This study aimed to test the validity of the 21-item Depression Anxiety Stress Scales (DASS-21) as a routine clinical outcome measure in the private in-patient setting. We hypothesized that it would be a suitable routine outcome instrument in this setting.

All in-patients treated at a private psychiatric hospital over a period of 24 months were included in the study. Data were collected on demographics, service utilization, diagnosis and a set of four routine measures both at admission and discharge. These measures consisted of the Clinical Global Impressions (CGI) scales, Health of the Nation Outcome Scales (HoNOS), the Mental Health Questionnaire (MHQ-14) and DASS-21. The results of these measures were compared.

Of 786 admissions in total, the number of fully completed (ie paired admission and discharge) data sets for the DASS-21 depression, anxiety and stress subscales were 337, 328 and 347, respectively. All subscales showed statistically significant reductions in mean scores from admission to discharge (P < 0.001) and were significantly correlated with all MHQ-14 subscales and significantly related to CGI scale categories. The total DASS-21 and total HoNOS scores were also significantly correlated.

The findings from the present study support the validity of DASS-21 as a routine clinical outcome measure in the private in-patient setting.

To provide a comprehensive review and evaluation of the psychological and neurophysiological literature pertaining to mindfulness meditation.

A search for papers in English was undertaken using PsycINFO (from 1804 onward), MedLine (from 1966 onward) and the Cochrane Library with the following search terms: Vipassana, Mindfulness, Meditation, Zen, Insight, EEG, ERP, fMRI, neuroimaging and intervention. In addition, retrieved papers and reports known to the authors were also reviewed for additional relevant literature.

Mindfulness-based therapeutic interventions appear to be effective in the treatment of depression, anxiety, psychosis, borderline personality disorder and suicidal/self-harm behaviour. Mindfulness meditation per se is effective in reducing substance use and recidivism rates in incarcerated populations but has not been specifically investigated in populations with psychiatric disorders. Electroencephalography research suggests increased alpha, theta and beta activity in frontal and posterior regions, some gamma band effects, with theta activity strongly related to level of experience of meditation; however, these findings have not been consistent. The few neuroimaging studies that have been conducted suggest volumetric and functional change in key brain regions.

Preliminary findings from treatment outcome studies provide support for the application of mindfulness-based interventions in the treatment of affective, anxiety and personality disorders. However, direct evidence for the effectiveness of mindfulness meditation per se in the treatment of psychiatric disorders is needed. Current neurophysiological and imaging research findings have identified neural changes in association with meditation and provide a potentially promising avenue for future research.

This paper reviews the magnetic resonance imaging (MRI) literature on the effects of prenatal alcohol exposure on the developing human brain.

A literature search was conducted through the following databases: PubMed, PsycINFO and Google Scholar. Combinations of the following search terms and keywords were used to identify relevant studies: ‘alcohol’, ‘fetal alcohol spectrum disorders’, ‘fetal alcohol syndrome’, ‘FAS’, ‘FASD’, ‘MRI’, ‘DTI’, ‘MRS’, ‘neuroimaging’, ‘children’ and ‘infants’.

A total of 64 relevant articles were identified across all modalities. Overall, studies reported smaller total brain volume as well as smaller volume of both the white and grey matter in specific cortical regions. The most consistently reported structural MRI findings were alterations in the shape and volume of the corpus callosum, as well as smaller volume in the basal ganglia and hippocampi. The most consistent finding from diffusion tensor imaging studies was lower fractional anisotropy in the corpus callosum. Proton magnetic resonance spectroscopy studies are few to date, but showed altered neurometabolic profiles in the frontal and parietal cortex, thalamus and dentate nuclei. Resting-state functional MRI studies reported reduced functional connectivity between cortical and deep grey matter structures.

There is a critical gap in the literature of MRI studies in alcohol-exposed children under 5 years of age across all MRI modalities. The dynamic nature of brain maturation and appreciation of the effects of alcohol exposure on the developing trajectory of the structural and functional network argue for the prioritisation of studies that include a longitudinal approach to understanding this spectrum of effects and potential therapeutic time points.

Inflammatory bowel disease (IBD) is a chronic relapsing and remitting disorder characterised by inflammation of the gastrointestinal tract. There is a growing consensus that IBD is associated with anxiety- and depression-related symptoms. Psychological symptoms appear to be more prevalent during active disease states with no difference in prevalence between Crohn’s disease and ulcerative colitis. Behavioural disturbances including anxiety- and depression-like symptoms have also been observed in animal models of IBD.

The likely mechanisms underlying the association are discussed with particular reference to communication between the gut and brain. The close bidirectional relationship known as the gut–brain axis includes neural, hormonal and immune communication links. Evidence is provided for a number of interacting factors including activation of the inflammatory response system in the brain, the hypothalamic–pituitary–adrenal axis, and brain areas implicated in altered behaviours, changes in blood brain barrier integrity, and an emerging role for gut microbiota and response to probiotics in IBD.

The impact of psychological stress in models of IBD remains somewhat conflicted, however, it is weighted in favour of stress or early stressful life events as risk factors in the development of IBD, stress-induced exacerbation of inflammation and relapse.

It is recommended that patients with IBD be screened for psychological disturbance and treated accordingly as intervention can improve quality of life and may reduce relapse rates.

Cognitive impairment is the most consistent neurological complication of acquired and degenerative brain disorders. Historically, most focus was on dementia but now has been broadened to include the important construct of mild cognitive impairment.

Systematic search and review of articles linked quality of life (QoL) and cognitive complications of neurological disorders. We excluded QoL in dementia.

Our search identified 249 publications. Most research examined patients with brain tumours, stroke, epilepsy, head injury, Huntington's disease, motor neuron disease, multiple sclerosis and Parkinson's disease. Results suggested that the majority of patients with epilepsy, motor neuron disease, multiple sclerosis, Parkinson's disease, stroke and head injury have subtle cognitive deficits early in their disease course. These cognitive complaints are often overlooked by clinicians. In many cases, the cognitive impairment is progressive but it can also be relapsing-remitting and in some cases reversible. Despite the importance of severe cognitive impairment in the form of dementia, there is now increasing recognition of a broad spectrum of impairment, including those with subclinical or mild cognitive impairment. Even mild cognitive difficulties can have functional and psychiatric consequences–especially when they are persistent and untreated. Specific cognitive deficits such an inattention, dysexecutive function and processing speed may affect a number of quality of life (QoL) domains. For example, cognitive impairment influences return to work, interpersonal relationships and leisure activities. In addition, fear of future cognitive decline may also impact upon QoL.

We recommend further development of simple tools to screen for cognitive impairments in each neurological condition. We also recommend that a thorough cognitive assessment should be a part of routine clinical practice in those caring for individuals with neurological disorders.

Background: The suggestion that the neurohormone oxytocin may have clinical application in the treatment of schizophrenia was first published in 1972. Since then, a considerable body of research on a variety of fronts – including several recent double-blind treatment trials – has buttressed these early reports, providing support for the assertion that the oxytocin system is a promising and novel therapeutic target for this devastating malady. Herein, we review the diverse, convergent lines of evidence supporting the therapeutic potential of oxytocin in psychotic illness.

Methods: We performed a systematic review of preclinical and clinical literature pertaining to oxytocin's role in schizophrenia.

Results: Multiple lines of evidence converge to support the antipsychotic potential of oxytocin. These include several animal models of schizophrenia, pharmacological studies examining the impact of antipsychotics on the oxytocin system, human trials in patients examining the aspects of the oxytocin system and several double-blind, placebo-controlled clinical treatment trials.

Conclusions: There exists considerable, convergent evidence that oxytocin has potential as a novel antipsychotic with a unique mechanism of action. Auspiciously, based on the few chronic trials to date, its safety profile and tolerability appear very good. That said, several critical clinical questions await investigation before widespread use is clinically warranted.

Oxidative stress is one of the suggested mechanisms in major depression.

To determine the oxidative and antioxidative status of plasma of patients with major depression and to investigate whether there is a relationship between the potency of oxidative stress and the severity of depression.

To determine the antioxidative status of plasma, total and individual antioxidant levels which are total antioxidant potential (TAOP), total protein, albumin, uric acid, vitamin C and total bilirubin were measured. To determine the oxidative status, total peroxide level of plasma was measured in patients with drug-free depressive patients and compared with those of controls. Per cent ratio of total peroxide to TAOP was evaluated as oxidative stress index (OSI).

Plasma TAOP and individual antioxidant levels were found to be lower in patients with depression than those of controls. On the contrary, the patients had high total plasma peroxide levels. OSI values of the patients were significantly higher than those of controls (P = 0.002), and a significant positive correlation between Hamilton Depression Rating Scale (HDRS) and OSI values was found (r = 0.54, P = 0.01).

The patients with major depression are exposed to oxidative stress, and OSI may be useful to reflect the severity of the disease.

Epilepsy is a chronic neurological disease characterised with seizures. The aetiology of the most generalised epilepsies cannot be explicitly determined and the seizures are pronounced to be genetically determined by disturbances of receptors in central nervous system. Besides, neurotransmitter distributions or other metabolic problems are supposed to involve in epileptogenesis. Lack of adequate data about pharmacological agents that have antiepileptogenic effects point to need of research on this field. Thus, in this review, inflammatory aspects of epileptogenesis has been focussed via considering several concepts like role of immune system, blood–brain barrier and antibody involvement in epileptogenesis.

We conducted an evidence-based review of the literatures in order to evaluate the possible participation of inflammatory processes to epileptogenesis and also, promising agents which are effective to these processes. We searched PubMed database up to November 2015 with no date restrictions.

In the present review, 163 appropriate articles were included. Obtained data suggests that inflammatory processes participate to epileptogenesis in several ways like affecting fibroblast growth factor-2 and tropomyosin receptor kinase B signalling pathways, detrimental proinflammatory pathways [such as the interleukin-1 beta (IL-1β)–interleukin-1 receptor type 1 (IL-1R1) system], mammalian target of rapamycin pathway, microglial activities, release of glial inflammatory proteins (such as macrophage inflammatory protein, interleukin 6, C–C motif ligand 2 and IL-1β), adhesion molecules that are suggested to function in signalling pathways between neurons and microglia and also linkage between these molecules and proinflammatory cytokines.

The literature research indicated that inflammation is a part of epileptogenesis. For this reason, further studies are necessary for assessing agents that will be effective in clinical use for therapeutic treatment of epileptogenesis.

A view that handedness is not a dichotomous, i.e. left–right, phenomenon is shared by majority of researchers. However, there are different opinions about the exact number of hand-preference categories and criteria that should be used for their classification.

This study examined hand-preference categories using the latent class analysis (LCA) and validated them against two external criteria (i.e. hand demonstration test and a series of arbitrary cut-off points).

The Edinburgh Handedness Inventory was applied to 354 individuals randomly selected from the general population, and the obtained data were analysed using the LatentGOLD software.

Three discrete hand-preference clusters were identified, i.e. left-, right- and mixed-handed category. Further subdivision of hand-preference clusters resulted in a non-parsimonious subcategorization of individuals. There was a good agreement between the LCA-based classification and classification based on hand-preference demonstration tests. The highest agreement between the LCA model and the different types of arbitrary classification criteria ranged between 0 ± 50 and 0 ± 70 of the laterality quotient.

The study findings supported the view that handedness is not a bimodal phenomenon. However, definitions and subcategorizations of mixed-handedness using the cut-off points that are outside of the recommended range may lead to misclassification of cases. It is hoped that the categorization and validation of handedness developed in the context of this study will make future research in this area less dependent on arbitrary values and criteria.

We undertook a non-targeted lipidomics analysis of post-mortem cerebrospinal fluid (CSF), frontal cortex grey matter, and subjacent white matter to define potential biomarkers that distinguish cognitively intact subjects from those with incipient or established dementia. Our objective was to increase our understanding of the role of brain lipids in pathophysiology of aging and age-related cognitive impairment.

Levels of 650 individual lipids, across 26 lipid subclasses, were measured utilising a high-resolution mass spectrometric analysis platform.

Monoacylglycerols (MAG), diacylglycerols (DAG), and the very-long-chain fatty acid 26:0 were elevated in the grey matter of the mild cognitive impairment (MCI) and old dementia (OD) cohorts. Ethanolamine plasmalogens (PlsEtn) were decreased in the grey matter of the young dementia (YD) and OD cohorts while and phosphatidylethanolamines (PtdEth) were lower in the MCI, YD and OD cohorts. In the white matter, decrements in sulphatide levels were detected in the YD group, DAG levels were elevated in the MCI group, and MAG levels were increased in the YD and OD groups.

The parallel changes in grey matter MAGs and DAGs in the MCI and OD groups suggest that these two cohorts may have a similar underlying pathophysiology; consistent with this, MCI subjects were more similar in age to OD than to YD subjects. While PlsEtn and phosphatidylethanolamine were decreased in the YD and OD groups they were unaltered in the MCI group indicating that alterations in plasmalogen synthesis are unlikely to represent an initiating event in the transition from MCI to dementia.

One of the main utilities of staging in bipolar disorder is enhancing the formulation of pharmacological and non-pharmacological treatment strategies. Hence, it is essential to ascertain whether the number of previous episodes influences treatment response. Hereby, we present a 5-year post hoc study on the efficacy of group psychoeducation for bipolar disorders according to the number of previous episodes.

For this subanalysis, we have compared the 5-year outcome of 120 euthymic psychoeducated versus non-psychoeducated bipolar patients according to the number of previous episodes at study entry.

Patients with more than seven episodes at study entry did not show any significant improvement with psychoeducation according to time to recurrence. Patients with more than 14 episodes did not benefit from psychoeducation in terms of a reduction of time spent ill. Patients with 7 or 8 episodes showed a benefit in terms of fewer days spent in hypomania, depression, mixed episodes or any episodes but not mania, while patients with 9–14 episodes showed a benefit in terms of fewer days spent in hypomania and depression but not in mixed states or mania. Only patients who presented up to 6 episodes showed reduction in time spent in any episode polarity.

The number of previous episodes clearly worsens response to psychoeducation, perhaps in a more subtle way than that observed with other psychological therapies. Psychoeducation should be delivered as soon as possible in the illness course, supporting the idea of early intervention.

Impaired social functioning and autistic symptoms are characteristics of schizophrenia. The social hormones oxytocin (OT) and arginine-vasopressin (AVP) both modulate social interaction and therefore may be involved in the pathogenesis of schizophrenia. We investigated whether men with schizophrenia show altered OT and AVP levels compared with healthy controls (HC) and whether autism symptoms are associated with OT levels.

Forty-one men with non-acute schizophrenia and 45 matched HC were enroled. Schizophrenia was assessed with the Positive and Negative Syndrome Scale (PANSS). Blood samples were collected on 2 days, and plasma OT and AVP levels were measured by ELISA immunoassay.

The schizophrenia patients had significantly lower plasma OT levels than the HC; a similar trend was found for AVP. Plasma OT levels were associated with severe life events, fewer important attached persons, and a higher score on the PANSS negative scale; the most dominant PANSS items were ‘preoccupation’, ‘emotional withdrawal’, and ‘passive/apathetic social withdrawal’.

These findings support an association between the social hormones OT and AVP and schizophrenia. We suggest that OT metabolism may be altered in schizophrenia, but other possible causes for decreased plasma OT levels in schizophrenia patients include decreased OT synthesis, mRNA expression, and translation. Especially the ‘autistic’ symptoms of schizophrenia seem to be closely linked to an altered metabolism of OT, the ‘attachment’ hormone.

The aim of the current study was to examine whether and to what extent mood disorders, comprising major depression and bipolar disorder, are accompanied by structural changes in the brain as measured using voxel-based morphometry (VBM).

We performed a VBM study using a 3Т MRI system (GE Discovery 750w) in patients with mood disorders (n=50), namely, 39 with major depression and 11 with bipolar disorder compared to 42 age-, sex- and education-matched healthy controls.

Our results show that depression was associated with significant decreases in grey matter (GM) volume of the regions located within the medial frontal and anterior cingulate cortex on the left side and middle frontal gyrus, medial orbital gyrus, inferior frontal gyrus (triangular and orbital parts) and middle temporal gyrus (extending to the superior temporal gyrus) on the right side. When the patient group was separated into bipolar disorder and major depression, the reductions remained significant only for patients with major depressive disorder.

Using VBM the present study was able to replicate decreases in GM volume restricted to frontal and temporal regions in patients with mood disorders, mainly major depression, compared with healthy controls.

Depression and pain are both burdensome ailments that affect a major proportion of the population. It is evident that depression and pain frequently coexist, with treatment and outcome implications.

To review the literature on the nature, prevalence and co-morbidity of depression and pain, the biological and psychological mechanisms involved and treatment options, thus presenting a broad overview of the current information available.

Relevant sources were identified from PubMed and Medline databases using a combination of keywords including depression, pain, prevalence, co-morbidity, biological and psychological mechanisms, serotonin (5-HT), norepinephrine (NE), hypothalamic-pituitary-adrenal (HPA) axis, amygdala, functional magnetic resonance imaging (fMRI), antidepressant and psychological therapy.

It is evident from the research that depression and pain are common co-morbidities. Pain as a physical symptom of depression affects approximately 65% of patients, leading to less favourable outcomes and greater health care utilization. Moreover, depression is a common feature in chronic pain patients and can affect pain threshold and tolerance. Evidence from biological and psychological studies has revealed mechanisms that link chronic pain to depression. Several classes of anti-depressants and psychological interventions have been used successfully in the treatment of somatic symptoms of depression and for a variety of pain syndromes.

Pain and depression are linked by overlapping phenomenology, neurobiology and therapy. They are mutually interacting, and the interaction has significant treatment and outcome implications.

Although monoaminergic-targeted drugs have prompted great advances in the development of treatments for depression, the need for new options persists, since these drugs still have a delayed clinical effect and most patients do not respond properly to them. Recently, the observation of the antidepressant effects of ketamine brought on a new wave of studies regarding the comprehension of the neurobiology of depression and the development of new and more effective antidepressant drugs.

Thus, in this paper, we present a historical review of the development of monoaminergic antidepressant drugs and the role of ketamine as the introductory agent of a new era in the research of the neurobiology of depression.

Firstly, we review how the pharmacological treatment for major depression started, and we point out the main drugs discovered, the researchers involved, and how the studies developed have contributed to the understanding of the neurobiology of depression. Secondly, the major problems regarding the clinical efficacy and acceptance of these drugs are discussed, and the introduction of the glutamatergic system as a target for antidepressant drugs is presented. Finally, we review how ketamine revealed itself as an exciting option towards obtaining pharmacological agents to treat depression, through the understanding of biological markers.

Ketamine contributed to confirm that different targets of the glutamatergic system and neurotrophic pathways are strictly related to the neurobiology of depression. There are several antidepressant drugs based on ketamine’s mechanism of action already in the pipeline, and glutamatergic-targeted antidepressants may be on the market in the near future.

Gut microbiota (GM) has previously been associated with alterations in rodent behaviour, and since the GM is affected by the diet, the composition of the diet may be an important factor contributing to behavioural changes. Interestingly, a magnesium restricted diet has been shown to induce anxiety and depressive-like behaviour in humans and rodents, and it could be suggested that magnesium deficiency may mediate the effects through an altered GM.

The present study therefore fed C57BL/6 mice with a standard diet or a magnesium deficient diet (MgD) for 6 weeks, followed by behavioural testing in the forced swim test (FST) to evaluate depressive-like behaviour. An intraperitoneal glucose tolerance test (GTT) was performed 2 day after the FST to assess metabolic alterations. Neuroinflammatory markers were analysed from hippocampus. GM composition was analysed and correlated to the behaviour and hippocampal markers.

It was found that mice exposed to MgD for 6 weeks were more immobile than control mice in the FST, suggesting an increased depressive-like behaviour. No significant difference was detected in the GTT. GM composition correlated positively with the behaviour of undisturbed C57BL/6 mice, feeding MgD diet altered the microbial composition. The altered GM correlated positively to the hippocampal interleukin-6.

In conclusion, we hypothesise that imbalances of the microbiota–gut–brain axis induced by consuming a MgD diet, contributes to the development of depressive-like behaviour.