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Gregory W. Albers, MD
Department of Neurology and Neurological Sciences Stanford University Medical Center Stanford, CA 94305

Arch Neurol. 1991;48(12):1215.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—A number of recent publications^1-3 have emphasized that small deep cerebral infarcts can be caused by a variety of etiologic factors including cardioembolism and large vessel occlusion. This has led some authors to conclude that the "lacune hypothesis," which suggests that lacunes are caused by lesions involving small perforating brain arteries, is a "fallacy"¹ and that the term lacunar "should be evicted from the bedside."²

In their recent article,⁴ Waterston and colleagues provide further evidence that the cause of small deep cerebral infarcts is diverse. In reviewing their study, as well as other reports of patients with lacunes of "atypical etiology,"⁵ it appears that a high percentage of these patients have unusually large lacunes.

Most lacunes are only 2 to 3 mm in maximal diameter,^6,7 and Fisher⁷ believed that lacunes greater than 10 mm in diameter should be designated as giant . . . [Full Text PDF of this Article]

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