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Transcranial midbrain sonography in narcoleptic subjects with and without concomitant REM sleep behaviour disorder

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Abstract

Substantia nigra (SN) hyperechogenicity—a sonographic vulnerability marker for Parkinson’s disease (PD)—has been recently described in patients with idiopathic REM sleep behaviour disorder (RBD). It is not known whether subjects with narcolepsy (who frequently have associated RBD) also show SN hyperechogenicity. The aim of this study was to (1) evaluate SN echogenicity in narcolepsy and (2) determine whether transcranial sonography (TCS) differs in narcoleptic subjects with and without RBD. A total of 16 patients with narcolepsy–cataplexy (7 had a concomitant, video-polysomnographically based diagnosis of RBD) were examined with TCS by two investigators blinded to the clinical data. The size of the SN echogenic area in both subgroups was within the range previously described for healthy subjects. The brainstem raphe, however, was reduced in five of seven narcoleptic subjects with RBD, whereas only two of nine narcoleptic subjects without RBD exhibited this TCS finding. We conclude that evaluation of SN echogenicity does not discriminate between both subgroups. The absence of SN hyperechogenicity in narcoleptic patients with RBD supports the hypothesis that SN hyperechogenicity in patients with presumed idiopathic RBD is an additional risk marker for subsequent evolvement of PD rather than an RBD-immanent finding. Reduced echogenicity of the brainstem raphe might indicate an involvement of the serotonergic system in narcoleptic subjects with RBD.

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Acknowledgments

This work was supported by grants from the BMBF (funding code: 01GI0401) and the Willy und Monika Pitzer Stiftung.

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The authors declare that there is no conflict of interest regarding this work.

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Correspondence to Marcus M. Unger.

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W.H. Oertel and G. Mayer contributed equally to this work.

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Unger, M.M., Möller, J.C., Ohletz, T. et al. Transcranial midbrain sonography in narcoleptic subjects with and without concomitant REM sleep behaviour disorder. J Neurol 256, 874–877 (2009). https://doi.org/10.1007/s00415-009-5032-7

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  • DOI: https://doi.org/10.1007/s00415-009-5032-7

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