Abstract Background and Hypothesis Sleep disturbance is a well-established risk factor for suicide, though few studies to date have examined whether sleep disturbance contributes to suicide risk among individuals at clinical high risk for psychosis (CHR). The current study addressed this gap in the literature. We hypothesized that sleep disturbance would have a unique relationship with suicidal ideation/attempts when accounting for other variables in the model. We also hypothesized that the interaction between sleep disturbance/attenuated positive symptoms and sleep disturbance/stress would be related to suicidal ideation/attempts in CHR. Study Design The current study used data generated by the Accelerating Medicines Partnership® Schizophrenia Observational Study. The total sample included 1,048 participants (827 CHR and 221 community controls). Participants completed measures of suicidal ideation/attempts, attenuated positive symptoms, depressive symptoms, perceived stress, and sleep disturbance. Study Results Results supported a relationship between sleep disturbance and suicidal ideation/attempts in CHR, with participants who had lifetime ideation and attempts experiencing more sleep disturbance than those with no ideation or attempts. We also found small, but significant positive correlations between sleep disturbance and suicide risk in CHR. When accounting for other variables in the model, the effect of sleep disturbance remained significant for past month ideation, but not lifetime ideation or attempts. Both interaction models were non-significant. Conclusions Our findings highlight the potential value of sleep measures in early identification and treatment of suicide risk in CHR. Further research in this area is warranted.
H. Wastler, Aubrey M. Moe, Alexandra M Blouin et al.· Schizophrenia Bulletin Open· 0 citations
Background: Cognitive impairment is the leading cause of disability in schizophrenia with limited treatments. A major barrier to treatment development is the absence of reproducible, mechanistically grounded neural targets. Cross-sectional studies have identified dorsomedial prefrontal cortex (DMPFC)-somatomotor connectivity as a neural marker of cognitive performance on the Auditory Continuous performance task (ACPT), a measure of attention. To test the stability of this marker, we tested the relationship between DMPFC-somatomotor connectivity and ACPT performance in a longitudinal psychosis sample. Methods: Individuals with early psychosis (n=251) and matched controls (n=90) were enrolled and underwent resting-state neuroimaging and neurocognitive assessment. A subset completed longitudinal assessments over 2-4 years. We calculated DMPFC-somatomotor resting-state functional connectivity using a previously identified DMPFC region and a seed in the somatomotor cortex. We performed linear mixed effects models to predict ACPT performance based on connectivity, time, psychosis type, and their interaction. Results: In the psychosis sample, time (p=.0037) and affective psychosis diagnosis (p<.0001) predicted better ACPT performance. In a model predicting ACPT performance, we observed a significant interaction effect of DMPFC-somatomotor connectivity*psychosis subtype (p=.0079) such that DMPFC-somatomotor connectivity predicted ACPT performance only in individuals with non-affective psychosis (p=.0051). We then tested the specificity of this connectivity-cognitive performance relationship. In a model predicting DMPFC-somatomotor connectivity, only ACPT performance (p=.017), but not fluid cognition, was a significant predictor. Conclusions: DMPFC-somatomotor connectivity is longitudinally associated with cognitive performance in early psychosis. This relationship is strongest in nonaffective psychosis, suggesting a novel, reliable target for intervention for cognitive deficits in early psychosis.
K. A. Mignondje, J. Connolly, A. Beermann et al.· medRxiv· 0 citations
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