Deficient inhibition in alcohol-dependence: a transcranial magnetic stimulation study.

Abstract

Event Abstract Back to Event Deficient inhibition in alcohol-dependence: a transcranial magnetic stimulation study. Caroline Quoilin1*, Philippe De Timary1 and Julie Duque1 1 Institute of Neuroscience, Catholic University of Leuven, Belgium Background: The development, maintenance, and relapse phenomena in alcohol-dependence has been related to an impaired inhibitory control, but the neural correlates of this deficit are still unclear1. As impaired inhibition has been classically understood as a pure cognitive deficit, most studies have focused on prefrontal areas, while little attention has been given to the role of more “primary” structures, such as the motor system. Importantly, recent transcranial magnetic stimulation (TMS) studies have observed profound inhibitory changes in the motor output pathway during the preparation of actions2-6; this neural motor inhibition is thought to assist goal-directed behaviors by suppressing neural activity that could cause premature or inappropriate responses7-9. Thus, as inhibition of the motor system supports the ability to subjugate inappropriate behaviors and because this aptitude is altered in alcohol-dependence, we tested the hypothesis that alcohol-dependent (AD) patients may suffer from a shortage of neural motor inhibition. Methods: Single TMS pulses were applied over the right and the left primary motor cortex to elicit motor-evoked potentials (MEPs) in the left and the right hand, respectively, of 20 detoxified ADs and 20 matched healthy subjects performing a choice reaction time task. In addition, behavioral inhibitory aptitudes and trait impulsivity were assessed in all participants. Finally, the patients were called back one year after the experiment to evaluate their relapse status and the potential relationship with motor inhibition. Results: As expected, AD patients exhibited poorer behavioral inhibition and higher trait impulsivity than control subjects. More importantly, the TMS experiment revealed a considerable shortage of neural motor inhibition in AD patients. Interestingly, the patients who resumed consuming alcohol within the year following the experiment were those displaying the strongest deficits, both at the behavioral and the neural levels, while the relapse status did not depend on the trait impulsivity measure. Conclusions: Our data suggest a strong motor component in the neural correlate of altered inhibitory control in AD patients. They also highlight an intriguing relationship with relapse and the perspective of a new biomarker to follow strategies aiming at reducing relapse in AD patients. Short lay summary: Impaired inhibitory control is a core element of alcohol-dependence. So far, most studies investigating the neural correlates of this deficit have focused on prefrontal areas, overlooking the contribution of more “primary” structures, such as the motor cortex. Yet, appropriate neural motor inhibition may be a central aspect of healthy behavior. Here, by using transcranial magnetic stimulation, we revealed a deficit in neural motor inhibition in alcohol-dependent patients relative to control subjects. Moreover, this alteration was stronger in patients who ended-up relapsing during the year following the experiment, suggesting that it may represent a new biomarker of the risk for relapse.