Despite the use of antihypertensive drugs, mortality (but not morbidity) from cerebrovascular diseases has been reduced significantly. As a consequence, an increasing number of patients suffer from recurring strokes and from the debilitating consequences of cerebrovascular diseases and develop progressive cognitive impairment. Its pathological substrates are regional alteration of cerebral perfusion, lacunae, white matter lesions, progressive cortical atrophy, even in the asymptomatic patient and in the absence of extracranial carotid artery stenosis. Lacunar infarction and white matter lesions are particularly frequent in the hypertensive diabetic patient. Lacunae and white matter lesions sometimes coexist and may favour the development of dementia in the hypertensive patient, through focal ischaemia, perivascular oedema, disruption of the blood-brain barrier, cerebral diaschisis and cortical deafferentation. Treatment with calcium channel blockers, angiotensin converting enzyme inhibitors and diuretics smooth the patchy hypoperfusion despite the fall in pressure. However, the time course and the extent of this effect vary according to the drug administered. In particular, only a calcium channel blocker increased perfusion of both cortical and subcortical areas, while diuretic treatment increased perfusion only after prolonged treatment, and this effect was limited to the cortical areas. Such differences may explain the discrepant results on risk reduction for dementia observed in large intervention trials.