Reduction of the behavioral complaints during thyroid hormone therapy is associated with a restoration of metabolic activity in brain areas that are integral to the regulation of affect and cognition. The findings suggest that thyroid hormone modulates regional glucose metabolism and psychiatric symptoms in the mature brain.
The effects of inadequate thyroid hormone availability to the brain on adult cognitive function are poorly understood. This study assessed the effects of hypothyroidism on cognitive function using a standard neuropsychological battery in 14 patients suffering from untreated hypothyroidism and complaining of subjective cognitive difficulties in comparison with 10 age-matched healthy comparison subjects. Significant differences between groups were limited to verbal memory retrieval as measured by the California Verbal Learning Test (CVLT). On short delay free recall, long delay free recall, and long delay cued recall, significant differences remained between groups despite the limited statistical power of this study. There were no significant results found between groups on attentional or nonverbal tasks. Results suggest that hypothyroid-related memory deficits are not attributable to an attentional deficit but rather to specific retrieval deficits.
To elucidate the mechanism of thyroglobulin (Tg) release in man, the effects of an iv injection of a submaximal dose of bovine TSH (bTSH) on the serum levels of Tg were compared with the effects on serum T3 and T4. After the administration of bTSH, short term kinetics (0-4 h) were studied in eight subjects receiving 0.5 IU bTSH and seven subjects receiving 1 IU bTSH. Serum Tg did not significantly increase in either of the short term studies. By contrast, serum T3 increased significantly and linearly after the administration of 0.5 and 1 IU bTSH; serum T4 also rose but only after 1 IU bTSH. Long term kinetics (0-120 h) were studied in seven additional subjects after the iv administration of 1 IU bTSH; serum bTSH was no longer detectable after 8 h. Maximum serum concentrations of T3 were obtained at about 4 h, maximum serum concentrations of T4 were obtained between 4-8 h. Serum Tg levels increased linearly with time during the first 24 h. Maximum serum Tg levels correlated well with basal serum Tg values (r = 0.97; P < 0.001). The maximal increment in Tg correlated inversely with the maximal increment in T3 (r = 0.71; P < 0.05). The half-life of Tg was estimated to be approximately 4 days by measuring the disappearance rate of Tg after its peak level was attained.
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