The purpose of this study was to investigate the contributions of altered resting-state functional connectivity (FC) of the cerebellar vermis to specific domains of gait impairment in Parkinson disease (PD).

Dementia and gait imbalance amplify mortality and morbidity in PD and their strong association suggests a common underlying pathophysiology.  Both respond inadequately to dopamine repletion, suggesting dysfunction of neurotransmitters and brain regions beyond nigrostriatal pathways. Most PD neuroimaging studies focus on dopaminergic nigrostriatal circuitry that do not adequately explain cognitive or gait impairments. We recently demonstrated that altered vermal FC with association cortex correlated with cognitive impairment in PD, but the gait correlates of vermal FC with sensorimotor cortex (SMC) remain unknown.

We conducted morphometric and FC-MRI analyses contrasting 45 PD and 32 age-matched healthy control participants using stringent quality assurance measures. Comprehensive quantitative spatiotemporal and dynamic gait measures were assessed for behavioral correlations.   

The PD participants had significantly altered FC between vermis and sensorimotor cortex compared to controls. The altered vermal FC with the paracentral lobules correlated with the dynamic measures of variability in stride length, cadence and single support time, even after controlling for confounding variables including local atrophy. Vermis volume did not correlate with any gait measure. No group differences in volume of vermis or regional cortical thickness of the significant clusters were observed.

These results demonstrate a correlation between significantly altered vermal FC with sensorimotor cortex and gait impairment in PD. The lack of relevant vermal or cortical atrophy suggests this effect could be secondary to local pathophysiology such as neurotransmitter dysfunction. This finding, combined with our recent demonstration of correlation between altered vermal FC with association cortex and cognition in PD, point to the vermis as one of the potential pathophysiologic links between gait imbalance and dementia, two deleterious domains of impairment in PD.