The variability in the response to antipsychotic medication in schizophrenia may reflect between-patient differences in neurobiology. Recent cross-sectional neuroimaging studies suggest that a poorer therapeutic response is associated with relatively normal striatal dopamine synthesis capacity but elevated anterior cingulate cortex (ACC) glutamate levels. We sought to test whether these measures can differentiate patients with psychosis who are antipsychotic responsive from those who are antipsychotic nonresponsive in a multicenter cross-sectional study. 1H-magnetic resonance spectroscopy (1H-MRS) was used to measure glutamate levels (Glucorr) in the ACC and in the right striatum in 92 patients across 4 sites (48 responders [R] and 44 nonresponders [NR]). In 54 patients at 2 sites (25 R and 29 NR), we additionally acquired 3,4-dihydroxy-6-[18F]fluoro-l-phenylalanine (18F-DOPA) positron emission tomography (PET) to index striatal dopamine function (Kicer, min−1). The mean ACC Glucorr was higher in the NR than the R group after adjustment for age and sex (F1,80 = 4.27; P = .04). This was associated with an area under the curve for the group discrimination of 0.59. There were no group differences in striatal dopamine function or striatal Glucorr. The results provide partial further support for a role of ACC glutamate, but not striatal dopamine synthesis, in determining the nature of the response to antipsychotic medication. The low discriminative accuracy might be improved in groups with greater clinical separation or increased in future studies that focus on the antipsychotic response at an earlier stage of the disorder and integrate other candidate predictive biomarkers. Greater harmonization of multicenter PET and 1H-MRS may also improve sensitivity.

Any item and its associated metadata held in the University of Cumbria's institutional repository Insight (unless stated otherwise on the metadata record) may be copied, displayed or performed, and stored in line with the JISC fair dealing guidelines (available here) for educational and not for profit activities provided that• the authors, title and full bibliographic details of the item are cited clearly when any part of the work is referred to verbally or in the written form• a hyperlink/URL to the original Insight record of that item is included in any citations of the work • the content is not changed in any way• all files required for usage of the item are kept together with the main item file. You may not• sell any part of an item• refer to any part of an item without citation • amend any item or contextualise it in a way that will impugn the creator's reputation• remove or alter the copyright statement on an item.The full policy can be found here. Alternatively contact the University of Cumbria Repository Editor by emailing insight@cumbria.ac.uk. AimsTo determine the prevalence of PTSD following asthma attack, and investigate whether agency beliefs mediate PTSD and comorbid psychiatric symptoms in this population. MethodWe recruited 110 adults with asthma from online peer support forums. Participants completed the Asthma Symptom Checklist, PTSD Checklist, GHQ-28, General Self-Efficacy scale, and Multidimensional Health Locus of Control scale. Results20% of our sample met criteria for PTSD. Regression results indicated that higher asthma severity significantly predicted PTSD and psychiatric co-morbidity. Lower selfefficacy significantly predicted PTSD symptoms while controlling for asthma severity, however Locus of Control (LoC) did not improve the model further. Self-efficacy, but not LoC, significantly partially mediated the effect of asthma severity on PTSD severity and psychiatric co-morbidity. Conclusions 2Pos$rauma)c Stress Disorder following asthma a$ack PTSD and other psychiatric symptoms in asthma populations are mediated in part by self-efficacy. Safeguarding and improving self-efficacy in this population is an important area for future research and intervention. Declaration of interestThe authors have no conflict of interest to declare.