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REM sleep behavior disorder is related to striatal monoaminergic deficit in MSA

From the Department of Neurology (Drs. Gilman, Chervin, Consens, and Junck, M. Heumann); Division of Nuclear Medicine (Dr. Koeppe), Department of Radiology; and Department of Biostatistics (Dr. Little, H. An); University of Michigan, Ann Arbor.

Address correspondence and reprint requests to Dr. S. Gilman, Department of Neurology, University of Michigan Health System, 1500 E. Medical Center Dr., Ann Arbor, MI 48109-0316; e-mail: sgilman{at}umich.edu

Objective: To explore the neurochemical basis of REM sleep behavior disorder (RBD) in multiple-system atrophy (MSA).

Methods: In 13 patients with probable MSA, nocturnal, laboratory-based polysomnography was used to rate the severity of REM atonia loss by the percentage of REM sleep with tonically increased electromyographic (EMG) activity and the percentage of REM sleep with phasic EMG bursts. PET with (+)-[¹¹C]dihydrotetrabenazine ([¹¹C]DTBZ) was employed to measure the density of striatal monoaminergic terminals and SPECT with (-)-5-[¹²³I]iodobenzovesamicol ([¹²³I]IBVM) to measure the density of thalamic cholinergic terminals. Data in the patient group were compared with data from 15 normal control subjects scanned with [¹¹C]DTBZ and 12 with [¹²³I]IBVM.

Results: Age and gender distributions were similar in patient and normal control groups. The MSA subjects showed decreased mean [¹¹C]DTBZ binding in the striatum (p < 0.0001) and decreased [¹²³I]IBVM binding in the thalamus (p < 0.001). Moreover, in the MSA group, striatal [¹¹C]DTBZ binding was inversely correlated with the severity of REM atonia loss (p = 0.003). Thalamic [¹²³I]IBVM binding, however, was not correlated to the severity of REM atonia loss.

Conclusion: Decreased nigrostriatal dopaminergic projections may contribute to RBD in MSA.

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