[Cerebral lacunae: still under debate].

During the last fifteen years, a new interest has been shown in cerebral lacunes due to the development of brain imagery using Magnetic Resonance Imaging (MRI). The concept of lacunar infarction as defined par Fisher (lacunar hypothesis) can no longer be accepted. Clinical data showed that the so-called lacunar clinical syndromes were far from being specific and could be observed in corticosubcortical infarcts. Epidemiological data pointed out that hypertensive disease was not found in many cases of lacunar infarction. Pathological studies suggest that there are two types of lacunar infarction. Lacunar infarcts resulting in clinical stroke syndromes (type 1 a lacunae) seem to be mainly due to obstruction of the trunk of a perforating artery by atherosclerosis. Silent lacunar infarcts (type 1 b lacunae) result from obstruction of small ramifications of the perforating arteries by a non specific microangiopathy related to age, atherosclerosis, cardiovascular disease as well as to hypertensive disease. Silent lacunar infarcts and dilatation of perivascular spaces (type 3 lacunae) are associated with the white matter hyperintensities shown by MRI in elderly subjects. Lacunar infarcts and diffuse white matter hyperintensities are related to small vessel changes and ischaemic damages resulting from (a) arteriolar occlusion and or (b) loss of autoregulation associated with variations in systemic blood pressure. Both lesions constitute a high risk to develop Vascular Cognitive Impairment (Hachinski) and are frequently associated with Alzheimer's disease. Cases of giant or expanding type 3 lacunae have been reported in the last ten years but the physiopathology of such lacunes and their relationship with clinical symptoms remain a puzzle.