As a risk factor for psychosis, childhood trauma rates are elevated in the clinical-high-risk (CHR) syndrome compared to the general population. However, it is unknown whether trauma is typically experienced in childhood or adolescence/young adulthood, whether it occurred prior to CHR syndrome onset, and how severe trauma relates to presenting symptoms. In this study, we examined the relationship of trauma history to symptoms and functioning in individuals diagnosed with the CHR syndrome on the Structured Interview for Psychosis-Risk Syndromes (N = 103). Trauma, defined as meeting the DSM-IV A1 criterion of actual or threatened death or injury, was assessed by semi-structured interview. A large proportion of CHR participants (61%) reported trauma exposure, including interpersonal trauma, trauma prior to CHR onset, and childhood trauma prior to age 12. Those with a trauma history (versus those without trauma) were rated as having more severe perceptual disturbances, general/affective symptoms and more impairment on the Global Assessment of Functioning Scale. The number of traumatic events correlated with more severe ratings in those three domains. Additionally, the number of interpersonal traumas was correlated with ratings of suspiciousness. Trauma was unrelated to specific measures of social and role functioning. A small proportion of CHR participants were diagnosed with formal PTSD (14%), which was unrelated to symptom severity or functioning. Thus, we demonstrate that trauma exposure is often early in life (before age 12), occurs prior to the onset of the CHR syndrome, and is related to both positive and affective symptoms.

Background Bipolar disorder (BD) is associated with inhibitory deficits characterized by a reduced ability to control inappropriate actions or thoughts. While aspects of inhibition such as exaggerated novelty-seeking and perseveration are quantified in rodent exploration of novel environments, similar models are rarely applied in humans. The human Behavioral Pattern Monitor (hBPM), a cross-species exploratory paradigm, has identified a pattern of impaired inhibitory function in manic BD participants, but this phenotype has not been examined across different BD phases. The objective of this study was to determine if euthymic BD individuals demonstrate inhibitory deficits in the hBPM, supporting disinhibition as an endophenotype for the disorder. Methods 25 euthymic BD outpatients and 51 healthy comparison subjects were assessed in the hBPM, where activity was recorded by a concealed videocamera and an ambulatory monitoring sensor. Results Euthymic BD individuals, similar to manic subjects, demonstrated increased motor activity, greater interaction with novel objects, and more frequent perseverative behavior relative to comparison participants. The quantity of locomotion was also reduced in BD individuals treated with mood stabilizers compared to other patients. Limitations Low sample size for treatment subgroups limits the evaluation of specific medication regimens. Conclusions Our results suggest that BD is distinguished by both trait- and state-dependent inhibitory deficits optimally assessed with sophisticated multivariate measures. These data support the use of the hBPM as a tool to elucidate the effects of BD across various illness states, facilitate the development of BD animal models, and advance our understanding of the neurobiology underlying the disorder.

Psychosis is linked to aberrant salience or to viewing neutral stimuli as self-relevant, suggesting a possible impairment in selfrelevance processing. Psychosis is also associated with increased dopamine in the dorsal striatum, especially the anterior caudate (Kegeles et al., 2010). Critically, the anterior caudate is especially connected to (a) the cortical default mode network (DMN), centrally involved in self-relevance processing, and (b) to a lesser extent, the cortical frontoparietal network (FPN; Choi, Yeo, & Buckner, 2012). However, no previous study has directly examined striatal-cortical DMN connectivity in psychosis risk. In Study 1, we examined resting-state functional connectivity in psychosis risk (n = 18) and control (n = 19) groups between (a) striatal DMN and FPN subregions and (b) cortical DMN and FPN. The psychosis risk group exhibited decreased connectivity between the striatal subregions and the cortical DMN. In contrast, the psychosis risk group exhibited intact connectivity between the striatal subregions and the cortical FPN. Additionally, recent distress was also associated with decreased striatal-cortical DMN connectivity. In Study 2, to determine whether the decreased striatal-cortical DMN connectivity was specific to psychosis risk or was related to recent distress more generally, we examined the relationship between connectivity and distress in individuals diagnosed with nonpsychotic emotional distress disorders (N = 25). In contrast to Study 1, here we found that distress was associated with evidence of increased striatal-cortical DMN connectivity. Overall, the present results suggest that decreased striatal-cortical DMN connectivity is associated with psychosis risk and could contribute to aberrant salience.

Psychosis risk was associated with both behavioral and striatal dysfunction during performance on the PCLT, suggesting that behavioral and imaging measures using this task could be a marker for psychosis risk.

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