Cognitive theory posits that core beliefs play an active role in developing and maintaining symptoms of depression, anxiety, and psychosis. This study sought to comprehensively examine core beliefs, their dimensionality, and their relationships to depression, anxiety, and attenuated psychotic symptoms in two groups of community youth: a group at ultrahigh risk for psychosis (UHR; n = 73, M age = 18.7) and a matched healthy comparison group (HC; n = 73, M age = 18.1). UHR youth reported significantly more negative beliefs about self and others, and significantly less positive beliefs about self and others. HC youth rarely endorsed negative self-beliefs. Exploratory factor analyses found that HC negative self-beliefs did not cohere as a single factor. We hypothesized specific links between core beliefs and symptoms based on cognitive models of each disorder, and tested these links through regression analyses. The results in the HC group were consistent with the proposed models of depression and anxiety. The results in the UHR group were consistent with proposed models of depression and negative psychotic symptoms, somewhat consistent with a proposed model of positive psychotic symptoms, and not at all consistent with a proposed model of anxiety. These findings add to a growing developmental literature on core beliefs and psychopathology, with important clinical implications.
Background: Although psychiatric comorbidity is the norm among individuals at clinical high risk for psychotic disorders (CHR), research has yet to examine transdiagnostic dimensional models of comorbidity in this critical population.Methods: This study analyzed quantitative measures of eleven psychiatric syndromes in a group at CHR (n = 71) and a matched healthy comparison group (n = 73) to determine these syndromes' dimensional structure and relationships to cognition, functioning, and risk of conversion to psychotic disorders.Results: Relative to the comparison group, the CHR group was elevated on all eleven psychiatric syndromes. Exploratory factor analysis found three psychopathology dimensions: internalizing, negative symptoms, and positive symptoms. Depression cross-loaded onto the internalizing and negative symptom dimensions. Hypomania loaded positively on positive symptoms but negatively on negative symptoms. The negative symptom factor was associated with poorer cognition and functioning and a higher risk of conversion to psychosis.Conclusions: These dimensions align with internalizing, detachment, and thought disorder, three of the five spectra in higher-order models such as the Hierarchical Taxonomy of Psychopathology (HiTOP). In the CHR state, detachment appears to be particularly insidious and predictive of psychosis. Further research is required to distinguish depression and hypomania from attenuated psychotic symptoms in this population.
Schizophrenia researchers may ask themselves-or be asked by others-whether their research is relevant in the face of the COVID-19 pandemic. This commentary argues that schizophrenia research is more relevant than ever during this public health crisis, because of the likelihood that the COVID-19 pandemic may lead to increased incidence of psychotic disorders. Journal Pre-proof J o u r n a l P r e -p r o o f SCHIZOPHRENIA RESEARCH AND COVID-19
Self-reference is impaired in psychotic disorders such as schizophrenia, associated with disability, and closely related to characteristic patterns of aberrant brain connectivity.However, at present, it is unclear whether self-reference is impacted in pathogenesis of the disorder. Alterations in connectivity during a self-reference task or resting-state in the psychosis risk (i.e., prodromal) period may yield important clues for biomarker development, as well as for novel treatment targets. This study examined a task-based and resting-state functional magnetic resonance imaging in individuals at clinical high risk (CHR) for psychosis (n = 22) and healthy control unaffected peers (n = 20). The selfreference task comprised three task conditions where subjects were asked if an adjective was relevant to themselves (self), a designated other individual (other), or to evaluate the word's spelling (letter). Connectivity analyses examined medial prefrontal cortex (mPFC) and posterior cingulate cortex (PCC), regions commonly found in conjunction analyses of self-reference, during both the self-reference task and rest. In task connectivity analyses, CHR individuals exhibited decreased mPFC-PCC connectivity when compared to controls. In resting-state analyses, CHR participants showed greater mPFC-PCC connectivity. Taken together, results suggest that psychosis-like alterations in mPFC-PCC connectivity is present prior to psychosis onset across both task and rest.
Negative symptoms are characteristic of schizophrenia and closely linked to numerous outcomes. A body of work has sought to identify homogenous negative symptom subgroups—a strategy that can promote mechanistic understanding and precision medicine. However, our knowledge of negative symptom subgroups among individuals at clinical high-risk (CHR) for psychosis is limited. Here, we investigated distinct negative symptom profiles in a large CHR sample (N = 244) using a cluster analysis approach. Subgroups were compared on external validators that are (1) commonly observed in the schizophrenia literature and/or (2) may be particularly relevant for CHR individuals, informing early prevention and prediction. We observed 4 distinct negative symptom subgroups, including individuals with (1) lower symptom severity, (2) deficits in emotion, (3) impairments in volition, and (4) global elevations. Analyses of external validators suggested a pattern in which individuals with global impairments and volitional deficits exhibited more clinical pathology. Furthermore, the Volition group endorsed more disorganized, anxious, and depressive symptoms and impairments in functioning compared to the Emotion group. These data suggest there are unique negative symptom profiles in CHR individuals, converging with studies in schizophrenia indicating motivational deficits may be central to this symptom dimension. Furthermore, observed differences in CHR relevant external validators may help to inform early identification and treatment efforts.
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