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Updated: Aug 16, 2026
Optimized System for Cerebral Perfusion Monitoring in the Rat Stroke Model of Intraluminal Middle Cerebral Artery Occlusion
Published on: February 17, 2013
Hemodynamic aspect of cerebral watershed infarction: assessment of perfusion reserve using iodine-123-iodoamphetamine
H Moriwaki1, M Matsumoto, K Hashikawa
1First Department of Medicine, Osaka University Medical School, Suita, Japan.
Unlabelled:
The mechanism whereby watershed (WS) infarcts develop remains controversial, although a hemodynamic cause is usually assumed. The aim of this study was to investigate the relationship between the site of WS infarcts and the hemodynamic status of the cerebral circulation.
Methods:
From among 96 consecutive patients with angiographically confirmed unilateral major cerebral artery obstruction (occlusion or > 70% stenosis), we investigated 29 patients with supratentorial WS infarcts on magnetic resonance imaging. The regional cerebral blood flow and perfusion reserve were quantified using the split-dose [123I]iodoamphetamine SPECT method, coupled with intravenous injection of 1 g of acetazolamide. Seven patients had a cortical WS infarct between the superficial branches of the anterior and middle cerebral arteries (MCAs) or between the middle and posterior cerebral arteries (Group C), and 22 had a deep WS infarct between the superficial branches and deep penetrating arteries of the MCA (Group D). Moreover, the patients in Group D were classified into two subgroups, i.e., Type A (n = 12), with lesions lying in the centrum semiovale above the level of the lateral ventricles, and Type B (n = 10), with lesions lying in the corona radiata adjacent to the lateral ventricles.
Results:
Comparison of the Type of WS infarct with the clinical course of onset showed that sudden onset was more frequent in Group C than in Group D (p < 0.05). The perfusion reserve in the affected MCA territory in Group D (20.1% +/- 15.6%) was significantly lower than that in Group C (43.8% +/- 10.8%; p < 0.01) and that in 20 hemispheres (10 control subjects) without a major arterial lesion (54.7% +/- 16.4%; p < 0.01). Among the Group D patients, the patients with Type A infarcts showed a significantly lower perfusion reserve compared with those with Type B infarcts (p < 0.05).
Conclusion:
Patients with deep WS infarcts, especially Type A infarcts, showed severe hemodynamic impairment, whereas patients with cortical WS infarcts showed preserved perfusion reserve which appeared to be secondary to the embolism. The mechanism of development of WS infarcts is multifactorial, and distinguishing among these WS infarcts and from other types of infarct is important, because different pathogenic mechanisms require different therapeutic strategies.
