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Neuropsychopharmacology. 2018 Aug;43(9):1851-1858. doi: 10.1038/s41386-018-0074-0. Epub 2018 Apr 26.

Deficient inhibition in alcohol-dependence: let's consider the role of the motor system!

Author information

1
Institute of Neuroscience, Université Catholique de Louvain, Brussels, Belgium. caroline.quoilin@uclouvain.be.
2
Laboratory for Experimental Psychopathology, Psychological Sciences Research Institute, Université Catholique de Louvain, Louvain-la-Neuve, Belgium. caroline.quoilin@uclouvain.be.
3
Institute of Neuroscience, Université Catholique de Louvain, Brussels, Belgium.
4
Laboratory for Experimental Psychopathology, Psychological Sciences Research Institute, Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
5
Research Institute for Psychological Sciences, Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
6
Unité Intégrée d'Hépatologie, Saint-Luc Academic Hospital, Université Catholique de Louvain, Brussels, Belgium.
7
Department of Adult Psychiatry, Saint-Luc Academic Hospital, Université Catholique de Louvain, Brussels, Belgium.

Abstract

Impaired inhibitory control contributes to the development, maintenance, and relapse of alcohol-dependence, but the neural correlates of this deficit are still unclear. Because inhibitory control has been labeled as an executive function, most studies have focused on prefrontal areas, overlooking the contribution of more "primary" structures, such as the motor system. Yet, appropriate neural inhibition of the motor output pathway has emerged as a central aspect of healthy behavior. Here, we tested the hypothesis that this motor inhibition is altered in alcohol-dependence. Neural inhibitory measures of motor activity were obtained in 20 detoxified alcohol-dependent (AD) patients and 20 matched healthy subjects, using a standard transcranial magnetic stimulation procedure whereby motor-evoked potentials (MEPs) are elicited in a choice reaction time task. Moreover, behavioral inhibition and trait impulsivity were evaluated in all participants. Finally, the relapse status of patients was assessed 1 year after the experiment. As expected, AD patients displayed poorer behavioral inhibition and higher trait impulsivity than controls. More importantly, the MEP data revealed a considerable shortage of neural motor inhibition in AD patients. Interestingly, this neural defect was strongest in the patients who ended up relapsing during the year following the experiment. Our data suggest a strong motor component in the neural correlates 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.

PMID:
29728650
PMCID:
PMC6046042
DOI:
10.1038/s41386-018-0074-0
[Indexed for MEDLINE]
Free PMC Article

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