Literature DB >> 24911989

Executive dysfunction and reward dysregulation: a high-density electrical mapping study in cocaine abusers.

Kristen P Morie1, Pierfilippo De Sanctis2, Hugh Garavan3, John J Foxe4.   

Abstract

Executive function deficits and reward dysregulation, which mainly manifests as anhedonia, are well documented in drug abusers. We investigated specific aspects of executive function (inhibitory control and cognitive control), as well as anhedonia, in a cohort of current cocaine abusers in order to ascertain to what extent these factors are associated with more severe drug dependence. Participants filled out questionnaires relating to anhedonia and their addiction history. Participants also performed a response inhibition task while high-density event-related potentials (ERPs) were recorded. Electrophysiological responses to successful inhibitions (N2/P3 components) and to commission errors (ERN/Pe components) were compared between 23 current users of cocaine and 27 non-using controls. A regression model was performed to determine the association of our measures of reward dysregulation and executive function with addiction severity. As expected, cocaine users performed more poorly than controls on the inhibitory control task and showed significant electrophysiological differences. They were also generally more anhedonic than controls. Higher levels of anhedonia were associated with more severe substance use, whereas the level of executive dysfunction was not associated with more severe substance use. However, N2 amplitude was associated with duration of drug use. Further, inhibitory control and anhedonia were correlated, but only in controls. These data suggest that while executive dysfunction characterizes drug abuse, it is anhedonia, independent of executive dysfunction, that is most strongly associated with more severe use.
Copyright © 2014 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Addiction; EEG; ERP; Executive function; Inhibition; Reward; Substance abuse

Mesh:

Substances:

Year:  2014        PMID: 24911989      PMCID: PMC4385568          DOI: 10.1016/j.neuropharm.2014.05.016

Source DB:  PubMed          Journal:  Neuropharmacology        ISSN: 0028-3908            Impact factor:   5.250


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