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.

Most people with bipolar disorder spend a significant percentage of their lifetime experiencing either subsyndromal depressive symptoms or major depressive episodes, which contribute greatly to the high levels of disability and mortality associated with the disorder. Despite the importance of bipolar depression, there are only a small number of recognised treatment options available. Consecutive treatment failures can quickly exhaust these options leading to treatment-resistant bipolar depression (TRBD). Remarkably few studies have evaluated TRBD and those available lack a comprehensive definition of multi-therapy-resistant bipolar depression (MTRBD).

To reach consensus regarding threshold definitions criteria for TRBD and MTRBD.

Based on the evidence of standard treatments available in the latest bipolar disorder treatment guidelines, TRBD and MTRBD criteria were agreed by a representative panel of bipolar disorder experts using a modified Delphi method.

TRBD criteria in bipolar depression was defined as failure to reach sustained symptomatic remission for 8 consecutive weeks after two different treatment trials, at adequate therapeutic doses, with at least two recommended monotherapy treatments or at least one monotherapy treatment and another combination treatment. MTRBD included the same initial definition as TRBD, with the addition of failure of at least one trial with an antidepressant, a psychological treatment and a course of electroconvulsive therapy.

The proposed TRBD and MTRBD criteria may provide an important signpost to help clinicians, researchers and stakeholders in judging how and when to consider new non-standard treatments. However, some challenging diagnostic and therapeutic issues were identified in the consensus process that need further evaluation and research.

In the past 3 years, M.B. has received grant/research support from the NIH, Cooperative Research Centre, Simons Autism Foundation, Cancer Council of Victoria, Stanley Medical Research Foundation, MBF, NHMRC, Beyond Blue, Rotary Health, Geelong Medical Research Foundation, Bristol Myers Squibb, Eli Lilly, Glaxo SmithKline, Meat and Livestock Board, Organon, Novartis, Mayne Pharma, Servier, Woolworths, Avant and the Harry Windsor Foundation, has been a speaker for Astra Zeneca, Bristol Myers Squibb, Eli Lilly, Glaxo SmithKline, Janssen Cilag, Lundbeck, Merck, Pfizer, Sanofi Synthelabo, Servier, Solvay and Wyeth and served as a consultant to Allergan, Astra Zeneca, Bioadvantex, Bionomics, Collaborative Medicinal Development, Eli Lilly, Grunbiotics, Glaxo SmithKline, Janssen Cilag, LivaNova, Lundbeck, Merck, Mylan, Otsuka, Pfizer and Servier. A.J.C. has in the past 3 years received honoraria for speaking from Astra Zeneca and Lundbeck, honoraria for consulting from Allergan, Janssen, Lundbeck and LivaNova and research grant support from Lundbeck. G.M.G. holds shares in P1Vital and has served as consultant, advisor or CME speaker for Allergan, Angelini, Compass pathways, MSD, Lundbeck, Otsuka, Takeda, Medscape, Minervra, P1Vital, Pfizer, Servier, Shire and Sun Pharma. J.G. has received research funding from National Institute for Health Research, Medical Research Council, Stanley Medical Research Institute and Wellcome. H.G. received grants/research support, consulting fees or honoraria from Gedeon Richter, Genericon, Janssen Cilag, Lundbeck, Otsuka, Pfizer and Servier. R.H.M.-W. has received support for research, expenses to attend conferences and fees for lecturing and consultancy work (including attending advisory boards) from various pharmaceutical companies including Astra Zeneca, Cyberonics, Eli Lilly, Janssen, Liva Nova, Lundbeck, MyTomorrows, Otsuka, Pfizer, Roche, Servier, SPIMACO and Sunovion. R.M. has received research support from Big White Wall, Electromedical Products, Johnson and Johnson, Magstim and P1Vital. S.N. received honoraria from Lundbeck, Jensen and Otsuka. J.C.S. has received funds for research from Alkermes, Pfizer, Allergan, J&J, BMS and been a speaker or consultant for Astellas, Abbott, Sunovion, Sanofi. S.W has, within the past 3 years, attended advisory boards for Sunovion and LivaNova and has undertaken paid lectures for Lundbeck. D.J.S. has received honoraria from Lundbeck. T.S. has reported grants from Pathway Genomics, Stanley Medical Research Institute and Palo Alto Health Sciences; consulting fees from Sunovion Pharamaceuticals Inc.; honoraria from Medscape Education, Global Medical Education and CMEology; and royalties from Jones and Bartlett, UpToDate and Hogrefe Publishing. S.P. has served as a consultant or speaker for Janssen, and Sunovion. P.T. has received consultancy fees as an advisory board member from the following companies: Galen Limited, Sunovion Pharmaceuticals Europe Ltd, myTomorrows and LivaNova. E.V. received grants/ research support, consulting fees or honoraria from Abbott, AB-Biotics, Allergan, Angelini, Dainippon Sumitomo, Ferrer, Gedeon Richter, Janssen, Lundbeck, Otsuka and Sunovion. L.N.Y. has received grants/research support, consulting fees or honoraria from Allergan, Alkermes, Dainippon Sumitomo, Janssen, Lundbeck, Otsuka, Sanofi, Servier, Sunovion, Teva and Valeant. A.H.Y. has undertaken paid lectures and advisory boards for all major pharmaceutical companies with drugs used in affective and related disorders and LivaNova. He has also previously received funding for investigator-initiated studies from AstraZeneca, Eli Lilly, Lundbeck and Wyeth. P.R.A.S. has received research funding support from Corcept Therapeutics Inc. Corcept Therapeutics Inc fully funded attendance at their internal conference in California USA and all related expenses. He has received grant funding from the Medical Research Council UK for a collaborative study with Janssen Research and Development LLC. Janssen Research and Development LLC are providing non-financial contributions to support this study. P.R.A.S. has received a presentation fee from Indivior and an advisory board fee from LivaNova.

There is an established relationship between depression and sexual functioning in women. However, there is limited research examining the relationship between perinatal depression and sexual functioning.

This study draws on the Mercy Pregnancy and Emotional Wellbeing Study and reports on 211 women recruited in early pregnancy and followed to 12 months postpartum. Women were assessed for depression using the Structured Clinical Interview for the DSM-IV, repeated measurement of depressive symptoms using the Edinburgh Postnatal Depression Scale and sexual functioning using the Female Sexual Functioning Inventory. Data were also collected on antidepressant use, mode of delivery, history of childhood trauma, breastfeeding and partner support.

Women showed a decline in sexual functioning over pregnancy and the first 6 months postpartum, which recovered by 12 months. For women with depression, sexual functioning was lower throughout pregnancy and continued to be lower at 6 months postpartum than those without depression. Ongoing depressive symptoms at 12 months were also associated with lower sexual functioning. Sexual functioning was not predicted by mode of delivery, antidepressant use or childhood trauma. Breastfeeding predicted lower sexual functioning only at 6 months. Higher partner support predicted higher female sexual functioning.

Pregnancy and the postpartum are a time of reduced sexual functioning for women; however, women with depression are more likely to have lower levels of sexual functioning and this was not predicted by antidepressant use. In women with perinatal depression, consideration of the impact on sexual functioning should be an integral part of care.

Sleep disturbance is common on in-patient psychiatry wards. This study explored subjective and objective patterns of sleep disturbance and contributory environmental factors. Participants were recruited from mental health acute admission wards and had a range of subjective and objective assessments of sleep. Light intensity and noise levels were measured to characterise potential environmental causes for poor sleep.

We recruited 20 patients; 15% were high risk for obstructive sleep apnoea. Nineteen participants reported poor sleep quality on the Pittsburgh Sleep Quality Index, and 90% had significant sleep fragmentation with objective measures. Inside light levels were low (day <200 lux and night <10 lux). Night sound levels were 40–90 db.

Sleep disturbance was highly prevalent. Increased awareness of sleep disorders is needed. Modifiable environmental factors on the ward were implicated, therefore increased awareness and a change of approach to sleep disturbance in in-patient psychiatry is recommended.

None.

Testosterone influences well-being, mood and cognition and may play a role in the pathophysiology of bipolar disorder.

To examine testosterone levels in patients with bipolar disorder compared with healthy controls.

We examined baseline total testosterone levels and current depression scores in male and female patients with bipolar disorder and mild to moderate depression and healthy controls.

A significant interaction between diagnosis and gender was observed (F(2,97)=9.791, P=0.002). Testosterone levels were significantly lower for male patients with bipolar disorder compared with male controls (P=0.001). Women with bipolar disorder had significantly higher testosterone levels than female controls (P=0.03).

Disturbances in testosterone levels may represent an important neurobiological abnormality in bipolar disorder and may differ by gender. If these findings are confirmed, the use of gender appropriate treatment strategies for the normalisation of testosterone levels in bipolar disorder depression should be further explored.