The classical “lacunar hypothesis ” based on pathological and CT studies states that particular clinical syndromes - “lacunar syndromes ” - are caused by small ( < 15 mm) subcortical infarcts due to the occlusion of a small perforating artery. In many cases however the clinical syndromes are not associated with any detectable changes on classsical CT imaging. Recent advances in neuroimaging help us to better visualize lesions with relevance to actual clinical syndromes and with respect to functional systems thus leading to earlier and more accurate etiologic diagnosis and refinement of clinico-anatomical correlations. Therefore we re-evaluate the lacunar hypothesis and the clinico-pathological entity of lacunar stroke. We summarize recent knowledge about the capacity of various imaging modalities 1. to identify and localize lacunar infarcts, 2. to judge their clinical relevance by establishing their age and following their time course, 3. to differentiate between lacunar and non-lacunar mechanisms producing small subcortical infarcts and 4. to differentiate lacunar infarcts from other small cerebral lesions like Unidentified Bright Objects and dilated Virchow-Robin spaces. On the other hand lesions may frequently be identified in patients with apparently no corresponding clinical syndromes. Therefore we discuss the clinical relevance of silent brain infarcts and other imaging abnormalities.
Keywords: Lacunar infarct, lacunar syndrome, MRI, DWI, stroke subtypes, silent brain infarct
Rights & PermissionsPrintExport