Drijkoningen, D., Chalavi, S., Sunaert, S., Duysens, J., Swinnen, S. P & Caeyenberghs, K. (2017). Regional gray matter volume loss is associated with gait impairments in young brain-injured individuals. Journal of Neurotrauma,34(5), 1022-1034. United States of America: Mary Ann Liebert, Inc., Publishers. Retrieved from https://doi.org/10.1089/neu.2016.4500
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 gray matter ( GM ) volume in young moderate-to-severe TBI participants ( n = 19; age 13 years 11 months ±3 years 1 month ), compared with typically developing ( TD ) participants ( n = 30; 14 years 10 months ±2 years 2 months ), 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 with 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.
Access may be restricted.