This Article Full Text Full Text (PDF) All Versions of this Article: 39/11/2921    most recent STROKEAHA.108.523795v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wardlaw, J. M. Search for Related Content PubMed PubMed Citation Articles by Wardlaw, J. M. Related Collections Acute Cerebral Infarction Cerebral Lacunes

(Stroke. 2008;39:2921.)
© 2008 American Heart Association, Inc.

Editorials

What Is a Lacune?

From the University of Edinburgh, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK.

Correspondence to Joanna M. Wardlaw, University of Edinburgh, Department of Clinical Neurosciences, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK. E-mail joanna.wardlaw@ed.ac.uk

Key Words: lacunar infarcts • lacunes • leukoaraiosis

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 stroke lesions, perhaps as few as a third, ever cavitate, with the majority that fail to cavitate retaining the appearance of a WML?⁶ Counting . . . [Full Text of this Article]

This article has been cited by other articles:

				J. Wardlaw Response to Letter by Landau Stroke, July 1, 2009; 40(7): e500 - e500. [Full Text] [PDF]

				P. Armario and A. de la Sierra Antihypertensive treatment and stroke prevention: are angiotensin receptor blockers superior to other antihypertensive agents? Therapeutic Advances in Cardiovascular Disease, June 1, 2009; 3(3): 197 - 204. [Abstract] [PDF]

				F. N. Doubal, T. J. MacGillivray, P. E. Hokke, B. Dhillon, M. S. Dennis, and J. M. Wardlaw Differences in retinal vessels support a distinct vasculopathy causing lacunar stroke Neurology, May 19, 2009; 72(20): 1773 - 1778. [Abstract] [Full Text] [PDF]