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Stroke: cerebrovascular disease 

Stroke: cerebrovascular disease

Chapter:
Stroke: cerebrovascular disease
Author(s):

J van Gijn

DOI:
10.1093/med/9780199204854.003.0241001

A relevant case history from Neurological Case Histories: Case Histories in Acute Neurology and the Neurology of General Medicine has been added to this chapter.

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date: 24 April 2017

Cerebrovascular diseases include many pathological conditions but the principal categories are (1) infarction—through occlusion of major arteries, small arteries or venous sinuses; and (2) haemorrhage—most often through rupture of small arteries, arterial aneurysms or capillaries.

Epidemiology

Strokes are common, with annual incidence rates for subjects aged over 55 ranging from 420 to over 1000 per 100 000. They are the most important case of disability in developed Western nations and the second most frequent cause of death after coronary heart disease. About 80% of strokes are caused by cerebral infarcts, with the remainder due to haemorrhage, with 20% of these attributable to a bleeding cerebral aneurysm. The incidence of transient ischaemic attacks (TIAs) is about 50 per 100 000.

General considerations

Strokes typically present with sudden onset of focal neurological deficit. Urgent imaging with CT or MRI allows rapid differentiation between haemorrhagic and ischaemic causes—with critical benefit for the introduction of appropriate treatment—and serial imaging may reveal the development of important complications such as rebleeding, ischaemia, or hydrocephalus that mandate specific interventions.

The consequences of stroke are often devastating: sudden loss of a large amount of brain tissue affects much more than specific, localized functions such as movement, sensation, vision, and language. Mood, initiative, sense of humour, and speed of thought are among the essential aspects of mental life that can be severely affected, but are often sadly ignored. Management of patients with stroke requires complex needs to be comprehensively addressed. The introduction of specialized clinical units for the multidisciplinary care of patients with stroke has been shown to improve clinical diagnosis and recovery, reducing the risk of death or institutionalized care by 14%.

Pathophysiology of arterial occlusive disease

Atherothrombosis is the main cause of occlusion of major arteries in the brain, typically by embolism from a source in the carotid artery, aorta, or heart. Whether occlusion of an artery supplying brain tissue actually leads to ischaemia depends on collateral pathways, which may be by (1) circle of Willis, (2) connections between extracranial and intracranial vessels, (3) leptomeningeal anastomoses.

Arterial occlusive disease—transient ischaemic attacks

These, by definition, are due to ischaemia of a part of the brain, producing symptoms/signs that last for <24 h (usually for minutes). The main presentations are with transient (1) hemiparesis, (2) dysphasia, (3) monocular visual loss, or (4) hemianopia. Without treatment (see ‘Secondary prevention’), the risk of stroke after a TIA is up to 20% in the first year and 7% in subsequent years.

Arterial occlusive disease—cerebral infarction

Classification—this has been attempted on the basis of time course (‘progressive’, ‘completed’), anatomy (which artery?), cause (e.g. large artery atherosclerosis, cardio-embolism) or functional deficit (e.g. modified Rankin scale). The Oxfordshire Community Stroke Project system provides a useful and widely accepted compromise, defining four types of cerebral infarction: (1) total anterior circulation infarcts (TACI)—with both cortical and subcortical involvement; (2) partial anterior circulation infarcts (PACI)—more restricted and predominantly cortical infarcts; (3) posterior circulation infarcts (POCI)—clearly associated with the vertebrobasilar arterial territory; (4) lacunar infarcts (LACI), confined to the territory of the deep perforating arteries.

Specific treatments—several medical interventions aim at dissolving the occluding clot, or at least preventing it from growing. Those of widest application are: (1) Thrombolysis—treatment of highly selected patients within 4.5 h of the stroke event (and the sooner the better) with intravenous recombinant tissue plasminogen activator (rt-PA) will avoid death or dependence in 55 patients per 1000 treated. (2) Antiplatelet agents—treatment with aspirin, started within 48 h of onset, will avoid death or dependence in 13 patients per 1000 treated.

Secondary prevention—aside from control of lifestyle factors (cessation of smoking, reducing overweight, daily exercise), specific measures to reduce the risk of threatened stroke include (1) Carotid endarterectomy—substantially decreases the risk of disabling or fatal stroke in patients with severe, symptomatic carotid stenosis. (2) Antiplatelet drugs—aspirin produces relative risk reduction of 13%, with addition of dipyridamole providing some further benefit; clopidogrel should be prescribed in patients who are intolerant to aspirin. (3) Anticoagulants—with embolic sources in the heart, mostly from atrial fibrillation, coumadin anticoagulants (INR 2.5–4) are the first choice in the absence of contraindications. (4) Statins—reduce the risk of stroke by about 20% per mmol/litre reduction in low-density lipoprotein (LDL) cholesterol. (5) Antihypertensive drugs—the level of blood pressure is by far the most powerful risk factor for stroke; in individuals with a history of stroke or TIA, a blood-pressure-lowering regimen reduces the risk of stroke by 25 to 50% depending on the degree of blood pressure lowering, regardless of whether or not the blood pressure at baseline was considered too high.

Venous occlusive disease

Aetiology—cerebral venous thrombosis usually occurs in the context of a combination of predisposing factors, e.g. the oral contraceptive pill, pregnancy, or postpartum, in combination with some inherited disorder of coagulation such as the factor V Leiden mutation.

Clinical features, investigation and treatment—manifestations include headache, focal deficits, seizures, and impairment of consciousness. Imaging with CT/MRI reveals ‘venous’ infarcts that do not correspond to a known arterial territory and evidence of the underlying sinus thrombosis. Most physicians treat with anticoagulants, but evidence for their efficacy is not strong. Mortality is 5 to 30%.

Primary intracerebral haemorrhage

Aetiology—primary intracerebral haemorrhage usually occurs in the context of a combination of (1) anatomical factors—cerebral vascular lesions or malformations, e.g. arteriovenous or cavernous malformations, ruptured perforating arteries, amyloid angiopathy; (2) haemodynamic factors—most notably blood pressure; and (3) haemostatic factors—relating to platelet function or the coagulation system, e.g. oral anticoagulants.

Clinical features, investigation and treatment—in most cases history and examination provide few clues to the cause of an intracerebral haemorrhage, but specific enquiry should always be made about use of oral anticoagulants and the possibility of malignant disease (with bleed into a metastasis), and evidence of a generalized haemostatic disorder should be sought. Brain imaging (CT or MRI) is the most important single investigation in patients with suspected intracerebral bleeding. There is no specific treatment for most patients, but therapeutic anticoagulation should be reversed, and surgical evacuation of cerebellar haematomas should be considered.

Subarachnoid haemorrhage

Aetiology—ruptured aneurysms cause 85% of nontraumatic subarachnoid haemorrhages.

Clinical features and investigation—presentation is with sudden, severe, and unusual headache, with loss of consciousness at onset in 50%. Imaging with CT is the most important investigation: scanning within 3 days reveals extravasation of blood in the basal cisterns in 95% of cases. Lumbar puncture is indicated if the history is convincing but the CT scan negative: xanthochromia of the supernatant after centrifugation of the cerebrospinal fluid sample is the diagnostic finding. CT and MR angiography are the methods of choice for demonstrating or excluding an aneurysm as the source of haemorrhage.

Treatment—aside from general nursing and supportive measures, key issues are (1) Prevention of rebleeding—without intervention, the risk of this is 30% in the month after presentation, with immediate mortality of 50%. Endovascular treatment (‘coiling’) is the preferred method to occlude the aneurysm and prevent rebleeding, but not all aneurysms can be treated in this way and operative clipping is still necessary for these patients. (2) Delayed cerebral ischaemia—occurs in up to 25% of patients with a ruptured aneurysm, most commonly 5 to 14 days after the initial bleed. Nimodipine reduces the frequency of cerebral ischaemia and poor outcome by about one-third.

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