Polysomnographic effects of thyroid hormones primary myxedema.

Nine primary myxedematous patients were subjected to all-night polysomnographic recordings under the following conditions: (1) basal or myxedematous state; (2) acute replacement therapy (treatment with thyroid hormones at doses that increased weekly to the maximal replacement dose, Mrd); and (3) chronic replacement therapy (maintenance on the Mrd; euthyroid state). The most striking abnormality found in the sleep pattern during the myxedematous state was observed in both young adult (greater than 20 years old) and adult (greater than 50 years old) patients, consisting of either a complete absence or very low levels of slow wave sleep (SWS). Replacement therapy was accompanied by a restoration of the normal sleep pattern in 3 of the 4 patients that were followed. In contrast, younger patients (14-18 years old with a bone age of less than or equal to 10 years) had normal levels of SWS, with the exception of an adolescent with a bone age of less than 3 years. The latency for rapid eye movement (REM) sleep tended to increase during acute replacement therapy and became normal when euthyroidism was reached. These results lend support to the proposal that thyroid hormones exert central effects on the adult CNS.

Neuroendocrine and electroencephalographic sleep changes due to acute amphetamine ingestion in human beings.

Amphetamine, a clinically used sympathomimetic central-acting drug, was administered in Spansule capsules in a blind schedule to 8 normal obse volunteers in a daily (8 a.m.) single 15 dose for 7 days. The study, conducted in the metabolic ward, included two 7 day placebo periods (pre- and post-drug). During the 1st placebo period, all subjects exhibited within the 1st 2 h of sleep a clear and significant nocturnal increase of growth hormone (GH) closely related with sleep stages 3 and 4. Thyrotropin (TSH) increase was observed between 01.00 to 04.00 h and was accompanied by a reduction of thyroxine (T4) levels. Cortisol levels presented their characteristic rhythm, clearly associated with paradoxical sleep (REM). Amphetamine significantly reduced stages 3 and 4, as well as REM sleep, and increased stage 2. GH and cortisol circadian profiles were preserved, although their magnitude was diminished. The extent of nocturnal TSH and T4 changes was significantly reduced. Drug withdrawal was accompanied by a rebound of REM sleep and a trend to recover the pretreatment TSH and T4 temporal profile. These results suggest that adrenergic neurotrasmitters may be a significant modulating system for TSH and cortisol, whereas GH nocturnal secretion may be influenced by different mechanisms.