The aetiopathogenesis of small, deep (lacunar) infarcts remains controversial. The view that they are caused by occlusive intrinsic small vessel disease is widely held, but is based on only a small number of detailed pathology studies. We describe and illustrate a variant of small, microvessel-associated basal ganglia lesion, the histopathological features of which are distinct from those of classical Types I, II and III lacunes. Their appearances suggest a state of incomplete infarction. The pathogenetic significance of such lesions is discussed, in particular the role of mechanisms causing temporary or only moderately severe ischaemia.