Stroke I

Published on 10/04/2015 by admin

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Last modified 22/04/2025

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Stroke I

Stroke refers to damage to the brain caused by abnormalities of blood supply. This presents with a rapidly developing focal neurological deficit, which may lead to coma or death. If this deficit lasts less than 24 h it is referred to as a transient ischaemic attack (TIA; p. 70).

Stroke is the third most common cause of death in developed countries. The incidence of first stroke is 2 per 1000 per year. The incidence increases with age. It is rare below 45 years of age and increases from 2 per 1000 per year for people aged 45–54 years to 10 per 1000 per year for those aged 65–74 years and to about 30 per 1000 per year in those aged over 80 years. About a quarter of these patients will be dead within 6 months (the majority of these within 1 month). Stroke is a major cause of disability; after their first stroke, 40% of surviving patients will be dependent at 6 months.

Stroke is not a single diagnosis. Strokes differ in terms of their aetiology and pathogenesis, the area of the brain affected and the resulting clinical deficit. These differences have implications for investigation, treatment and prognosis.

Pathogenesis

Cerebral infarction accounts for 80% of strokes, 15% are primary intracerebral haemorrhages and 5% are due to subarachnoid haemorrhages (p. 72).

Cerebral infarction

Cerebral infarction results from an interruption in blood supply to an area of the brain. This can be due to (Fig. 1):

image emboli (30% of all strokes)
image thrombosis (30%)
image small vessel disease (20%).
image

Fig. 1 Pathophysiology of common causes of cerebral infarction.

Atheroma

Atheroma is an important factor in both embolic and thrombotic strokes. A similar pathological process, occurring in patients with the same risk factors, produces intracerebral small vessel disease.

The risk factors for atheroma, and other disease resulting from it, are given in Table 1. The most important risk factor is hypertension, with the risk increasing with the blood pressure.

Table 1 Risk factors for atheroma and relative risk of stroke

Risk factors for atheroma Relative risk of stroke
Hypertension 5
Diabetes 2
Smoking 3
Family history  
Cholesterol  
Excess alcohol intake 1–4

Atheroma commonly arises at the junctions of arteries, for example the carotid bifurcation and the point where the two vertebral arteries join to form the basilar artery (Fig. 2).

image

Fig. 2 Circle of Willis.

The build up of atheroma may lead to narrowing of the arteries. This is usually a gradual process and anastomotic channels can develop, either around the circle of Willis (Fig. 2) or with enlargement of meningeal anastomoses. Stenosis can develop and proceed to occlusion of a vessel without resulting in cerebral ischaemia. However, the atheromatous plaque can lead to cerebral ischaemia in several ways:

image It can produce a stenosis that is not compensated for by anastomoses.
image The plaque may ulcerate and fragments can act as emboli.
image The base of an ulcerated plaque is irregular and may act as a focus for propagation of thrombus.
image Haemorrhage into an ulcerated plaque can produce a rapidly developing stenosis or occlusion.

Embolic strokes

An embolus is an abnormal particle within the bloodstream that can lodge in, and block, blood vessels. Emboli commonly arise from either the heart or the proximal arteries in the neck. The most common sources of emboli from the heart include thrombus from atrial fibrillation, mural thrombus following myocardial infarction and left ventricular dilatation. Rare embolic sources include bacterial vegetations in subacute bacterial endocarditis, calcium from heart valves or fragments from an atrial myxoma. Emboli from the heart account for about 10% of all strokes.

Emboli can come from the proximal neck vessels (artery to artery emboli) and these usually relate to atheromatous disease. The emboli consist of plaque debris, cholesterol crystals or platelet emboli, which arise from ulcerated atheromatous plaque. Other types include fat (from trauma) and air (from surgery).

Thrombotic strokes

Thrombosis arises in three main circumstances.

Abnormality in the vessel wall

Thrombosis usually occurs in the context of atheroma, which produces stenosis and irregularities in the vessel wall from which thrombosis can propagate. More rarely, thrombosis can occur in inflammatory arterial diseases, such as temporal arteritis, systemic lupus erythematosus, rheumatoid arthritis and other rarer diseases.

Abnormal tendency of the blood to thrombose

Thrombosis can also occur when there is a predisposition to clotting, for example polycythaemia, thrombocythaemia, sickle cell disease and coagulation disorders that result in thrombophilia (e.g. protein C and S deficiencies and antiphospholipid syndrome).

Stasis of the blood flow

Stasis usually occurs in association with severe atheromatous stenosis. An arterial dissection can arise if the intimal lining of an artery is torn, then blood can track beneath this layer in the wall. This produces a stenosis of the vessel and potential stasis and may lead to thrombosis. This is the commonest identifiable cause of stroke in young adults.

Small vessel disease

Intracerebral small vessel disease refers to the process of lipohyalinosis (or microatheroma) that occurs in penetrating and branch arteries, resulting in their occlusion. Patients with small vessel disease usually have a predisposition to atheroma.

Intracerebral haemorrhage

Intracerebral haemorrhage is usually due to hypertension (primary intracerebral haemorrhage). This occurs when small penetrating arteries within the brain rupture at sites of weakness, as a result of lipohyalinosis and microaneurysms (Charcot–Bouchard aneurysms). Intracerebral haemorrhages occur most frequently in the basal ganglia (50%; Fig. 3), lobar white matter (20%), pons (10%) and cerebellum (10%).

image

Fig. 3 CT scan showing massive intracerebral haemorrhage.

Ruptured saccular aneurysms produce subarachnoid haemorrhage (p. 72). However, sometimes the direction of rupture of an aneurysm can result in most of the haemorrhage being intracerebral rather than subarachnoid. Arteriovenous malformations can rupture and produce intracerebral haemorrhage. Patients with bleeding disorders, particularly related to drugs (anticoagulants and thrombolytics such as streptokinase), can develop intracerebral haemorrhages.

Development of an ischaemic stroke

Cerebral infarction occurs after a few minutes of ischaemia. The consequence of ischaemia depends on its duration and severity. This will vary within the affected area of the brain, with areas on the edge of the vascular territory of the affected vessel being relatively less affected, sometimes called the ischaemic penumbra. Severe ischaemia will lead to cell death while less-affected cells may have the potential to survive. There is increasing evidence that excitotoxic amino acids may be involved in the pathogenesis of the cell death. Other biochemical factors, such as the blood glucose, will also affect cell survival.

Areas of necrosis will then swell, so-called cytotoxic oedema, which may interfere with the perfusion of areas in the penumbra. This swelling increases over 5 days and then gradually clears. If large areas of brain are affected (e.g. a middle cerebral artery occlusion; p. 66), this may produce a significant mass effect causing a further deterioration due to cerebral herniation. This is also seen in intracerebral haemorrhage where the haematoma increases the mass effect.

By 3 weeks, the haemodynamic changes that led to the stroke are stable and the recovery phase of the stroke is dependent on recovery of the ischaemic penumbra and remodelling of brain function. The area of infarction shrinks, undergoing the process of gliosis. In patients who have had strokes affecting small deep perforating vessels, this process of gliosis leads to the formation of small lakes of fluid, so-called ‘lacunes’.

Some rarer types of stroke

Hypotensive/watershed strokes

A period of systemic hypotension, for example during a cardiac arrest, can result in ischaemia in areas on the edge of two vascular territories (e.g. between the middle and posterior cerebral arteries). This can produce strokes sometimes referred to as watershed infarcts.

Intracranial venous thrombosis

This occurs when there is an abnormality in haemostasis or when there is some irritation of the venous sinuses (e.g. surgery, infection, inflammation or tumour). These usually result in headaches, seizures and confusion, sometimes with focal signs. It may also present with raised intracranial pressure.

Stroke I

image Stroke is a common cause of death and disability.
image Stroke is caused by cerebral infarction (80%), intracranial haemorrhage (15%) and subarachnoid haemorrhage (5%).
image Atheroma is the most important cause of ischaemic stroke.
image Ischaemic stroke can result from thrombosis or embolism.

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