Insomnia inflicts mental burden and decreases physical productivity and affects life quality. Transcutaneous vagus nerve stimulation (ta-VNS) may be an effective treatment option for insomnia. This study aims to evaluate the effect and safety of ta-VNS and compare it with transcutaneous nonvagus nerve stimulation (tn-VNS). A multicenter, randomized, clinical trial was conducted at 3 hospitals in China enrolling 72 insomnia participants from May 2016 to June 2017. Participants were randomly assigned (1 : 1) to receive 40 sessions of ta-VNS or tn-VNS treatment. 63 participants completed the trial. ta-VNS treatment significantly decreased the Pittsburgh Sleep Quality Index score, Epworth Sleepiness Scale score, Flinders Fatigue Scale score, Hamilton Depression Scale score, and Hamilton Anxiety Scale score over 4 weeks compared with those of the baseline. Moreover, it also significantly increased the 36-item Short-Form Health Survey Questionnaire scores compared with that of the baseline. However, it did not show significant differences compared with tn-VNS in changes of primary and secondary outcomes. The incidence of adverse events was low. ta-VNS significantly relieved insomnia over 4 weeks. Moreover, it also alleviated fatigue and improved participants’ quality of life as well as other concomitant symptoms such as depression and anxiety. This trial is registered at Chinese Clinical Trial Registry (http://www.chictr.org.cn) with the registration number: ChiCTR-TRC-13003519.

Objective: To clarify the effects of escitalopram on sleep EEG power in patients with Major depressive disorder (MDD).Method: Polysomnography (PSG) was detected overnight, and blood samples were collected at 4 h intervals over 24 h from 13 male healthy controls and 13 male MDD patients before and after treatment with escitalopram for 8 weeks. The outcome measures included plasma melatonin levels, sleep architecture, and the sleep EEG power ratio.Results: Compared with healthy controls, MDD patients presented abnormalities in the diurnal rhythm of melatonin secretion, including peak phase delayed 3 h and a decrease in plasma melatonin levels at night and an increase at daytime, accompanied by sleep disturbances, a decrease in low-frequency bands and an increase in high-frequency bands, and the dominant right-side brain activity. Several of these abnormalities (abnormalities in the diurnal rhythm of melatonin secretion, partial sleep architecture parameters) persisted for at least the 8-week testing period.Conclusions: Eight weeks of treatment with escitalopram significantly improved subjective sleep perception and depressive symptoms of patients with MDD, and partially improved objective sleep parameters, while the improvement of circadian rhythm of melatonin was limited.

We used an optimized isocratic reversed-phase high-performance liquid-chromatographic procedure to separate and measure 12 steroid hormones, and studied the steroid hormone profiles in sera from three patients with 17-hydroxylase deficiency (17-OHD). Two of the patients were sisters, one of whom (II-3), expressing normotension and primary amenorrhea, was diagnosed on the basis of chromatographic data and followed up for seven years. The untreated patients had obvious abnormalities on chromatograms of serum extracts, characterized by markedly increased corticosterone (B) and decreased or undetectable cortisol (F) and cortisone (E). The concentration of 11-deoxycorticosterone was much greater in the patient with classical symptoms than in the normotensive patient. In all three patients, concentrations of aldosterone were within the normal range, but concentrations of progesterone were much lower than in the patients with 21-hydroxylase deficiency. We evaluated the responses to corticotropin and dexamethasone. HPLC evaluation of the serum steroid profiles before and after corticotropin stimulation in the affected family showed that in the parents and one other sibling, concentrations of F before and after stimulation were within the normal ranges. The sums of the ratio of B to F before and the ratio of B to F after corticotropin stimulation (sigma B/F) in the parents and the other sibling were 0.292, 0.496, and 0.614, respectively, all much higher than the normal value (mean +/- SD: 0.164 +/- 0.038). Thus the sigma B/F value may be a hormonal marker of heterozygotes carrying this defect.