmolar nonketotic hyperglycemia, may present in stroke like fashion. The serum glucose level should therefore be determined in all patients with apparent stroke.

31. Treatment of Cerebral Thrombosis and Transient Ischemic Attacks • The current treatment of it may be divided into four parts: Management in the acute phase Measures to restore the circulation and arrest the pathologic process 1. Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs ) 2.Anticoagulant drugs ( Heparin, LMWH & warfarin) 3. Antiplatelet drugs ( Aspirin or Clopidogrel, Dipyridamole or Ticlopidine ) 4. Neuroprotective agents: barbiturates, opioid antagonist naloxone, Manitol

32. Treatment • Treatment of cerebral edema and raised intracranial pressure • Acute surgical revascularization • Surgery for symptomatic carotid stenosis • Carotid endarterectomy, intralumenal stents, extracranial-intracranial bypass • Physical therapy and rehabilitation • Measures to prevent further strokes and progression of vascular disease.

33. Treatment • Since the primary objective in the treatment of atherothrombotic disease is prevention , efforts to control the risk factors must continue. • Aspirin • Hypotensive agents • Oversedation should be avoided • Systemic hypotension, severe anemia should be treated promptly • Particular care should be taken to maintain the systemic blood pressure, oxygenation and intracranial blood flow during surgical procedures, especially in elderly patient.

34. Course and Prognosis • When the patient is seen early in the cerebral thrombosis, it is difficult to give an accurate prognosis. • As for the eventual or long-term prognosis of the neurologic deficit , there are many possibilities. • It must be mentioned that having had one thrombotic stroke, the patient is at risk in the ensuing months and years of having a stroke at the same or another site, especially if there is hypertension or diabetes mellitus.

35. Embolic infarction • This is one of the most common cause of stroke. In most cases of cerebral embolism, the embolic material consists of a fragment that has broken away from a thrombus within the heart. Embolism due to fat, tumor cells, fibrocartilage, amniotic fluid, or air is a rare occurrence and seldom enters into the differential diagnosis of stroke.

36. Clinical Picture • Of all strokes, those due to cerebral embolism develop most rapidly.The embolus strikes at any time of the day or night. Getting up to go to the bathroom is a time of danger.The neurologic picture will depend on the artery involved and the site of obstruction.

37. Clinical Picture • It is important to repeat that an embolus may produce a severe neurologic deficit that is only temporary; symptoms disappear as the embolus fragments. In other words , embolism is a common cause of a single evanescent stroke that may reasonably be called a prolonged TIA. Also as already pointed out, several emboli can give rise to two or three transient attacks of differing pattern or , rarely , of almost identical pattern.

38. Causes of cerebral embolism: • Cardiac originNoncardiac originUndetermined origin

39. Laboratory Findings • Not infrequently the first sign of myocardial infarction is the occurrence of embolism; therefore it is advisable that an ECG and echocardiogram be obtained in all patients with stroke of uncertain origin.Prolonged study of heart rhythm with Holter monitoring should be undertaken.

40. Laboratory Findings • In some 30 percent of cases, cerebral embolism produces a hemorrhagic infarction. CT scanning or MRI may be helpful in showing the more intense hemorrhagic infarcts, particularly if the scan is repeated on the second or third day.

41. Course and prognosis • Most patients survive the initial insult, and in many the neurologic deficit may recede relatively rapidly, as indicated above. The eventual prognosis is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis and so on.

42. Treatment and prevention Three phases of therapy : • General medical management in the acute phase, • Measures directed to restoring the circulation • Physical therapy and rehabilitation • These are much the same as described above the prevention of atherothrombotic infarction.

43. Lacunar infarct • As one might surmise, small penetrating branches of the cerebral arteries may become occluded, and the resulting infarcts may be so small or so situated as to cause no symptoms whatever. As the softened tissue is removed, it leaves a small cavity, or lacune.

44. Lacunar infarct • In our clinical and pathologic material, there has always been a strong correlation of the lacunar state with a combination of hypertension and atherosclerosis and, to a lesser degree, with diabetes.In all the cases of lacunar infarction, the diagnosis depends essentially on the occurrence of the certain unique stroke syndromes of limited proportions.

45. Lacunar infarct • As mentioned above, CT scanning is less reliable than MRI in demonstrating the lacunes. The EEG may be helpful in a negative sense; in the case of lacunes in the pons or the internal capsule, there is a notable discrepancy between the unilateral paralysis or sensory loss and the negligible electrical changes over the affected hemisphere.

46. Lacunar infarct • Recognition of lacunar stroke is important • Future lacunar stroke can be reduced by treating HTN Anticoagulation is not indicated (No evidence) Aspirin is also of uncertainty

47. Intracranial Hemorrhage • This is the common, well-known “spontaneous” brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries. • Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema.

48. Intracranial Hemorrhage • Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually caused by arterial bleeding.

49. Intracranial Hemorrhage • The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues . Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death.

50. Intracerebral Hemorrhage • Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic.It has been given its own name, “apoplexy”.