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NEIL H. RASKIN, MD; ROBERT A. FISHMAN, MD

Arch Neurol. 1966;14(1):21-30.

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

THE SYNDROMES that may result from a great excess or deficiency of thyroid hormone in man, thyroid storm,¹ and myxedema coma,² are both characterized neurologically by apathy, somnolence, psychosis, confusion, and, ultimately, coma— clinical expressions of profound alterations in cerebral function. The pathophysiology of these metabolic encephalopathies is poorly understood and, though nonspecific atrophic changes have been described in adult hypothyroid brains,³ these are inconsistent; no definite lesions have been observed in hyperthyroid brain.⁴ Although brain oxygen consumption has been shown to be diminished in human myxedema,⁵ it is normal in thyrotoxicosis.⁶ This study was undertaken, then, to elucidate thyroidal effects upon brain function. Myxedema and thyrotoxicosis were simulated in rats by thyroidectomy and thyroxine intoxication; brain permeability, composition and electrolyte metabolism were studied using sucrose¹⁴C, sulfate³⁵S, sodium 24 and potassium 42.

Methods

Adult male Sherman rats were used . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Neurological Clinical Research Center, Department of Neurology, College of Physicians and Surgeons, and the Neurological Institute, Presbyterian Hospital.

Footnotes
Submitted for publication July 30, 1965; accepted Aug 15.

Presented in part before the meeting of the American Association of Neuropathologists, June, 1965.

Reprint requests to 710 W 168th St, New York, NY 10032 (Dr. Fishman).

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