Cognitive behavioral therapy (CBT) with exposure and response prevention (ERP) is the psychotherapeutic treatment of choice for obsessive–compulsive disorder (OCD). However, little is known about the impact of CBT on frontostriatal dysfunctioning, known to be the neuronal correlate of OCD.

A probabilistic reversal learning (RL) task probing adaptive strategy switching capabilities was used in 10 unmedicated patients with OCD and 10 healthy controls during an event-related functional magnetic resonance imaging (fMRI) experiment. Patients were scanned before and after intensive CBT, controls twice at comparable intervals.

Strategy change within the RL task involved activity in a broad frontal network in patients and controls. No significant differences between the groups or in group by time interactions were detected in a whole-brain analysis corrected for multiple comparisons. However, a reanalysis with a more lenient threshold revealed decreased responsiveness of the orbitofrontal cortex and right putamen during strategy change before treatment in patients compared with healthy subjects. A group by time effect was found in the caudate nucleus, demonstrating increased activity for patients over the course of time. Patients with greater clinical improvement, reflected by greater reductions in Yale–Brown Obsessive Compulsive Scale (YBOCS) scores, showed more stable activation in the pallidum.

Although these findings are preliminary and need to be replicated in larger samples, they indicate a possible influence of psychotherapy on brain activity in core regions that have been shown to be directly involved both in acquisition of behavioral rules and stereotypes and in the pathophysiology of OCD, the caudate nucleus and the pallidum.

Many studies have reported an increased incidence of psychiatric disorder (particularly psychotic disorders) among first generation adult immigrants, along with an increasing risk for ethnic minorities living in low-minority concentration neighborhoods. These studies have depended mostly on European case-based databases. In contrast, North American studies have suggested a lower risk for psychiatric disorder in immigrants, although the effect of neighborhood immigrant concentration has not been studied extensively.

Using multi-level modeling to disaggregate individual from area-level influences, this study examines the influence of first generation immigrant status at the individual level, immigrant concentration at the neighborhood-level and their combined effect on 12-month prevalence of mood, anxiety and substance-dependence disorders and lifetime prevalence of psychotic disorder, among Canadians.

Individual-level data came from the Canadian Community Health Survey (CCHS) 1.2, a cross-sectional study of psychiatric disorder among Canadians over the age of 15 years; the sample for analysis was n=35 708. The CCHS data were linked with neighborhood-level data from the Canadian Census 2001 for multi-level logistic regression. Immigrant status was associated with a lower prevalence of psychiatric disorder, with an added protective effect for immigrants living in neighborhoods with higher immigrant concentrations. Immigrant concentration was not associated with elevated prevalence of psychiatric disorder among non-immigrants.

The finding of lower 12-month prevalence of psychiatric disorder in Canadian immigrants, with further lessening as the neighborhood immigrant concentration increases, reflects a model of person–environment fit, highlighting the importance of studying individual risk factors within environmental contexts.

The apolipoprotein E4 allele (ApoE4) is an established genetic risk factor for Alzheimer's disease (AD). However, its effects on cognitive performance and brain structure in healthy individuals are complex. We investigated the effect of ApoE4 on cognitive performance and medial temporal lobe volumetric measures in cognitively unimpaired young elderly with and without subjective memory impairment (SMI), which is an at-risk condition for dementia.

Altogether, 40 individuals with SMI and 62 without were tested on episodic memory and on tasks of speed and executive function. All participants were ApoE genotyped. 21 subjects with SMI and 47 without received additional structural magnetic resonance imaging. Volumetric measures of the hippocampus, the entorhinal cortex and the amygdala were obtained manually.

In the SMI group, ApoE4 carriers performed worse on the episodic memory (p=0.049) and showed smaller left hippocampal volumes (p=0.030). In the individuals without SMI, the ApoE4 carriers performed better on episodic memory (p=0.018) and had larger right hippocampal volumes (p=0.039). The interaction of group (SMI/no SMI) and ApoE genotype was significant for episodic memory (p=0.005) and right and left hippocampal volumes (p=0.042; p=0.035). There were no within-group differences or interaction effects on speed and executive function composite measures or other volumetric measures.

The negative effect of ApoE4 on episodic memory and hippocampal volume in SMI supports SMI as a prodromal condition of AD. The positive effects of ApoE4 in subjects without SMI adds to a number of reports on positive ApoE4 effects in young and very old individuals.

We conducted a meta-analysis of voxel-based morphometry (VBM) studies in autism spectrum disorder (ASD) to clarify the changes in regional white-matter volume underpinning this condition, and generated an online database to facilitate replication and further analyses by other researchers.

PubMed, ScienceDirect, Web of Knowledge and Scopus databases were searched between 2002 (the date of the first white-matter VBM study in ASD) and 2010. Manual searches were also conducted. Authors were contacted to obtain additional data. Coordinates were extracted from clusters of significant white-matter difference between patients and controls. A new template for white matter was created for the signed differential mapping (SDM) meta-analytic method. A diffusion tensor imaging (DTI)-derived atlas was used to optimally localize the changes in white-matter volume.

Thirteen datasets comprising 246 patients with ASD and 237 healthy controls met inclusion criteria. No between-group differences were found in global white-matter volumes. ASD patients showed increases of white-matter volume in the right arcuate fasciculus and also in the left inferior fronto-occipital and uncinate fasciculi. These findings remained unchanged in quartile and jackknife sensitivity analyses and also in subgroup analyses (pediatric versus adult samples).

Patients with ASD display increases of white-matter volume in tracts known to be important for language and social cognition. Whether the results apply to individuals with lower IQ or younger age and whether there are meaningful neurobiological differences between the subtypes of ASD remain to be investigated.

Psychiatry and clinical psychology are the two dominant disciplines in mental health research, but the structure of scientific influence and information flow within and between them has never been mapped.

Citations among 96 of the highest impact psychiatry and clinical psychology journals were examined, based on 10 052 articles published in 2008. Network analysis explored patterns of influence between journal clusters.

Psychiatry journals tended to have greater influence than clinical psychology journals, and their influence was asymmetrical: clinical psychology journals cited psychiatry journals at a much higher rate than the reverse. Eight journal clusters were found, most dominated by a single discipline. Their citation network revealed an influential central cluster of ‘core psychiatry’ journals that had close affinities with a ‘psychopharmacology’ cluster. A group of ‘core clinical psychology’ journals was linked to a ‘behavior therapy’ cluster but both were subordinate to psychiatry journals. Clinical psychology journals were less integrated than psychiatry journals, and ‘health psychology/behavioral medicine’ and ‘neuropsychology’ clusters were relatively peripheral to the network.

Scientific publication in the mental health field is largely organized along disciplinary lines, and is to some degree hierarchical, with clinical psychology journals tending to be structurally subordinate to psychiatry journals.

In people with bulimic eating disorders, exposure to high-calorie foods can result in increases in food craving, raised subjective stress and salivary cortisol concentrations. This cue-induced food craving can be reduced by repetitive transcranial magnetic stimulation (rTMS). We investigated whether rTMS has a similar effect on salivary cortisol concentrations, a measure of hypothalamic–pituitary–adrenal axis (HPAA) activity.

We enrolled twenty-two female participants who took part in a double-blind randomized sham-controlled trial on the effects of rTMS on food craving. Per group, eleven participants were randomized to the real or sham rTMS condition. The intervention consisted of one session of high-frequency rTMS delivered to the left dorsolateral prefrontal cortex (DLPFC). Salivary cortisol concentrations were assessed at four time points throughout the 90-min trial. To investigate differences in post-rTMS concentrations between the real and sham rTMS groups, a random-effects model including the pre-rTMS cortisol concentrations as covariates was used.

Salivary cortisol concentrations following real rTMS were significantly lower compared with those following sham rTMS. In this sample, there was also a trend for real rTMS to reduce food craving more than sham rTMS.

These results suggest that rTMS applied to the left DLPFC alters HPAA activity in people with a bulimic disorder.

Recent genetic studies found the A allele of the variant rs1006737 in the alpha 1C subunit of the L-type voltage-gated calcium channel (CACNA1C) gene to be over-represented in patients with psychosis, including schizophrenia, bipolar disorder and major depressive disorder. In these disorders, attention deficits are among the main cognitive symptoms and have been related to altered neural activity in cerebral attention networks. The particular effect of CACNA1C on neural function, such as attention networks, remains to be elucidated.

The current event-related functional magnetic resonance imaging (fMRI) study investigated the effect of the CACNA1C gene on brain activity in 80 subjects while performing a scanner-adapted version of the Attention Network Test (ANT). Three domains of attention were probed simultaneously: alerting, orienting and executive control of attention.

Risk allele carriers showed impaired performance in alerting and orienting in addition to reduced neural activity in the right inferior parietal lobule [Brodmann area (BA) 40] during orienting and in the medial frontal gyrus (BA 8) during executive control of attention. These areas belong to networks that have been related to impaired orienting and executive control mechanisms in neuropsychiatric disorders.

Our results suggest that CACNA1C plays a role in the development of specific attention deficits in psychiatric disorders by modulation of neural attention networks.

Cognitive behaviour therapies (CBTs) have through several trials been demonstrated to reduce symptoms and disability in irritable bowel syndrome (IBS) patients, but the mechanisms responsible for the changes are still unknown. The aim of this study was to test a theoretical model of CBT and investigate if cognitions and/or behaviour mediated the changes seen in CBT for IBS.

To assess for possible mediating effects, we applied path analysis to the dataset of 149 diagnosed participants randomized to mebeverine hydrochloride plus CBT or mebeverine hydrochloride alone. Primary outcome was symptom severity, while secondary outcomes were work and social adjustment and anxiety.

The path analyses supported mediational paths for all outcomes. Changes in behaviour and cognitions mediated all three outcomes, with models placing behaviour change ‘upstream’ of cognition change having best fit. The analyses of model fits revealed best fit for the anxiety model and hence provide increased confidence in the causal model of anxiety.

Changes in behaviour and cognitions mediate the change in CBT given to IBS patients. The results strengthen the validity of a theoretical model of CBT by confirming the interaction of cognitive, emotional and behavioural factors in IBS.