RESUMEN
Predicting mood disorders in adolescence is a challenge that motivates research to identify neurocognitive predictors of symptom expression and clinical profiles. This study used machine learning to test whether neurocognitive variables predicted future manic or anhedonic symptoms in two adolescent samples risk-enriched for lifetime mood disorders (Sample 1, n = 73, ages = 13-25, M [SD] = 19.22 [2.49] years, 68% lifetime mood disorder) or familial mood disorders (Sample 2, n = 154, ages = 13-21, M [SD] = 16.46 [1.95] years, 62% first-degree family history of mood disorder). Participants completed cognitive testing and functional magnetic resonance imaging at baseline, for behavioral and neural measures of reward processing and executive functioning. Next, participants completed a daily diary procedure for 8-16 weeks. Penalized mixed-effects models identified neurocognitive predictors of future mood symptoms and stress-reactive changes in mood symptoms. Results included the following. In both samples, adolescents showing ventral corticostriatal reward hyposensitivity and lower reward performance reported more severe stress-reactive anhedonia. Poorer executive functioning behavior was associated with heightened anhedonia overall in Sample 1, but lower stress-reactive anhedonia in both samples. In Sample 1, adolescents showing ventral corticostriatal reward hypersensitivity and poorer executive functioning reported more severe stress-reactive manic symptoms. Clustering analyses identified, and replicated, five neurocognitive subgroups. Adolescents characterized by neural or behavioral reward hyposensitivities together with average-to-poor executive functioning reported unipolar symptom profiles. Adolescents showing neural reward hypersensitivity together with poor behavioral executive functioning reported a bipolar symptom profile (Sample 1 only). Together, neurocognitive phenotypes may hold value for predicting symptom expression and profiles of mood pathology. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
Asunto(s)
Anhedonia , Trastornos del Humor , Adolescente , Humanos , Trastornos del Humor/diagnóstico , Trastornos del Humor/psicología , Afecto , Pruebas Neuropsicológicas , Función Ejecutiva , ManíaRESUMEN
BACKGROUND: Life stressors confer risk for depressive symptoms, but individuals vary in the extent of their sensitivity to life stressors. One protective factor may be an individual's level of reward sensitivity, e.g., a stronger neurobiological response to environmental rewards may mitigate emotional responses to stressors. However, the nature of neurobiological reward sensitivity that corresponds with stress resilience is unknown. Further, this model is untested in adolescence, when life stressor frequency and depression increase. METHODS: We tested the hypothesis that stronger reward-related activation in the left and right nucleus accumbens (NAc), amygdala, and medial prefrontal cortex (mPFC) attenuates the strength of the stress-depression relation. We measured BOLD activation throughout Win and Lose blocks of a monetary reward task, as well as during anticipation and outcome phases of the task. Participants (N = 151, ages 13-19) were recruited to be stratified on risk for mood disorders to enhance variance in depressive symptoms. RESULTS: Activation during anticipation of rewards in the bilateral amygdala and NAc, but not mPFC, buffered the association between life stressors and depressive symptoms. This buffering effect was not found for reward outcome activation or activation across Win blocks. CONCLUSIONS: Results highlight the importance of reward anticipation activation of subcortical structures in attenuating the stress-depression link, suggesting that reward motivation may be a cognitive mechanism through which this stress buffering occurs.
Asunto(s)
Amígdala del Cerebelo , Anticipación Psicológica , Depresión , Núcleo Accumbens , Recompensa , Estrés Psicológico , Amígdala del Cerebelo/fisiología , Núcleo Accumbens/fisiología , Depresión/fisiopatología , Depresión/psicología , Estrés Psicológico/fisiopatología , Estrés Psicológico/psicología , Humanos , Masculino , Femenino , Adolescente , Adulto Joven , Revisión de MedicamentosRESUMEN
Background: Maladaptive and adaptive emotion regulation are putative risk and protective factors for depression and anxiety, but most prior research does not differentiate within-person effects from between-person individual differences. The current study does so during the early part of the Covid-19 pandemic when internalizing symptoms were high. Methods: A sample of emerging adult undergraduate students (N = 154) completed online questionnaires bi-weekly on depression, anxiety, and emotion regulation across eight weeks during the early days of the Covid-19 pandemic (April 2nd to June 27th, 2020). Results: Depression demonstrated significantly positive between-person correlations with overall maladaptive emotion regulation, catastrophizing, and self-blame, and negative correlations with overall adaptive emotion regulation and reappraisal. Anxiety demonstrated significantly positive between-person correlations with overall maladaptive emotion regulation, rumination, and catastrophizing, and a negative correlation with reappraisal. After controlling for these between-person associations, however, there were generally no within-person associations between emotion regulation and internalizing symptoms. Conclusions: Emotion regulation and internalizing symptoms might be temporally stable individual differences that cooccur with one another as opposed to having a more dynamic relation. Alternatively, these dynamic mechanisms might operate over much shorter or longer periods compared to the two-week time lag in the current study. Supplementary Information: The online version contains supplementary material available at 10.1007/s10608-023-10366-9.
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Adolescence is critical period of neurocognitive development as well as increased prevalence of mood pathology. This cross-sectional study replicated developmental patterns of neurocognition and tested whether mood symptoms moderated developmental effects. Participants were 419 adolescents (n=246 with current mood disorders) who completed reward learning and executive functioning tasks, and reported on age, puberty, and mood symptoms. Structural equation modeling revealed a quadratic relationship between puberty and reward learning performance that was moderated by symptom severity: in early puberty, adolescents reporting higher manic symptoms exhibited heightened reward learning performance (better maximizing of rewards on learning tasks), whereas adolescents reporting elevated anhedonia showed blunted reward learning performance. Models also showed a linear relationship between age and executive functioning that was moderated by manic symptoms: adolescents reporting higher mania showed poorer executive functioning at older ages. Findings suggest neurocognitive development is altered in adolescents with mood pathology and suggest directions for longitudinal studies.
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The COVID-19 pandemic significantly disrupted daily life for undergraduates and introduced new stressors (e.g., campus closures). How individuals respond to stressors can interact with stress to increase disorder risk in both unique and transdiagnostic ways. The current study examined how maladaptive and adaptive stress response styles moderated the perceived severity of COVID-related stressors effect on general and specific internalizing dimensions at the beginning of the COVID-19 pandemic in a combined undergraduate sample across two universities (N = 451) using latent bifactor modeling and LASSO modeling to identify optimal predictors. Results showed that perceived stress severity and maladaptive response styles (not adaptive response styles or interactions between stress and response styles) were associated with both common and specific internalizing dimensions. Results suggest additive associations of stress severity and maladaptive coping with internalizing symptoms during the pandemic's beginning, and provide important insights for screening, prevention, and intervention during future public health crises. Supplementary Information: The online version contains supplementary material available at 10.1007/s10862-022-09975-7.
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Both unipolar and bipolar depression have been linked with impairments in executive functioning (EF). In particular, mood symptom severity is associated with differences in common EF, a latent measure of general EF abilities. The relationship between mood disorders and EF is particularly salient in adolescence and young adulthood when the ongoing development of EF intersects with a higher risk of mood disorder onset. However, it remains unclear if common EF impairments have associations with specific symptom dimensions of mood pathology such as blunted positive affect, mood instability, or physiological arousal, or if differences in common EF more broadly relate to what is shared across various symptom domains, such as general negative affect or distress. To address this question, bifactor models can be applied to simultaneously examine the shared and unique contributions of particular mood symptom dimensions. However, no studies to our knowledge have examined bifactor models of mood symptoms in relation to measures of common EF. This study examined associations between common EF and general vs. specific symptom dimensions (anhedonia, physiological arousal, and mania) using structural equation modeling in adolescents and young adults with varying severity of mood symptoms (n = 495, ages = 13-25 years, 68.69% female). A General Depression factor capturing shared variance across symptoms statistically predicted lower Common EF. Additionally, a factor specific to physiological arousal was associated with lower Common EF. Anhedonia-specific and Mania-specific factors were not significantly related to Common EF. Altogether, these results indicate that deficits in common EF are driven by, or reflect, general features of mood pathology that are shared across symptom dimensions but are also specifically associated with physiological arousal.
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BACKGROUND: Stress is a risk factor for unipolar and bipolar mood disorders, but the mechanisms linking stress to specific symptoms remain elusive. Behavioral responses to stress, such as impulsivity and social withdrawal, may mediate the associations between stress and particular mood symptoms. METHODS: This study evaluated behavioral mediators of the relationship between self-reported intensity of daily stress and mood symptoms over up to eight weeks of daily diary surveys. The sample included individuals with unipolar or bipolar disorders, or with no psychiatric history (n = 113, ages 15-25). RESULTS: Results showed that higher daily stress was related to higher severity of mania, and this pathway was mediated by impulsive behaviors. Higher stress also predicted higher severity of anhedonic depression, and social withdrawal mediated this relationship. A k-means clustering analysis revealed six subgroups with divergent profiles of stress-behavior-symptom pathways. LIMITATIONS: Given the observational study design, analyses cannot determine causal relationships amongst these variables. Further work is needed to determine how relationships between these variables may vary based on stressor type, at different timescales, and within different populations. CONCLUSIONS: Findings support a theoretical model in which impulsivity and social withdrawal act as behavioral mediators of the relationship between stress and mood symptoms. Additionally, distinct patterns of reactivity distinguished subgroups of people vulnerable to particular types of mood symptoms. These results provide novel information about how stress-reactive behaviors relate to specific mood symptoms, which may have clinical relevance as targets of intervention.