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The current study used a paired stimulus paradigm to investigate the P1 midlatency auditory evoked potential in Vietnam combat veterans with posttraumatic stress disorder (PTSD) and three comparison groups: alcohol dependents, combat-exposed normals, and combat-unexposed normals. Compared to each comparison group, PTSD subjects exhibited significantly diminished habituation of the P1 potential. P1 potential habituation within the PTSD group, correlated significantly with intensity of PTSD reexperiencing symptoms, such as trauma-related nightmares and flashbacks. These findings are discussed as consistent with a sensory gating defect at the brainstem level in PTSD, and are further discussed in the context of other psychophysiological measures in PTSD and of P1 potential findings in psychiatric disorders other than PTSD.

A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been reported in both alcoholic and depressed men. To discern whether the pathophysiological basis of a reduced TSH response is similar in these two disorders, the present study compares the dose-response patterns of TSH and prolactin (PRL) to TRH in depressed, alcoholic, and control men. Four doses of TRH (25, 100, 500, and 800 micrograms) were given at several day intervals to 6 men with major depression, 8 men with alcohol dependence, and 7 control men. Examination of the pattern of TRH-induced TSH and PRL response revealed differences for each paired group comparison: depressed versus control, depressed versus alcoholic, and alcoholic versus control. Compared with controls, depressed men had low TSH and low PRL responses to TRH, whereas alcoholic men had low TSH responses and normal PRL responses. Levels of neither thyroid hormones, cortisol, or sex steroids, nor age or body size, explained these differences. These findings suggest that the pathophysiological basis of a reduced TSH response to TRH is different in alcoholism, compared with depression.

Background: A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (protirelin [TRH]) has been found consistently in a portion of patients with major depression. One hypothesis to explain this observation is that pituitary TRH receptors are down-regulated in major depression. One prediction stemming from this hypothesis is that prolactin (PRL) as well as TSH responses to TRH should be attenuated. To adequately test the pattern of protirelin-induced TSH and PRL responses with a protirelin dose-response design is necessary., Methods: Four doses of protirelin (25, 100, 500, and 800 micrograms) were infused in an ascending schedule at intervals of 3 to 7 days in patients with major depression and in control subjects. Seven women and six men with major depression were compared with age- and gender-matched controls (five women and seven men). The TSH and PRL responses were measured at regular intervals following each dose of protirelin., Results: No significant group differences in baseline levels of thyroid hormones or cortisol were present. Depressed men exhibited significant reductions in both TSH and PRL responses to protirelin across all doses compared with control men. Depressed women exhibited significant reductions in TSH responses but not in PRL responses compared with control women., Conclusions: The findings that men with major depression exhibit reductions in both protirelin-induced TSH and PRL responses support the hypothesis that TRH receptors are downregulated in depression. The findings in women are less clear and may represent the greater variance in the protirelin-induced PRL responses found in women.

We investigated the relationship between suicidality, agitation, panic attacks, and the thyrotropin-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH), and tested the hypothesis that panic would account for the association between a reduced TSH response and the other conditions. Twenty-seven euthyroid primary unipolar depressed inpatient women received a TRH test and systematic psychiatric assessment. Panic attacks were insufficient to explain the link between the TSH response and suicidal intent, lethality, and agitation; each condition was independently associated with a lower TSH response. In an additive fashion, copresence of conditions further reduced TSH response. The symptom constellation of panic, agitation, and suicidality in depression may correlate with the greatest reduction in TSH response.

A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been reported in subjects with a history of alcoholism whereas prolactin (PRL) responses have generally been normal. One hypothesis proposed to explain the reduced TSH response is down-regulation of pituitary TRH receptors. If this is correct, PRL response should also be diminished. To account for the different dose-response characteristics of TSH/PRL we have given four dosages of TRH (25, 100, 500 and 800 micrograms) to eight noncirrhotic, male alcoholics abstinent from ethanol a minimum of 28 days and to seven male control subjects. Across the TRH dose range the alcoholic subjects exhibited reduced basal TSH (p = .01) and a reduced TSH response (p = .0023) but no differences in basal and stimulated PRL levels. Alcoholic subjects had higher basal T4, T3 and FT4I values than did control subjects but covarying for T4, T3 and FT4I did not change the significance of either TSH or PRL findings. No significant differences in estradiol, estrone, testosterone, cortisol or glucose were noted between groups. The present study confirms the observation of a lower TSH response to TRH in abstinent alcoholics and indicates that the lower response cannot be overcome by increasing TRH dosage. The similar PRL response between groups suggests normal lactotroph function in noncirrhotic abstinent alcoholics and argues against the pituitary TRH receptor down-regulation hypothesis.

Low thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) has been repeatedly described in approximately 25% of patients with major depression. Panic disorder appears related to depression along several dimensions, including prevalence of low TSH response to TRH. The authors divided 46 patients with primary unipolar depression by gender and by presence or absence of concurrent panic attacks and compared their TRH test results with those of 106 normal control subjects, controlling for confounding variables. Depressed patients with panic had higher prevalence of low TSH response and significantly lower mean TSH response than depressed patients without panic. The latter were indistinguishable from normal control subjects.

A 64-year-old woman with long-standing bipolar illness was treated with carbamazepine and clonazepam with minimal success. Discontinuation of carbamazepine and clonazepam was followed by episodic amnesia, purposeless behavior, déjà vu, and confusion. Although her EEG was normal, the episodes were compatible with complex partial seizures and ceased after carbamazepine and clonazepam were reinstituted. This case raises the question of whether discontinuing carbamazepine and clonazepam can induce complex partial seizures in bipolar patients.

A 30-year-old man with a 3-year history of tardive dyskinesia developed a neuroleptic malignant syndrome while having reserpine and lithium; his symptoms worsened following three doses of neuroleptic medication and improved with bromocriptine. The pre-existing dyskinesia made the presentation confused, and delayed proper diagnosis.

Four patients whose depressions were failing to respond to administration of tricyclic antidepressants were given separate trials of T3 and lithium. In all four cases, T3 failed to potentiate the antidepressant, whereas the lithium did.