Citation

Drijkoningen D, Chalavi S, Sunaert S, Duysens J, Swinnen SP, Caeyenberghs K. J. Neurotrauma 2016; 34(5): 1022-1034.

Affiliation

Australian Catholic University, 95359, School of Psychology, Melbourne, Victoria, Australia ; Karen.caeyenberghs@acu.edu.au.

Copyright

(Copyright © 2016, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2016.4500

PMID

27673741

Abstract

Traumatic brain injury (TBI) often leads to impairments in gait performance. However, the underlying neurostructural pathology of these gait deficits is poorly understood. We aimed to investigate regional grey matter (GM) volume in young moderate-to-severe TBI participants (n=18, age 13y11m ± 3y1m) as compared to typically developing participants (TD; n=30, 14y10m ± 2y2m) and assess whether reduced volume was related to impaired gait performance in TBI participants. Cortical and subcortical GM structures, involved in the neural control of gait, were selected as regions of interest (ROIs) and their volume was extracted using Freesurfer. Moreover, established spatiotemporal markers of gait impairments in TBI participants, including step length asymmetry, step length variability and double support time, were obtained using an electronic walkway. Compared to TD participants, TBI participants showed increased double support time, step length asymmetry and step length variability suggesting a reduced gait control. Secondly, in TBI participants, reduced volumes were demonstrated in overall subcortical GM and individual subcortical ROIs, including the hippocampus, cerebellar cortex, putamen and thalamus. Moreover, in the TBI group, volume losses in subcortical ROIs were highly inter-correlated, indicating that atrophy tends to occur in combined subcortical structures. Finally, it was demonstrated, for the first time, that gait abnormalities in TBI subjects were associated with reduced volume in specific GM structures including the hippocampus, thalamus and the cerebellar, superior frontal, paracentral, posterior cingulate and superior parietal cortices. The present study is an important first step in the understanding of the neurostructural pathology underlying impaired gait in TBI patients.

Language: en