Although it seems obvious that excessive intravascular pressure is the caus
e of spontaneous intracerebral haemorrhage, the available evidence instead
suggests that haemorrhage arises from previous ischaemic damage to the wall
s of small blood vessels. This interpretation unifies the aetiology of cere
bral infarction and intracerebral haemorrhage. It is supported by much path
ological evidence and also fits with observations on spontaneous stroke-pro
ne hypertensive rats, which have smaller cerebral arteries than Wistar-Kyot
o rats. Ischaemic damage to the brain probably occurs during spontaneous di
ps in aortic pressure in the presence of atheromatous arterial lesions and
arteriolar narrowing by lipohyaline deposits. It may also follow long-lasti
ng arterial spasm provoked by sudden pressure elevations. Local factors, es
pecially unevenness of cerebral perfusion, probably determine the site of a
n infarct and whether it becomes haemorrhagic or not In the long term, hypo
tensive drugs will lessen atheroma deposition. In the short term, they may
act by reducing or preventing damaging arteriolar spasm. (C) 2001 Lippincot
t Williams & Wilkins.