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(Stroke. 2004;35:616.)
© 2004 American Heart Association, Inc.
Original Contributions |
From the Department of Neurology, University Hospital Charité, Berlin (S.W., B.G., G.J.J., P.B., B.M., A.B., N.A., A.V.); Department of Neurology, Heinrich-Heine University, Düsseldorf (V.J., M.S.); Departments of Neurology (R.K., J.R.) and Neuroradiology (T.K.), University of Hamburg, Eppendorf; Departments of Neuroradiology (J.B.F.) and Neurology (P.D.S.), Ruprecht-Karls University, Heidelberg; Institute of Medical Biometrics, Humboldt University, Berlin (K.D.W.); and Medical Faculty, Albert-Ludwigs University, Freiburg (M.W.), Germany.
Correspondence to Susanne Wegener, MD, Department of Neurology, University Hospital Charité, Schumannstrasse 20/21, 10117 Berlin, Germany. E-mail susanne.wegener{at}charite.de
Background and Purpose We investigated whether transient ischemic attacks (TIAs) before stroke can induce tolerance by raising the threshold of tissue vulnerability in the human brain.
Methods Sixty-five patients with first-ever ischemic territorial stroke received diffusion- and perfusion-weighted MRI within 12 hours of symptom onset. Epidemiological and clinical data, lesion volumes in T2, apparent diffusion coefficient (ADC) maps and perfusion maps, and cerebral blood flow and cerebral blood volume values were compared between patients with and without a prodromal TIA.
Results Despite similar size and severity of the perfusion deficit, initial diffusion lesions tended to be smaller and final infarct volumes were significantly reduced (final T2: 9.1 [interquartile range, 19.7] versus 36.5 [91.2] mL; P=0.014) in patients with a history of TIA (n=16). This was associated with milder clinical deficits.
Conclusions The beneficial effect of TIAs on lesion size in ADC and T2 suggests the existence of endogenous neuroprotection in the human brain.
Key Words: ischemic attack, transient ischemic preconditioning magnetic resonance imaging neuroprotection stroke
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