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The association between executive dysfunction, brain dysconnectivity, and inflammation is a prominent feature across major psychiatric disorders (MPDs), schizophrenia, bipolar disorder, and major depressive disorder. A dimensional approach is warranted to delineate their mechanistic interplay across MPDs.
This single site study included a total of 1543 participants (1058 patients and 485 controls). In total, 1169 participants underwent diffusion tensor and resting-state functional magnetic resonance imaging (745 patients and 379 controls completed the Wisconsin Card Sorting Test). Fractional anisotropy (FA) and regional homogeneity (ReHo) assessed structural and functional connectivity, respectively. Pro-inflammatory cytokine levels [interleukin (IL)-1β, IL-6, and tumor necrosis factor-α] were obtained in 325 participants using blood samples collected with 24 h of scanning. Group differences were determined for main measures, and correlation and mediation analyses and machine learning prediction modeling were performed.
Executive deficits were associated with decreased FA, increased ReHo, and elevated IL-1β and IL-6 levels across MPDs, compared to controls. FA and ReHo alterations in fronto-limbic-striatal regions contributed to executive deficits. IL-1β mediated the association between FA and cognition, and IL-6 mediated the relationship between ReHo and cognition. Executive cognition was better predicted by both brain connectivity and cytokine measures than either one alone for FA-IL-1β and ReHo-IL-6.
Transdiagnostic associations among brain connectivity, inflammation, and executive cognition exist across MPDs, implicating common neurobiological substrates and mechanisms for executive deficits in MPDs. Further, inflammation-related brain dysconnectivity within fronto-limbic-striatal regions may represent a transdiagnostic dimension underlying executive dysfunction that could be leveraged to advance treatment.
In the past decade, neuroimaging research has identified key components in the neural system that underlies bipolar disorder (BD). The ventral prefrontal cortex (VPFC) and amygdala are highly interconnected structures that jointly play a central role in emotional regulation. Numerous research groups have reported prominent structural and functional abnormalities within the VPFC and amygdala supporting their essential role in a neural system underlying the emotional dysregulation that is a core feature of BD. Findings in BD also include those in brain regions interconnected with the VPFC and amygdala, including the ventral striatum, hippocampus and the cerebellum. Abnormalities in these regions may contribute to symptoms that reflect disruption in functions sub-served by these structures, including motivational, mnemonic and psychomotor functions.
This article will first review leads from behavioural neurology that implicated these neural system abnormalities in BD. It will then review findings from structural and functional imaging studies to support the presence of abnormalities within these neural system components in BD. It will also review new findings from studies using diffusion tensor imaging (DTI) that provide increasing evidence of abnormalities in the connections between these neural system components in BD. Emerging data supporting differences in this neural system during adolescence, as well as potential beneficial effects of treatment on structure and function will also be presented. Finally, the article will discuss the implications for future investigations, including those for early identification and treatment of BD.
Objective: Increased impulsivity has been shown to be a trait feature of adults with bipolar disorder (BD), yet impulsivity has received little study in adolescents with BD. Thus, it is unknown whether it is a trait feature that is present early in the course of the disorder. We tested the hypotheses that self-reported impulsiveness is increased in adolescents with BD, and that it is present during euthymia, supporting impulsiveness as an early trait feature of the disorder.
Methods: Impulsiveness was assessed in 23 adolescents with BD and 23 healthy comparison (HC) adolescents using the self-report measure of impulsivity, the Barratt Impulsiveness Scale (BIS), comprised by attentional, motor and non-planning subscale scores. Effects of subscale scores and associations of scores with mood state and course features were explored.
Results: Total and subscale BIS scores were significantly higher in adolescents with BD than HC adolescents. Total, attentional and motor subscale BIS scores were also significantly higher in the subset of adolescents with BD who were euthymic, compared to HC adolescents. Adolescents with BD with rapid-cycling and chronic mood symptoms had significantly higher total and motor subscale BIS scores than adolescents with BD without these course features.
Conclusion: These results suggest increased self-reported impulsiveness is a trait feature of adolescents with BD. Elevated impulsivity may be especially prominent in adolescents with rapid-cycling and chronic symptoms.
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