Citation

Hall JM, Shine JM, Ehgoetz Martens KA, Gilat M, Broadhouse KM, Szeto JYY, Walton CC, Moustafa AA, Lewis SJG. J. Neurol. 2018; 265(6): 1353-1364.

Affiliation

Brain and Mind Centre, University of Sydney, 100 Mallett Street, Camperdown, NSW, 2050, Australia. profsimonlewis@gmail.com.

Copyright

(Copyright © 2018, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s00415-018-8846-3

PMID

29616302

Abstract

Freezing of gait (FOG) is a common symptom in advanced Parkinson's disease (PD). Despite current advances, the neural mechanisms underpinning this disturbance remain poorly understood. To this end, we investigated the structural organisation of the white matter connectome in PD freezers and PD non-freezers. We hypothesized that freezers would show an altered network architecture, which could hinder the effective information processing that characterizes the disorder. Twenty-six freezers and twenty-four well-matched non-freezers were included in this study. Using diffusion tensor imaging, we investigated the modularity and integration of the regional connectome by calculating the module degree z score and the participation coefficient, respectively. Compared to non-freezers, freezers demonstrated lower participation coefficients in the right caudate, thalamus, and hippocampus, as well as within superior frontal and parietal cortical regions. Importantly, several of these nodes were found within the brain's 'rich club'. Furthermore, group differences in module degree z scores within cortical frontal and sensory processing areas were found. Together, our results suggest that changes in the structural network topology contribute to the manifestation of FOG in PD, specifically due to a lack of structural integration between key information processing hubs of the brain.

Language: en

Keywords

Connectome; Diffusion imaging; Freezing of gait; Parkinson’s disease