Sustained polyphasic sleep restriction abolishes human growth hormone release.

STUDY OBJECTIVES: Voluntary sleep restriction is a common phenomenon in industrialized societies aiming to increase time spent awake and thus productivity. We explored how restricting sleep to a radically polyphasic schedule affects neural, cognitive, and endocrine characteristics. METHODS: Ten young healthy participants were restricted to one 20-minute nap opportunity at the end of every 4 hours (i.e. six sleep episodes per 24 hours) without any extended core sleep window, which resulted in a cumulative sleep amount of just 2 hours per day (i.e. ~20 minutes per bout). RESULTS: All but one participant terminated this schedule during the first month. The remaining participant (a 25-year-old male) succeeded in adhering to a polyphasic schedule for five out of the eight planned weeks. Cognitive and psychiatric measures showed modest changes during polyphasic as compared to monophasic sleep, while in-blood cortisol or melatonin release patterns and amounts were apparently unaltered. In contrast, growth hormone release was almost entirely abolished (>95% decrease), with the residual release showing a considerably changed polyphasic secretional pattern. CONCLUSIONS: Even though the study was initiated by volunteers with exceptional intrinsic motivation and commitment, none of them could tolerate the intended 8 weeks of the polyphasic schedule. Considering the decreased vigilance, abolished growth hormone release, and neurophysiological sleep changes observed, it is doubtful that radically polyphasic sleep schedules can subserve the different functions of sleep to a sufficient degree.

Increased Aperiodic Neural Activity During Sleep in Major Depressive Disorder.

Background: In major depressive disorder (MDD), patients often express subjective sleep complaints, while polysomnographic studies report only subtle alterations of the electroencephalographic signal. We hypothesize that differentiating the signal into its oscillatory and aperiodic components may bring new insights into our understanding of sleep abnormalities in MDD. Specifically, we investigated aperiodic neural activity during sleep and its relationships with sleep architecture, depression severity, and responsivity to antidepressant treatment. Methods: Polysomnography was recorded in 38 patients with MDD (in unmedicated and 7-day-medicated states) and 38 age-matched healthy control subjects (N= 76). The aperiodic power component was calculated using irregularly resampled auto-spectral analysis. Depression severity was assessed with the Hamilton Depression Rating Scale. We replicated the analysis using 2 independently collected datasets of medicated patients and control subjects (N = 60 and N = 80, respectively). Results: Unmedicated patients showed flatter aperiodic slopes compared with control subjects during non-rapid eye movement (non-REM) stage 2 sleep (p = .009). Medicated patients showed flatter aperiodic slopes compared with their earlier unmedicated state (p values < .001) and control subjects during all sleep stages (p values < .03). In medicated patients, flatter aperiodic slopes during non-REM sleep were linked to the higher proportion of N1, lower proportion of REM, delayed onset of N3 and REM, and shorter total sleep time. Conclusions: Flatter slopes of aperiodic electroencephalographic power may reflect noisier neural activity due to increased excitation-to-inhibition balance, representing a new disease-relevant feature of sleep in MDD.

Non-REM sleep in major depressive disorder.

Disturbed sleep is a key symptom in major depressive disorder (MDD). REM sleep alterations are well described in the current literature, but little is known about non-REM sleep alterations. Additionally, sleep disturbances relate to a variety of cognitive symptoms in MDD, but which features of non-REM sleep EEG contribute to this, remains unknown. We comprehensively analyzed non-REM sleep EEG features in two central channels in three independently collected datasets (N = 284 recordings of 216 participants). This exploratory and descriptive study included MDD patients with a broad age range, varying duration and severity of depression, unmedicated or medicated, age- and gender-matched to healthy controls. We explored changes in sleep architecture including sleep stages and cycles, spectral power, sleep spindles, slow waves (SW), and SW-spindle coupling. Next, we analyzed the association of these sleep features with acute measures of depression severity and overnight consolidation of procedural memory. Overall, no major systematic alterations in non-REM sleep architecture were found in patients compared to controls. For the microstructure of non-REM sleep, we observed a higher spindle amplitude in unmedicated patients compared to controls, and after the start of antidepressant medication longer SWs with lower amplitude and a more dispersed SW-spindle coupling. In addition, long-term, but not short-term medication seemed to lower spindle density. Overnight procedural memory consolidation was impaired in medicated patients and associated with lower sleep spindle density. Our results suggest that alterations of non-REM sleep EEG in MDD might be more subtle than previously reported. We discuss these findings in the context of antidepressant medication intake and age.

[Sleep medicine in psychiatry and psychotherapy]. / Schlafmedizin in der Psychiatrie und Psychotherapie.

Sleep medicine is a cross-disciplinary subject with high relevance for psychiatry and psychotherapy. The three most common sleep disorders (insomnia, sleep apnea syndrome and restless legs syndrome) are presented here with practical relevance. Cognitive behavioral therapy is the treatment of choice for insomnia, whereas symptomatic drug treatment (especially with GABA receptor agonists) should be used with caution. Sleep-related breathing disorders have a high prevalence of around 24% among psychiatric inpatients in Germany. Typical symptoms of obstructive sleep apnea syndrome should lead to a staged diagnostic process and, if necessary, cardiorespiratory polysomnography. It is not unusual for restless legs syndrome to be caused by psychopharmacological treatment. The primary form was usually treated with dopamine or dopamine agonists but due to the risk of augmentation, alternatives should be considered more often.

A set of composite, non-redundant EEG measures of NREM sleep based on the power law scaling of the Fourier spectrum.

Features of sleep were shown to reflect aging, typical sex differences and cognitive abilities of humans. However, these measures are characterized by redundancy and arbitrariness. Our present approach relies on the assumptions that the spontaneous human brain activity as reflected by the scalp-derived electroencephalogram (EEG) during non-rapid eye movement (NREM) sleep is characterized by arrhythmic, scale-free properties and is based on the power law scaling of the Fourier spectra with the additional consideration of the rhythmic, oscillatory waves at specific frequencies, including sleep spindles. Measures derived are the spectral intercept and slope, as well as the maximal spectral peak amplitude and frequency in the sleep spindle range, effectively reducing 191 spectral measures to 4, which were efficient in characterizing known age-effects, sex-differences and cognitive correlates of sleep EEG. Future clinical and basic studies are supposed to be significantly empowered by the efficient data reduction provided by our approach.

Sleep in pituitary insufficient patients compared to patients with depression and healthy controls at baseline and after challenge with CRH.

Sleep disturbances are prevalent in both patients with pituitary insufficiency and with depression. The role of corticotropin releasing hormone (CRH), involved in sleep regulation, has not been fully clarified. Pituitary insufficiency is an ideal model for studying sleep-endocrine effects since no consecutive hormone releases and feedback effects occur after hormone administration. 11 male patients with a chronic insufficiency of the anterior pituitary gland (PI) and under stable hormonal substitution were studied during three consecutive nights in the sleep laboratory. The first night served for adapting to laboratory setting, during the second night placebo was administered and during the third night 4 × 50 µg CRH were injected in pulsatile fashion. Sleep parameters were additionally compared with those of 15 healthy male controls (C) and 15 male patients with depression (D). CRH administration was associated with a numerical increase of wake time (115 ± 15 to 131 ± 13 min) and a decrease of REM sleep (89 ± 8 to 80 ± 8 min), REM latency (69 ± 14 to 55 ± 9 min) and slow wave sleep (66 ± 16 to 57 ± 15 min). Yet, none of these changes reached statistical significance. PI showed a worse sleep profile as compared to both control groups, e.g. indicated by a significantly lower sleep efficiency index (PI:0.80 ± 0.03 vs. C:0.94 ± 0.01 vs. D:0.87 ± 0.03). In conclusion sleep-EEG changes after CRH in PI patients resemble those found in in part in patients with depression. Sleep in anterior pituitary insufficiency was impaired despite full hormonal substitution possibly suggesting an alteration of the receptor organisation of brain structures involved in sleep regulation.