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Stroke. 2003;34:e87-e88
Published online before print June 19, 2003, doi: 10.1161/01.STR.0000078660.31648.3C
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(Stroke. 2003;34:e87.)
© 2003 American Heart Association, Inc.


Research Reports

Editorial Comment—ADC and Metabolites in Stroke: Even More Confusion About Diffusion?

Jens Fiehler, MD, Guest Editor

Department of Neuroradiology, University Hospital Eppendorf, University of Hamburg, Hamburg, Germany


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

Recently, permanent and transient early ADC renormalization has been reported in stroke patients.1–3 Several other articles with different focus report on patients with substantial decrease of lesion volume from initial DWI to outcome T2-weighted imaging. Differences in the reported rates of patients showing ADC normalization may be due to varieties in imaging time points and application of thrombolytic therapy. These reports resulted in some confusion among stroke physicians about the clinical value of the ADC.

The accompanying article by Nicoli et al provides novel insights into the pathophysiological basis of DWI in patients with acute ischemic stroke. Using spectroscopic imaging, the authors describe a heterogeneous cellular metabolic injury within the region of decreased ADC values. This finding may help us to understand why severe ADC decreases do not necessarily predict irreversible tissue damage in stroke patients.1,2

What do we know about the ADC? Diffusion in tissues is referred to as random walk of water molecules restricted by fibers, membranes, and macromolecules. Despite some lack of understanding about the biophysical background of ADC decrease, we have learned much about its pathophysiological correlates from stroke models.4 It has been shown by different experimental modalities that cerebral ischemia results in failure of ion pumps and anoxic cell membrane depolarization. Water shifts from the extracellular to the intracellular space with consecutive cell swelling. The increase of the intracellular osmolarity as a result of lactate accumulation is considered the reason for cell swelling beyond depolarization. The time course of these changes corresponds to the evolution . . . [Full Text of this Article]




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