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(Stroke. 2004;35:1778.)
© 2004 American Heart Association, Inc.

Controversies in Stroke

Lacunar Infarction

Embolism is the Key

From the Intermountain Stroke Center, Salt Lake City, Utah.

Correspondence to Dr Nancy Futrell, Intermountain Stroke Center, 5292 College Drive, Suite 204, Salt Lake City, UT 84123. E-mail nancyfutrell@yahoo.com

Geoffrey A. Donnan MD, FRACP Stephen M. Davis MD, FRACEP Section Editors:

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

Lacunes are small deep infarcts which cavitate, producing "lacunes" (French for lake).¹ "Lacunar infarcts" have been thought of as strokes caused by intrinsic disease of small vessels called lipohyalinosis, resulting from hypertension² and diabetes.³ Contrary to this established dogma, the literature demonstrates that emboli are the cause of lacunes.

Almost all of the histopathological evaluation of blood vessels associated with lacunes has been done by C. Miller Fisher. In 11 patients with lacunes there was only a single case of lipohyalinosis compared with 2 cases of cerebral emboli.² Although not commonly cited this way, Fisher’s own writing demonstrates emboli are more common than lipohyalinosis in patients with lacunes.

Fisher was also responsible for the hypothesis of hypertension as a cause of lacunes, based on his report of hypertension in 111/114 of his patients with lacunes. This has not been documented by subsequent studies, which showed hypertension in 24% to 73% of patients with lacunes, similar to that found in stroke patients in general.⁴ Fisher’s inflated report of hypertension may be in part because transient reactive hypertension was misinterpreted as hypertension. In addition, 13 of these patients were assumed to have hypertension based on heart weight >400 g, in the absence of any documented elevated blood pressure recording!⁵ It is surprising that a nonreproducible result such as this has remained highly quoted, rather than actively refuted.

Animal models of both hypertension and diabetes exist. The pathology in the spontaneously hypertensive rats includes glial scars and focal cortical atrophy,⁶ not lacunes. There . . . [Full Text of this Article]

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