Although it seems obvious that excessive intravascular pressure is the cause of spontaneous intracerebral haemorrhage, the available evidence instead suggests that haemorrhage arises from previous ischaemic damage to the walls of small blood vessels. This interpretation unifies the aetiology of cerebral infarction and intracerebral haemorrhage. It is supported by much pathological evidence and also fits with observations on spontaneous stroke-prone hypertensive rats, which have smaller cerebral arteries than Wistar-Kyoto rats. Ischaemic damage to the brain probably occurs during spontaneous dips in aortic pressure in the presence of atheromatous arterial lesions and arteriolar narrowing by lipohyaline deposits. It may also follow long-lasting arterial spasm provoked by sudden pressure elevations. Local factors, especially unevenness of cerebral perfusion, probably determine the site of an infarct and whether it becomes haemorrhagic or not. In the long term, hypotensive drugs will lessen atheroma deposition. In the short term, they may act by reducing or preventing damaging arteriolar spasm.