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Dennis L. Murphy, MD; Jerry R. Mendell, MD; W. King Engel, MD

Arch Neurol. 1973;28(4):239-242.

Abstract
Since lesions characteristic of Duchenne muscular dystrophy (DMD) are reproduced in animals by vascular ischemia from aortic ligation plus serotonin (5-HT) injections, 5-HT levels and serotonin 14C cellular transport mechanisms were studied in 14 boys with DMD. Plasma 5-HT levels were no different from those of 23 controls, but platelet 5-HT content was moderately reduced. No abnormalities were found in serotonin ¹⁴C efflux or monoamine oxidase activity. These studies suggest that a simple increase in circulating 5-HT or decrease in its enzymatic degradation is not present in DMD. The major finding was a markedly reduced initial rate of accumulation of serotonin ¹⁴C into platelets from DMD patients. This finding may be of significance to the proposed vascular pathogenesis for DMD in raising the possibility of an alteration in biogenic amine deactivation at the microvascular level.

Author Affiliations
Bethesda, Md

From the Laboratory of Clinical Science, National Institute of Mental Health, and the Medical Neurology Branch, National Institute of Neurological Diseases and Stroke, Bethesda, Md.

Footnotes
Accepted for publication Nov 24, 1972.

Read before the annual meeting of the American Academy of Neurology, St. Louis, April 28, 1972.

Reprint requests to NIH Clinical Center, 10-3S229, 9000 Rockville Pike, Bethesda, Md 20014 (Dr. Murphy).

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