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Neurology 2003;61:823-825
© 2003 American Academy of Neurology
Brief Communications

CSF hypocretin levels in Guillain–Barré syndrome and other inflammatory neuropathies

S. Nishino, MD PhD, T. Kanbayashi, MD PhD, N. Fujiki, MD PhD, M. Uchino, MD PhD, B. Ripley, BS, M. Watanabe, MD PhD, G. J. Lammers, MD PhD, H. Ishiguro, MD PhD, S. Shoji, MD PhD, Y. Nishida, MD, S. Overeem, MSc, I. Toyoshima, MD PhD, Y. Yoshida, MD PhD, T. Shimizu, MD PhD, S. Taheri, MD PhD and E. Mignot, MD PhD

From the Stanford University Center for Narcolepsy (Drs. Nishino, Fujiki, Yoshida, Taheri, and Mignot, B. Ripley), Palo Alto, CA; Departments of Neuropsychiatry (Drs. Kanbayashi and Shimizu) and Neurology (Dr. Toyoshima), Akita University School of Medicine, and Department of Neurology (Dr. Ishiguro), Akita Red Cross Hospital, Department of Neurology (Drs. Uchino and Nishida), Kumamoto University School of Medicine, and Department of Neurology (Drs. Watanabe and Shoji), Tsukuba University School of Medicine, Japan; and Department of Neurology and Clinical Neurophysiology (Dr. Lammers, S. Overeem), Leiden University Medical Center, the Netherlands.

Address correspondence and reprint requests to Dr. S. Nishino, Stanford University Center for Narcolepsy, 701B Welch Rd., Rm. 142, Palo Alto, CA 94304; e-mail: nishino{at}stanford.edu

CSF hypocretin-1 was measured in 28 Guillain–Barré syndrome (GBS), 12 Miller–Fisher syndrome, 12 chronic inflammatory demyelinating polyneuropathy (CIDP), and 48 control subjects. Seven GBS subjects had undetectably low hypocretin-1 levels (<100 pg/mL). Hypocretin-1 levels were moderately reduced in an additional 11 GBS, 5 Miller–Fisher syndrome, and 1 CIDP subject. Low levels in GBS occurred early in the disease and were associated with upper CNS level abnormalities.




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Correspondence:

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CSF hypocretin levels in Guillain–Barré syndrome and other inflammatory neuropathies
Christian R. Baumann, et al.
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