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This study evaluates the relationship between stress of captivity and subsequent presence of Post Traumatic Stress Disorder (PTSD) has been evaluated in a homogeneous population of 817 Alsatian World War II veterans who were imprisoned in the USSR during and after the war. Data were collected in 1988 by a questionnaire structured to investigate the presence of DSM-III-R criteria for PTSD as well as events experienced in captivity. The presumptive diagnosis of PTSD was found to be significantly associated with longer internment and with higher scores on a severity of POW experience index.
We studied circadian thyrotropin (TSH) and prolactin (PRL) response to synthetic thyrotropin-releasing-hormone (protirelin) infusion (200μg IV) at 8 am and 11 pm in 35 drug-free inpatients with DSM III-R Major Depressive Episode and in 22 hospitalized controls. In each group, maximum TSH and PRL responses were lower at 8 am than at 11 pm. The difference between 11 pm-ΔTSH and 8 am-ΔJTSH (ΔΔTSH) was significantly lower in depressed patients compared to controls. No such blunting was observed in PRL responses to protirelin in depressed patients. In the overall population, TSH response to protirelin (ie8 am-ΔTSH, 11 pm-ΔTSH, ΔΔTSH) correlated significantly with TSH circadian parameters (ie mesor and amplitude). These correlations were also observed with PRL (except for ΔΔPRL). TSH mesor and amplitude were lower in depressives than in controls. In contrast, PRL mesor and amplitude were not significantly different between diagnostic groups. ΔΔTSH is thus a chronobiological refinement to the measure of thyroid axis dysfunction in major depression. The blunted TSH response to protirelin suggests that the TRH receptors of the pituitary thyrotrophs are hyposensitive in major depression.
A stimulating variety of papers on genetic and clinical research in psychiatry was discussed at the latest meeting of the American Psychiatric Association and the Society of Biological Psychiatry in May 1990 in New York. Conflicting results point out that extreme caution must be taken in interpreting linkage studies of psychiatric disorders. Difficulties stem from complex models on inheritance as well as the genetic heterogeneity of psychiatric disorders. Progress has been made in the approach to the regulation of receptor genes that have been implicated in the pathogenesis of psychiatric disorders. In some cases, gene regulation may be tissue-dependent, as is suggested by the alternative splicing of D2 receptor mRNA.
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