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Violence in schizophrenia is best investigated within the broader context of violent behavior in the general population. Two important domains of general pathology which allow us to take such an approach include impairment in emotion processing, as manifested by faulty facial emotion recognition, and aggressive reactivity which consists of heightened sensitivity to provocation. To test this approach, we included 135 subjects: 38 violent (VS's) and 33 nonviolent patients with schizophrenia, 32 healthy controls and 32 non-psychotic violent subjects (NPV's). We measured violence with the Life History of Aggression Scale, recognition of facial emotions with the Emotion Recognition Task, and aggressive reactivity through the Buss-Perry Aggression Questionnaire. Adolescent antisocial behavior was evaluated as a potential precursor to these deficits. We found that impairment in fear recognition (IFR) and aggressive reactivity have a significant effect on violence in the violent groups. These two impairments interact in different ways in these groups. In NPV's they contribute in an additive fashion to violence, whereas in VS's they represent separate pathways; aggressive reactivity leads to violence only when there is no IFR. Adolescent antisocial behavior has a differential effect on these 2 impairments in the 2 groups. Thus, these findings provide insights on the differential role of IFR and aggressive reactivity for violence in schizophrenia compared to the general population. In NPV's, both dysfunctions represent antisocial features and contribute jointly to violence. In schizophrenia, they have different etiologies and constitute alternative pathways to violence. This has important implications for the conceptualization and treatment of violence. [Display omitted] • Violence in schizophrenia studied in the context of violence in general population. • Violent patients with schizophrenia and non-psychotic violent subjects are compared. • Fear recognition impairment and aggressive reactivity lead to violence in both groups. • In non-psychotic subjects these two impairments contribute additively to violence. • In schizophrenia these impairments constitute separate pathways to violence. [ABSTRACT FROM AUTHOR]

False suffocation alarm hypothesis has been widely used to explain carbon dioxide hypersensitivity in panic disorder (PD). However, hypersensitivity to carbon dioxide has been observed in other psychiatric disorders. We explored the specificity of carbon dioxide inhalation as a panic provocation test among psychiatric disorders via network meta-analysis. A systematic literature search on PubMed, EMBASE, and PsycNET was performed to acquire the studies using the carbon dioxide provocation test in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and checklists. Odds ratios (OR) for a panic attack (PA) induced by the carbon dioxide inhalation tests were extracted from each of the original studies and were pooled using the random-effects model. Network meta-analysis on a pool of 2181 participants from 41 studies was used to compare the efficacy of carbon dioxide provocation tests among psychiatric disorders. The network meta-analysis showed that the odds for PA in response to carbon dioxide inhalation are higher in patients with PD, premenstrual dysphoric syndrome (PMDD), and social anxiety disorder (SAD) than healthy controls (HC). The odds for PA were not significantly different among patients with generalized anxiety disorder (GAD), obsessive-compulsive disorder (OCD), major depressive disorder (MDD), and healthy controls (HC). The vulnerability to the carbon dioxide provocation test is not limited to PD. The specificity of the test for PD is questionable, as individuals suffering from PMDD and SAD are also significantly more responsive to carbon dioxide inhalation compared to HC, OCD, MDD, and GAD. There may be shared underpinning biological mechanisms between PD, PMDD, and SAD. [ABSTRACT FROM AUTHOR]

Anhedonia is a salient transdiagnostic psychiatric symptom associated with increased illness severity and chronicity. Anhedonia is also present to varying degrees in non-clinical cohorts. Here, we sought to examine factors influencing expression of anhedonia. Participants (N = 335) were recruited through the Nathan Kline Institute-Rockland Sample, an initiative to deeply phenotype a large community sample across the lifespan. Utilizing a data-driven approach, we evaluated associations between anhedonia severity, indexed by Snaith-Hamilton Pleasure Scale (SHAPS), and 20 physical, developmental, and clinical measures, including Structured Clinical Interview for DSM-IV, Beck Depression Inventory, State-Trait Anxiety Inventory, NEO Five-Factor Inventory-3 (NEO–FFI–3), BMI, Hemoglobin A1C, and demography. Using a bootstrapped AIC-based backward selection algorithm, seven variables were retained in the final model: NEO–FFI–3 agreeableness, extraversion, and openness to experience; BMI; sex; ethnicity; and race. Though median SHAPS scores were greater in participants with psychiatric diagnoses (18.5) than those without (17.0) (U = 12238.5, z = 2.473, p = 0.013), diagnosis and symptom measures were not retained as significant predictors in the final robust linear model. Participants scoring higher on agreeableness, extraversion, and openness to experience reported significantly lower anhedonia. These results demonstrate personality as a mild-to-moderate but significant driver of differences in experiencing pleasure in a community sample. • Self-reported hedonic capacity is heterogenous in individuals without diagnosis. • Hedonic capacity correlated with personality characteristics and not psychiatric diagnosis. • Clinical symptom measures were not correlated with hedonic capacity after accounting for personality characteristics. [ABSTRACT FROM AUTHOR]