Event-Related Potential Study of Executive Dysfunctions in a Speeded Reaction Task in Cocaine Addiction

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Abstract
This study used a flanker task with NoGo elements to investigate frontal executive function deficits in 19 cocaine abusers. The executive functions of interest in this study were cortical inhibition or ability to withhold motor response, the ability to select an appropriate response among several competing ones, the ability to inhibit inappropriate responses, and the ability to detect error and exercise corrective control. These processes were evaluated with specific frontal and parietal event-related potentials (ERP) registered during performance on this speeded reaction time task with conflicting motor response demands. Specifically we used behavioral response measures, stimulus-locked anterior (frontal N200, N450) ERP markers of conflict detection, response inhibition (NoGo-N2 and NoGo-P3), and response-locked error-related negativity (ERN) that represent different time points of signal classification, motor response conflict detection, response inhibition, and error monitoring processes. The results revealed that the higher-level executive motor control attributed to the prefrontal cortex is hypoactive in cocaine abusers, and therefore is incapable to effectively resolve response conflicts arising between the competing motor response alternatives. It was also demonstrated that the mesial frontal structures, such as the anterior cingulate cortex, implicated in motor response conflict detection and error monitoring functions were also compromised in addicts. It is reasonable to propose that a ‘hypofunctional’ prefrontal and midfrontal processing results in a diminished ability to effectively override strong habitual automated response tendencies controlled by the lower-level neural mechanisms triggered by the external stimuli. The results propose a neurobiological basis for the understanding why cocaine abusers are facing difficulties in controlling their drug-seeking and drug-taking behaviors, and why their drug-related habitual behavior is so vulnerable to be triggered by external (e.g., drug-related items and environment) cues.