Lammie G A, Brannan F, Wardlaw J M
Department of Pathology, Edinburgh University, Western General Hospital, UK.
Acta Neuropathol. 1998 Aug;96(2):163-71. doi: 10.1007/s004010050877.
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.
小而深（腔隙性）梗死的病因发病机制仍存在争议。它们由闭塞性原发性小血管疾病引起的观点被广泛认可，但仅基于少数详细的病理学研究。我们描述并展示了一种与微血管相关的基底节小病变的变体，其组织病理学特征与经典的I、II和III型腔隙不同。它们的表现提示为不完全梗死状态。本文讨论了此类病变的发病学意义，尤其是导致短暂或仅中度严重缺血的机制所起的作用。
