Drijkoningen David, Chalavi Sima, Sunaert Stefan, Duysens Jacques, Swinnen Stephan P, Caeyenberghs Karen
1 University Medical Center Utrecht , Utrecht, the Netherlands .
2 Movement Control and Neuroplasticity Research Group , Group Biomedical Sciences, Leuven, Belgium .
J Neurotrauma. 2017 Mar 1;34(5):1022-1034. doi: 10.1089/neu.2016.4500. Epub 2016 Oct 18.
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.
创伤性脑损伤（TBI）常导致步态表现受损。然而，这些步态缺陷背后的神经结构病理学仍知之甚少。我们旨在研究年轻的中度至重度TBI参与者（n = 19；年龄13岁11个月±3岁1个月）与正常发育（TD）参与者（n = 30；14岁10个月±2岁2个月）的区域灰质（GM）体积，并评估TBI参与者中体积减少是否与步态表现受损有关。选择参与步态神经控制的皮质和皮质下GM结构作为感兴趣区域（ROI），并使用Freesurfer提取其体积。此外，使用电子步道获得TBI参与者中已确定的步态损伤时空标志物，包括步长不对称、步长变异性和双支撑时间。与TD参与者相比，TBI参与者的双支撑时间、步长不对称和步长变异性增加，表明步态控制能力下降。其次，在TBI参与者中，整体皮质下GM和个体皮质下ROI的体积减少，包括海马体、小脑皮质、壳核和丘脑。此外，在TBI组中，皮质下ROI的体积损失高度相互关联，表明萎缩倾向于在联合皮质下结构中发生。最后，首次证明TBI受试者的步态异常与特定GM结构的体积减少有关，包括海马体、丘脑以及小脑、额上回、中央旁小叶、后扣带回和顶上叶皮质。本研究是理解TBI患者步态受损背后神经结构病理学的重要第一步。
