| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2008;39:494.)
© 2008 American Heart Association, Inc.
Case Reports |
From the Departments of Neurology (Y.N., T.O., K. Yoshikawa, N.K., N.T., T.K., N.Y., T.M., M.N.) and Radiology (K. Yamada, T.N.), Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Correspondence to Yoshinari Nagakane, MD, PhD, Department of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan. E-mail nagakane{at}koto.kpu-m.ac.jp
Abstract
Background and Purpose— Symptomatic progression is frequently observed in lacunar infarcts. The exact mechanisms of this phenomenon have not yet been clarified.
Summary of Cases— We report 2 patients with lenticulostriate artery infarcts that presented with skip lesions that were restricted to gray matter. One of the patients subsequently developed symptomatic deterioration; the other experienced no further neurological events.
Conclusions— A possible mechanism of differential vulnerability to ischemia of gray and white matter is considered. White matter may have a longer therapeutic time window for neuroprotective treatment than gray matter.
Key Words: cerebral ischemia lacunar infarction MRI white matter
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2008 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |