Circadian rhythms of prolactin and thyroid-stimulating hormone during the menstrual cycle and early versus late sleep deprivation in premenstrual dysphoric disorder.

The present study extended previous work by examining whether disturbances in the circadian rhythms of prolactin (PRL) and thyroid-stimulating hormone (TSH) distinguish patients with premenstrual dysphoric disorder (PMDD) from normal volunteers. In addition, the effects of therapeutic interventions with early and late partial sleep deprivation were explored. Both PRL and TSH levels were measured every 30 min from 18:00 h to 09:00 h during midfollicular and late luteal menstrual cycle phases in 23 PMDD patients and 18 normal volunteers. Hormone levels were measured again after a randomized crossover trial of early (sleep 03:00-07:00 h) versus late (sleep 21:00-01:00 h) partial sleep deprivation administered in two separate luteal phases. Compared with normal volunteers, PMDD patients had higher PRL concentrations, consistent with previous findings. TSH rhythms occurred earlier in PMDD than in normal subjects. PRL levels decreased and TSH levels increased with sleep deprivation compared with baseline conditions. The timing of PRL secretion shifted earlier with late sleep deprivation and later with early sleep deprivation. Although circadian disturbances of PRL and TSH were found in PMDD patients compared with normal volunteers, the therapeutic effects of early and late sleep deprivation do not appear to be mediated by correcting these disturbances.

Early versus late partial sleep deprivation in patients with premenstrual dysphoric disorder and normal comparison subjects.

OBJECTIVE: The aim of this study was to compare the clinical effects of early-night and late-night partial sleep deprivation in patients with premenstrual dysphoric disorder and normal comparison subjects. METHOD: In the premenstrual phase of two menstrual cycles, 23 subjects with DSM-IV premenstrual dysphoric disorder and 18 normal comparison subjects underwent a randomized crossover trial of 1) early-night sleep deprivation, in which subjects slept from 3:00 a.m. to 7:00 a.m., followed by a night of recovery sleep (11:00 p.m. to 7:00 a.m.), and 2) late-night sleep deprivation, in which subjects slept from 9:00 p.m. to 1:00 a.m., followed by a night of recovery sleep. RESULTS: For the subjects with premenstrual dysphoric disorder, in both partial sleep deprivation conditions the Hamilton and Beck depression ratings were significantly lower after recovery sleep than at baseline. Ratings on the day after early or late partial sleep deprivation tended to be lower than at baseline but were not statistically different. The normal comparison subjects showed no clinically important mood changes. A factor analytic approach used with the Hamilton depression scores showed that depressive retardation symptoms were the most responsive to sleep deprivation in the premenstrual dysphoric disorder subjects. CONCLUSIONS: These results are consistent with the reported efficacy of sleep deprivation for major depressive disorder. However, the premenstrual dysphoric disorder subjects improved after the recovery sleep rather than directly after partial sleep deprivation. That late-night sleep deprivation did not have greater benefit than did the hypothesized sham treatment, early-night sleep deprivation, also suggests that placebo effects cannot be ruled out.

Immunity and depression: insomnia, retardation, and reduction of natural killer cell activity.

Depressed patients show a reduction of natural killer (NK) cell activity which may be associated with specific depressive symptoms. The present study demonstrated that sleep disturbance and retardation, but not other depressive symptoms, were negatively correlated with NK activity in 38 depressed patients. Specific behavioral changes in depression such as sleep disturbance and retardation were found to predict 16% of the variance of cytotoxicity levels in depression.