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  • Updated 09.29.2022
  • Released 09.01.1995
  • Expires For CME 09.29.2025

Lacunar infarction



In this article, the authors summarize the epidemiology, pathophysiology, clinical manifestations, and management of lacunar infarction. The authors report developments, including clinical MRI correlations and distinct imaging patterns associated with gender, age, vascular risk factors, genetic makeup, race, and ethnicity.

Key points

• A lacune is typically between 3 and 15 mm in size and is observed on imaging as a round or ovoid and fluid-filled cavity consistent with a previous acute subcortical brain infarct or, less commonly, previous hemorrhage.

• A lacunar infarct is a common manifestation of cerebral small vessel disease and is usually the end result of the occlusion of a perforating artery.

• The clinical stroke subtype associated with lacunar infarction often presents as a classic lacunar syndrome.

• Lacunar infarction can be caused by multiple pathological mechanisms, including lipohyalinosis, atherosclerosis, and, rarely, embolic disease.

• Lacunes contribute to cerebral small vessel disease burden overall, which can lead to cognitive impairment and functional disability that is often independent of the occurrence of a clinical stroke event.

• Acute management of lacunar infarction includes intravenous thrombolytic therapy, and secondary prevention includes risk factor management and antithrombotic therapy.

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 (58). 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 (22; 23). 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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