Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Published Online
on March 9, 2006

Stroke. 2006
Published online before print March 9, 2006, doi: 10.1161/01.STR.0000209330.73175.34
A more recent version of this article appeared on April 1, 2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
37/4/1129    most recent
01.STR.0000209330.73175.34v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rogalewski, A.
Right arrow Articles by Schäbitz, W.-R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rogalewski, A.
Right arrow Articles by Schäbitz, W.-R.
Related Collections
Right arrow Emergency treatment of Stroke
Right arrow Neuroprotectors

Submitted on October 29, 2005
Revised on January 11, 2006
Accepted on January 20, 2006

Toward a Multimodal Neuroprotective Treatment of Stroke

Andreas Rogalewski MD; Armin Schneider MD; E. Bernd Ringelstein MD; and Wolf-Rüdiger Schäbitz MD*

From the Department of Neurology (A.R., E.B.R., W.-R.S.), University of Muenster, Germany; and Axaron Bioscience (A.S.), Heidelberg, Germany.

* To whom correspondence should be addressed. E-mail: schabitz{at}uni-muenster.de.

Background and Purpose--Stroke remains a common medical problem with importance attributable to the demographic changes in industrialized societies.

Summary of Review--After years of setbacks, acute stroke therapy has finally emerged, including thrombolysis with tissue plasminogen activator (t-PA). However, t-PA treatment is limited by a narrow time window and side effects, so that only 3% of all stroke patients receive thrombolysis. Unimodal targeting of key events in stroke pathophysiology was not effective in providing long-term benefits, leading to negative results in previous clinical neuroprotective stroke trials. A successful future stroke therapy should approach multiple pathophysiological mechanisms besides revascularization at once, including reduction of t-PA-related side effects, prevention of cell death, stimulation of neuroregeneration, and plasticity.

Conclusions--Strategies targeting these processes include multiple combination therapies as well as treatment with multimodal drugs that interact with these mechanisms. Here, we review such combination approaches, and outline how this concept could be developed into future stroke treatment.


Key words: apoptosis • clinical trials • excitotoxicity • growth factors • inflammation • neuroprotection • stroke




This article has been cited by other articles:


Home page
StrokeHome page
S. I. Savitz and W.-R. Schabitz
A Critique of SAINT II: Wishful Thinking, Dashed Hopes, and the Future of Neuroprotection for Acute Stroke
Stroke, April 1, 2008; 39(4): 1389 - 1391.
[Full Text] [PDF]


Home page
StrokeHome page
T. M. Hemmen and P. D. Lyden
Induced Hypothermia for Acute Stroke
Stroke, February 1, 2007; 38(2): 794 - 799.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
M. Wiart, N. Davoust, J.-B. Pialat, V. Desestret, S. Moucharrafie, T.-H. Cho, M. Mutin, J.-B. Langlois, O. Beuf, J. Honnorat, et al.
MRI Monitoring of Neuroinflammation in Mouse Focal Ischemia
Stroke, January 1, 2007; 38(1): 131 - 137.
[Abstract] [Full Text] [PDF]