This article includes discussion of lacunar infarction, lacunar infarct, and lacunar stroke. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
In this article, the author reports developments including clinical MRI correlations and distinct imaging patterns associated with gender, age, vascular risk factors, genetic make up, and race-ethnicity. A possible implication of vascular stiffness and involvement of the blood brain barrier in the pathogenesis of lacunar infarction is also emphasized.
• Blood brain barrier permeability increases in small vessel disease in the setting of lacunar strokes with evidence to suggest that new pharmacological targeting of the blood brain barrier for the prevention and treatment of small vessel disease.
• Genetic correlation with the COL4A2 and PCSK9 is associated with lacunar ischemic stroke.
• The presence of small vessel disease is associated with increased blood pressure variability and increases the likelihood of stroke in those with large vessel disease.
Historical note and terminology
In 1838, Deschambre coined the term “lacune” to describe small cavities caused by the resorption of small deep brain infarcts. Durand-Fardel noted that some small cerebral cavities contained a small blood vessel and were not infarcts but enlarged perivascular spaces. He introduced the term état criblé to describe multiple enlarged perivascular spaces. Subsequent authors often called any small hole in the brain a “lacune” and failed to distinguish between lacunar infarcts and enlarged perivascular spaces. In 1901, Pierre Marie made a distinction between lacunar infarcts, état cribilé, and état porose (cerebral porosis), holes in the brain caused by postmortem gas formation. He established the morphological characteristics and the common association of lacunes with isolated hemiplegia (Pullicino et al 1993). He called multiple lacunar infarcts état lacunaire, a term that is now also referred to as the “lacunar state." Marie did not fully understand the pathogenesis of lacunar infarcts and thought that some were due to an inflammatory process, “vaginalite destructive." In 1960, Charles Miller Fisher stressed the major role of arterial hypertension and intracranial atherosclerosis in the pathogenesis of lacunes and redefined lacunes as “small, deep cerebral infarcts” due to occlusion of a single perforating vessel (Fisher 1965; Fisher 1969). He coined the term “lipohyalinosis” for the segmental arterial pathology that affects small penetrating arteries and causes lacunar infarcts. He also showed that atherosclerosis of the origins of penetrating arteries, “microatheroma,” is a frequent cause of lacunar infarcts.
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