Impulse control problems may predict dyskinesia in Parkinson’s

Impulse control problems and involuntary movements may be linked through changes in brain networks, according to a new study. The findings could help researchers understand who is more likely to develop dyskinesia. Published in Translational Psychiatry in October 2026, the study examined whether people with Parkinson’s who had impulse control disorders were more likely to later develop levodopa-induced dyskinesia. Dyskinesia is involuntary movement that can occur after long-term levodopa treatment. $1 Researchers analysed data from 464 people with Parkinson’s who participated in the Parkinson’s Progression Markers Initiative. Participants were grouped according to whether they had an impulse control disorder at the start of the study. These disorders can involve gambling, compulsive shopping, binge eating or other repetitive urges. They may occur as part of Parkinson’s or be associated with dopamine-based treatments, including dopamine agonists. Participants were followed for more than four years. Those with an impulse control disorder at the start were more likely to develop dyskinesia. After adjustment for age, sex and dopamine transporter availability in the putamen, the group had a 33.8% higher relative rate of developing dyskinesia. This is a relative increase, not a 33.8 percentage-point increase in the number of people affected. It also does not mean that everyone with an impulse control disorder will develop dyskinesia. $1 The researchers used brain scans to examine differences in brain organisation. They focused on morphological similarity, which compares structural features across brain regions. This measure provides clues about network organisation but does not directly measure communication between neurons. People with impulse control disorders showed reduced morphological similarity across a network of cortical regions, including both paracentral lobules and the left caudal anterior cingulate cortex. These areas contribute to movement control and behavioural regulation. Statistical analysis suggested that organisation of the left paracentral lobule helped explain the association between the altered network and later dyskinesia. Dopamine transporter availability in the putamen did not show the same mediating relationship. The findings suggest that dyskinesia risk may involve more than dopamine loss in movement-related regions. Wider differences in brain network organisation may also contribute. $1 The results could eventually help clinicians assess dyskinesia risk when planning treatment. They also highlight the importance of monitoring impulse control problems as part of Parkinson’s care. However, the study does not show that impulse control disorders cause dyskinesia, or that treating them would prevent involuntary movements. The brain network findings are exploratory and require confirmation in independent patient groups. The researchers did not develop a clinically usable prediction tool or identify a treatment to prevent dyskinesia in people with impulse control problems. For now, the study provides evidence of a possible link between two Parkinson’s complications, supported by longitudinal clinical data and brain imaging. If confirmed, impulse control problems could become one of several factors considered when assessing dyskinesia risk. The findings are not sufficient to change clinical practice.