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(Stroke. 2006;37:2713.)
© 2006 American Heart Association, Inc.
Original Contributions |
From the Department of Neurology (D.S., C.W.), University Medical Center Freiburg, Freiburg, Germany; the Departments of Nuclear Medicine (R.B.) and Neurology (R.K.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany; and the Department of Neurology (J.R.), Klinikum Minden, Academic Teaching Hospital, Hannover Medical School, Minden, Germany.
Correspondence to Dorothee Saur, MD, Department of Neurology, University Medical Center Freiburg, Breisacher Strasse 64, 79106 Freiburg, Germany. E-mail dorothee.saur{at}uniklinik-freiburg.de
Background and Purpose The mismatch of hypoperfused tissue on perfusion imaging and ischemic tissue on diffusion-weighted imaging is used as a surrogate marker for thrombolytic therapy in the extended time window. Mismatch tissue may recover completely, progress toward infarction, or proceed toward incomplete infarction with selective loss of cortical neurons. We used [123I]iomazenilsingle-photon emission computed tomography (IMZ-SPECT) to characterize the neuronal integrity of reperfused "tissue at risk of infarction" that appeared morphologically intact on follow-up magnetic resonance imaging (MRI).
Methods Twelve patients with acute stroke with striatocapsular (SC) infarctions were examined with multimodal MRI at days 0, 1, and 7; IMZ-SPECT was performed at days 5 to 15. The PI at day 0, fluid-attenuated inversion recovery (FLAIR) image at day 7, and IMZ-SPECT were coregistered and stereotactically normalized. The mismatch volume of interest (VOI) was defined as the initial PI lesion subtracted by the FLAIR lesion at day 7. An asymmetry ratio (AR) was computed by dividing the mean IMZ uptake of the mismatch VOI by the unaffected mirror VOI. The same AR was computed for signal intensity on FLAIR images at day 7. Three patients with cortical infarctions were included for calibration of the AR. In this group, the VOI consisted of the FLAIR lesion at day 7.
Results All patients with SC infarctions had a large mismatch of initially hypoperfused (112±31 mL; mean±SD) and finally infarcted tissue (19±14 mL). Mean AR of cortical IMZ uptake was 0.85±0.01 in cortical infarctions and 0.95±0.03 in SC infarctions; thereby AR showed a continuous distribution from clearly reduced (0.89) to normal (1.01) in SC infarctions. Mean AR for FLAIR signal intensity was 1.84±0.14 for cortical infarctions and normal (1.01+0.03) for SC infarctions.
Conclusions IMZ-SPECT detected a selective loss of cortical neurons in patients with SC infarctions in transient hypoperfused tissue, which was morphologically intact on MRI.
Key Words: cerebral ischemia diffusion and perfusion imaging incomplete infarction iomazenil-SPECT mismatch tissue
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