Available online 11 September 2021.Impulse control disorder is a prevalent side-effect of Parkinson’s disease (PD) medication, with a strong negative
impact on the quality of life of those affected. Although impulsivity has classically been associated with response
inhibition deficits, previous evidence from PD patients with impulse control disorder (ICD) has not revealed
behavioral dysfunction in response inhibition. In this study, 18 PD patients with ICD, 17 PD patients without this
complication, and 15 healthy controls performed a version of the conditional Stop Signal Task during functional
magnetic resonance imaging. Whole-brain contrasts, regions of interest, and functional connectivity analyses
were conducted. Our aim was to investigate the neural underpinnings of two aspects of response inhibition:
proactive inhibition, inhibition that has been prepared beforehand, and restrained inhibition, inhibition of an
invalid inhibitory tendency. We observed that, in respect to the other two groups, PD patients with ICD exhibited
hyperactivation of the stopping network bilaterally while performing proactive inhibition. When engaged in
restrained inhibition, they showed hyperactivation of the left inferior frontal gyrus, an area linked to action
monitoring. Restrained inhibition also resulted in changes to the functional co-activation between inhibitory
regions and left inferior parietal cortex and right supramarginal gyrus. Our findings indicate that PD patients
with ICD completed the inhibition task correctly, showing altered engagement of inhibitory and attentional
areas. During proactive inhibition they showed bilateral hyperactivation of two inhibitory regions, while during
restrained inhibition they showed additional involvement of attentional areas responsible for alerting and
orienting.This work was supported by grants from the Carlos III Institute of
Health (PI11/02109) and the ERA-Neuron program (PIM2010ERN-
0033). Additionally, the authors received the following grants and
honoraria: T.E.-P. received a grant from the Spanish Ministry of Economy
and Competitiveness (BES-2016-079489). P.M.P.-A. was supported
by grants from the Spanish Ministry of Economy and Competitiveness
(RYC-2014-15440), the Spanish Ministry of Science and Innovation
(PGC2018-093408-B-I00), and the Fundación Tatiana Pérez de Guzmán
el Bueno. I.N.-G. was the recipient of a Rio Hortega grant (CM16/00033)
from the Carlos III Institute of Health. I.N.-G. received honoraria from
Zambon and TEVA for travel and accommodation to attend scientific
meetings. M.C.R.-O. received financial support for her research from
national and local government institutions in Spain (Carlos III Institute
of Health, Basque Country Government, Diputacion Foral Guipuzcoa,
and CIBERNED). M.C.R.-O. received honoraria from Zambon, Bial, and
Boston Scientific for lectures, travel, and accommodation to attend scientific
meetings. BCBL acknowledges support from the Basque Government
through the BERC 2018-2021 program
