TY - JOUR
T1 - Common dimensional reward deficits across mood and psychotic disorders
T2 - A connectome-wide association study
AU - Sharma, Anup
AU - Wolf, Daniel H.
AU - Ciric, Rastko
AU - Kable, Joseph W.
AU - Moore, Tyler M.
AU - Vandekar, Simon N.
AU - Katchmar, Natalie
AU - Daldal, Aylin
AU - Ruparel, Kosha
AU - Davatzikos, Christos
AU - Elliott, Mark A.
AU - Calkins, Monica E.
AU - Shinohara, Russell T.
AU - Bassett, Danielle S.
AU - Satterthwaite, Theodore D.
N1 - Funding Information:
Dr. Bassett further acknowledges support from the John D.and Catherine T. MacArthur Foundation, the Alfred P. Sloan Foundation, and the National Institute of Child Health and Human Development (grant 1R01HD086888-01).
PY - 2017/7/1
Y1 - 2017/7/1
N2 - Objective: Anhedonia is central to multiple psychiatric disorders and causes substantial disability. A dimensional conceptualization posits that anhedonia severity is related to a transdiagnostic continuum of reward deficits in specific neural networks. Previous functional connectivity studies 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 heterogeneous psychopathology. Method: 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 control subjects, N=53), the authors conducted a connectome-wide analysis examining the relationship between a dimensional measure of reward responsivity (the reward sensitivity subscale of the Behavioral Activation Scale) and resting-state functional connectivity using multi-variate distance-based matrix regression. Results: The authors identified foci of dysconnectivity associated with reward responsivity inthe nucleus accumbens, the default mode network, and the cingulo-opercular network. Follow-up analyses revealed dysconnectivity among specific large-scale functional networks and their connectivity with the nucleus accumbens. Reward deficits were associated with decreased connectivity between the nucleus accumbens and the default mode network and increased connectivity between the nucleus accumbens and the cingulo-opercular network. In addition, impaired reward responsivity was associated with default mode network hyperconnectivity and diminished connectivity between the default mode network and the cingulo-opercular network. Conclusions: 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.
AB - Objective: Anhedonia is central to multiple psychiatric disorders and causes substantial disability. A dimensional conceptualization posits that anhedonia severity is related to a transdiagnostic continuum of reward deficits in specific neural networks. Previous functional connectivity studies 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 heterogeneous psychopathology. Method: 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 control subjects, N=53), the authors conducted a connectome-wide analysis examining the relationship between a dimensional measure of reward responsivity (the reward sensitivity subscale of the Behavioral Activation Scale) and resting-state functional connectivity using multi-variate distance-based matrix regression. Results: The authors identified foci of dysconnectivity associated with reward responsivity inthe nucleus accumbens, the default mode network, and the cingulo-opercular network. Follow-up analyses revealed dysconnectivity among specific large-scale functional networks and their connectivity with the nucleus accumbens. Reward deficits were associated with decreased connectivity between the nucleus accumbens and the default mode network and increased connectivity between the nucleus accumbens and the cingulo-opercular network. In addition, impaired reward responsivity was associated with default mode network hyperconnectivity and diminished connectivity between the default mode network and the cingulo-opercular network. Conclusions: 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.
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U2 - 10.1176/appi.ajp.2016.16070774
DO - 10.1176/appi.ajp.2016.16070774
M3 - Article
C2 - 28135847
AN - SCOPUS:85021708292
SN - 0002-953X
VL - 174
SP - 657
EP - 666
JO - American Journal of Psychiatry
JF - American Journal of Psychiatry
IS - 7
ER -