The heterogeneity of vascular dementia depends on the cause, size, location and nature of the vascular lesions (36, 62). Magnetic resonance imaging (MRI) techniques are of major interest to detect the vascular origin of dementia: the lack of focal lesions or leukoencephalopathy excludes the vascular origin of dementia (36). Occlusions of large extra-cerebral arteries usually lead to cortical or large subcortical infarcts or both (28). Dementia may be due to multiple infarcts or to a single infarct located in a strategic area (47). Lacunar infarcts are due to the occlusion of one single deep perforator with a thickening of the arterial wall due to lipohyalinosis (25), usually in a patient with arterial hypertension; lacunes are located in a territory supplied by the deep perforators. They appear as hyperintense in T2-weighted sequences and hypo-intense in T1-weighted sequences. Old small hemorrhages have the same appearance than infarcts on CT-scans but their center appears hypo-intense in T2-weighted sequences. In normal subjects, age and arterial hypertension are risk factors for hemispheric white matter hyperintensities (59, 60). Their vascular origin is likely because of the evidence of lesions of the wall of deep perforators (17, 21), their association with lacunes (17, 21, 30, 37) or deep hemorrhages (30, 32, 37), and their frequency in amyloid angiopathy (26). Their prevalence is higher in vascular dementia than in Alzheimer's disease (59). They sometimes fulfill criteria for Binswanger's disease (5). Even after exclusion of predisposing factors they remain frequent in healthy subjects over 50 years (39, 56); however, whether they herald subsequent dementia remains unsettled.(ABSTRACT TRUNCATED AT 250 WORDS)