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January 1966

Effects of Thyroid on Permeability, Composition, and Electrolyte Metabolism Of Brain and Other Tissues

Author Affiliations

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

Arch Neurol. 1966;14(1):21-30. doi:10.1001/archneur.1966.00470070025003

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

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