Neural Correlates of Drug-Related Attentional Bias in Heroin Dependence.

Qinglin Zhao,Dante Mantini,Yonghui Li,Hongqian Li,Quanying Liu,Bin Hu,Céline R Gillebert

doi:10.3389/fnhum.2017.00646

Abstract

The attention of drug-dependent persons tends to be captured by stimuli associated with drug consumption. This involuntary cognitive process is considered as attentional bias (AB). AB has been hypothesized to have causal effects on drug abuse and drug relapse, but its underlying neural mechanisms are still unclear. This study investigated the neural basis of AB in abstinent heroin addicts (AHAs), combining event-related potential (ERP) analysis and source localization techniques. Electroencephalography data were collected in 21 abstinent heroin addicts and 24 age- and gender-matched healthy controls (HCs) during a dot-probe task. In the task, a pair of drug-related image and neutral image was presented randomly in left and right side of the cross fixation, followed by a dot probe replacing one of the images. Behaviorally, AHAs had shorter reaction times (RTs) for the congruent condition compared to the incongruent condition, whereas this was not the case in the HCs. This finding demonstrated the presence of AB towards drug cues in AHAs. Furthermore, the image-evoked ERPs in AHAs had significant shorter P1 latency compared to HCs, as well as larger N1, N2, and P2 amplitude, suggesting that drug-related stimuli might capture attention early and overall require more attentional resources in AHAs. The target-related P3 had significantly shorter latency and lower amplitude in the congruent than incongruent condition in AHAs compared to HCs. Moreover, source localization of ERP components revealed increased activity for AHAs as compared to HCs in the dorsal posterior cingulate cortex (dPCC), superior parietal lobule and inferior frontal gyrus (IFG) for image-elicited responses, and decreased activity in the occipital and the medial parietal lobes for target-elicited responses. Overall, the results of our study confirmed that AHAs may exhibit AB in drug-related contexts, and suggested that the bias might be related to an abnormal neural activity, both in early and late attention processing stages.

Highlights

Drug-related attentional bias (AB), the effect for which substance-addicted patients involuntarily orient their attention toward drug-related cues, has been considered a fundamental factor in substance abuse, addiction development and maintenance (Mckay, 1999; Franken et al, 2003; Field and Cox, 2008; Robinson and Berridge, 2008)
abstinent heroin addicts (AHAs) tended to have quicker response to targets preceded by drug-related cues compared to targets preceded by neutral images, whereas the opposite pattern was observed in healthy controls (HCs) (Figure 2)
For P3 amplitude, the congruent or incongruent condition showed a significant effect on P3 amplitude for the AHA group [F(1,43) = 8.08, p = 0.007], but not the HC group [F(1,43) = 0.76, p = 0.388] (Figure 4C)

Summary

Introduction

Drug-related attentional bias (AB), the effect for which substance-addicted patients involuntarily orient their attention toward drug-related cues, has been considered a fundamental factor in substance abuse, addiction development and maintenance (Mckay, 1999; Franken et al, 2003; Field and Cox, 2008; Robinson and Berridge, 2008). AB has been observed in various types of addictions, Drug-Related Attentional Bias in Heroin Dependence including alcohol (Townshend and Duka, 2001), cigarette (Chanon et al, 2010), heroin (Waters et al, 2012), and cocaine (Mayer et al, 2016), even in abstinent individuals (Noël et al, 2006; Rahmanian et al, 2006; Wang et al, 2007). Previous studies have shown that abstinent heroin addicts (AHAs) exhibit AB to heroin-related stimuli (Marissen et al, 2006). Few studies investigated the underlying neural correlates of AB for heroin-related stimuli in AHAs. The dot-probe task, developed by MacLeod et al (1986), is a widely used paradigm to investigate AB (Norman et al, 2014; Ursache and Blair, 2015). The task has been extended to investigate AB in cigarette (Ehrman et al, 2002; Spencer, 2015), alcohol (Klein et al, 2013; Mcateer et al, 2015; Clerkin et al, 2016), as well as drug dependence (Lubman et al, 2000; Bradley et al, 2003; Field et al, 2009; Gardini, 2009)

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