title: Neural Circuitry of Impaired Emotion Regulation in Substance Use Disorders.
abstract: Impaired emotion regulation contributes to the development and severity of substance use disorders (substance disorders). This review summarizes the literature on alterations in emotion regulation neural circuitry in substance disorders, particularly in relation to disorders of negative affect (without substance disorder), and it presents promising areas of future research. Emotion regulation paradigms during functional magnetic resonance imaging are conceptualized into four dimensions: affect intensity and reactivity, affective modulation, cognitive modulation, and behavioral control. The neural circuitry associated with impaired emotion regulation is compared in individuals with and without substance disorders, with a focus on amygdala, insula, and prefrontal cortex activation and their functional and structural connectivity. Hypoactivation of the rostral anterior cingulate cortex/ventromedial prefrontal cortex (rACC/vmPFC) is the most consistent finding across studies, dimensions, and clinical populations (individuals with and without substance disorders). The same pattern is evident for regions in the cognitive control network (anterior cingulate and dorsal and ventrolateral prefrontal cortices) during cognitive modulation and behavioral control. These congruent findings are possibly related to attenuated functional and/or structural connectivity between the amygdala and insula and between the rACC/vmPFC and cognitive control network. Although increased amygdala and insula activation is associated with impaired emotion regulation in individuals without substance disorders, it is not consistently observed in substance disorders. Emotion regulation disturbances in substance disorders may therefore stem from impairments in prefrontal functioning, rather than excessive reactivity to emotional stimuli. Treatments for emotion regulation in individuals without substance disorders that normalize prefrontal functioning may offer greater efficacy for substance disorders than treatments that dampen reactivity.
authors.affiliation: From the Department of Psychiatry and the Department of Psychology, University of New Mexico, Albuquerque; the Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas; and the VA North Texas Health Care System, Dallas.
authors.forename: Claire E
authors.initials: CE
authors.lastname: Wilcox
authors.affiliation: From the Department of Psychiatry and the Department of Psychology, University of New Mexico, Albuquerque; the Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas; and the VA North Texas Health Care System, Dallas.
authors.forename: Jessica M
authors.initials: JM
authors.lastname: Pommy
authors.affiliation: From the Department of Psychiatry and the Department of Psychology, University of New Mexico, Albuquerque; the Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas; and the VA North Texas Health Care System, Dallas.
authors.forename: Bryon
authors.initials: B
authors.lastname: Adinoff
mesh_terms: D000339:Affect; D000679:Amygdala / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology*; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology; D003071:Cognition; D004644:Emotions / Q000502:physiology*; D059907:Functional Neuroimaging; D006179:Gyrus Cinguli / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D009434:Neural Pathways / Q000503:physiopathology*; D017397:Prefrontal Cortex / Q000503:physiopathology; D000068356:Self-Control / Q000523:psychology*; D019966:Substance-Related Disorders / Q000503:physiopathology* / Q000523:psychology