Psychological factors contribute to bipolar disorder illness course, representing targets for psychological intervention. Research to date has focused on bipolar I disorder, extrapolating results to bipolar II disorder. The current study addresses this discrepancy by exploring cognitive and coping styles in patients diagnosed with bipolar I or II disorder.

Participants were recruited from the Sydney-based Black Dog Institute. Diagnoses were derived via the MINI International Neuropsychiatric Interview. Baseline cognitive and coping style measures were completed, and mood symptoms assessed over a 6-month period. Clinician-rated mood status was assessed at follow-up to determine the predictive utility of cognitive and coping styles.

The follow-up sample comprised 151 participants. Differential relationships between cognitive style, coping styles and mood symptoms emerged across the bipolar sub-types. Some key differences were that a broader set of negative cognitive styles were associated with bipolar II depression symptoms; while few relationships were observed between coping styles and bipolar II symptoms.

Differences in cognitive and coping style relationships with symptom expression across bipolar I and II disorder may provide clinicians with fruitful guides for directing treatment interventions when relevant maladaptive styles are observed. Further exploration of differences in cognitive and coping styles in bipolar I and II disorder is warranted.

Here, we examined the cingulum bundle, a long-range white matter tract mediating dorsal limbic connectivity, using diffusion tensor imaging (DTI) tractography, in children and adolescents with autism spectrum disorder (ASD) versus controls. We hypothesised that cingulum bundle microstructure would be altered in ASD, based on evidence implicating abnormal white matter connectivity in this disorder.

DTI data were acquired for 19 ASD participants (IQ ⩾ 70; 7–18 years; mean = 12.4 ± 3.1) and 16 age-matched controls (7–18 years; mean = 12.3 ± 3.6) on a 3 T magnetic resonance imaging system. Deterministic tractography was used to isolate the cingulum bundle. Left and right cingulum bundles were examined for differences in several DTI metrics in ASD children/adolescents versus controls, including: fractional anisotropy (FA), mean, axial, and radial diffusivity.

Significant age × group interaction effects were found for all DTI metrics (mean diffusivity: F1,28 = 9.5, p = 0.005, radial diffusivity: F1,28 = 7.8, p = 0.009, axial diffusivity: F1,28 = 5.2, p = 0.03, FA: F1,28 = 4.4, p = 0.04). Interaction effects were driven by increases in cingulum bundle diffusivity (mean, radial, and axial diffusivity), and decreased FA, in younger ASD participants within our sample versus controls.

Our results point to immature microstructural organisation of the cingulum bundle in ASD, particularly during the early years of life, with implications for limbic network synchronisation and complex socio-emotional performance.

This study aimed to explore effects of adjunctive N-acetylcysteine (NAC) treatment on inflammatory and neurogenesis markers in unipolar depression.

We embarked on a 12-week clinical trial of NAC (2000 mg/day compared with placebo) as an adjunctive treatment for unipolar depression. A follow-up visit was conducted 4 weeks following the completion of treatment. We collected serum samples at baseline and the end of the treatment phase (week 12) to determine changes in interleukin-6 (IL6), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following NAC treatment.

NAC treatment significantly improved depressive symptoms on the Montgomery–Asberg Depression Rating Scale (MADRS) over 16 weeks of the trial. Serum levels of IL6 were associated with reductions of MADRS scores independent of treatment response. However, we found no significant changes in IL6, CRP and BDNF levels following NAC treatment.

Overall, this suggests that our results failed to support the hypothesis that IL6, CRP and BDNF are directly involved in the therapeutic mechanism of NAC in depression. IL6 may be a useful marker for future exploration of treatment response.

This study investigated immersive virtual reality (IVR), as a novel technique to test executive function of healthy younger and older adults. We predicted IVR tasks to have greater predictive power than traditional measures when assessing age-related cognitive functioning due to the real-world validity of the tasks.

Participants (n=40) completed the Stroop colour–word test and the trail-making test (TMT) as traditional and commonly used assessments of executive functioning. Participants then completed three IVR tasks; a seating arrangement task, an item location task (both set in a virtual chemistry lab), and a virtual parking simulator.

Younger adults completed significantly more parking simulator levels (p<0.001), placed significantly more objects (p<0.001), and located significantly more items than older adults (p<0.01), demonstrating higher levels of performance. Significant correlations were found between performance on traditional neuropsychological measures and IVR measures. For example, Stroop CW performance significantly correlated with the number of parking simulator levels completed (τ=0.43, p<0.01). This suggests that IVR measures assess the same underlying cognitive constructs as traditional tasks. In addition, IVR measures contributed a significant percentage of the explained variance in age.

IVR measures (i.e. number of parking simulator levels completed and number of objects placed in the seating arrangement task) were found to be stronger contributors than existing traditional neuropsychological tasks in predicting age-related cognitive decline. Future research should investigate the implementation of these real-world-based tasks in clinical groups given this promising initial work.

Pain perception is reported to be altered in patients with depression and schizophrenia. However, few studies have investigated the pain perception in patients with bipolar disorders. We therefore aimed to compare pain sensitivity between patients with bipolar disorder, schizophrenia and controls.

Study groups consisted of 30 patients with bipolar disorder, and control groups consisted of 27 patients with schizophrenia and 59 healthy subjects. Pain perception was assessed with cold pressor test (CPT) by exposure to ice-water.

Patients with schizophrenia had significantly higher pain thresholds (PTh) than patients with bipolar disorder. There were no differences between the PTh of patients with schizophrenia and healthy control subjects. However, patients with bipolar disorder had significantly lower pain tolerance (PT) in the CPT than patients with schizophrenia and corresponding healthy control subjects.

The higher PTh in the schizophrenia group compared with the bipolar group found in this study supports further investigation of a potential difference in the pain perception between patients with schizophrenia and bipolar disorder. Theoretical implications of these findings and possible relevant behavioural and neurochemical mechanisms are discussed.

Emotion regulation involves the initiation of new emotional responses and continual alteration of current emotions in response to rapidly changing environmental and social stimuli. The capacity to effectively implement emotion regulation strategies is essential for psychological health; impairments in the ability to regulate emotions may be critical to the development of clinical levels of depression, anxiety and mania.

This review provides a summary of findings from current research examining the neural mechanisms of emotion regulation by means of conscious cognitive strategies of reappraisal. These findings are considered in the context of related concepts of emotion perception and emotion generation, with discussion of the likely cognitive neuropsychological contributions to emotion regulation and the implications for psychiatric disorders.

Convergent evidence implicates an inhibitory role of prefrontal cortex and cingulate regions upon subcortical and cortical emotion generation systems in the cognitive control of emotional experience. Concurrent modulation of cortical activity by the peripheral nervous system is highlighted by recent studies using simultaneous physiological and neuroimaging techniques. Individual differences in emotion perception, generation of affect and neuropsychological skills are likely to have direct consequences for emotion regulation.

Emotion regulation relies on synergy within brain stem, limbic and cortical processes that promote the adaptive perception, generation and regulation of affect. Aberrant emotion processing in any of these stages may disrupt this self-sustaining regulatory system, with the potential to manifest in distinct forms of emotion dysregulation as seen in major psychiatric disorders such as depression, bipolar disorder and schizophrenia.

An area of recent interest in psychiatric research is the application of neuroimaging techniques to investigate neural events associated with the development and the treatment of symptoms in a number of psychiatric disorders.

To examine whether psychological therapies modulate brain activity and, if so, to examine whether these changes similar to those found with relevant pharmacotherapy in various mental disorders.

Relevant data were identified from Pubmed and PsycInfo searches up to July 2005 using combinations of keywords including ‘psychological therapy’, ‘behaviour therapy’, ‘depression’, ‘panic disorder’, ‘phobia’, ‘obsessive compulsive disorder’, ‘schizophrenia’, ‘psychosis’, ‘brain activity’, ‘brain metabolism’, ‘PET’, ‘SPECT’ and ‘fMRI’.

There was ample evidence to demonstrate that psychological therapies produce changes at the neural level. The data, for example in depression, panic disorder, phobia and obsessive compulsive disorder (OCD), clearly suggested that a change in patients' symptoms and maladaptive behaviour at the mind level with psychological techniques is accompanied with functional brain changes in relevant brain circuits. In many studies, cognitive therapies and drug therapies achieved therapeutic gains through the same neural pathways although the two forms of treatment may still have different mechanisms of action.

Empirical research indicates a close association between the ‘mind’ and the ‘brain’ in showing that changes made at the mind level in a psychotherapeutic context produce changes at the brain level. The investigation of changes in neural activity with psychological therapies is a novel area which is likely to enhance our understanding of the mechanisms for therapeutic changes across a range of disorders.

The aim of this paper was to provide a systematic review and update on the pharmacotherapy of social anxiety disorder (SAD), including the efficacy and tolerability of these agents, the ranking of interventions, and the grading of results by quality of evidence.

The Common Mental Disorder Controlled Trial Register and two trial registries were searched for randomised controlled trials (RCTs) comparing any pharmacological intervention or placebo in the treatment of SAD. We performed a standard pairwise meta-analysis using a random effects model and carried out a network meta-analysis (NMA) using the statistical package, R. Quality of evidence was also assessed.

We included 67 RCTs in the review and 21 to 45 interventions in the NMA. Paroxetine was most effective in the reduction of symptom severity as compared to placebo. Superior response to treatment was also observed for paroxetine, brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline. Higher dropout rates were found for fluvoxamine. Brofaromine, escitalopram, fluvoxamine, paroxetine, pregabalin, sertraline, and venlafaxine performed worse in comparison to placebo for the outcome of dropouts due to adverse events. Olanzapine yielded a relatively high rank for treatment efficacy and buspirone the worse rank for dropouts due to any cause.

The differences between drugs and placebo were small, apart from a significant reduction in symptom severity and response for paroxetine. We suggest paroxetine as a first-line treatment of SAD, with the consideration of future research on the drug olanzapine as well as brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline because we observed a response to treatment.

Our understanding of the neural circuitry involved in mood disorders is rapidly expanding through the ever-increasing application of functional brain imaging techniques.

A selective review of functional neuroimaging studies in patients with primary mood disorders was undertaken in order to identify points of commonality and controversy in the existing literature.

Articles published between 1980 and July 2005 were identified using a range of keywords from relevant on-line databases and key journals.

Increased activity within limbic regions has been consistently associated with depressive states and may also be present in manic states too. Dorsal and ventral prefrontal regions appear compromised as suggested by emerging evidence of cortical inefficiency within prefrontal regions or reductions in their connectivity with limbic areas. Most of the functional changes observed are at least partly reversible following clinical remission although deficits in prefrontal regions may be state-related.

Despite the use of disparate functional imaging modalities, there is a convergence of findings, and the results described do not appear to differ between unipolar and bipolar depression. However, further data are required in order to fully determine the functional changes occurring during manic states. Future work will also need to elucidate the effects of medication, the utility of specific cognitive tasks, and blood oxygenation level-dependent interactions within these affective states.

Severely malnourished patients with anorexia nervosa (AN) are reported to show fewer symptomatic viral infections and a poorer response to bacterial infection than controls. They are also reported to show mild immune system changes, although the relevance of these to altered infection disease presentation in AN and AN pathophysiology is unknown. Thus, in this paper, we suggest a range of immune system changes that might underpin these altered responses to common pathogens, and review a number of recent infectious disease findings for their utility in explaining the pathophysiology of AN.

A systematic review of the literature pertaining to immunity and infectious disease in AN was performed.

AN is associated with leucopenia, and the increased spontaneous and stimulated levels of proinflammatory cytokines [i.e. interleukin (IL)-1β, IL-6 and tumour necrosis factor α). A range of less consistent findings are also reviewed. Most of these data were not controlled for length of illness, degree of malnutrition, micronutrient or vitamin deficiencies or recent refeeding and starvation.

Cytokine disturbances have been suggested to be causally related to AN symptomatology and pathophysiology of AN, although the evidence supporting this assertion is lacking. Immune and cytokine changes in AN do, however, occur in association with a decreased incidence of symptomatic viral infection, decreased clinical response to bacterial infection leading to delayed diagnosis and increased morbidity and mortality associated with the infections.

This study provides a comprehensive review of the literature on memory impairment and the potential effective factors in patients with chronic pain.

A literature search of databases PubMed, EMBASE, SpringerLink, and PsycINFO until September 2012 was conducted using the keywords ‘memory’ and ‘chronic pain’. The study emphasises on publications over the past 20 years.

Memory impairment in chronic pain patients is substantial, but the aspects of memory (e.g. working memory, long-term memory, and autobiographical memory) in chronic pain patients and the potentially related factors (e.g. age, level of education, pain conditions, emotion, neural network, and use of analgesics) are modest. Memory impairment is interpreted with the attention-narrowing hypothesis and the capacity-reduction hypothesis.

The currently available data and theory have explained memory impairment in chronic pain patients, but many controversies remain. Future research should focus on the subclinical characteristics of chronic pain, enlarging the sample size, and emphasise on the experimental intervention method and the cognitive neuroscience method.

Cardiac autonomic dysregulation has been reported in major depressive disorder (MDD), but scarce studies investigated that in fully remitted MDD.

To examine cardiac autonomic function in remitted MDD, 470 unmedicated individuals with a diagnosis of MDD earlier in life and 462 healthy volunteers, aged 18–65 years, were recruited for a case–control analysis. Cardiac autonomic function was evaluated by measuring heart rate variability (HRV) parameters. Frequency-domain indices of HRV were obtained. The obtained results were evaluated in association with personality traits assessed by the Tridimensional Personality Questionnaire.

In patients with remitted MDD, no differences in RR intervals and all frequency-domain indices of HRV could be detected as compared with controls. Stratified analyses by the presence of a history of suicide ideation (the SI+ vs. the SI-subgroup) revealed decreased cardiac vagal control in the SI+ subgroup. The correlation analysis revealed an inverse relation between HRV levels and the harm avoidance score (which has been suggested to be associated with serotonergic activity), mainly attributable to the robust association in the SI+ subgroup.

Our study shows that cardiac autonomic dysregulation is not shown in remitted MDD patients as a whole but is limited to the subgroup of remitted MDD patients with a history of suicidal ideation. In view of the higher risk for cardiac complications in these vulnerable individuals, one might consider the treatment to restore their autonomic function.

Negative symptoms in schizophrenia have been associated with structural and functional alterations of the amygdala. We hypothesised that there would be between-group differences in amygdala volume and neural activation patterns during processing of affective stimuli among patients with schizophrenia and healthy controls. We further hypothesised correlations between neuroimaging metrics and clinical ratings of negative symptoms in patients with schizophrenia.

We used structural and functional magnetic resonance imaging to assess volume and neural activation of the amygdala in 28 patients with schizophrenia and 28 healthy controls.

We found no between-group differences in amygdala volume or neural activation. However, we found a significant negative correlation between emotional blunting and neural activation in the left amygdala during processing of positive affect. We also found a significant negative correlation between stereotyped thinking and the volume of right amygdala.

Our findings implicate the amygdala in a subgroup of negative symptoms in schizophrenia that are characterised by reduced expression with blunted affect and stereotyped thinking.

Review efficacy, safety, and tolerability of brexpiprazole in patients with schizophrenia in short- and long-term phase 3 studies.

Patients experiencing a current exacerbation of schizophrenia received brexpiprazole in two fixed-dose (2 and 4 mg), 6-week, placebo-controlled studies, one flexible-dose (2–4 mg), 6-week, placebo-control and active reference study, and one fixed-dose (1–4 mg), 52-week, placebo-controlled maintenance study.

The efficacy of brexpiprazole was demonstrated in the two short-term fixed-dose studies with statistically significant improvements from baseline in Positive and Negative Syndrome Scale (PANSS) total score compared with placebo. In the flexible-dose short-term study, treatment with brexpiprazole resulted in numerically greater improvements in PANSS total score than with placebo that approached statistical significance (p=0.056). A meta-analysis of these short-term studies showed a mean change in PANSS total score of −20.1, reflecting a clinically meaningful reduction in symptoms. In the maintenance study, brexpiprazole had a beneficial effect relative to placebo on time to exacerbation of psychotic symptoms/impending relapse (p<0.0001). For all studies, brexpiprazole demonstrated clinically meaningful treatment effects on the Personal and Social Performance scale. Brexpiprazole had a favourable safety profile, with a relatively low prevalence of activating and sedating side effects. Weight gain in the short-term studies was ~1 kg greater than placebo. No safety concerns were observed with brexpiprazole in laboratory values, electrocardiogram, or vital signs.

Overall, the results indicate brexpiprazole, used either short-term or as part of a long-term maintenance treatment programme, is an efficacious therapy option in adults with schizophrenia and has a favourable safety/tolerability profile.

The clinical and etiologic implications of comorbid psychiatric and substance-use disorders are relevant across countries and cultures. The DSM-IV now places greater emphasis on the clinical and research utility of the substance-induced disorders classification, and clarifies several important diagnostic issues specific to primary and substance-induced disorders. However, no research consensus exists over the core problem of identifying and differentiating the drug and alcohol intoxication and withdrawal symptoms that can mimic psychiatric symptoms in heavy drinkers and drug users.

To investigate how various diagnostic instruments have measured comorbid psychiatric and substance-use disorders and how each instrument operationalizes the DSM-IV classification.

We review the evolution of the concept of comorbidity beginning with its formalization as the ‘primary–secondary’ distinction in the Feighner Criteria. We address the ‘organic–non-organic’ distinction found in the RDC, DSM-III, and DSM-III-R; and finally, review the ‘primary’ and ‘substance-induced’ categories of DSM-IV, DSM-IV-TR and ICD-10. We describe how these distinctions have been operationalized in widely used diagnostic instruments.

Further understanding of these classifications and the relationship of co-occurring psychiatric and substance disorders can be accomplished with the range of available measures, particularly the Psychiatric Research Interview for Substance and Mental Disorders (PRISM), which reliably utilizes and refines DSM-IV classification distinctions.