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NEUROLOGY 2004;63:2416-2418
© 2004 American Academy of Neurology
Brief Communications

Dissociation in circadian rhythms in a pseudohypersomnia form of fatal familial insomnia

Y. Dauvilliers, MD, K. Cervena, MD, B. Carlander, MD, F. Espa, BSc, C. Bassetti, MD, B. Claustrat, MD, PhD, J. L. Laplanche, MD, PhD, M. Billiard, MD and J. Touchon, MD

From the Service de Neurologie B (Drs. Dauvilliers, Cervena, Carlander, Billiard, and Touchon, F. Espa), Gui-de-Chauliac Hospital, Montpellier, France; INSERM E0361 Hospital la Colombière (Drs. Dauvilliers and Touchon), Montpellier, France; Neurology Department (Dr. Bassetti), University Hospital Zurich, Switzerland; Radioanalysis Unit (Dr. Claustrat), Neuro-Cardiological Hospital, Lyon, France; and Service of Biochemistry and Molecular Biology (Dr. Laplanche), Lariboisière Hospital, Paris, France.

Address correspondence and reprint requests to Dr. Yves Dauvilliers, Service de Neurologie B, Hôpital Gui-de-Chauliac, 80 avenue Augustin Fliche, 34295 Montpellier Cedex 5, France; e-mail: ydauvilliers{at}yahoo.fr

The authors present clinical, sleep, and neuroendocrine features of a patient with genetically confirmed fatal familial insomnia (D178N mutation with heterozygosity at codon 129 of the prion protein gene). The patient exhibited pseudohypersomnia behavior instead of insomnia. There was profound alteration in the sleep-wake cycle with a clear dissociation in the disappearance of circadian and neuroendocrine rhythms, findings unrelated to abnormalities in the hypocretinergic system.

Received February 5, 2004. Accepted in final form July 26, 2004.






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