| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2007;38:1718.)
© 2007 American Heart Association, Inc.
Editorials |
From the Georgetown University (C.S.K.), Washington, DC; the Washington Hospital Center (C.S.K., S.W.), Washington, DC; and the National Institute of Neurological Disorders and Stroke (S.W.), National Institutes of Health, Bethesda, Md.
Correspondence to Chelsea S. Kidwell, MD, 110 Irving St NW, East Building Rm 6126, Washington, DC 20010. E-mail Ck256@georgetown.edu
See related article, pages 1826–1830.
Key Words: acute stroke magnetic resonance thrombolysis
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The goal of acute stroke evaluation is to determine not only stroke type (ischemic versus hemorrhagic) and localization (anatomical and vascular), but perhaps more importantly, to determine reversibility (presence of an ischemic penumbra that may be salvaged with acute therapy). Traditionally, neurologists have relied on history and neurological examination to provide much of this information. However, long experience has demonstrated that the neurological examination is imperfect at best in determining lesion localization and grossly limited in its ability to provide insights into the presence of penumbral tissue. This is evidenced by the only modest correlations between National Institutes of Health Stroke Scale (NIHSS) score and perfusion-weighted imaging lesion volume.1,2
The last decade has seen a striking growth in neuroimaging techniques that provide important real-time information about acute stroke pathophysiology. In the mid-1990s the advent of diffusion-weighted imaging revolutionized the role of MRI in acute stroke evaluation. Not only could diffusion-weighted imaging provide evidence of tissue injury within minutes of symptom onset, but also the diffusion-perfusion mismatch model offered a simple and practical means of identifying the ischemic penumbra and thus patients most likely to respond to reperfusion therapies, particularly in the late time window (>3 hours from symptom onset).3 Multiple prior studies have shown that if blood flow is not restored, the diffusion lesion will grow into the mismatch region and become a permanent infarct.4 Although this model continues to offer an imperfect approach to defining the penumbra, it has clearly been shown to provide a good approximation of penumbral
Related Article:
Stroke 2007 38: 1826-1830.
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |