Objective: We evaluated the role of inhibition in freezing of gait, and related performance on a behavioral stopping task to the structural integrity of the neural stopping network.

Background: Recent studies suggest that patients with Parkinson’s disease (PD) with freezing of gait (FOG) are impaired in response inhibition (e.g. Stroop task, GoNoGo task). Moreover, neuroimaging studies show that patients with FOG have loss of white matter in nodes that are part of the ‘stopping’ network, comprising the presupplementary motor area (preSMA), right inferior frontal gyrus (rIFG) and subthalamic nuclei (STN). This network is particularly mportant for global stopping of motor actions as assessed in stop signal reaction tasks (SSRT).

Methods: 15 patients with FOG (FOG+) and 15 PD patients without (FOG-) completed the SSRT. FOG severity was objectively measured during 360 deg turns and quantified as the ratio between the spectral power in freezing band and power in locomotor band (FOG ratio). Probabilistic structural connectivity of the right hemisphere’s stopping network was performed to identify quantity and quality of fiber tract connections between 1) preSMA IFG, 2) preSMA STN and 3) IFG STN.

Results: There were no significant differences between FOG+ and FOG- patients on the SSRT, nor did the FOG ratio correlate with the SSRT performance. Interestingly, more severe freezing of gait was associated with stronger structural connectivity of preSMA and STN nodes in the stopping network.

Conclusions: Our results do not support a global stopping deficit related to FOG in PD. Stronger integrity of white matter tracts in the stopping network was observed in PD freezers. In line with evidence of less functional connectivity between (pre)SMA and STN in freezers, we suggest that excessive inhibitory drive along the hyperdirect pathway may be an integral component underlying FoG.

Presented at Neuroscience 2015 and ASNR Annual Meeting 2015 (Chicago) as poster.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/freezing-of-gait-in-parkinsons-disease-a-stopping-deficit/