Perinatal maternal depression may affect fetal neurodevelopment directly or indirectly via exposures such as smoking, alcohol, or antidepressant use. The relative contribution of these risk factors on child executive function (EF) has not been explored systematically.

A prospective pregnancy cohort of 197 women and their children was studied to determine whether maternal depression diagnosis and the trajectory of maternal depressive symptoms (MDSs) from early pregnancy to 12 months postpartum predicts child EF at age 4 (measured using the preschool age psychiatric assessment, NEPSY-II, and Shape School task) using latent growth curve modeling. Indirect effects of smoking, alcohol, and antidepressant use were also formally tested.

Increasing maternal perinatal depressive symptoms over time predicted more inattentive symptoms, poorer switching, and motor inhibition, but not cognitive inhibition. When adjusted for multiple comparison, and after accounting for maternal cognition and education, the association with child inattentive symptoms remained significant. However, diagnosed depression did not predict child EF outcomes. Prenatal exposure to smoking, alcohol, and antidepressants also did not mediate pathways from depressive symptoms to EF outcomes. Our findings were limited by sample size and statistical power to detect outcome effects of smaller effect size.

This study suggests that increasing MDSs over the perinatal period is associated with poorer EF outcomes in children at age 4 – independent of prenatal smoking, drinking, or antidepressant use. Depressive chronicity, severity, and postpartum influences may play crucial roles in determining childhood outcomes of EF.

Surgically implanted vagus nerve stimulation (VNS) is a recognised treatment for depression. The vagus nerve can also be stimulated non-invasively via its auricular branch, using transauricular vagus nerve stimulation (taVNS). Heart rate variability (HRV) is a putative biomarker of autonomic nervous system (ANS) engagement. We aimed to test the impact of taVNS on the ANS of healthy volunteers by measuring HRV using a double-blind, sham-controlled, longitudinal design to acquire data over 7 days using wearable cardiac sensors.

taVNS was delivered to the left ear of healthy volunteers using a transcutaneous electrical nerve stimulation (TENS) device via a custom clip electrode (developed at Newcastle University). All participants were stimulated at 10 Hz, with pulse widths of 300 ms and variable current outputs, depending on perceptual thresholds. We delivered double-blinded active and sham taVNS for hour-long periods, in the morning and evening. We also recorded an electrocardiogram (ECG) lead I using a VitalPatch for 7 consecutive days. Python scripts were developed to produce HRV timeseries and plot data. ECG frequency domain parameters – low- (LF) (0.05–0.15 Hz) and high-frequency (HF) power (0.15–0.4 Hz) – were calculated for each stimulation period. The LF/HF ratio was used as a marker of autonomic modulation. The Wilcoxon signed-rank test was used to compare LF/HF ratio distributions.

Initial data from the wearable sensors were used to develop interpolation scripts to improve the processing of noise, missed R waves and ectopic beats, to reduce errors when estimating HRV from the heart rate signal. Initial results from 97 individual 1-hour long stimulation periods, from 18 participants, show that active stimulation in the morning, when compared with sham stimulation in the same period, significantly reduces the LF/HF ratio. The median and interquartile range (IQR) of the LF/HF ratio for the active and sham periods was, respectively, 1.72 (1.99) and 2.75 (2.82), a statistically significant difference (p = 0.043).

taVNS modulates HRV frequency domains, suggestive of vagal cardiac effects, and replicates findings from previous taVNS studies. Reductions in the LF/HF ratio are suggestive of increased parasympathetic tone. As the auricular branch of the vagus does not have any direct cardiac efferents, this suggests central ANS modulation using taVNS. Secondly, it suggests that cardiac ANS modulation could be used as a proxy measure of afferent vagal stimulation, which could be of clinical utility. These effects warrant exploration in a larger cohort study, including wider demographics (including age range) and improved processing pipelines.

Autonomic nervous system (ANS) dysregulation might be relevant to the pathophysiology of fatigue and cognitive impairment in depression and perhaps should be considered when making prescribing decisions.

To determine the relationship of self-reported ANS symptoms with fatigue, cognition and prescribed medication in people with a diagnosis of depression, in comparators without depression but with other mental health, neurodevelopmental or neurodegenerative disorders (active controls) and in healthy controls.

Cross-sectional analysis of an opportunistic sample from England. Self-reported data were collected on demographics, diagnosis, medication, ANS symptoms (Composite Autonomic Symptom Scale-31, COMPASS-31) and fatigue (Visual Analogue Scale for Fatigue, VAS-F). A subsample completed cognitive tests (THINC-it), including the subjective Perceived Deficits Questionnaire five-item version (PDQ-5). Spearman's correlation and mediation models were used to explore the relationship between COMPASS-31, VAS-F and PDQ-5 scores.

Data were obtained for 3345 participants, 22% with depression. The depression group had significantly (P < 0.01) more severe autonomic dysregulation as measured by COMPASS-31 scores (median 30) than active (median 23) and healthy controls (median 10). The depression group had significantly higher symptom severity (P < 0.01) than both control groups on the VAS-F and PDQ-5. Overall, there was a significantly positive correlation (P < 0.01) between COMPASS-31, VAS-F scores (Spearman's rho rs = 0.44) and PDQ-5 scores (rs = 0.56). COMPASS-31 scores mediated greater symptom severity on the VAS-F and PDQ-5 for those with depression. COMPASS-31 scores remained significantly different between the depression group and both control groups independently of medication.

People with a diagnosis of depression report worse fatigue and cognition than active and healthy comparators; this appears to be mediated by ANS dysregulation.

Recent developments in computational psychiatry have led to the hypothesis that mood represents an expectation (prior belief) on the likely interoceptive consequences of action (i.e. emotion). This stems from ideas about how the brain navigates its external world by minimising an upper bound on surprisal (free energy) of sensory information and echoes developments in other perceptual domains.

In this paper we aim to present a simple partial observable Markov decision process that models mood updating in response to stressful or non-stressful environmental fluctuations while seeking to minimise surprisal in relation to prior beliefs about the likely interoceptive signals experienced with specific actions (attenuating or amplifying stress and pleasure signals).

We examine how, by altering these prior beliefs we can model mood updating in depression, mania and anxiety.

We discuss how these models provide a computational account of mood and its related psychopathology and relate it to previous research in reward processing.

Models such as this can provide hypotheses for experimental work and also open up the potential modelling of predicted disease trajectories in individual patients.

Psychiatric disorders are associated with fatigue and with impairment to a range of cognitive domains, including executive functioning, learning, memory and complex attention. Similar impairments are seen in autonomic nervous system (ANS) dysfunction. The aetipathogenic significance of this for psychiatric disorders is unknown. The main aim of the cap-mem study was to characterize the relationships between ANS and cognitive function in a sample of none-clinical controls and people with mental health, neurodevelopmental and neurodegenerative disorders. The potentially confounding role of medication was included within this analysis.

The sample was recruited via secondary care mental health trusts. ANS function was assessed using self-report measures of ANS dysfunction symptoms (COMPASS-31) and fatigue (VAFS). Cognitive ability in various domains was measured using a validated, computerised assessment tool (THINC-IT). Psychiatric status and medication status were self-reported, and where possible, disorder severity measured using a rating scale (CGI-S).

Participants with depression had a significantly higher COMPASS-31 and VAFS scores (higher being more severe), with effect sizes being medium to large. Medication did not fully explain the associations observed. Overall, participants with mental health disorders, when compared to healthy controls, had significantly higher levels of cognitive impairment. Levels of ANS dysfunction significantly and positively correlated with cognitive impairment. The severity of the psychiatric disorder significantly correlated with both ANS dysfunction (p < 0.001) and cognitive impairment. These results were found across all cognitive tests (p < 0.05), other than reaction times in the N-back test, a measure of working memory.

Our results show significant association between ANS dysfunction, psychiatric disorders and cognitive impairments. This is consistent with previously published data. There is now a need to understand the underlying mechanisms and the directionality of the associations. If these mechanisms are shared and relate to autonomic dysfunction, targeted treatments addressing this directly could be helpful with mental health disorders and associated burdensome symptoms, such as cognitive impairments and fatigue. This study is part of a wider project assessing cognitive ability and autonomic functioning in psychiatric populations, and investigating treatments that directly address autonomic dysfunction in psychiatric samples, such as non-invasive transauricular vagus nerve stimulation (taVNS).

Sleep difficulties are often reported in practice, and are part of the diagnostic criteria for depression and bipolar disorder.

To inform the understanding of the relationship between sleep and both depression and bipolar disorder.

We conducted a narrative literature review of affective disorders and sleep difficulties in children and young people.

Specific sleep disorders, such as parasomnias, narcolepsy and sleep-related movement disorders, are associated with depression, whereas insomnia, obstructive sleep apnoea and circadian rhythm disorders are associated with both depression and bipolar disorder in children and young people. Conversely, children and young people with depression can present with a number of sleep difficulties, and these are associated with higher depression severity and greater fatigue, suicidal ideation, physical complaints, pain and decreased concentration. Sleep disturbances among adolescents with bipolar disorder can affect the severity of depressive and manic symptoms, are a poor prognostic indicator and have been associated with social and academic impairment. Antidepressants and antipsychotics can directly affect sleep architecture, which clinicians need to be aware of. Non-pharmacological interventions for sleep problems could prevent and/or minimise the risk of relapse in affective disorders.

Sleep difficulties can occur before, during and after an episode of depression or bipolar disorder, and have a higher prevalence in affective disorders compared with the general population. A multi-modal approach would include the treatment of both the affective and specific sleep disorder. Further research is needed in this field to understand the impact of combined interventions on clinical outcomes.

To assess the feasibility and utility of introducing the following changes on to in-patient units:

Structural and cultural adaptation to create a sleep friendly ward environment

A “Protected Sleep Time” between midnight and 6am

Routine screening for sleep disorders, including obstructive sleep apnoea and restless leg syndrome

Insomnia and other sleep disturbances are cause, correlate and consequence of psychiatric disorders. Routine hourly night time observations, ward noise, bright lights at night time, sleep disorders, insufficient exercise, insufficient day light exposure, too much caffeine and inappropriate psychotropic use are all causes of disturbed sleep (Horne 2018).

Seven wards participated in a pilot (SleepWell). These consisted of one male and two female Acute Wards (General Adult), a High Dependency Unit, a Neurorehabilitation ward, an in-patient dementia service and one rehabilitation ward. These wards were supported via an existing trust management structure and the pilot was specifically supported by two trust managers (RW and RB) and by a clinical director (PK). The expectation was that each ward would identify a sleep champion from existing staff to facilitate the changes. A “product” was developed which identified core sleep management features but, in addition, wards were not confined to these. The existing policy that all inpatients should be checked each hour over night was suspended for the pilot wards and the patients had protected sleep time (PST) if the MDT agreed that it was clinically appropriate.

Quantitative and qualitative techniques were used to identify facilitators of change, impact on sleep and, outcome.

Protected sleep was viewed positively by all staff and approximately 50% of patients on the pilot wards were able to have PST at some point in their admission. Routine sleep disorder assessments were harder to implement and 33% of patients were screened. There were no deaths or significant events on patients due to PST. Hypnotic use on the pilot wards reduced. It is anticipated that PST where it is safe will be rolled out across all adult and old age wards in the trust.

With support, it has been feasible to change many aspects of sleep management across a breadth of inpatient units in a large NHS trust.

In-patients on mental health wards are commonly prescribed hypnotics for the long-term management of disturbed sleep. Specific sleep disorders remain underdiagnosed and effective behavioural interventions are underused. We developed a suite of three educational interventions (a video, poster and handbook) about sleep, sleep disorders, the safe prescribing of hypnotics and use of psychological strategies (sleep hygiene and cognitive–behavioural therapy for insomnia, CBTi) using co-design and multiprofessional stakeholder involvement. This controlled before-and-after study evaluated the effectiveness of these interventions across seven in-patient psychiatric wards, examining their impact on hypnotic prescribing rates and staff confidence scores (data collected by retrospective drug chart analysis and survey respectively).

A marked reduction was seen in the percentage of patients prescribed hypnotics on in-patient prescription charts (−24%), with a 41% reduction in the number of hypnotics administered per patient (mean reduction −1.142 administrations/patient).

These simple educational strategies about the causes and treatment of insomnia can reduce hypnotic prescribing rates and increase staff confidence in both the medical and psychological management of insomnia.

Bipolar disorder is a chronic mental health condition, which can result in functional impairment despite medication. A large evidence base supports use of psychological therapies and structured care in the treatment of mood disorders, but these are rarely implemented. e-Pathways are digital structures that inform and record patient progress through a healthcare system, although these have not yet been used for bipolar disorder.

To assess the perceived benefits and costs associated with implementing a collaborative NICE-informed e-pathway for bipolar disorder.

Healthcare professionals and people with bipolar disorder attended a workshop to share feedback on e-pathways. Data were collected through questionnaires (n = 26) and transcription of a focus group, analysed qualitatively by a framework analysis.

Patients and healthcare professionals welcomed the development of an e-pathway for bipolar disorder. There were five elements to the framework: quality and delivery of care, patient–clinician collaboration, flexibility and adaptability, impact on staff and impact on healthcare services.

Identification of benefits and costs ensures that future development of e-pathways addresses concerns of healthcare professionals and people with bipolar disorder, which would be essential for successful implementation. Recommendations for this development include making e-pathways less complicated for patients, ensuring sufficient training and ensuring clinicians do not feel their skills become invalidated. Limitations of the study, and directions for future research, are discussed.

The development of childhood anxiety disorders (CADs) is likely to depend on pathways that can be programmed by early-life risk factors. We test the hypothesis that early-life maternal factors can predict this programming effect on CAD.

Data were obtained from 198 women and children from the Mercy Pregnancy and Emotional Wellbeing Study (MPEWS), a cohort study with data collected across pregnancy, postpartum and until 4 years of age. Maternal antenatal depression was measured using the Structured Clinical Interview for DSM-IV (SCID-IV), together with antenatal hair cortisol concentrations, maternal childhood trauma and parenting stress at 6 months postpartum. CAD was assessed with the Preschool Age Psychiatric Assessment and the Child Behaviour Checklist.

Antenatal depression, a history of maternal childhood trauma and lower gestational age at birth were each associated with anxiety disorders at 4 years of age in their children. A multivariate binary logistic model with these early predictors explained approximately 9% of variance in CAD outcome at 4 years of age; however, only maternal trauma and gestational age were significant predictors in the model. The effect of early parenting stress on CAD was found to vary by the concentration of maternal antenatal hair cortisol, whereby postpartum parenting stress was associated with CAD only when there were higher maternal antenatal cortisol levels.

This study suggests the importance of maternal factors pre-conception, pregnancy and in the postnatal period, which predict CADs and this is consistent with a developmental programming hypothesis for CAD.

Sleep disturbance is common in psychiatry wards despite poor sleep worsening mental health. Contributory factors include the ward environment, frequent nightly checks on patients and sleep disorders including sleep apnoea. We evaluated the safety and feasibility of a package of measures to improve sleep across a mental health trust, including removing hourly checks when safe, sleep disorder screening and improving the ward environment.

During the pilot there were no serious adverse events; 50% of in-patients were able to have protected overnight sleep. Hypnotic issuing decreased, and feedback from patients and staff was positive. It was possible to offer cognitive–behavioural therapy for insomnia to selected patients.

Many psychiatry wards perform standardised, overnight checks, which are one cause of sleep disruption. A protected sleep period was safe and well-tolerated alongside education about sleep disturbance and mental health. Future research should evaluate personalised care rather than blanket observation policies.

Childhood maltreatment is one of the strongest predictors of adulthood depression and alterations to circulating levels of inflammatory markers is one putative mechanism mediating risk or resilience.

To determine the effects of childhood maltreatment on circulating levels of 41 inflammatory markers in healthy individuals and those with a major depressive disorder (MDD) diagnosis.

We investigated the association of childhood maltreatment with levels of 41 inflammatory markers in two groups, 164 patients with MDD and 301 controls, using multiplex electrochemiluminescence methods applied to blood serum.

Childhood maltreatment was not associated with altered inflammatory markers in either group after multiple testing correction. Body mass index (BMI) exerted strong effects on interleukin-6 and C-reactive protein levels in those with MDD.

Childhood maltreatment did not exert effects on inflammatory marker levels in either the participants with MDD or the control group in our study. Our results instead highlight the more pertinent influence of BMI.

D.A.C. and H.W. work for Eli Lilly Inc. R.N. has received speaker fees from Sunovion, Jansen and Lundbeck. G.B. has received consultancy fees and funding from Eli Lilly. R.H.M.-W. has received consultancy fees or has a financial relationship with AstraZeneca, Bristol-Myers Squibb, Cyberonics, Eli Lilly, Ferrer, Janssen-Cilag, Lundbeck, MyTomorrows, Otsuka, Pfizer, Pulse, Roche, Servier, SPIMACO and Sunovian. I.M.A. has received consultancy fees or has a financial relationship with Alkermes, Lundbeck, Lundbeck/Otsuka, and Servier. S.W. has sat on an advisory board for Sunovion, Allergan and has received speaker fees from Astra Zeneca. A.H.Y. has received honoraria for speaking from Astra Zeneca, Lundbeck, Eli Lilly, Sunovion; honoraria for consulting from Allergan, Livanova and Lundbeck, Sunovion, Janssen; and research grant support from Janssen. A.J.C. has received honoraria for speaking from Astra Zeneca, honoraria for consulting with Allergan, Livanova and Lundbeck and research grant support from Lundbeck.