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.

l-theanine, an amino acid uniquely contained in green tea (Camellia sinensis), has been suggested to have various psychotropic effects. This study aimed to examine whether l-theanine is effective for patients with major depressive disorder (MDD) in an open-label clinical trial.

Subjects were 20 patients with MDD (four males; mean age: 41.0±14.1 years, 16 females; 42.9±12.0 years). l-theanine (250 mg/day) was added to the current medication of each participant for 8 weeks. Symptoms and cognitive functions were assessed at baseline, 4, and 8 weeks after l-theanine administration by the 21-item version of the Hamilton Depression Rating Scale (HAMD-21), State-Trait Anxiety Inventory (STAI), Pittsburgh Sleep Quality Index (PSQI), Stroop test, and Brief Assessment of Cognition in Schizophrenia (BACS).

HAMD-21 score was reduced after l-theanine administration (p=0.007). This reduction was observed in unremitted patients (HAMD-21>7; p=0.004) at baseline. Anxiety-trait scores decreased after l-theanine administration (p=0.012) in the STAI test. PSQI scores also decreased after l-theanine administration (p=0.030) in the unremitted patients at baseline. Regarding cognitive functions, response latency (p=0.001) and error rate (p=0.036) decreased in the Stroop test, and verbal memory (p=0.005) and executive function (p=0.016) were enhanced in the BACS test after l-theanine administration.

Our study suggests that chronic (8-week) l-theanine administration is safe and has multiple beneficial effects on depressive symptoms, anxiety, sleep disturbance and cognitive impairments in patients with MDD. However, since this is an open-label study, placebo-controlled studies are required to consolidate the effects.

The purpose of this study was to investigate deficient inhibitory control in individuals with pathological Internet use (PIU) using a visual go/no-go task by event-related potentials (ERPs).

Subjects were 26 individuals with PIU and 26 controls. Barratt Impulsiveness Scale-11 (BIS-11) was used for measures of impulsivity. A go/no-go task involved eight different two-digit numerical stimuli. The response window was 1000 ms and the inter-trial-interval (ITI) was 1500 ms. Electroencephalography (EEG) was recorded when participants performed the task. Brain electrical source analysis (BESA) 5.2.0 was used to perform data analysis and the no-go N2 amplitude was analysed for investigation of inhibitory control.

BIS-11 total scores, attentional key and motor key scores in PIU group were higher than that of the control group. In the go/no-go task, false alarm rate of PIU group was higher, and hit rate was lower than that of the control group. A repeated measure ANOVA revealed a significant group, frontal electrode sites and group × frontal electrode sites main effect for N2 amplitudes of no-go conditions (for group: F = 3953, df = 1, p = 0.000; for frontal electrode sites: F = 541, df = 9, p = 0.000; for group × frontal electrode sites: F = 306, df = 9, p = 0.000), and a significant group, central electrode sites and group × central electrode sites main effect for N2 amplitudes of no-go conditions (for group: F = 9074, df = 1, p = 0.000; for central electrode sites: F = 163, df = 2, p = 0.000; for group × central electrode sites: F = 73, df = 2, p = 0.000). N2 amplitudes of no-go conditions were lower than those at control group.

Individuals with PIU were more impulsive than controls and shared neuropsychological and ERPs characteristics of compulsive-impulsive spectrum disorder, which supports that PIU is an impulse disorder or at least related to impulse control disorder.

Psychopathological, neuropsychological and genetic findings indicate an association between ASD Spectrum Disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). The goal of this study was to compare the neuropsychological profiles of attention functions in children with ADHD and with ASD and without comorbid ADHD. The hypothesis was that either ADHD and autistic children with comorbid ADHD symptoms were more impaired in inhibition and sustained attention performance and that all individuals with ASD show more deficits in divided attention.

Children aged 6 to 18 years old with ADHD (n = 30) or ASD with (n = 21) and without comorbid ADHD (n = 20) and 30 healthy children were included consecutively. Psychopathology was evaluated using the KIDDIE-SADS and symptom checklists for ADHD and ASD according to DSM-IV. Assessed neuropsychological functioning included inhibition, sustained as well as divided attention and alertness tasks.

Age and IQ-corrected z-scores were used. Statistically significant group effects were found for the variables sustained attention median (F = 3.2, = .02), hits (F = 3.3, p = .02) and false alarms (F = 3.9, p = .01), divided attention hits (F = 3.3, p = .02), errors (F = 3.1, p = .03) and false alarms (F = 3.3, p = .03) and alertness false alarms (F = 2.9, p = .04). Pearson Correlations revealed associations between ADHD symptoms and sustained attention in the ADHD group and between ADHD symptoms and inhibition in the ASD+ group.

Our hypothesis was partly confirmed as ADHD children showed more deficits in sustained attention and ASD children in divided attention tasks. However there was no evidence that children with ASD and comorbid ADHD symptoms have a specific profile in comparison to pure ASD children.

Depression may be difficult to treat and with comorbid diabetes mellitus (DM) it is an even bigger challenge. This article aims to evaluate antidepressants most suitable for patients with depression and comorbid DM.

Initially we searched for randomised, controlled double-blind trials of treatment with antidepressants in depressed with DM but there were only a few studies and many of them were small trials. Thus, we decided to include studies that were not only randomised-controlled trials. In total, we ended up with 18 articles for our purposes.

The combination of depression and DM may be harmful as depression has a strong impact on psychosocial and medical outcomes in patients with DM. Almost all of the trials in this review showed a reduction in depressive symptoms after treatment with an antidepressant in the acute as well as during maintenance phase. It showed that depression improvement had a favourable effect on glycaemic control that was weight independent. Some studies included only subjects with minor depression or with suboptimal-controlled diabetes making it difficult to show an effect.

From these data, we will recommend choosing an selective serotonin reuptake inhibitor (SSRI) if possible to treat a depression among patients with diabetes. If treatment with a tricyclic antidepressant is needed, closer glycaemic monitoring is recommended. Bear in mind that there is a possible risk of hypoglycemia when using SSRIs. Agomelatine and bupropion have shown promising results, but need to be investigated in more trials.

Deep brain stimulation (DBS) was approved by Food and Drug Administration for Parkinson’s disease, essential tremor, primary generalised or segmental dystonia and obsessive-compulsive disorder (OCD) treatment. The exact mechanism of DBS remains unclear which causes side effects. The aim of this review was to assess variables causing stimulation-induced chronic psychiatric/personality-changing side effects.

The analysis of scientific database (PubMed, Cochrane Library, EMBASE) was conducted. The included articles had to be research study or case report and DBS to be conducted in therapeutic purposes. The researches with mental disorders in patients’ medical histories were excluded.

Seventeen articles were used in the review. In the group of movement disorders the characteristic of side effects was strongly related to the placement of the electrode implantation. Tiredness/fatigue was correlated with DBS in thalamus. Implantations in subthalamic nucleus were mostly followed by affective side effects such as depression or suicide. The higher voltage of electrode was connected with more severe depression after implantation. The analysis of affective disorder contained only three articles – two about OCD and one about depression. Forgetfulness and word-finding problems as activities connected with cognition may be an inevitable side effect if obsessive thoughts are to be inhibited.

DBS of subthalamic nucleus should be seen as the most hazardous place of implantation. As a result there is a strong need of ‘gold standards’ based on the connectivity research and closer cooperation of scientists and clinicians.

The United Nations, WHO and the World Bank have called the current prevalence rate of neuro-psychiatric disorder approaches of 1 in 4 individuals worldwide and ‘unheralded public health crisis’. Rates are driven by an early onset, high impairment and high chronicity of these disorders. Most importantly, detection and treatment rates are low, estimated at les than 10% worldwide resulting in 500 million people underserved. The related economic costs soared in 1999 to 120 billion dollars in Europe and North America, with over 60 billion dollars assigned to stress related disorders. Contributing factors are bio-psycho-social and include rapid social change as well as the time compression of modern life resulting in the experience of increased work-life stress that parallels a decade long intensification of activities in the workplace. Coping with the requirements of the new economy of mental performance has lagged behind at many individual and social levels as we cling to adjustments made during the industrial economy of the last century. A climate of transition, and more recently, terror and fear have stressed the landscape of mental health and work already ravaged by the destructive forces of stigma.

This presentation will examine the other side of prosperity from the point of view of stress in the workplace as two global problems converge at this time in history, the escalation of neuro-psychiatric disorders and the increasing dependence on the mental faculties of the world's citizens.

In this paper we also discuss how the international community can work together to help reduce the burden of mental disorders worldwide and sketch the implications for research and policy.

Ultimately the media will need to be enlisted to educate the public on the value of investments in mental health.

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.

Objective: Alexithymia refers to an ineffective regulation and expression of emotions. It constitutes a major risk factor for a range of medical and psychiatric problems, including chronic pain, somatisation, anxiety and depression. Alexithymia is a multi-faceted concept, described in terms of cognitive and affective aspects. From a neuropsychological perspective, alexithymia can be defined as a disturbance in affective information processing and social cognition. As the growing literature on brain structures involved in alexithymia is fragmented and sometimes even contradictory, the aim of this article was to review findings on neural substrates with regard to their convergence.

Methods: A narrative review was performed, including both early neuropsychological and more recent imaging studies, in order to achieve a better understanding of the aetiology of alexithymia.

Results: Corpus callosum, cingulate cortex and insula are clearly involved in alexithymia. The amygdala and the orbitofrontal part of the cortex appear to be implicated as mediators, because of their broader involvement in emotional processing and executive control.

Conclusion: Notwithstanding the diffuse neural representation, the alexithymia construct can be usefully applied in the clinical and empirical studies of social cognition, particularly when adopting a dimensional neuropsychological approach.

Fluid intelligence (Gf) has been related to executive functioning (EF) in previous studies, and it is also known to be correlated with crystallized intelligence (Gc). The present study includes representative measures of Gf, Gc, and EF frequently used in clinical practice to examine this Gf–EF relation. It is hypothesised that the Gf–EF relation is higher than the Gc–EF relation, and that working memory in particular (as a measure of EF) shows a high contribution to this relation.

Confirmatory factor analysis was performed on a mixed neuropsychiatric and non-clinical sample consisting of 188 participants, using the Kaufman Adolescent and Adult Intelligence Test, and three executive tasks of the Cambridge Neuropsychological Test Automated Battery, covering working memory, planning skills, and set shifting.

The model fitted the data well [χ2(24)=35.25, p=0.07, RMSEA=0.050]. A very high correlation between Gf and EF was found (0.91), with working memory being the most profound indicator. A moderate to high correlation between Gc and EF was present. Current results are consistent with findings of a strong relation between Gf and working memory.

Gf and EF are highly correlated. Gf dysfunction in neuropsychiatric patients warrants further EF examination and vice versa. It is discussed that results confirm the need to distinguish between specific versus general fluid/executive functioning, the latter being more involved when task complexity and novelty increase. This distinction can provide a more refined differential diagnosis and improve neuropsychiatric treatment indication.

Objective: The mechanisms involved in the dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, especially in the functioning of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) in depressed patients, are not well elucidated. The objective of this study was to conduct a systematic review of articles that assess the HPA axis activity from GR and MR in depressed patients and healthy controls with or without early life stress.

Methods: We conducted a systematic review of articles in PubMed, SCOPUS and SciELO published between 2000 and 2011, using the following search terms: child abuse, depression, HPA axis, dexamethasone, prednisolone, fludrocortisone and spironolactone. Thirty-four papers were selected for this review.

Results: Most studies identified in this review used the dexamethasone/corticotropin-releasing hormone test and dexamethasone suppression test. In these studies, hypercortisolaemia was associated with depression. We identified three studies with the Prednisolone suppression test, only one study with the use of fludrocortisone and one with spironolactone. This review found nine studies that evaluated the HPA axis in individuals with early life stress.

Conclusions: The majority of the studies assessed in this review show that early life stress leads to permanent changes in the HPA axis and may lead to development of depression in adults. The most consistent findings in the literature show increased activity of the HPA axis in depression associated with hypercortisolaemia and reduced inhibitory feedback. These findings suggest that this dysregulation of the HPA axis is partially attributable to an imbalance between GR and MR. Evidences have consistently showed that GR function is impaired in major depression, but few studies have assessed the activity of MR in depression and early life stress.

Background: Yoga therapy (YT) improves cognitive function in healthy individuals, but its impact on cognitive function among persons with schizophrenia (SZ) has not been investigated.

Objective: To evaluate the adjunctive YT for cognitive domains impaired in SZ.

Methods: Patients with SZ received YT or treatment as usual (TAU; n = 65, n = 23, respectively). Accuracy and speed for seven cognitive domains were assessed using a computerised neurocognitive battery (CNB), thus minimising observer bias. Separately, YT was evaluated among patients with bipolar I disorder (n = 40), major depressive disorder (n = 37) and cardiology outpatients (n = 68). All patients also received routine pharmacotherapy. Patients were not randomised to YT or TAU.

Results: In comparison with the SZ/TAU group, the SZ/YT group showed significantly greater improvement with regard to measures of attention following corrections for multiple comparisons; the changes were more prominent among the men. In the other diagnostic groups, differing patterns of improvements were noted with small-to-medium effect sizes.

Conclusions: Our initial analyses suggest nominally significant improvement in cognitive function in SZ with adjunctive therapies such as YT. The magnitude of the change varies by cognitive domain and may also vary by diagnostic group.

This study aims to document the nature and progression of spontaneous speech impairment suffered by patients with Alzheimer's disease (AD) over a 12-month period, using both cross-sectional and prospective longitudinal design.

Thirty one mild–moderate AD patients and 30 controls matched for age and socio-cultural background completed a simple and complex oral description task at baseline. The AD patients then underwent follow-up assessments at 6 and 12 months.

Cross-sectional comparisons indicated that mild–moderate AD patients produced more word-finding delays (WFDs) and empty and indefinite phrases, while producing fewer pictorial themes, repairing fewer errors, responding to fewer WFDs, produce shorter and less complex phrases and produce speech with less intonational contour than controls. However, the two groups could not be distinguished on the basis of phonological paraphasias. Longitudinal follow-up, however, suggested that phonological processing deteriorates over time, where the prevalence of phonological errors increased over 12 months.

Consistent with findings from neuropsychological, neuropathological and neuroimaging studies, the language deterioration shown by the AD patients shows a pattern of impairment dominated by semantic errors, which is later joined by a disruption in the phonological aspects of speech.

Caloric vestibular stimulation (CVS) has traditionally been used as a tool for neurological diagnosis. More recently, however, it has been applied to a range of phenomena within the cognitive neurosciences. Here, we provide an overview of such studies and review our work using CVS to investigate the neural mechanisms of a visual phenomenon – binocular rivalry. We outline the interhemispheric switch model of rivalry supported by this work and its extension to a metarivalry model of interocular-grouping phenomena. In addition, studies showing a slow rate of binocular rivalry in bipolar disorder are discussed, and the relationship between this finding and the interhemispheric switch model is described. We also review the effects of CVS in various clinical contexts, explain how the technique is performed and discuss methodological issues in its application.

A review of CVS and related literature was conducted.

Despite CVS being employed with surprising effect in a wide variety of cognitive and clinical contexts, it has been a largely underutilized brain stimulation method for both exploratory and therapeutic purposes. This is particularly so given that it is well tolerated, safe, inexpensive and easy to administer.

CVS can be used to investigate various cognitive phenomena including perceptual rivalry, attention and mood, as well as somatosensory representation, belief, hemispheric laterality and pain. The technique can also be used to investigate clinical conditions related to these phenomena and may indeed have therapeutic utility, especially with respect to postlesional disorders, mania, depression and chronic pain states. Furthermore, we propose that based on existing reports of the phenomenological effects of CVS and the brain regions it is known to activate, the technique could be used to investigate and potentially treat a range of other clinical disorders. Finally, the effects of CVS (and its potential effects) on several phenomena of interest to philosophy suggest that it is also likely to become a useful tool in experimental neurophilosophy.

Although cognitive behavioural therapy (CBT) has been shown to be an effective treatment for depression, the biological mechanisms underpinning it are less clear. This review examines if it is associated with changes identifiable with current brain imaging technologies.

To better understand the mechanisms by which CBT exerts its effects, we undertook a systematic review of studies examining brain imaging changes associated with CBT treatment of depression.

Ten studies were identified, five applying functional magnetic resonance imaging, three positron emission tomography, one single photon emission computer tomography, and one magnetic resonance spectroscopy. No studies used structural MRI. Eight studies included a comparator group; in only one of these studies was there randomised allocation to another treatment. CBT-associated changes were most commonly observed in the anterior cingulate cortex (ACC), posterior cingulate, ventromedial prefrontal cortex/orbitofrontal cortex (VMPFC/OFC) and amygdala/hippocampus.

The evidence, such as it is, suggests resting state activity in the dorsal ACC is decreased by CBT. It has previously been suggested that treatment with CBT may result in increased efficiency of a putative ‘dorsal cognitive circuit’, important in cognitive control and effortful regulation of emotion. It is speculated this results in an increased capacity for ‘top-down’ emotion regulation, which is employed when skills taught in CBT are engaged. Though changes in activity of the dorsal ACC could be seen as in-keeping with this model, the data are currently insufficient to make definitive statements about how CBT exerts its effects. Data do support the contention that CBT is associated with biological brain changes detectable with current imaging technologies.

Yoga and physical exercise have been used as adjunctive intervention for cognitive dysfunction in schizophrenia (SZ), but controlled comparisons are lacking.

A single-blind randomised controlled trial was designed to evaluate whether yoga training or physical exercise training enhance cognitive functions in SZ, based on a prior pilot study.

Consenting, clinically stable, adult outpatients with SZ (n=286) completed baseline assessments and were randomised to treatment as usual (TAU), supervised yoga training with TAU (YT) or supervised physical exercise training with TAU (PE). Based on the pilot study, the primary outcome measure was speed index for the cognitive domain of ‘attention’ in the Penn computerised neurocognitive battery. Using mixed models and contrasts, cognitive functions at baseline, 21 days (end of training), 3 and 6 months post-training were evaluated with intention-to-treat paradigm.

Speed index of attention domain in the YT group showed greater improvement than PE at 6 months follow-up (p<0.036, effect size 0.51). In the PE group, ‘accuracy index of attention domain showed greater improvement than TAU alone at 6-month follow-up (p<0.025, effect size 0.61). For several other cognitive domains, significant improvements were observed with YT or PE compared with TAU alone (p<0.05, effect sizes 0.30–1.97).

Both YT and PE improved attention and additional cognitive domains well past the training period, supporting our prior reported beneficial effect of YT on speed index of attention domain. As adjuncts, YT or PE can benefit individuals with SZ.

Although alterations in the dendritic spine density in the brain regions may play a role in the stress-induced depression-like phenotype, the precise mechanisms are unknown. The aim was to investigate the role of spine density in the brain regions after chronic social defeat stress (CSDS).

We examined dendritic spine density in the medial prefrontal cortex (mPFC), CA1, CA3, dentate gyrus (DG) of hippocampus, nucleus accumbens (NAc), and ventral tegmental area (VTA) of susceptible and resilient mice after CSDS.

Spine density in the prelimbic area of mPFC, CA3, and DG in the susceptible group, but not resilient group, was significantly lower than control group. In contrast, spine density in the NAc and VTA in the susceptible group, but not resilient group, was significantly higher than control group.

The results suggest that regional differences in spine density may contribute to resilience versus susceptibility in mice subjected to CSDS.