Should thyroid augmentation precede lithium augmentation--a pilot study.

BACKGROUND: It has not been investigated whether thyroid augmentation should precede lithium augmentation or vice versa. METHODS: In 22 outpatients with major depression not responsive to 4 weeks of antidepressant treatment, the effect of subsequent 4 weeks of thyroxine administration followed by 4 weeks of lithium augmentation was compared with the effect of the same treatments in reverse order. RESULTS: The percentage reduction in MADRS score was significantly greater in patients who started on thyroxine. CONCLUSIONS: Thyroxine augmentation should precede lithium augmentation. LIMITATIONS: We used relatively small doses of lithium. CLINICAL RELEVANCE: Thyroxine is effective in augmenting antidepressant responses.

Do reversed depressive symptoms occur together as a syndrome?

Although the DSM-IIIR diagnostic criteria for major depression include hypersomnia, increase in appetite, and in children and in adolescents irritability, there is no general agreement on the existence of a depressive syndrome with reversed vegetative symptoms. Our findings suggest that these reversed depressive symptoms may not occur together as a syndrome. However, they may share an enhanced responsiveness to moclobemide treatment.

Prolactin response to submaximal stimulation by TRH in nonaffective psychoses.

Nonaffective psychotic symptoms are heterogeneous and probably caused by mixed biopathology. A preliminary investigative tool to study pituitary dopamine activity, the prolactin response to submaximal stimulation by thyrotropin-releasing hormone (TRH) (mini-TRH test) was correlated in 20 subjects with nonaffective psychoses to positive psychotic symptoms as assessed by the Comprehensive Psychiatric Rating Scale psychosis subscale. A significant positive correlation was observed between the response and ratings of nonparanoid symptoms, especially nonparanoid delusions and disrupted thoughts. Because, in addition to pituitary dopamine activity, there is evidence to suggest that the response reflects extrapituitary dopamine activity as well, the results extend the evidence that nonparanoid acute productive psychotic symptoms may be associated with hypoactivity rather than with hyperactivity of brain dopaminergic systems.

Plasma endogenous opioids and dexamethasone suppression test in depression.

Plasma levels of beta-endorphin plus beta-lipotropin were determined in 35 hospital patients with depression and in 23 controls before and after administration of 1 mg of dexamethasone (dxm). Dxm suppressed opioid secretion in both groups. The opioid levels of the patients were significantly higher than those of the controls both before and after dxm. All the controls were cortisol suppressors. Among the patients the post-dxm opioid levels of cortisol nonsuppressors (n = 14) were higher than those of cortisol suppressors (n = 21). A significant correlation between the opioid and cortisol levels was found in the patients. There was a significant association between the use of neuroleptics and high opioid levels, but the difference between the patients and the controls was not explained by the effect of any single class of drugs. The results support the concept of hypersecretion of corticotropin-releasing factor in depression.

Plasma prolactin response to submaximal stimulation by TRH and endogenous corticosteroids in man.

Recent studies suggest that submaximal plasma prolactin responses to TRH may reflect the effects of endogenous dopamine on prolactin release more accurately than basal plasma prolactin levels or maximal plasma prolactin responses to TRH. In the present study the plasma prolactin response to 12.5 micrograms i.v. TRH in 25 male subjects was significantly correlated with 24-hour urinary 17-ketogenic steroid excretion (= "total" 17-hydroxy corticosteroids). With regard to the basal plasma prolactin level or the prolactin response to 200 micrograms i.v. TRH, no such relation with corticosteroid excretion was detected. It is concluded that the plasma prolactin response to 12.5 micrograms i.v. TRH may provide a new, useful investigative tool with which to study corticosteroid-dopamine interactions and central dopamine activity in man.

Submaximal plasma prolactin response to TRH and dopamine activity in man.

Submaximal plasma prolactin responses to TRH were evaluated as a measure of endogenous dopamine activity in man. In 25 male subjects, plasma prolactin responses to 0.5 mg i.m. haloperidol were significantly correlated with plasma prolactin responses to 12.5 micrograms i.v. TRH but not with plasma prolactin responses to 200 micrograms i.v. TRH or with basal plasma prolactin levels. The results suggest that submaximal plasma prolactin responses to TRH may reflect the effects of endogenous dopamine activity on prolactin release more accurately than the prolactin measures previously used.