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AJNR - American Journal of Neuroradiology

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American Journal of Neuroradiology 24:1355-1363, August 2003
© 2003 American Society of Neuroradiology

BRAIN

Assessment of Diffusion and Perfusion Deficits in Patients with Small Subcortical Ischemia

Claudia A. Doege^a, Christian M. Kerskens^a, Berenice I. Romero^a, Peter Brunecker^a, Jan Junge-Hülsing^a, Wolfram von Pannwitz^a, Bianca Müller^a and Arno Villringer^a

^a From the Department of Neurology, Humboldt University, Charité, Berlin, Germany

Address correspondence to Professor Arno Villringer, Klinik und Poliklinik für Neurologie, Universitätsklinikum Charité, Campus Mitte, Medizinische Fakultät der Humboldt-Universität zu Berlin, Schumannstraße 20/21, D-10117 Berlin, Germany

BACKGROUND AND PURPOSE: Using perfusion- and diffusion-weighted MR imaging in acute ischemic stroke of the middle cerebral artery (MCA), previous studies have shown a typical pathophysiologic pattern that is characterized by a perfusion deficit larger than the diffusion lesion (mismatch), with the final lesion usually comprising the initial diffusion lesion (core) plus parts of the initial mismatch area. Little is known about underlying pathophysiology in small ischemic stroke. In this study, we used perfusion- and diffusion-weighted MR imaging to investigate the underlying pathophysiology of small subcortical ischemia.

METHODS: Six consecutive patients (age range, 42–76 years) with small subcortical ischemia were examined by using a 1.5-T MR system 2–5, 22–55, and 144–392 hours after the onset of symptoms. T2-weighted, diffusion-weighted imaging at b=0 s/mm² and b=1000 s/mm², and bolus-track perfusion-weighted imaging were performed. Lesion sizes were determined on the basis of T2-weighted findings as well as those of apparent diffusion coefficient (ADC) maps and CBF.

RESULTS: In every patient, the initial CBF lesion was smaller than the initial ADC lesion. Both the CBF lesion and the ADC lesion increased in size from first to second examination. In all instances, however, the CBF lesion remained smaller than the ADC lesion. The CBF lesion observed during the acute phase and the one seen on the following days were both smaller than the final T2 lesion.

CONCLUSION: Our data suggest that in contrast to previous findings in MCA ischemia in small subcortical infarcts tissue damage may spread beyond the area of the initial perfusion disturbance. In light of the small number of patients, further studies will have to address the relevance of this observation.

This article has been cited by other articles:

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