Brain and behavior · 2026
Neurofunctional Correlates of Emotional Dysregulation: Systematic Review and ALE Meta-Analysis.
СтатьяСистематический обзорМетаанализНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wong Ern, Loconte Riccardo, Terigi Francesca, Giani Elisa, Bucci Matteo, De Rossi Maurilio Menduni, Coraci Davide, Milone Annarita, Masi Gabriele, Cecchetti Luca, Sesso Gianluca
Аннотация
BACKGROUND: Emotional dysregulation (ED) is a transdiagnostic feature of several psychiatric and neurodevelopmental disorders, characterized by heightened emotional reactivity, mood instability, and difficulties regulating emotional responses.
METHODS: In this study, an activation likelihood estimation (ALE) meta-analysis was conducted to examine the neural underpinnings of ED across different clinical populations. A systematic search based on preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines identified 35 task-based fMRI studies (n = 1989 subjects), including patients with borderline personality disorder (BPD), attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), and other conditions.
RESULTS: Hyper-activation was observed in emotion-related regions, particularly bilateral amygdala and left insula, indicating heightened emotional sensitivity and reactivity. Hypo-activation, detected through Bayesian thresholding, was found in areas such as the anterior cingulate cortex and supplementary motor area, suggesting impairments in cognitive control and emotional regulation. Functional connectivity analysis revealed distinct patterns of coactivation, with the amygdala showing isolated activity and the left insula coactivating with regions related to sensory processing and cognitive control.
CONCLUSIONS: These findings provide new insights into the neural circuitry of transdiagnostic ED and suggest that disorders, such as BPD, ADHD, and BD, share common neural mechanisms, particularly in regions involved in emotional reactivity and cognitive regulation. The results have important clinical implications for developing targeted interventions to address both emotional and cognitive deficits in ED. Future research should explore causal mechanisms and incorporate diverse clinical populations to further understand neurobiological basis of ED.
METHODS: In this study, an activation likelihood estimation (ALE) meta-analysis was conducted to examine the neural underpinnings of ED across different clinical populations. A systematic search based on preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines identified 35 task-based fMRI studies (n = 1989 subjects), including patients with borderline personality disorder (BPD), attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), and other conditions.
RESULTS: Hyper-activation was observed in emotion-related regions, particularly bilateral amygdala and left insula, indicating heightened emotional sensitivity and reactivity. Hypo-activation, detected through Bayesian thresholding, was found in areas such as the anterior cingulate cortex and supplementary motor area, suggesting impairments in cognitive control and emotional regulation. Functional connectivity analysis revealed distinct patterns of coactivation, with the amygdala showing isolated activity and the left insula coactivating with regions related to sensory processing and cognitive control.
CONCLUSIONS: These findings provide new insights into the neural circuitry of transdiagnostic ED and suggest that disorders, such as BPD, ADHD, and BD, share common neural mechanisms, particularly in regions involved in emotional reactivity and cognitive regulation. The results have important clinical implications for developing targeted interventions to address both emotional and cognitive deficits in ED. Future research should explore causal mechanisms and incorporate diverse clinical populations to further understand neurobiological basis of ED.