Common Dimensional Reward Deficits Across Mood and Psychotic Disorders: A Connectome-Wide Association Study.
Common Dimensional Reward Deficits Across Mood and Psychotic Disorders: A Connectome-Wide Association Study.
复制标题
DOI:
10.1176/appi.ajp.2016.16070774
复制
发表时间:
2017-07-01
期刊:
影响因子:
--
通讯作者:
Satterthwaite TD
中科院分区:
文献类型:
--
作者:
Sharma A;Wolf DH;Ciric R;Kable JW;Moore TM;Vandekar SN;Katchmar N;Daldal A;Ruparel K;Davatzikos C;Elliott MA;Calkins ME;Shinohara RT;Bassett DS;Satterthwaite TD
Anhedonia is central to multiple psychiatric disorders and causes substantial disability. A dimensional conceptualization posits that anhedonia severity relates to a trans-diagnostic continuum of reward deficits in specific neural networks. Prior investigations of functional connectivity related to anhedonia have focused on case-control comparisons in specific disorders, using region-specific seed-based analyses. Here, the authors explore the entire functional connectome in relation to reward responsivity across a population of adults with hetereogenous psychopathology. In a sample of 225 adults from five diagnostic groups (major depressive disorder, n=32; bipolar disorder, n=50; schizophrenia, n=51, psychosis risk, n=39; and healthy controls, n=53), the authors conducted a connectome-wide analysis examining the relationship between a dimensional measure of reward responsivity (reward sensitivity subscale of the Behavioral Activation Scale) and resting-state functional connectivity using multivariate distance-based matrix regression. This connectome-wide analysis identified foci of dysconnectivity associated with reward responsivity in the nucleus accumbens (NAc), default mode network (DMN) and cingulo-opercular network (CON). Follow-up analyses revealed dysconnectivity among specific large-scale functional networks and their connectivity with the NAc. Reward deficits were associated with decreased connectivity between the NAc and DMN and increased connectivity between the NAc and CON. In addition, impaired reward responsivity was associated with DMN hyper-connectivity and diminished connectivity between DMN and CON. These results emphasize the centrality of the nucleus accumbens in the pathophysiology of reward deficits and suggest that dissociable patterns of connectivity among large-scale networks are critical to the neurobiology of reward dysfunction across clinical diagnostic categories.