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Cerebellar Vasoreactivity in Stroke Patients with Crossed Cerebellar Diaschisis Assessed by Acetazolamide and ^99mTc-HMPAO SPECT

Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul
Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul, Korea

Correspondence: For correspondence or reprints contact: Sang Eun Kim, MD, Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Kangnam-ku, Seoul 135-710, Korea.

ABSTRACT

Crossed cerebellar diaschisis (CCD) tends to persist or even worsen after supratentorial infarction. Several studies have shown impairment of cerebral vasomotor responsiveness in the hemispheric area of diaschisis in patients with hemispheric infarction. This finding has led to the concern that the lack of CCD reversibility might be associated with chronic circulatory abnormalities. We therefore assessed the vasoreactivity in the cerebellar hemisphere in which diaschisis is manifested using acetazolamide (ACZ) and SPECT. Methods: Eight stroke patients with CCD (5 with unilateral hemispheric infarcts and 3 with unilateral intracerebral hemorrhage) had ^99mTc-HMPAO SPECT scanning at rest and 20 min after intravenous injection of 1.0 g ACZ. The time interval after stroke ranged from 25 to 904 d. From the total counts obtained from each cerebellar hemisphere, the asymmetry index (Al) was calculated as (unaffected – affected cerebellar hemispherej/unaffected cerebellar hemisphere x 100. Results: After ACZ, the mean Al (8.7 ± 6.6) was significantly decreased (P < 0.05) compared with that at rest (17.7 ± 5.8). Seven of the 8 patients showed decrease in the Al after ACZ. In 1 patient, the direction of the asymmetry was reversed after ACZ so that the Al was negative. The ACZ-induced change in the Al did not show a significant correlation with the time interval after stroke, whether calculated in absolute terms or as a percentage change. Conclusion: This study shows that normal vascular supply is maintained in the CCD-affected cerebellar hemisphere over king periods of time after a stroke. Thus, the lack of CCD reversibility may not be attributed to a chronic circulatory insufficiency. The results lend support to the concept of functional deactivation and subsequent transneuronal degeneration as a likely explanation for CCD. It is unclear whether decreased Al after ACZ indicates a higher vascular response of the affected cerebellar hemisphere than that of the normal side.

Key Words: crossed cerebellar diaschisis • cerebellar vasoreactivity • acetazolamide • ^99mTc-HMPAO • SPECT

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