Ischaemic stroke

Infarction from ischaemia accounts for approximately 80% of strokes. There are many causes, but these can be divided into three main groups: local arterial obstruction (the commonest), a generalized reduction in perfusion and local venous obstruction.

Local arterial obstruction causes infarction in the territory supplied by the obstructed artery if there is not an adequate collateral supply. For example, even if one internal carotid artery is occluded, the circle of Willis provides anastomotic connections that can allow adequate blood flow. This event is most likely if occlusion develops slowly, allowing the collateral vessels time to enlarge and compensate for the changed pattern of circulation. By comparison, the arteries within the brain parenchyma have poorly developed collaterals and are end-arteries. Causes of obstruction include:

emboli, usually from atheromatous plaques of the proximal aorta or carotid arteries (Fig. 3.57.1) or from mural thrombi of left atrium or left ventricle; other sources include vegetations of the mitral or aortic valve, and fat embolism following major trauma

atheroma of cerebral arteries, especially if complicated by thrombosis (Fig. 3.57.1)

vasculitis.

Fig. 3.57.1 Atheroma can produce ischaemic strokes in two ways: by acting as a source of emboli (A) or by directly obstructing the flow of blood (B).

A generalized reduction in cerebral perfusion can occur if systolic blood pressure falls or intercerebral pressure rises. Autoregulation normally keeps the cerebral blood flow relatively constant over a wide range of systemic arterial pressures. However, this flow will fall below a critical threshold and the blood supply will be inadequate if the systolic blood pressure falls below approximately 50mmHg or if the intracerebral pressure rises to a level at which the arterial pressure cannot push blood into the cranial cavity. The neurons are most sensitive to hypoxia and are the first to suffer ischaemic injury. The watershed areas of the brain are particularly prone to hypoxia when there is global ischaemia. The watershed zones represent the boundaries between arterial territories (Fig. 3.57.2). For example, the junction of the areas supplied by the anterior and middle cerebral arteries lies along the superior cerebral convexity. These zones are especially likely to become ischaemic if there is a failure of oxygenation either in hypotension (e.g. shock, arrhythmia) or in respiratory failure. The term ‘watershed infarct’ is used when these border areas become necrotic as a result.

Fig. 3.57.2 Lateral view of the left hemisphere showing the territories supplied by the three major cerebral arteries. The borders between the territories are the watershed areas.