Lammie G Alistair
Department of Pathology, University of Wales College of Medicine, Cardiff, United Kingdom.
Brain Pathol. 2002 Jul;12(3):358-70. doi: 10.1111/j.1750-3639.2002.tb00450.x.
Lacunar infarcts and "hypertensive" primary intracerebral hemorrhages, collectively often referred to as hypertensive small vessel strokes, constitute about one third of all strokes. However, despite their public health importance, their etiopathogenesis remains ill-understood. Like all strokes, they are a heterogeneous entity, but the autopsy pathology evidence suggests that the majority are caused by a limited number of cerebral small vessel lesions. Small vessel atherosclerosis is causally implicated in a proportion of lacunar infarcts, although modern concepts of atherosclerotic plaque biology and natural history have yet to be applied to small cerebral vessels. A lesion characterized in its acute form by fibrinoid necrosis appears to be important in causing both lacunar infarcts and primary intracerebral bleeds. Advances in molecular genetics may prove instrumental in understanding the cause of this lesion and therefore in designing its targeted prevention.
腔隙性梗死和“高血压性”原发性脑出血，统称为高血压性小血管性卒中，约占所有卒中的三分之一。然而，尽管它们对公众健康很重要，但其病因发病机制仍未被充分理解。与所有卒中一样，它们是异质性疾病，但尸检病理证据表明，大多数是由数量有限的脑小血管病变引起的。小血管动脉粥样硬化在一定比例的腔隙性梗死中起因果作用，尽管动脉粥样硬化斑块生物学和自然史的现代概念尚未应用于脑小血管。一种以急性形式表现为纤维蛋白样坏死的病变似乎在导致腔隙性梗死和原发性脑出血方面都很重要。分子遗传学的进展可能有助于理解这种病变的原因，从而有助于设计针对性的预防措施。
