Higher daytime cortisol levels because of a hyperactive hypothalamic–pituitary–adrenal axis have been reported in patients with major depressive disorder (MDD). The elevated glucocorticoids inhibit the proliferation of the oligodendrocytes that are responsible for myelinating the axons of white matter fibre tracts.

To evaluate the relationship between white matter integrity and serum cortisol levels during a first depressive episode in drug-naive patients with MDD (MDD group) using a tract-based spatial statistics (TBSS) method.

The MDD group (n = 29) and a healthy control group (n = 47) underwent diffusion tensor imaging (DTI) scans and an analysis was conducted using TBSS. Morning blood samples were obtained from both groups for cortisol measurement.

Compared with the controls, the MDD group had significantly reduced fractional anisotropy values (P<0.05, family-wise error (FWE)-corrected) in the inferior fronto-occipital fasciculus, uncinate fasciculus and anterior thalamic radiation. The fractional anisotropy values of the inferior fronto-occipital fasciculus, uncinate fasciculus and anterior thalamic radiation had significantly negative correlations with the serum cortisol levels in the MDD group (P<0.05, FWE-corrected).

Our findings indicate that the elevated cortisol levels in the MDD group may injure the white matter integrity in the frontal–subcortical and frontal–limbic circuits.

People with psychotic disorders account for most acute admissions to psychiatric wards. Psychological therapies are a treatment adjunct to standard medication and nursing care, but the evidence base for such therapies within in-patient settings is unclear.

To conduct a systematic scoping review of the current evidence base for psychological therapies for psychosis delivered within acute in-patient settings (PROSPERO: CRD42015025623).

All study designs, and therapy models, were eligible for inclusion in the review. We searched PubMed, PsycINFO, EThOS, ProQuest, conference abstracts and trial registries.

We found 65 studies that met criteria for inclusion in the review, 21 of which were randomised controlled trials (RCTs). The majority of studies evaluated cognitive–behavioural interventions. Quality was variable across all study types. The RCTs were mostly small (n<25 in the treatment arm), and many had methodological limitations including poorly described randomisation methods, inadequate allocation concealment and non-masked outcome assessments. We found studies used a wide range of different outcome measures, and relatively few studies reported affective symptoms or recovery-based outcomes. Many studies described adaptations to treatment delivery within in-patient settings, including increased frequency of sessions, briefer interventions and use of single-session formats.

Based on these findings, there is a clear need to improve methodological rigour within in-patient research. Interpretation of the current evidence base is challenging given the wide range of different therapies, outcome measures and models of delivery described in the literature.

None.

None.

Studies of light therapy have not been conducted previously in primary care.

To evaluate light therapy in primary care.

Fifty-seven participants with seasonal affective disorder were randomly allocated to 4 weeks of bright white or dim red light. Baseline expectations for treatment were assessed. Outcome was assessed with the Structured Interview Guide for the Hamilton Depression Scale, Seasonal Affective Disorder Version.

Both groups showed decreases in symptom scores of more than 40%. There were no differences in proportions of responders in either group, regardless of the remission criteria applied, with around 60% (74% white light, 57% red light) meeting broad criteria for response and 31% (30% white light, 33% red light) meeting strict criteria. There were no differences in treatment expectations.

Primary care patients with seasonal affective disorder improve after light therapy, but bright white light is not associated with greater improvements.

Identifying neurocognitive subtypes in schizophrenia may help establish neurobiologically meaningful subtypes of the disorder, but is frequently confounded by differences in intellectual function between individuals with schizophrenia and controls.

To examine neuropsychological performance in individuals with epidemiologically based, first-onset schizophrenia and intellectually matched controls.

Using standard IQ and reading tests, we examined the proportions of 101 people with epidemiologically derived, first-onset schizophrenia/schizoaffective disorder and 317 community controls, falling into three a priori defined intellectual categories: ‘stable good’, ‘deteriorated poor’ and ‘stable poor’. Neuropsychological function was compared between intellectually matched participants with schizophrenia and control subgroups.

Multiple deficits in executive function, processing speed and verbal memory, but not visual/spatial perception/memory, were detected in all participant groups with schizophrenia compared with controls. The average effect size across the affected domains ranged from small to medium to large in the stable good, deteriorated poor and stable poor subgroups of participants with schizophrenia, respectively.

Compared with intellectually matched controls, people with epidemiologically derived, first-onset schizophrenia/schizoaffective disorder show multiple deficits in executive function, processing speed and verbal memory.

It is unclear to what extent the traditional distinction between neurological and psychiatric disorders reflects biological differences.

To examine neuroimaging evidence for the distinction between neurological and psychiatric disorders.

We performed an activation likelihood estimation meta-analysis on voxel-based morphometry studies reporting decreased grey matter in 14 neurological and 10 psychiatric disorders, and compared the regional and network-level alterations for these two classes of disease. In addition, we estimated neuroanatomical heterogeneity within and between the two classes.

Basal ganglia, insula, sensorimotor and temporal cortex showed greater impairment in neurological disorders; whereas cingulate, medial frontal, superior frontal and occipital cortex showed greater impairment in psychiatric disorders. The two classes of disorders affected distinct functional networks. Similarity within classes was higher than between classes; furthermore, similarity within class was higher for neurological than psychiatric disorders.

From a neuroimaging perspective, neurological and psychiatric disorders represent two distinct classes of disorders.

A limited number of studies have demonstrated changes in cerebral blood flow (CBF) in older individuals with depression, but there are considerable inconsistencies between studies.

To investigate changes in CBF using arterial spin labelling (ASL) magnetic resonance imaging (MRI) in people with late-life depression and in a similarly aged healthy control group.

Sixty-eight participants (30 healthy individuals, 38 with depression) underwent ASL and T1-weighted MRI scanning. For each individual, regional estimates of separate grey and white matter CBF were obtained. Group differences in CBF and their associations with clinical features were examined.

Significant increases were observed in white matter CBF in patients with depression relative to the control group (F1,65 = 9.7, P = 0.003). Grey matter CBF in lateral frontal, medial frontal, cingulate, central and parietal regions did not significantly differ between groups (F1,65≤2.1, P≥0.2). A significant correlation was found between white matter CBF and Montgomery–Åsberg Depression Rating Scale (MADRS) scores in depression (r’ =–0.42, P = 0.03). Further analyses revealed that compared with controls, significant elevation of white matter CBF was apparent in participants whose depression was in remission (n = 21, MADRS≤10, P = 0.001) but not in those with current depression (n = 17, MADRS≥11, P = 0.80).

Findings suggest a compensatory response to white matter pathological change or a response to (or a predictor of) successful antidepressant treatment, perhaps by facilitating neurotransmission in specific circuits and so reducing depressive symptoms.

The Mental Health Act 1983 (MHA) is due to be revised by Parliament in the near future.

To explore changes in the use of the Act since its introduction.

The Department of Health and the Home Office routinely collect data on the numbers of patients admitted to psychiatric hospitals under the MHA. We present absolute figures, by year, for the total numbers admitted under each section of the Act. We used the total psychiatric hospital admissions and total prison populations as denominator data.

Formal admissions rose from 16 044 in 1984 to 26 308 in 1996, a 63% increase. Admissions under the MHA have increased as a proportion of all admissions. The increase is mainly accounted for by changes in the use of Part II of the Act, in particular sections 2 and 3. The use of forensic sections (Part III) has also increased, with a marked increase of sections 47 and 48. Use of Part X of the Act (sections 135 and 136) declined in the late 1980s but rose again in the 1990s.

Formal admissions are more common than they were in 1984, despite there being fewer psychiatric beds. This is probably due to changes in the provision of psychiatric services, and changing societal pressures on psychiatrists away from libertarianism and towards coercion.

After exposure to traumatic stressors, a subgroup of survivors (20–30%) will develop post-traumatic stress disorder (PTSD).

Since the incidence and prevalence rates for PTSD in the community are significant, it is important that general practitioners and psychiatrists be familiar with possible therapeutic options. In this review we shall look at the published evidence about the effectiveness of psychological treatments for PTSD.

The psychopathological mechanisms involved in PTSD are discussed. Studies of the effectiveness of different psychological therapies are reviewed.

The review suggests that persistent fear or shame reactions are key aspects of PTSD. Evidence from systematic reviews suggests that psychotherapeutic treatments are effective in the therapy of reactions based on fear, and may increase the effectiveness of pharmacological therapy. There is less systematic evidence for the efficacy of interventions for symptoms based on shame.

Although a proportion of patients with complex or chronic PTSD may require specialist interventions, most patients can be treated effectively by a general psychiatric service which can offer both pharmacological and psychological interventions.