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REM sleep behavior disorder (RBD) is characterized by dream enactment behaviors (DEB) and REM sleep without atonia (RSWA). A key structure in REM sleep muscle tone regulation in the rodent model is the sublateral dorsal (SLD) tegmental nucleus in the dorsomedial pons.1 Lesions of an analogous structure, the subceruleus (SC) nucleus are thought to mediate RSWA in humans, enabling DEB.1,2 However, in vivo human studies of discrete dorsomedial pontine lesions causing RBD in isolation have been limited.2–4 We report such a case of lesional RBD due to vasculitis. The Mayo Clinic Institutional Review Board approved this study.
Acknowledgments
Acknowledgment: The authors thank Lori Lynn Reinstrom, Department of Neurology, Mayo Clinic, for assistance with copyediting and manuscript submission.
Footnotes
Supplemental data at Neurology.org
Author contributions: Erik K. St. Louis: study concept and design, acquisition of data, data analysis and interpretation, authorship and critical revision of the manuscript, study supervision. Stuart J. McCarter: acquisition of data, analysis, authorship and critical revision of manuscript. Bradley F. Boeve: critical revision of the manuscript for important intellectual content. Michael H. Silber: critical revision of the manuscript for important intellectual content. Kejal Kantarci: critical revision of the manuscript for important intellectual content. Eduardo E. Benarroch: critical revision of the manuscript for important intellectual content. Alora Rando: analysis of data and critical revision of manuscript. Maja Tippmann-Peikert: critical revision of the manuscript for important intellectual content. Eric J. Olson: critical revision of the manuscript for important intellectual content. Michelle Mauermann: critical revision of the manuscript for important intellectual content.
Study funding: Supported by the National Center for Research Resources and the National Center for Advancing Translational Sciences, NIH, through grant 1 UL1 RR024150-01. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Disclosure: E. St. Louis receives research support from the Mayo Clinic Center for Translational Science Activities (CTSA), supported by the National Center for Research Resources and the National Center for Advancing Translational Sciences, NIH, through grant 1 UL1 RR024150-01, and a Mayo Clinic Alzheimer's Disease Research Center Grant Award from the National Institute on Aging (P50 AG016574). S. McCarter reports no disclosures relevant to the manuscript. B. Boeve is an investigator in clinical trials sponsored by Cephalon, Inc., Allon Pharmaceuticals, and GE Healthcare. He receives royalties from the publication of Behavioral Neurology of Dementia (Cambridge Medicine, 2009). He has received honoraria from the American Academy of Neurology. He serves on the board of the Tau Consortium. He receives research support from the National Institute on Aging (P50 AG16574 [coinvestigator], U01 AG06786 [coinvestigator], RO1 AG32306 [coinvestigator]) and the Mangurian Foundation. M. Silber, K. Kantarci, E. Benarroch, A. Rando, M. Tippmann-Peikert, E. Olson, and M. Mauermann report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures.
- Received February 26, 2014.
- Accepted in final form May 27, 2014.
- © 2014 American Academy of Neurology
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