The aetiopathogenesis of small, deep (lacunar) infarcts remains contro
versial. The view that they are caused by occlusive intrinsic small ve
ssel disease is widely held, but is based on only a small number of de
tailed pathology studies. We describe and illustrate a variant of smal
l, 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 infarcti
on. The pathogenetic significance of such lesions is discussed, in par
ticular the role of mechanisms causing temporary or only moderately se
vere ischaemia.