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(Stroke. 2005;36:530-a.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Adverse Effects of the Intraluminal Filament Model of Middle Cerebral Artery Occlusion

Michael S. Dittmar, MD

Department of Anesthesiology

Nando P. Fehm, MD; Bijan Vatankhah, MD; Ulrich Bogdahn, MD Felix Schlachetzki, MD

Department of Neurology, University of Regensburg, Regensburg, Germany.

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

To the Editor:

Animal models of ischemic stroke are of major importance for experimental stroke research. Comprehensive knowledge of the methodological aspects of the different stroke models available is crucial for data interpretation and correlation to human stroke. We therefore appreciate the recent work of Gerriets et al on complications in different models of focal ischemia in rats, taking advantage of high-resolution magnetic resonance imaging (MRI) and magnetic resonance angiography.¹

In addition to their findings of subarachnoid hemorrhage and hypothalamic infarction as a cause of hyperthermia, the appearance of ipsilateral masticatory hyperintensities in early MRI associated with temporal muscle necrosis (Figure) has also been identified recently as a complication of the intraluminal filament model of middle cerebral artery occlusion (MCAO). These lesions resulted in impaired body weight evolution and delayed restoration of neurological function in Wistar rats.² This is neither a laboratory-specific nor a rat strain-specific problem, as can be learned from a publication of Palmer et al.³ Sprague–Dawley rats MRI on day 2 after temporary MCAO (suture technique) depicted extracranial lesions in the temporal muscle that are identical to those found in our laboratory. Unfortunately, the authors do not comment on this finding.

View larger version (127K): [in this window] [in a new window]   Hyperintense signal changes in T2-weighted MRI of the ipsilateral temporal muscle (arrow) 1 day after surgery for filament MCAO.

The cause of the masticatory lesions is yet obscure. Although acute ischemic myopathy caused by transection of the external carotid artery had been discussed,² further experiments revealed that protection of the external carotid artery was . . . [Full Text of this Article]

Tibo Gerriets, MD; Erwin Stolz, MD Manfred Kaps, MD

Department of Neurology, University Giessen, Germany

Maureen Walberer, DVM; Clemens Mueller, PhD Georg Bachmann, MD

Department of Radiology and, Experimental Neurology Research Group, Kerckhoff Klinik Bad Nauheim, Germany

Marc Fisher, MD

Department of Neurology, University of Massachusetts Medical School, Worcester, Mass