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From the Department of Neurology (Drs. Scammell and Saper), Beth Israel Deaconess Medical Center, Boston, MA; and the Center for Narcolepsy (Drs. Nishino and Mignot), Department of Psychiatry, Stanford University School of Medicine, CA.
Address correspondence and reprint requests to Dr. T.E. Scammell, Department of Neurology, Beth Israel Deaconess Medical Center, 77 Ave. Louis Pasteur, Boston, MA 02115; e-mail: tscammel{at}caregroup.harvard.edu
Idiopathic narcolepsy usually results from a loss of the hypothalamic neuropeptide orexin (hypocretin), but the cause of secondary narcolepsy resulting from focal brain lesions is unknown. The authors describe a young man who developed narcolepsy after a large hypothalamic stroke. His lesion included much of the hypothalamic region in which orexin is produced, and his CSF concentration of orexin was low. The authors hypothesize that a loss of orexin neurons or their relevant targets may be the specific neuropathology causing this and many other cases of secondary narcolepsy.
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