See related article, pages 3083–3085.
The terms “lacune”, “lacunar infarct” and “lacunar stroke” are often used interchangeably, but they are not the same thing. Lacunes are 3 to 15 mm cerebrospinal fluid (CSF)-filled cavities in the basal ganglia or white matter, frequently observed coincidentally on imaging in older people, often not clearly associated with discrete neurological symptoms. “Lacunar stroke” describes a clinical stroke syndrome with the typical symptoms and signs referable to a small subcortical or brain stem lesion.1,2 “Lacunar infarct” should refer to a clinical stroke syndrome of lacunar type where the underlying lesion is an infarct on brain-imaging. On CT or MR T2-weighted and fluid-attenuated inversion recovery (FLAIR) imaging, an acute lacunar infarct can look just like a white matter lesion (WML), difficult to distinguish from an asymptomatic WML without diffusion-imaging to show a hyperintense signal (reduced on ADC), or a prior scan for comparison, especially in patients with WMLs. Some clinically evident acute lacunar infarcts may evolve with time into lacunes. These points are well-established.
Less well-established is how many clinically evident lacunar infarcts ever cavitate to become “lacunes”. It seems generally assumed that all lacunes start life as an infarct, even if the patient did not notice anything, and therefore share the same risk factors, etiology, prognosis, pathogenesis, etc, as clinically evident lacunar infarcts.3–5 However, suppose only a proportion of lacunar …
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