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NEUROLOGY 1980;30:98
© 1980 American Academy of Neurology

Norepinephrine and gamma-aminobutyric acid in amyotrophic lateral sclerosis

Michael G. Ziegler, M. D., Benjamin R. Brooks, M. D., C. Raymond Lake, M. D., Ph. D., James H. Wood, M. D. and S. J. Enna, Ph. D.

Departments of Medicine and Pharmacology, University of Texas Medical Branch, Galveston, TX (Dr. Ziegler), the Division of Neurology, Johns Hopkins Medical School, Baltimore, MD (Dr. Brooks), the Laboratory of Clinical Science, National Institutes of Health, Bethesda, MD (Dr. Lake), the Division of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia, PA (Dr. Wood), and the Departments of Pharmacology, Neurobiology, and Anatomy, University of Texas Medical School at Houston, Houston, TX (Dr. Enna).

Patients with amyotrophic lateral sclerosis have increased levels of the neurotransmitter norepinephrine in blood and cerebrospinal fluid and depressed levels of the inhibitory neurotransmitter gamma-aminobutyric acid in cerebrospinal fluid. These neurochemical alterations are most marked in patients bedridden with advanced disease, appear interrelated, and lead to cardiovascular alterations in patients with amyotrophic lateral sclerosis.

Address reprint requests to Dr. Ziegler, Room 457 Gail Borden, University of Texas Medical Branch, Galveston, TX 77550.

Accepted for publication May 25, 1979.

Supported in part by NHLBI grant HL 21817, USPHS Research Career Development Award NS-00335 (S. J. E.) and grants from the Pharmaceutical Manufacturers Association, Huntington's Chorea Foundation, and Merck Sharp & Dohme.






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