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JOSEPH F. FAZEKAS, M.D.; ANDREE THOMAS, M.D.; JULIA V. V. JOHNSON, M.S.; WILLIAM K. YOUNG, M.S.

AMA Arch Neurol. 1960;2(4):435-438.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

There is considerable uncertainty regarding the role of sympathetic amines in the central nervous system; although some have postulated that they may be concerned with neural transmission, supporting evidence is not entirely conclusive. Nevertheless, Vogt¹ has noted the presence of relatively high concentrations of sympathin in the hypothalamus and in the area postrema, with less in the midbrain and in the aqueduct, and has further demonstrated that their local concentrations may be reduced by drugs which stimulate these centers. It has long been recognized that the administration of epinephrine stimulates the waking state and increases spontaneous motor activity. It has been suggested that these effects of circulating epinephrine may in part be due to direct stimulation of ascending and descending reticular systems (Bonvallet, Dell, and Hiebel²; Dell, Bonvallet, and Hugelin³). Sensenbach et al.⁴ were unable to demonstrate significant alteration of cerebral oxygen consumption by the administration . . . [Full Text PDF of this Article]

Author Affiliations
Boston

From the District of Columbia General Hospital, Washington, D.C., and the Department of Neurology, Neurosurgery, and Psychiatry (Neurology), New England Center Hospital.

Footnotes
Accepted for publication Jan. 6, 1959.

This investigation was supported in part by a research grant (PHS B-178) from the National Institute of Neurological Diseases and Blindness of the National Institutes of Health, U.S. Public Health Service.

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