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Background Entrustable professional activities (EPAs) are increasingly used in undergraduate medical education (UME). We conducted a scoping review to summarize the evidence for the use of EPAs in clinical rotations in UME. Methods We searched multiple databases for scoping reviews based on the PRISMA guidelines for articles reporting qualitative and quantitative research, as well as conceptual and curriculum development reports, on EPAs in UME clinical rotations. Results We identified 3309 records by searching through multiple databases. After the removal of duplicates, 1858 reports were screened. A total of 36 articles were used for data extraction. Of these, 47% reported on EPA and EPA-based curriculum development for clerkships, 50% reported on implementation strategies, and 53% reported on assessment methods and tools used in clerkships. Validity frameworks for developing EPAs in the context of clerkships were inconsistent. Several specialties reported feasible implementation strategies for EPA-based clerkship curricula, however, these required additional faculty time and resources. Limited exposure to clinical activities was identified as a barrier to relevant learning experiences. Educators used nationally defined, or specialty-specific EPAs, and a range of entrustability and supervision scales. We found only one study that used an empirical research approach for EPA assessment. One article reported on the earlier advancement of trainees from UME to graduate medical education based on summative entrustment decisions. Conclusions There is emerging evidence concerning how EPAs can be effectively introduced to clinical training in UME. Specialty-specific, nested EPAs with context-adapted, entrustment-supervision scales might be helpful in better leveraging their formative assessment potential.

Background Therapeutic sleep deprivation (SD) presents a unique paradigm to study the neurobiology of major depressive disorder (MDD). However, the rapid antidepressant mechanism, which differs from today's slow first-line treatments, is not sufficiently understood. We recently integrated two prominent hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, into a synaptic plasticity model of therapeutic SD in MDD. Here, we further tested this model positing that homeostatically elevating net synaptic strength through therapeutic SD shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP)-like plasticity in patients with MDD into a more favorable window of associative plasticity. Methods We used paired associative stimulation (PAS), a transcranial magnetic stimulation protocol (TMS), to quantify cortical LTP-like plasticity after one night of therapeutic sleep deprivation in 28 patients with MDD. Results We demonstrate a significantly different inducibility of associative plasticity in clinical responders to therapeutic SD (> 50% improvement on the 6-item Hamilton-Rating-Scale for Depression, n=13) compared to non-responders (n=15), which was driven by a long-term depression (LTD)-like response in SD-non-responders. Indices of global net synaptic strength (wake EEG theta activity, intracortical inhibition and BDNF serum levels) were increased after SD in both groups, with responders showing a generally lower intracortical inhibition than non-responders. Limitations Repetitive assessments prior to and after treatment would be needed to further determine potential mechanisms. Conclusion After a night of therapeutic SD, clinical responders show a significantly higher inducibility of associative LTP-like plasticity than non-responders.

Die Insomnie, d. h. eine Ein- und/oder Durchschlafstörung, die sich negativ auf die Leistungsfähigkeit und Tagesbefindlichkeit auswirkt, ist eine der häufigsten Erkrankungen in der Allgemeinbevölkerung. Sie wird derzeit meistens pharmakologisch und/oder psychotherapeutisch behandelt, wobei die pharmakologische Behandlung mit Benzodiazepin-Rezeptor-Agonisten zu Abhängigkeit führen kann und die Verfügbarkeit von für die Insomnie-Therapie ausgebildeten Psychotherapeuten momentan nicht in ausreichendem Maße gegeben ist. Durch innovative Behandlungsmethoden könnte hier eine Versorgungslücke effektiv geschlossen werden. Hierzu zählt die auditorische Stimulation, welche vorhandene Sinneskanäle nutzt, um den Schlaf zu beeinflussen. Bisher wurde die auditorische Stimulation vor allem zur Untersuchung von Prozessen der Gedächtniskonsolidierung bei gesunden Probanden angewendet, wobei erfolgreich eine Erhöhung langsamer Oszillationen erreicht wurde, welche vor allem während des Tiefschlafs auftreten. Erste Befunde und sekundäre Outcome-Parameter liefern Hinweise, dass die Potenzierung langsamer Oszillationen durch auditorische Stimulation den Schlaf vertiefen kann, jedoch wurde hierzu bislang keine Studie mit Insomniepatienten durchgeführt. Weitere Forschung bezüglich des Einflusses der Potenzierung langsamer Oszillationen auf die Linderung von Ein- und Durchschlafproblemen bei vorliegender nichtorganischer Insomnie erscheint daher geboten zu sein, um der hohen Beschwerdelast dieser Patientengruppe entgegenzuwirken., Insomnia is considered among the most prevalent health conditions in western communities. Treatment regularly consists of pharmacology and/or psychotherapy. However, pharmacological treatments bear a high risk of development of tolerance and addiction, whereas the availability of specifically qualified psychotherapists to treat insomnia is scarce. Innovative treatments have the capability to fill this supply gap. One of these new methods is called auditory stimulation and uses external stimuli that travel through existing sensory networks to influence sleep. This stimulation method has so far been mainly used to assess overnight memory consolidation in healthy participants in which slow oscillations, neuronal events occurring prominently in deep sleep, were enhanced successfully. Initial findings and secondary outcome parameters indicate that the potentiation of slow oscillations can deepen sleep, however there are currently no studies assessing efficacy in patients with insomnia. Further research is recommended.

Background:Arousal and sleep represent basic domains of behavior, and alterations are of high clinical importance. Objective/hypothesis:The aim of this study was to further elucidate the neurobiology of insomnia disorder (ID) and the potential for new treatment developments, based on the modulation of cortical activity through the non-invasivebrain stimulationtechnique transcranial direct current stimulation (tDCS). Specifically, we tested the hypotheses that bi-frontal anodal tDCS shortens and cathodal tDCS prolongs total sleep time in patients with ID, compared to sham stimulation. Furthermore, we tested for differences in indices of arousal between ID patients and healthy controls and explored their potential impact on tDCS effects. Methods:Nineteen ID patients underwent a within-subject repeated-measures sleep laboratory study with adaptation, baseline and three experimental nights. Bifrontal anodal, cathodal and sham tDCS was delivered in a counterbalanced order immediately prior to sleep. WakeEEGwas recorded prior to and after tDCS as well as on the following morning. Subsequently, we compared patients with ID to a healthy control group from an earlier dataset. Results:Against our hypothesis, we did not observe any tDCS effects on sleep continuity or sleep architecture in patients with ID. Further analyses of nights without stimulation demonstrated significantly increased levels of arousal in ID patients compared to healthy controls, as indexed by subjective reports, reduced total sleep time, increased wake after sleep onset and increased high frequency EEG power during wakefulness andNREM sleep. Of note, indices of increased arousal predicted the lack of effect of tDCS in ID patients. Conclusions:Our study characterizes for the first time differential effects of tDCS on sleep in patients with ID and healthy controls, presumably related to persistent hyperarousal in ID. These findings suggest that adapted tDCS protocols need to be developed to modulate arousal and sleep dependent on baseline arousal levels.

Severin Pinilla,1,2 Andrea Cantisani,3 Stefan Klöppel,1 Werner Strik,3 Christoph Nissen,3 Sören Huwendiek2 1University Hospital of Old Age Psychiatry and Psychotherapy, University of Bern, Bern, Switzerland; 2Institute for Medical Education, Department for Assessment and Evaluation, University of Bern, Bern, Switzerland; 3University Hospital of Psychiatry and Psychotherapy, University of Bern, Bern, SwitzerlandCorrespondence: Severin Pinilla Email severin.pinilla@upd.unibe.chBackground: Learning management systems (LMSs) have not been explored from an educational design research (EDR) perspective for developing clinical curricula and supporting novice clinical students with self-regulated learning during their early clinical rotations.Methods: An EDR approach was used to inform a de novo implementation of an LMS during an early clinical rotation of medical students. The EDR consisted of three phases: analysis and exploration; design and construction; and evaluation and reflection. Process and evaluation data (including academic years 2018 and 2019) from two student cohorts (total n = 190, 107 without and 83 with LMS exposure) at one academic teaching hospital were analyzed.Results: Learning theories and concepts of self-regulated learning were used to develop and implement an LMS clerkship prototype. For design and construction, the maturing prototype design included flipped-classroom elements, in-class activation, voluntary digital self-assessments, and clinical teaching videos. For evaluation and reflection, global satisfaction improvement was significant (from 3.9 to 4.4 on a 5-point Likert scale, p < 0.05). There was a positive evaluation trend for all evaluation items related to learning climate, self-regulated learning, and perceived usefulness of the LMS prototype; however, these changes were not statistically significant. The teaching hospital also improved its ranking after the introduction of the LMS prototype. Nearly all students (94%) used the LMS material. The average number of times the LMS course was accessed per student was 70 (range: 7– 172), and the average duration students spent online was 58 minutes (range: 9– 165).Conclusion: Our data indicate that using an EDR approach was helpful for systematically introducing an LMS in a clerkship curriculum informed by learning theory. Our evidence-oriented curriculum reform was associated with higher student satisfaction and appeared to support self-regulated learning in the workplace. Further research should explore which elements of an LMS most effectively help to achieve educational outcomes.Keywords: learning-management system, self-regulated learning, clinical education, educational research design, psychiatry

Study Objectives Insomnia is defined by the subjective complaint of poor sleep as well as daytime impairments. Since polysomnography (PSG) typically shows only modest sleep impairment, some still unidentified property of sleep, not mirrored in PSG, may be modified in insomnia. One possible mechanistic hypothesis is that insomnia patients may be more sensitive to inevitably occurring internal or external stimuli during the night, causing brief sleep disruptions then perceived as wake time. Methods Auditory event-related potentials (ERP) to low intensity (50 dB SPL) synthesized guitar tones played continuously throughout two nights of polysomnographically registered sleep were obtained in fifty patients with insomnia disorder (ID, without comorbidities) and 50 age- and sex-matched good sleeper controls (GSC) for each sleep stage and NREM/REM cycle. Phasic and tonic REM were treated as separate stages. Latencies and amplitudes of components P1, N1 and P2 were measured and analyzed by multivariate repeated-measures ANCOVA including effects of group, night, cycle, and age. Results ID showed reduced P2 amplitudes relative to GSC specifically in phasic REM sleep. The same reduction also correlated with the amount of sleep misperception across groups. Independent component analysis showed a frontal negativity to contribute most to this group difference. Conclusions The present finding can be interpreted as increased mismatch negativity (MMN) in ID, reflecting automated detection of change in the auditory system and a concomitant orienting response. Specifically phasic REM sleep appears to be vulnerable to sensory afferences in ID patients, possibly contributing to the perception of being awake. Clinical Trial Information Short name “PERSLEEP 2,” URL https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00008965, Registration DRKS00008965.

Background and purpose: Insomnia is a common and debilitating disorder that is frequently associated with important consequences for physical health and well-being. Methods: An international expert group considered the current state of knowledge based on the most relevant publications in the previous 5 years, discussed the current challenges in the field of insomnia and identified future priorities. Results: The association of trajectories of insomnia with subsequent quality of life, health and mortality should be investigated in large populations. Prospective health economics studies by separating the costs driven specifically by insomnia and costs attributable to its long-term effects are needed. Ignoring the heterogeneity of insomnia patients leads to inadequate diagnosis and inefficient treatment. Individualized interventions should be promoted. More data are needed on both the impact of sleep on overnight effects, such as emotion regulation, and the potential compensatory effort to counteract diurnal impairments. Another gap is the definition of neurocognitive deficits in insomnia patients compared to normal subjects after chronic sleep loss. There are also a number of key gaps related to insomnia treatment. Expert guidelines indicate cognitive–behavioural therapy for insomnia as first-line treatment. They neglect, however, the reality of major healthcare providers. The role of combined therapy, cognitive–behavioural therapy for insomnia plus pharmacological treatment, should be evaluated more extensively. Conclusion: Whilst insomnia disorder might affect large proportions of the population, there are a number of significant gaps in the epidemiological/clinical/research studies carried out to date. In particular, the identification of different insomnia phenotypes could allow more cost-effective and efficient therapies.

Background Entrustable professional activities (EPAs) in competency-based, undergraduate medical education (UME) have led to new formative workplace-based assessments (WBA) using entrustment-supervision scales in clerkships. We conducted an observational, prospective cohort study to explore the usefulness of a WBA designed to assess core EPAs in a psychiatry clerkship. Methods We analyzed changes in self-entrustment ratings of students and the supervisors’ ratings per EPA. Timing and frequencies of learner-initiated WBAs based on a prospective entrustment-supervision scale and resultant narrative feedback were analyzed quantitatively and qualitatively. Predictors for indirect supervision levels were explored via regression analysis, and narrative feedback was coded using thematic content analysis. Students evaluated the WBA after each clerkship rotation. Results EPA 1 (“Take a patient’s history”), EPA 2 (“Assess physical & mental status”) and EPA 8 (“Document & present a clinical encounter”) were most frequently used for learner-initiated WBAs throughout the clerkship rotations in a sample of 83 students. Clinical residents signed off on the majority of the WBAs (71%). EPAs 1, 2, and 8 showed the largest increases in self-entrustment and received most of the indirect supervision level ratings. We found a moderate, positive correlation between self-entrusted supervision levels at the end of the clerkship and the number of documented entrustment-supervision ratings per EPA (p n = 214) of the WBAs. Most narratives addressed the Medical Expert role (77%, n = 208) and used reinforcement (59%, n = 161) as a feedback strategy. Students perceived the feedback as beneficial. Conclusions Using formative WBAs with an entrustment-supervision scale and prompts for written feedback facilitated targeted, high-quality feedback and effectively supported students’ development toward self-entrusted, indirect supervision levels.

Purpose Clinical learning contexts influence how medical students engage with entrustment decisions. However, it is unclear how students and health care team members perceive the entrustment decision process. This study explored which factors students and team members consider relevant to entrustment decisions in early clinical rotations. Methods The authors conducted a case study at an academic teaching hospital, interviewing 28 medical students and four health care team members during the clerkship year. Within a social constructivist epistemology, we explored students' and health care team members' perceptions of ad hoc entrustment decisions using semi-structured interviews. Transcripts from the interviews and notes from feedback rounds with students were used for analysis. Results Medical students in their core clerkship year perceived clinical residents as critical educational gatekeepers and key facilitators of entrustment decisions. Another important theme emerged around students' motivation, initiative and willingness to engage with the health care team and patients. Students actively engaged in trust formation processes with different health care team members. The entrustment decision process was perceived as multilateral and dynamic, involving all health care team members and patients. Multiple entrusting supervisors for clerkship students, including nurses and psychologists, emerged from our interview data. They assumed an active role in negotiating entrustment decisions both with and for clerkship students, either facilitating or hindering opportunities. The entrustment decisions emerged as a result of a multifaceted supervisor network interaction. Conclusions Supervising residents' ability to integrate students into clinical teams seems to be a critical factor in facilitating entrustment opportunities for clinical activities. Students' active management of informal supervisor networks of health care team members and these team members' willingness to assume responsibility for the students' education emerged as relevant aspects for ad hoc entrustment. Our data suggest that supervision from different health professionals is beneficial for clinical education of medical students and merits further exploration.

Study Objectives The low-frequency high-amplitude oscillations of slow-wave sleep (SWS) are considered to promote the consolidation of episodic memory. Previous research suggests that sleep slow waves can be entrained and enhanced by presenting short acoustic stimuli to the up-states of endogenous waves. Several studies have investigated the effects of these increases in slow-wave activity on overnight memory consolidation, with inconsistent results. The aim of this meta-analysis was to evaluate the accumulated evidence connecting acoustic stimulation during sleep to episodic memory consolidation. Methods A systematic literature search was conducted in October 2020 using PubMed, Web of Science, and PsycInfo. The main study inclusion criteria were the application of acoustic slow wave enhancement in healthy participants and an assessment of pre- and post-sleep episodic memory performance. Effect sizes were pooled using a random-effects model. Results A total of 10 primary studies with 11 experiments and 177 participants were included. Results showed a combined effect size (Hedges’ g) of 0.25 (p = 0.07). Subgroup models based on young adults (n = 8), phase-locked stimulation approaches (n = 8), and their combination (n = 6) showed combined effect sizes of 0.31 (p = 0.051), 0.36 (p = 0.047), and 0.44 (p = 0.01), respectively. There was no indication of publication bias or bias in individual studies. Conclusions Acoustic enhancement of SWS tends to increase the overnight consolidation of episodic memory but effects remain small and—with the exception of subgroup models—at trend levels. Currently, the evidence is not sufficient to recommend the use of commercially available devices.

The current study was designed to further clarify the influence of brain morphology, sleep oscillatory activity and age on memory consolidation. Specifically, we hypothesized, that a smaller volume of hippocampus, parahippocampal and medial prefrontal cortex negatively impacts declarative, but not procedural, memory consolidation. Explorative analyses were conducted to demonstrate whether a decrease in slow-wave activity negatively impacts declarative memory consolidation, and whether these factors mediate age effects on memory consolidation. Thirty-eight healthy participants underwent an acquisition session in the evening and a retrieval session in the morning after night-time sleep with polysomnographic monitoring. Declarative memory was assessed with the paired-associate word list task, while procedural memory was tested using the mirror-tracing task. All participants underwent high-resolution magnetic resonance imaging. Participants with smaller hippocampal, parahippocampal and medial prefrontal cortex volumes displayed a reduced overnight declarative, but not procedural memory consolidation. Mediation analyses showed significant age effects on overnight declarative memory consolidation, but no significant mediation effects of brain morphology on this association. Further mediation analyses showed that the effects of age and brain morphology on overnight declarative memory consolidation were not mediated by polysomnographic variables or sleep electroencephalogram spectral power variables. Thus, the results suggest that the association between age, specific brain area volume and overnight memory consolidation is highly relevant, but does not necessarily depend on slow-wave sleep as previously conceptualized.

Objectives: A proposed replay of memory traces between the hippocampus and frontal cortical brain areas during sleep is of high relevance for overnight memory consolidation. Recently, we demonstrated that bi-frontal anodal transcranial direct current stimulation (tDCS) prior to sleep increases waking EEG gamma power and decreases total sleep time during the night. It is unclear whether this effect on cortical excitability has an influence on overnight memory consolidation. We hypothesized that bi-frontal evening tDCS interferes with overnight memory consolidation with a polarity specific impairment following anodal tDCS. Materials and methods: Nineteen healthy participants underwent a within-subject, repeated-measures protocol in the sleep laboratory with bi-frontal tDCS applied prior to sleep according to the experimental protocol (anodal, cathodal, sham stimulation). Memory tasks for declarative and procedural memory were assessed prior to tDCS and on the following morning. Results: No deterioration of overnight memory consolidation following evening offline bi-frontal tDCS could be detected. Conclusion(s): The application of tDCS can be considered safe regarding overnight memory consolidation and represents a promising treatment approach in conditions of decreased vigilance and arousal.

The increasing incidence rate of dementia underlines the necessity to identify early biomarkers of imminent cognitive decline. Recent findings suggest that cognitive decline and the pathophysiology of Alzheimer's disease are closely linked to disruptions in slow wave sleep (SWS) – the deepest sleep stage. SWS is essential for memory functions and displays a potentially causal and bidirectional link to the accumulation of amyloid beta deposition. Accordingly, improving SWS in older adults – especially when at risk for dementia – might slow down the rate of cognitive decline. Recent work suggests that SWS can be improved by specifically targeting the electrophysiological peaks of the slow waves with acoustic stimulation. In older adults, this approach is still fairly new and accompanied by challenges posed by the specific complexity of their sleep physiology, like lower amplitude slow waves and fragmented sleep architecture. We suggest an approach that tackles these issues and attempts to re-instate a sleep physiology that resembles a younger, healthier brain. With enough SWS of high quality, metabolic clearance and memory functions could benefit and help slowing the process of cognitive aging. Ultimately, acoustic stimulation to enhance SWS could serve as a cost-effective, non-invasive tool to combat cognitive decline.

Arousal and sleep represent fundamental physiological domains, and alterations in the form of insomnia (difficulty falling or staying asleep) or hypersomnia (increased propensity for falling asleep or increased sleep duration) are prevalent clinical problems. Current first-line treatments include psychotherapy and pharmacotherapy. Despite significant success, a number of patients do not benefit sufficiently. Progress is limited by an incomplete understanding of the ­neurobiology of insomnia and hypersomnia. This work summarizes current concepts of the regulation of arousal and sleep and its modulation through noninvasive brain stimulation (NIBS), including transcranial magnetic, current, and auditory stimulation. Particularly, we suggest: (1) characterization of patients with sleep problems – across diagnostic entities of mental disorders – based on specific alterations of sleep, including alterations of sleep slow waves, sleep spindles, cross-frequency coupling of brain oscillations, local sleep-wake regulation, and REM sleep and (2) targeting these with specific NIBS techniques. While evidence is accumulating that the modulation of specific alterations of sleep through NIBS is feasible, it remains to be tested whether this translates to clinically relevant effects and new treatment developments.

Sleep promotes adaptation of behavior and underlying neural plasticity in comparison to active wakefulness. However, the contribution of its two main characteristics, sleep-specific brain activity and reduced stimulus interference, remains unclear. We tested healthy humans on a texture discrimination task, a proxy for neural plasticity in primary visual cortex, in the morning and retested them in the afternoon after a period of daytime sleep, passive waking with maximally reduced interference, or active waking. Sleep restored performance in direct comparison to both passive and active waking, in which deterioration of performance across repeated within-day testing has been linked to synaptic saturation in the primary visual cortex. No difference between passive and active waking was observed. Control experiments indicated that deterioration across wakefulness was retinotopically specific to the trained visual field and not due to unspecific performance differences. The restorative effect of sleep correlated with time spent in NREM sleep and with electroencephalographic slow wave energy, which is thought to reflect renormalization of synaptic strength. The results indicate that sleep is more than a state of reduced stimulus interference, but that sleep-specific brain activity restores performance by actively refining cortical plasticity.

We investigated the prevalence and treatment of patients with chronic insomnia presenting to Swiss primary care physicians (PCPs) part of "Sentinella", a nationwide practice-based research network. Each PCP consecutively asked 40 patients if they had sleep complaints, documented frequency, duration, comorbidities, and reported ongoing treatment. We analysed data of 63% (83/132) of the PCPs invited. The PCPs asked 76% (2,432/3,216) of included patients about their sleep (51% female); 31% (761/2,432) of these had had insomnia symptoms; 36% (875/2,432) had current insomnia symptoms; 11% (269/2,432) met the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria for chronic insomnia (61% female). In all, 75% (201/269) of patients with chronic insomnia had comorbidities, with 49% (99/201) reporting depression. Chronic insomnia was treated in 78% (209/269); 70% (188/268) took medication, 38% (102/268) benzodiazepines or benzodiazepine receptor agonists, 32% (86/268) took antidepressants. Only 1% (three of 268) had been treated with cognitive behavioural therapy for insomnia (CBT-I). A third of patients presenting for a non-urgent visit in Swiss primary care reported insomnia symptoms and 11% met the DSM-5 criteria for chronic insomnia. Hypnotics were the most common treatment, but almost no patients received first-line CBT-I. Reducing the burden of insomnia depends on disseminating knowledge about and access to CBT-I, and encouraging PCPs to discuss it with and offer it as a first-line treatment to patients with chronic insomnia.

Study Objectives The majority of patients with mental disorders suffer from insomnia, associated with adverse health outcomes. Cognitive behavioral therapy for insomnia (CBT-I) represents the first-line treatment, but is too complex for severely ill patients and not systematically implemented in inpatient psychiatric care. This project aimed to develop a pragmatic behavioral treatment program that empowers inpatients with severe mental disorders to take care of their own sleep health. Methods CBT-I was adapted based on implementation research involving 24 inpatients with psychiatric disorders across diagnostic entities and comorbid insomnia and 30 health care providers at the University Hospital of Psychiatry and Psychotherapy, Bern. The program was implemented and evaluated by 15 patients and 22 health care providers based on interviews and questionnaires before participation and prior to discharge. Results Implementation research resulted in the SLEEPexpert intervention, centering on bedtime restriction and circadian adaptation in three phases; therapist-guided treatment initiation, self-management with nursing support, and self-management. Evaluative pre-post assessments in 15 patients demonstrated feasibility. Time in bed decreased by 60 minutes (520 ± 105.3 vs. 460 ± 78.1, p = 0.031, d = 0.6) and total sleep time increased by around 45 minutes (331 ± 110.6 vs. 375 ± 74.6, p = 0.09, d = 0.5), resulting in increased sleep efficiency (65.3 ± 21.8 vs. 81.9 ± 11.2%, p = 0.011, d = 0.8). Patients improved on the Insomnia Severity Index (18.3 ± 4.6 vs. 11.4 ± 4.4, p < 0.001, d = 1.2) and Pittsburgh Sleep Quality Index (12.9 ± 3.8 vs. 10.3 ± 3.3, p = 0.031, d = 0.6). Conclusions We propose a new pragmatic behavioral treatment program (SLEEPexpert) customized to the needs of patients and health care providers in inpatient psychiatric care. Data demonstrate feasibility. An improvement of insomnia severity was observed, but a control comparison is needed to further test for efficacy.

Ageing involves significant neurophysiological changes that are both systematic while at the same time exhibiting divergent trajectories across individuals. These changes underlie cognitive impairments in elderly while also affecting the response of aged brains to interventions like transcranial direct current stimulation (tDCS). While the cognitive benefits of tDCS are more variable in elderly, older adults also respond differently to stimulation protocols compared to young adults. The age-related neurophysiological changes influencing the responsiveness to tDCS remain to be addressed in-depth. We review and discuss the premise that, in comparison to the better calibrated brain networks present in young adults, aged systems perform further away from a homoeostatic set-point. We argue that this age-related neurophysiological deviation from the homoeostatic optimum extends the leeway for tDCS to modulate the aged brain. This promotes the potency of immediate tDCS effects to induce directional plastic changes towards the homoeostatic equilibrium despite the impaired plasticity induction in elderly. We also consider how age-related neurophysiological changes pose specific challenges for tDCS that necessitate proper adaptations of stimulation protocols. Appreciating the distinctive properties of aged brains and the accompanying adjustment of stimulation parameters can increase the potency and reliability of tDCS as a treatment avenue in older adults. Special Issue:SI

Insomnia, the most prevalent sleep disorder worldwide, confers marked risks for both physical and mental health. Furthermore, insomnia is associated with considerable direct and indirect healthcare costs. Recent guidelines in the US and Europe unequivocally conclude that cognitive behavioural therapy for insomnia (CBT‐I) should be the first‐line treatment for the disorder. Current treatment approaches are in stark contrast to these clear recommendations, not least across Europe, where, if any treatment at all is delivered, hypnotic medication still is the dominant therapeutic modality. To address this situation, a Task Force of the European Sleep Research Society and the European Insomnia Network met in May 2018. The Task Force proposed establishing a European CBT‐I Academy that would enable a Europe‐wide system of standardized CBT‐I training and training centre accreditation. This article summarizes the deliberations of the Task Force concerning definition and ingredients of CBT‐I, preconditions for health professionals to teach CBT‐I, the way in which CBT‐I should be taught, who should be taught CBT‐I and to whom CBT‐I should be administered. Furthermore, diverse aspects of CBT‐I care and delivery were discussed and incorporated into a stepped‐care model for insomnia. publishedVersion

Since ancient times it is known that melancholia and sleep disturbances co-occur. The introduction of polysomnography into psychiatric research confirmed a disturbance of sleep continuity in patients with depression, revealing not only a decrease in Slow Wave Sleep, but also a disinhibition of REM (rapid eye movement) sleep, demonstrated as a shortening of REM latency, an increase of REM density, as well as total REM sleep time. Initial hopes that these abnormalities of REM sleep may serve as differential-diagnostic markers for subtypes of depression were not fulfilled. Almost all antidepressant agents suppress REM sleep and a time-and-dose-response relationship between total REM sleep suppression and therapeutic response to treatment seemed apparent. The so-called Cholinergic REM Induction Test revealed that REM sleep abnormalities can be mimicked by administration of cholinomimetic agents. Another important research avenue is the study of chrono-medical timing of sleep deprivation and light exposure for their positive effects on mood in depression. Present day research takes the view on insomnia, i.e., prolonged sleep latency, problems to maintain sleep, and early morning awakening, as a transdiagnostic symptom for many mental disorders, being most closely related to depression. Studying insomnia from different angles as a transdiagnostic phenotype has opened many new perspectives for research into mechanisms but also for clinical practice. Thus, the question is: can the early and adequate treatment of insomnia prevent depression? This article will link current understanding about sleep regulatory mechanisms with knowledge about changes in physiology due to depression. The review aims to draw the attention to current and future strategies in research and clinical practice to the benefits of sleep and depression therapeutics.

Objective The primary aim of this study was to further characterize the acute effects of amitriptyline (AMI) and escitalopram (ESC) on serum levels of ghrelin, leptin, cortisol and prolactin in healthy humans. Methods Eleven healthy male participants received a single dose of AMI 75 mg, ESC 10 mg, or placebo (PLA) at 9:00 PM in a double blind, randomized, controlled, repeated measures study separated by one week. Fasting morning serum levels (7:00 AM) of ghrelin, leptin, cortisol and prolactin were assessed. Results A repeated measures multivariate analysis of variance revealed a significant main effect for the factor condition (AMI, ESC, PLA). Subsequent univariate analyses demonstrated significant condition effects for ghrelin and cortisol. Post-hoc analyses demonstrated a significant reduction of ghrelin levels after AMI in comparison to PLA, and a significant reduction of cortisol levels after AMI in comparison to both ESC and PLA. Other contrasts did not reach statistical significance. Conclusion Administration of a single dose of AMI, but not of ESC, leads to a significant reduction in morning serum ghrelin and cortisol levels. No effects on leptin and prolactin levels were observed. The differential impact of AMI and ESC on hormones might contribute to different adverse effect profiles of both substances.

According to the World Health Organization, cardiovascular diseases are the leading cause of death in the world. Therefore, early prevention of these diseases is a public health priority. Epidemiological data suggest that insomnia may be a modifiable risk factor for cardiovascular diseases. A randomized controlled trial in a sample of insomnia patients without cardiovascular disease was conducted to investigate the effects of insomnia treatment on early markers of cardiovascular diseases assessed by 24-hr ambulatory blood pressure, heart rate and heart rate variability monitoring, and morning fasting blood samples. Forty-six patients with insomnia disorder were randomized to cognitive behavioural therapy for insomnia (CBT-I; n = 23) or a waitlist control condition (n = 23). Contrary to the hypothesis, intention-to-treat analyses did not show any significant treatment effects on early markers of cardiovascular disease (d = 0.0-0.6) despite successful insomnia treatment (d = 1.3). Potential methodological and conceptual reasons for these negative findings are discussed. Future studies might include larger sample sizes that are at risk of cardiovascular diseases and focus on other cardiovascular markers.

Background Long-term synaptic plasticity is a basic ability of the brain to dynamically adapt to external stimuli and regulate synaptic strength and ultimately network function. It is dysregulated by behavioral stress in animal models of depression and in humans with major depressive disorder. Antidepressants have been shown to restore disrupted synaptic plasticity in both animal models and humans; however, the underlying mechanism is unclear. Methods We examined modulation of synaptic plasticity by selective serotonin reuptake inhibitors (SSRIs) in hippocampal brain slices from wild-type rats and serotonin transporter (SERT) knockout mice. Recombinant voltage-gated calcium (Ca2+) channels in heterologous expression systems were used to determine the modulation of Ca2+ channels by SSRIs. We tested the behavioral effects of SSRIs in the chronic behavioral despair model of depression both in the presence and in the absence of SERT. Results SSRIs selectively inhibited hippocampal long-term depression. The inhibition of long-term depression by SSRIs was mediated by a direct block of voltage-activated L-type Ca2+ channels and was independent of SERT. Furthermore, SSRIs protected both wild-type and SERT knockout mice from behavioral despair induced by chronic stress. Finally, long-term depression was facilitated in animals subjected to the behavioral despair model, which was prevented by SSRI treatment. Conclusions These results showed that antidepressants protected synaptic plasticity and neuronal circuitry from the effects of stress via a modulation of Ca2+ channels and synaptic plasticity independent of SERT. Thus, L-type Ca2+ channels might constitute an important signaling hub for stress response and for pathophysiology and treatment of depression.

Reference data for sleep are needed for the interpretation of clinical sleep parameters. This analysis aimed to provide polysomnography-measured, spectral analytic and subjective reference data based on a sample of healthy adults. In addition, effects of age and sex were investigated.The sample was selected from the archival database of the Sleep Center at the University Medical Center Freiburg and consisted of 206 healthy adults aged 19 to 73 years. For an adaptation and a second examination night, polysomnography parameters, spectral analytic data, and subjective sleep estimations are presented.With increasing age, sleep became shorter (less total sleep time, more wake time after sleep onset) and lighter (eg, more percentage of stage N1 sleep, increase in fast activity in the beta range). Sleep in females was deeper than sleep in males (eg, higher percentage of stage N3 sleep). Females had higher overall power density than males. Altogether, it is apparent that sleep parameters exhibit high standard deviations, suggesting a high variability within healthy adults and complicating the specification of reference values.Our data suggest that the informative value of sleep reference data in healthy individuals is limited because of high interindividual and intraindividual variation within sleep variables. More research, preferably in the form of meta-analyses and/or large international databases, is needed to further investigate the relevance of such reference data for mental and physical health. In the absence of such knowledge, giving patients feedback about deviations from the norm in their sleep profile may give rise to ill-founded concerns and worry.

Sleep modulates motor learning, but its detailed impact on performance curves remains to be fully characterized. This study aimed to further determine the impact of brief daytime periods of NREM sleep on ‘offline’ (task discontinuation after initial training) and ‘on-task’ (performance within the test session) changes in motor skill performance (finger tapping task). In a mixed design (combined parallel group and repeated measures) sleep laboratory study (n = 17 ‘active’ wake vs. sleep, n = 19 ‘passive’ wake vs. sleep), performance curves were assessed prior to and after a 90 min period containing either sleep, active or passive wakefulness. We observed a highly significant, but state- (that is, sleep/wake)-independent early offline gain and improved on-task performance after sleep in comparison to wakefulness. Exploratory curve fitting suggested that the observed sleep effect most likely emerged from an interaction of training-induced improvement and detrimental ‘time-on-task’ processes, such as fatigue. Our results indicate that brief periods of NREM sleep do not promote early offline gains but subsequent on-task performance in motor skill learning.

The experimental study of electroencephalographic slow wave sleep (SWS) stretches over more than half a century and has corroborated its importance for basic physiological processes, such as brain plasticity, metabolism and immune system functioning. Alterations of SWS in aging or pathological conditions suggest that modulating SWS might constitute a window for clinically relevant interventions. This work provides a systematic and integrative review of SWS modulation through non-invasive brain stimulation in humans. A literature search using PubMed, conducted in May 2020, identified 3220 studies, of which 82 fulfilled inclusion criteria. Three approaches have been adopted to modulate the macro- and microstructure of SWS, namely auditory, transcranial electrical and transcranial magnetic stimulation. Our current knowledge about the modulatory mechanisms, the space of stimulation parameters and the physiological and behavioral effects are reported and evaluated. The integration of findings suggests that sleep slow wave modulation bears the potential to promote our understanding of the functions of SWS and to develop new treatments for conditions of disrupted SWS.

Mammalian sleep emerges from attenuated activity in the ascending reticular arousal system (ARAS), the main arousal network of the brain. This system originates in the brainstem and activates the thalamus and cortex during wakefulness via a well-characterized 'bottom-up' pathway. Recent studies propose that a less investigated cortico-thalamic 'top-down' pathway also regulates sleep. The present work integrates the current evidence on sleep regulation with a focus on the 'top-down' pathway and explores the potential to translate this information into clinically relevant interventions. Specifically, we elaborate the concept that arousal and sleep continuity in humans can be modulated by non-invasive brain stimulation (NIBS) techniques that increase or decrease cortical excitability. Based on preclinical studies, the modulatory effects of the stimulation are thought to extend to subcortical arousal networks. Further exploration of the 'top-down' regulation of sleep and its modulation through non-invasive brain stimulation techniques may contribute to the development of novel treatments for clinical conditions of disrupted arousal and sleep, which are among the major health problems worldwide.

Therapeutic sleep deprivation (SD) is a rapid acting treatment for major depressive disorder (MDD). Within hours, SD leads to a dramatic decrease in depressive symptoms in 50-60% of patients with MDD. Scientifically, therapeutic SD presents a unique paradigm to study the neurobiology of MDD. Yet, up to now, the neurobiological basis of the antidepressant effect, which is most likely different from today's first-line treatments, is not sufficiently understood. This article puts the idea forward that sleep/wake-dependent shifts in synaptic plasticity, i.e., the neural basis of adaptive network function and behavior, represent a critical mechanism of therapeutic SD in MDD. Particularly, this article centers on two major hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, and on how they can be integrated into a novel synaptic plasticity model of therapeutic SD in MDD. As a major component, the model proposes that therapeutic SD, by homeostatically enhancing cortical synaptic strength, shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP) in patients with MDD in a more favorable window of associative plasticity. Research on the molecular effects of SD in animals and humans, including observations in the neurotrophic, adenosinergic, monoaminergic, and glutamatergic system, provides some support for the hypothesis of associative synaptic plasticity facilitation after therapeutic SD in MDD. The model proposes a novel framework for a mechanism of action of therapeutic SD that can be further tested in humans based on non-invasive indices and in animals based on direct studies of synaptic plasticity. Further determining the mechanisms of action of SD might contribute to the development of novel fast acting treatments for MDD, one of the major health problems worldwide.

Objective Entrustable professional activities (EPAs) represent discrete clinical tasks that can be entrusted to trainees in psychiatry. They are increasingly being used as educational framework in several countries. However, the empirical evidence available has not been synthesized in the field of psychiatry. Therefore, the authors conducted a systematic review in order to summarize and evaluate the available evidence in the field of EPAs in undergraduate and graduate medical education in psychiatry. Methods The authors searched PubMed, Cochrane Library, ERIC, Embase, PsycINFO, all Ovid journals, Scopus, Web of Science, MedEdPORTAL and the archives of Academic Psychiatry for articles reporting quantitative and qualitative research as well as educational case reports on EPAs in undergraduate and graduate psychiatry education published since 2005. All included articles were assessed for content (development, implementation and assessment of EPAs) and quality using the Quality Assessment Tool for Studies with Diverse Designs. Results The authors screened 2,807 records and included a total of 20 articles in the final data extraction. Most studies were expert consensus reports (n = 6, 30%) and predominantly conducted in English-speaking countries (n = 17, 85%). Papers reported mainly EPA-development and/or EPA-implementation studies (n = 14, 70%), whereas EPA-assessment studies were less frequent (n = 6, 30%). Publications per year showed an increasing trend both in quantity (from 1 in 2011 to 7 in 2018) and quality (from a QATSDD-score of 27 in 2011 to an average score of 39 in 2018). The main focus of the articles was the development of individual EPAs on different levels of training for psychiatry or on curricular frameworks based on EPAs in psychiatry (n = 10, 50%). The lack of empirical controlled studies does currently not allow for meta-analyses of educational outcomes. Conclusion The concept of EPA-based curricula seems to become increasingly present a focus in the specialty of psychiatry both in UME and GME. The lack of empirical research in this context is an important limitation for educational practice recommendations. Currently there is only preliminary but promising data available for using EPAs with regards to educational outcomes. EPAs seem to be effectively used from a curriculum design perspective for UME and GME in psychiatry.

Transcranial magnetic stimulation (TMS) is a well-established tool in probing cortical plasticity in vivo. Changes in corticomotor excitability can be induced using a paired associative stimulation (PAS) protocol, in which TMS stimulation over the primary motor cortex is conditioned with an electrical peripheral nerve stimulation of the contralateral hand. PAS with an inter-stimulus interval of 25 ms induces long-term potentiation (LTP)-like effects in cortical excitability. However, the response to a PAS protocol tends to vary substantially across individuals. In this study, we used univariate and multivariate data-driven methods to investigate various previously proposed determinants of inter-individual variability in PAS efficacy, such as demographic, cognitive, clinical, neurophysiological, and neuroimaging measures. Forty-one right-handed participants, comprising 22 patients with amnestic mild cognitive impairment and 19 healthy controls, underwent the PAS protocol. Prior to stimulation, demographic, genetic, clinical, as well as structural and resting-state functional MRI data were acquired. The two groups did not differ in any of the variables, except by global cognitive status. Univariate analysis showed that only 61 % of all participants were classified as PAS responders, irrespective of a group membership. Higher PAS response was associated with lower TMS intensity and with higher resting-state connectivity within the sensorimotor network, but only in responders, as opposed to non-responders. We also found an overall positive correlation between PAS response and structural connectivity within the corticospinal tract, which did not differ between groups. A multivariate random forest (RF) model identified age, gender, education, IQ, global cognitive status, sleep quality, alertness, TMS intensity, genetic factors, and neuroimaging measures (functional and structural connectivity, grey matter volume, and cortical thickness) as poor predictors of PAS response. The model resulted in low accuracy of the RF classifier (58 %; 95% CI: 42% - 74%), with a higher relative importance of brain connectivity measures compared to the other variables. We conclude that PAS variability in our sample was not well explained by factors known to influence PAS efficacy, emphasizing the need for future replication studies.

Animals and humans spend on average one third of their lives in sleep, but its functions remain to be specified. Distinct lines of research propose that sleep promotes local strengthening of information-bearing synapses (plasticity) and global downscaling of synaptic strength (stability) in neural networks-prerequisites for adaptive behavior in a changing environment. However, the potential orchestration of these processes, particularly in humans, needs to be further characterized. Here, we use electrophysiological, behavioral, and molecular indices to noninvasively study cortical plasticity and network stability in humans. We observe indices of local strengthening of prior induced long-term potentiation-like plasticity (paired associative stimulation induced change in motor-evoked potential) and global network stabilization (homeostatic regulation of wake EEG theta activity) after brief periods of nonrapid eye movement sleep compared with wakefulness. The interplay of local sleep slow oscillations and spindle activity, previously related to synaptic refinements during sleep, is identified as a potential mechanism. Our findings are consistent with the notion that sleep-specific brain activity patterns reduce the plasticity-stability dilemma by orchestrating local plasticity and global stability of neural assemblies in the human cortex. Future studies are needed to further decipher the neural mechanisms underlying our indirect observations.

Initially independent lines of research suggest that sleep-specific brain activity patterns, observed as electroencephalographic slow oscillatory and sleep spindle activity, promote memory consolidation and underlying synaptic refinements. Here, we further tested the emerging concept that specifically the coordinated interplay of slow oscillations and spindle activity (phase-amplitude coupling) support memory consolidation. Particularly, we associated indices of the interplay between slow oscillatory (0.16-1.25 Hz) and spindle activity (12-16 Hz) during non-rapid eye movement sleep (strength [modulation index] and phase degree of coupling) in 20 healthy adults with parameters of overnight declarative (word-list task) and procedural (mirror-tracing task) memory consolidation. The pattern of results supports the notion that the interplay between oscillations facilitates memory consolidation. The coincidence of the spindle amplitude maximum with the up-state of the slow oscillation (phase degree) was significantly associated with declarative memory consolidation (r = .65, p = .013), whereas the overall strength of coupling (modulation index) correlated with procedural memory consolidation (r = .45, p = .04). Future studies are needed to test for potential causal effects of the observed association between neural oscillations during sleep and memory consolidation, and to elucidate ways of modulating these processes, for instance through non-invasive brain-stimulation techniques.

Background In spite of the availability of effective treatments for obsessive-compulsive disorder (OCD), many patients do not respond sufficiently or relapse. Treatments using other potentially effective methods such as experiential techniques need to be investigated. We developed a 12-week inpatient treatment augmenting exposure and response prevention (ERP) with schema therapy (ST) called STERP. The feasibility and effectiveness of STERP was tested.. Methods In a pilot study, 10 inpatients with OCD who failed to respond to Cognitive Behavioral Therapy (CBT) with ERP received STERP. The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) served as primary outcome. Secondary outcome measures were the Obsessive Compulsive Inventory-revised (OCI-R) and the Beck Depression Inventory (BDI-II). Treatment effects were assessed with t-tests for paired samples. Results Significant reductions of the Y-BOCS, OCI-R and the BDI-II were found, with very large effect sizes (Cohen's d = 1.48–2.25). Results remained stable at 6 months follow-up. Five prior non-responders responded according to the 35% Y-BOCS symptom reduction criterion.. Limitations Lack of control group, small sample size and lack of repeated outcome measures during baseline. Conclusions STERP may be a feasible and potentially effective treatment for prior non-responders among OCD patients and thus worth further investigation in randomized controlled trials..

Acetylcholine is critically involved in modulating learning and memory function, which both decline in neurodegeneration. It remains unclear to what extent structural and functional changes in the cholinergic system contribute to episodic memory dysfunction in mild cognitive impairment (MCI), in addition to hippocampal degeneration. A better understanding is critical, given that the cholinergic system is the main target of current symptomatic treatment in mild to moderate Alzheimer's disease. We simultaneously assessed the structural and functional integrity of the cholinergic system in 20 patients with MCI and 20 matched healthy controls and examined their effect on verbal episodic memory via multivariate regression analyses. Mediating effects of either cholinergic function or hippocampal volume on the relationship between cholinergic structure and episodic memory were computed. In MCI, a less intact structure and function of the cholinergic system was found. A smaller cholinergic structure was significantly correlated with a functionally more active cholinergic system in patients, but not in controls. This association was not modulated by age or disease severity, arguing against compensational processes. Further analyses indicated that neither functional nor structural changes in the cholinergic system influence verbal episodic memory at the MCI stage. In fact, those associations were fully mediated by hippocampal volume. Although the cholinergic system is structurally and functionally altered in MCI, episodic memory dysfunction results primarily from hippocampal neurodegeneration, which may explain the inefficiency of cholinergic treatment at this disease stage.

Sleep is ubiquitous in animals and humans, but its function remains to be further determined. The synaptic homeostasis hypothesis of sleep–wake regulation proposes a homeostatic increase in net synaptic strength and cortical excitability along with decreased inducibility of associative synaptic long-term potentiation (LTP) due to saturation after sleep deprivation. Here we use electrophysiological, behavioural and molecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans after sleep and sleep deprivation. We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined amplitude of motor-evoked potential and EEG theta activity) and decreased LTP-like plasticity (paired associative stimulation induced change in motor-evoked potential and memory formation) after sleep deprivation. Changes in plasma BDNF are identified as a potential mechanism. Our study indicates that sleep recalibrates homeostatic and associative synaptic plasticity, believed to be the neural basis for adaptive behaviour, in humans., Sleep deprivation is believed to lead to homeostatic increases in synaptic strength and reduced inducibility of associative LTP, based mainly on findings from animal studies. Here, Kuhn et al. demonstrate similar sleep-dependent synaptic plasticity changes in humans along with altered plasma BDNF levels.

Objective Paired associative stimulation (PAS) is a widely used transcranial magnetic stimulation (TMS) paradigm to induce synaptic long-term potentiation (LTP)-like plasticity in the intact human brain. The PAS effect is reduced in Alzheimer’s dementia (AD) but has not yet been assessed in patients with mild cognitive impairment (MCI). Methods PAS was assessed in a group of 24 MCI patients and 24 elderly controls. MCI patients were further stratified by their cognitive profile as well as hippocampal atrophy and Apolipoprotein E (ApoE) genotype. Results There was no difference in PAS effects between MCI patients and healthy controls. MCI patients tended to show a higher response rate and an average PAS effect. PAS effects were not correlated with markers of disease severity or ApoE genotype but were more pronounced in individuals with shorter sleep duration and in MCI subjects with higher ratings of subjective alertness. Conclusions Contrary to our initial hypothesis, there was no clear difference in PAS between MCI patients and healthy controls. Significance Our results argue against a continuous reduction of LTP-like plasticity along the spectrum of clinical MCI when stratified by MCI-subtype, APOE genotype or hippocampus atrophy.

The disorder insomnia represents a relevant and frequent condition in clinical care. Cognitive behavioral therapy of insomnia (CBT-I) is regarded as first line treatment. Pharmacotherapy can be considered if CBT-I is not available or effective. Therefore, pharmacological approaches for disturbed sleep are still among the most widely prescribed pharmacological treatments in clinical care.In this review, the authors highlight basic physiological pathways of sleep regulation to understand fundamental pharmacological principles of sleep medicine. Available guidelines and reviews are summarized and recommendations formulated regarding the use of benzodiazepines and hypnotic benzodiazepine receptor agonists, melatonin and melatonin receptor agonists, sedating antidepressants, antipsychotics and antihistamines, and orexin receptor antagonists in insomnia disorder. Variations in the treatment of insomnia disorder in subpopulations with increased prevalence of sleep disorders - childhood, pregnancy and old age - are specified.The well-established off-label use of hypnotic drugs should evocate a debate about a better alignment of clinical practice and scientific evidence and guidelines. Better understanding of sleep regulation could help in the development of completely new substance classes. Focusing subjective sleep disturbances, such as superficial sleep perception might help identify novel pathways.

Questionnaire studies suggest that stroke patients experience sustained problems with sleep and daytime sleepiness, but physiological sleep studies focussing specifically on the chronic phase of stroke are lacking. Here we report for the first time physiological data of sleep and daytime sleepiness obtained through the two gold-standard methods, nocturnal polysomnography and the Multiple Sleep Latency Test. Data from community-dwelling patients with chronic right-hemispheric stroke (>12 months) were compared to sex- and age-matched controls. Behavioural and physiological measures suggested that stroke patients had poorer sleep with longer sleep latencies and lower sleep efficiency. Patients further spent more time awake during the night, and showed greater high-frequency power during nonREM sleep than controls. At the same time the Multiple Sleep Latency Test revealed greater wake efficiency in patients than controls. Importantly these findings were not due to group differences in sleep disordered breathing or periodic limb movements. Post-stroke insomnia is presently not adequately addressed within the care pathway for stroke. A holistic approach to rehabilitation and care provision, that includes targeted sleep interventions, is likely to enhance long-term outcome and quality of live in those living with chronic deficits after stroke.

The left dorsolateral prefrontal cortex (DLPFC) is involved in encoding and retrieval of episodic memories, and thus, is frequently targeted in non-invasive brain stimulation paradigms, aiming for its functional modulation. Anodal transcranial direct current stimulation (tDCS), that boosts neuronal excitability in stimulated cortical areas, has been found to increase cognitive skills differentially, depending on the initial performance. We hypothesize that the benefit of tDCS on verbal episodic memory can be extrapolated from the participants’ baseline performance. In the present randomized, double-blind, parallel group study, healthy young adults (n = 43) received either real anodal or sham tDCS over their left DLPFC during the encoding phase of a verbal episodic memory task. Forty words were presented visually thrice with immediate vocal retrieval after each block and an additional delayed recall. We conducted a moderation analysis to test the modulating effect of initial episodic memory retrieval, adjusted for primacy and recency effects, on delayed recall under real or sham stimulation. Despite the absence of a significantly beneficial tDCS effect at the group level, we found that the number of remembered midlist words in the first retrieval significantly moderated the stimulation effect in such a way that initially low performers experienced the highest gain from real stimulation. These results suggest that anodal tDCS to the left DLPFC improves memory functions only so far. While only marginal stimulation-induced gains occur in cognitively unimpaired populations, greater stimulation benefits might be expected in individuals with clinically relevant deficiencies in the verbal episodic memory domain.

Study Objectives: Perfectionism has been suggested to represent a predisposing factor for poor sleep. However, previous studies have relied upon self-report measures and the association between perfectionism and polysomnographic sleep warrants further investigation. Methods: The current retrospective exploratory study used the Frost Multidimensional Perfectionism Scale (FMPS) and polysomnography (PSG) in an unselected sample of 334 consecutive sleep laboratory patients (140 males, 194 females, 44.6 ± 15.9 years). Data was analysed using linear regression analyses. Results: High levels of perfectionism were associated with polysomnographically determined markers of poor sleep in the first sleep laboratory night. The total FMPS score was significantly associated with the number of nocturnal awakenings in the first sleep laboratory night. The sub-scales “concern over mistakes” and “personal standards” of perfectionism were significantly associated with markers of poor sleep. In contrast, there were only few associations between perfectionism and polysomnographic variables of the second sleep laboratory night. Conclusions: This pattern of results suggests that high levels of perfectionism may predispose individuals to sleep disturbances in the context of acute stressors. Thus the influence of perfectionism on poor sleep should be further investigated to improve treatment.

Aim: Empathy is a core element in the doctor–patient relationship. This study examined whether empathy in medical students can be improved by specific training.Methods: 158 medical students were randomized into two groups. The intervention group participated in an empathy skills training with simulated patients (SPs). The control group participated in a history course. After the intervention, empathy was assessed by blinded SPs and experts in an Objective Structured Clinical Examination (OSCE). Students also filled out a self-assessment concerning their attitude on empathy (Jefferson Scale of Physician Empathy Student Version, JSPE-S-S).Results and Conclusions: Participants of the intervention group showed significantly higher levels of empathy when rated by SPs and experts than the control group. In contrast to that, no significant group differences were observed in self-rated empathy. The results underpin the value of empathy skills trainings in medical school study programs.

This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta-analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co-morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate-to high-quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders), in treatment-resistant insomnia, for professional at-risk populations and when substantial sleep state misperception is suspected (strong recommendation, high-quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (strong recommendation, high-quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short-term treatment of insomnia (

Objective/Background: Sleep-related attentional bias has been suggested to represent an important factor for the maintenance of chronic insomnia. However, little is known about potentially underlying psychological mechanisms such as threat or craving. As these are associated with distinguishable brain activation patterns, we performed a functional neuroimaging study. Participants/Methods: Functional magnetic resonance imaging was used to investigate brain reactivity to sleep-related words in 20 patients with primary insomnia according to DSM-IV criteria and 35 good sleeper controls according to Research Diagnostic Criteria. In addition, an emotional Stroop task was performed in all participants outside the scanner to investigate sleep-related attentional bias. Results: Contrary to the hypotheses, patients with chronic insomnia did not differ from good sleeper controls in terms of threat- or craving-related brain reactivity to sleep-related words. In addition, the emotional Stroop task did not reveal any significant group difference in sleep-related attentional bias. Exploratory analyses did not show any significant correlations between brain reactivity/selective attention to sleep-related words and questionnaire scores/PSG parameters. Conclusions: The results from the present study call into question that attentional bias to sleep-related stimuli is a core feature of chronic insomnia. Future studies may use pictorial stimuli and larger sample sizes for investigating sleep-related information processing in insomnia.

Mental disorders are among the most prevalent and impairing disorders worldwide. According to the WHO (World Health Organization), about a third of the population will suffer from a mental disorder across the lifespan. Current guidelines include psychotherapy, or at least psychoeducation, as a first-line treatment component for all mental disorders. Psychotherapy represents an interpersonal process that involves the modification of cognition, emotion and behavior. As such, it can, at least in part, be conceptualized as the quantitative strengthening and qualitative reorganization of novel and more adaptive memory representations. Given that sleep substantially modulates learning, memory and underlying neural refinements, this chapter centers on the idea that sleep-related interventions can be used to augment the treatment effects of psychotherapy. The first part identifies basic memory processes with particular relevance for psychotherapy. The second part evaluates the potential of sleep-related interventions prior to and after psychotherapy, as well as the modulation of distinct aspects of sleep to augment these memory processes in psychotherapy and discusses further directions.

Insomnia and circadian rhythm sleep disorders affect large proportions of the population and have pronounced effects on quality of life and daytime performance. While the neurobiology of insomnia is not yet fully understood, circadian rhythm sleep disorders are assumed to be caused by a mismatch between the individual circadian phase position and the desired sleep–wake schedule. Benzodiazepines and non-benzodiazepine positive allosteric GABAA receptor modulators improve sleep onset and maintenance in the short-term treatment of insomnia. However, tolerance and dependence are important side effects. Sedating antidepressants are frequently prescribed for insomnia, however, only few randomised controlled trials have been published so far. Melatonin and melatonin receptor agonists are considered to be an option for the treatment of insomnia especially because of their minimal abuse potential and safety. First data on orexin (aka hypocretin) receptor antagonists are promising, however, the risk-benefit ratio needs to be further evaluated. With respect to circadian rhythm sleep disorders, there is solid evidence from meta-analyses supporting the use of melatonin in jet lag disorder to accelerate entrainment to the new time zone, and in delayed sleep phase disorder to advance sleep–wake rhythms. In addition to that, there is evidence supporting the use of melatonin in patients with shift work disorder in order to promote daytime sleep after night shifts.

PURPOSE OF REVIEW: This review discusses current concepts on the relationship between sleep, memory formation and underlying neural refinements, with a particular focus on possible ways to use or modulate sleep in a targeted manner to augment psychiatric and psychotherapeutic treatments. RECENT FINDINGS: The most promising lines of research with regard to psychiatry and psychotherapy center on the targeted implementation or modulation of sleep to augment existing or create novel forms of treatment. SUMMARY: The modulation of sleep and interconnected neural plasticity processes provides a window of opportunity for developing novel treatments in psychiatry and psychotherapy.

Schlaf ist ein Zustand, der die Konsolidierung kurzlich erworbener Gedachtnisinhalte optimiert. Daher konnten Schlafstorungen zu Gedachtnisverminderungen bei psychiatrischen Erkrankungen wie der Depression oder der Schizophrenie beitragen. Dieser Beitrag gibt einen Uberblick uber die aktuelle Forschung zum Thema Schlaf und Gedachtnis mit dem Fokus auf psychiatrische Erkrankungen. Storungen in der Schlafstruktur sind assoziiert mit bestimmten Gedachtnisdefiziten bei Patienten mit unterschiedlichen psychischen Erkrankungen. Wirksame Behandlungen von Schlafverminderungen sollten nicht nur den Schlaf an sich, sondern auch die assoziierten Gedachtniseinschrankungen verbessern. Erste Beispiele dafur werden genannt.