Cognitive behavior therapy (CBT) is effective for most patients with a social anxiety disorder (SAD) but a substantial proportion fails to remit. Experimental and clinical research suggests that enhancing CBT using imagery-based techniques could improve outcomes. It was hypothesized that imagery-enhanced CBT (IE-CBT) would be superior to verbally-based CBT (VB-CBT) on pre-registered outcomes.

A randomized controlled trial of IE-CBT v. VB-CBT for social anxiety was completed in a community mental health clinic setting. Participants were randomized to IE (n = 53) or VB (n = 54) CBT, with 1-month (primary end point) and 6-month follow-up assessments. Participants completed 12, 2-hour, weekly sessions of IE-CBT or VB-CBT plus 1-month follow-up.

Intention to treat analyses showed very large within-treatment effect sizes on the social interaction anxiety at all time points (ds = 2.09–2.62), with no between-treatment differences on this outcome or clinician-rated severity [1-month OR = 1.45 (0.45, 4.62), p = 0.53; 6-month OR = 1.31 (0.42, 4.08), p = 0.65], SAD remission (1-month: IE = 61.04%, VB = 55.09%, p = 0.59); 6-month: IE = 58.73%, VB = 61.89%, p = 0.77), or secondary outcomes. Three adverse events were noted (substance abuse, n = 1 in IE-CBT; temporary increase in suicide risk, n = 1 in each condition, with one being withdrawn at 1-month follow-up).

Group IE-CBT and VB-CBT were safe and there were no significant differences in outcomes. Both treatments were associated with very large within-group effect sizes and the majority of patients remitted following treatment.

Even in cases with complexity, simple techniques can be useful to target a specific symptom. Intrusive mental images are highly disruptive, drive emotion, and contribute to maintaining psychopathology. Cognitive science suggests that we might target intrusive images using competing tasks.

We describe an imagery competing task technique within cognitive behavioural therapy (CBT) with a patient with bipolar disorder and post-traumatic stress disorder (PTSD) symptoms. The intervention – including Tetris computer game-play – was used (1) to target a specific image within one therapy session, and (2) to manage multiple images in daily life.

A single case (AB) design was used. (1) To target a specific image, the patient brought the image to mind and, after mental rotation instructions and game-play practice, played Tetris for 10 minutes. Outcomes, pre- and post-technique, were: vividness/distress ratings when the image was brought to mind; reported intrusion frequency over a week. (2) To manage multiple images, the patient used the intervention after an intrusive image occurred. Outcomes were weekly measures of: (a) imagery characteristics; (b) symptoms of PTSD, anxiety, depression and mania.

(1) For the target image, there were reductions in vividness (80% to 40%), distress (70% to 0%), and intrusion frequency (daily to twice/week). (2) For multiple images, there were reductions from baseline to follow-up in (a) imagery vividness (38%), realness (66%) and compellingness (23%), and (b) PTSD symptoms (Impact of Events Scale-Revised score 26.33 to 4.83).

This low-intensity intervention aiming to directly target intrusive mental imagery may offer an additional, complementary tool in CBT.

To describe the initial results of implementing pharmacogenomics testing in a community-based psychiatry practice and potential impacts on medication management.

Retrospective chart review of prospectively maintained medical records of all adult patients with pharmacogenomics results from 9/01/2017 to 6/30/2019 under the care of psychiatrist and clinical pharmacist.

A total of 51 patients met inclusion criteria. A total of 7 pharmacokinetic genes and, due to changes in the test report over time, a range of 6-10 pharmacodynamic genes relevant to psychotropic medications were evaluated per patient. Every patient had genetic variations, with an average of 6.1 per patient (range 3-9; SD= 1.5). Patients were taking an average of 3.6 (range 1-8; SD=1.7) psychiatric medications at the time of the genetic test, to treat an average of 5 psychiatric conditions (range 1-9; SD=2.2). An average of 1.2 (range 0-4; SD=1.0) gene-drug interactions were uncovered per patient. Following review by psychiatrist and pharmacist, medication adjustments resulted in patients remaining on an average of 3.6 psychiatric medications, but decreasing the average number of gene-drug interactions per patient to 0.8 (range 0-3, SD=0.8).

The large number of genetic variations observed per patient is consistent with previous findings 1-2. The decrease in number of gene-drug interactions following testing demonstrates the practical utility of pharmacogenomics information to guide medication therapy. This study did not examine outcomes such as improvement in psychiatric condition or reduction in medication adverse effects; however, these endpoints have been evaluated in other trials 3-4.

Pharmacogenomics testing presents an opportunity for a personalized medicine approach in a community-based psychiatry practice.

There is demand for new, effective and scalable treatments for depression, and development of new forms of cognitive bias modification (CBM) of negative emotional processing biases has been suggested as possible interventions to meet this need.

We report two double blind RCTs, in which volunteers with high levels of depressive symptoms (Beck Depression Inventory ii (BDI-ii) > 14) completed a brief course of emotion recognition training (a novel form of CBM using faces) or sham training. In Study 1 (N = 36), participants completed a post-training emotion recognition task whilst undergoing functional magnetic resonance imaging to investigate neural correlates of CBM. In Study 2 (N = 190), measures of mood were assessed post-training, and at 2-week and 6-week follow-up.

In both studies, CBM resulted in an initial change in emotion recognition bias, which (in Study 2) persisted for 6 weeks after the end of training. In Study 1, CBM resulted in increases neural activation to happy faces, with this effect driven by an increase in neural activity in the medial prefrontal cortex and bilateral amygdala. In Study 2, CBM did not lead to a reduction in depressive symptoms on the BDI-ii, or on related measures of mood, motivation and persistence, or depressive interpretation bias at either 2 or 6-week follow-ups.

CBM of emotion recognition has effects on neural activity that are similar in some respects to those induced by Selective Serotonin Reuptake Inhibitors (SSRI) administration (Study 1), but we find no evidence that this had any later effect on self-reported mood in an analogue sample of non-clinical volunteers with low mood (Study 2).

Despite a reported high rate of mental disorders in refugees, scientific knowledge on their risk of suicide attempt and suicide is scarce. We aimed to investigate (1) the risk of suicide attempt and suicide in refugees in Sweden, according to their country of birth, compared with Swedish-born individuals and (2) to what extent time period effects, socio-demographics, labour market marginalisation (LMM) and morbidity explain these associations.

Three cohorts comprising the entire population of Sweden, 16–64 years at 31 December 1999, 2004 and 2009 (around 5 million each, of which 3.3–5.0% refugees), were followed for 4 years each through register linkage. Additionally, the 2004 cohort was followed for 9 years, to allow analyses by refugees' country of birth. Crude and multivariate hazard ratios (HRs) with 95% confidence intervals (CIs) were computed. The multivariate models were adjusted for socio-demographic, LMM and morbidity factors.

In multivariate analyses, HRs regarding suicide attempt and suicide in refugees, compared with Swedish-born, ranged from 0.38–1.25 and 0.16–1.20 according to country of birth, respectively. Results were either non-significant or showed lower risks for refugees. Exceptions were refugees from Iran (HR 1.25; 95% CI 1.14–1.41) for suicide attempt. The risk for suicide attempt in refugees compared with the Swedish-born diminished slightly across time periods.

Refugees seem to be protected from suicide attempt and suicide relative to Swedish-born, which calls for more studies to disentangle underlying risk and protective factors.

Subclinical delusional ideas, including persecutory beliefs, in otherwise healthy individuals are heritable symptoms associated with increased risk for psychotic illness, possibly representing an expression of one end of a continuum of psychosis severity. The identification of variation in brain function associated with these symptoms may provide insights about the neurobiology of delusions in clinical psychosis.

A resting-state functional magnetic resonance imaging scan was collected from 131 young adults with a wide range of severity of subclinical delusional beliefs, including persecutory ideas. Because of evidence for a key role of the amygdala in fear and paranoia, resting-state functional connectivity of the amygdala was measured.

Connectivity between the amygdala and early visual cortical areas, including striate cortex (V1), was found to be significantly greater in participants with high (n = 43) v. low (n = 44) numbers of delusional beliefs, particularly in those who showed persistence of those beliefs. Similarly, across the full sample, the number of and distress associated with delusional beliefs were positively correlated with the strength of amygdala-visual cortex connectivity. Moreover, further analyses revealed that these effects were driven by those who endorsed persecutory beliefs.

These findings are consistent with the hypothesis that aberrant assignments of threat to sensory stimuli may lead to the downstream development of delusional ideas. Taken together with prior findings of disrupted sensory-limbic coupling in psychosis, these results suggest that altered amygdala-visual cortex connectivity could represent a marker of psychosis-related pathophysiology across a continuum of symptom severity.