Goudriaan Marije, Shuman Benjamin R, Steele Katherine M, Van den Hauwe Marleen, Goemans Nathalie, Molenaers Guy, Desloovere Kaat
Department of Rehabilitation Sciences, University of Leuven, Leuven, Belgium.
Clinical Motion Analysis Laboratory, University Hospitals Leuven, Pellenberg, Belgium.
Front Hum Neurosci. 2018 Jan 31;12:5. doi: 10.3389/fnhum.2018.00005. eCollection 2018.
Cerebral palsy (CP) and Duchenne muscular dystrophy (DMD) are neuromuscular disorders characterized by muscle weakness. Weakness in CP has neural and non-neural components, whereas in DMD, weakness can be considered as a predominantly non-neural problem. Despite the different underlying causes, weakness is a constraint for the central nervous system when controlling gait. CP demonstrates decreased complexity of motor control during gait from muscle synergy analysis, which is reflected by a higher total variance accounted for by one synergy (tVAF). However, it remains unclear if weakness directly contributes to higher tVAF in CP, or whether altered tVAF reflects mainly neural impairments. If muscle weakness directly contributes to higher tVAF, then tVAF should also be increased in DMD. To examine the etiology of increased tVAF, muscle activity data of gluteus medius, rectus femoris, medial hamstrings, medial gastrocnemius, and tibialis anterior were measured at self-selected walking speed, and strength data from knee extensors, knee flexors, dorsiflexors and plantar flexors, were analyzed in 15 children with CP [median (IQR) age: 8.9 (2.2)], 15 boys with DMD [8.7 (3.1)], and 15 typical developing (TD) children [8.6 (2.7)]. We computed tVAF from 10 concatenated steps with non-negative matrix factorization, and compared tVAF between the three groups with a Mann-Whiney -test. Spearman's rank correlation coefficients were used to determine if weakness in specific muscle groups contributed to altered tVAF. No significant differences in tVAF were found between DMD [tVAF: 0.60 (0.07)] and TD children [0.65 (0.07)], while tVAF was significantly higher in CP [(0.74 (0.09)] than in the other groups (both < 0.005). In CP, weakness in the plantar flexors was related to higher tVAF ( = -0.72). In DMD, knee extensor weakness related to increased tVAF ( = -0.50). These results suggest that the non-neural weakness in DMD had limited influence on complexity of motor control during gait and that the higher tVAF in children with CP is mainly related to neural impairments caused by the brain lesion.
脑性瘫痪（CP）和杜氏肌营养不良症（DMD）是具有肌肉无力特征的神经肌肉疾病。CP中的无力有神经和非神经成分，而在DMD中，无力可被视为主要是一个非神经问题。尽管潜在病因不同，但在控制步态时，无力对中枢神经系统来说是一种限制。从肌肉协同分析来看，CP在步态期间运动控制的复杂性降低，这表现为一个协同作用所解释的总方差更高（tVAF）。然而，尚不清楚无力是否直接导致CP中tVAF升高，或者tVAF的改变是否主要反映神经损伤。如果肌肉无力直接导致tVAF升高，那么DMD中的tVAF也应该升高。为了研究tVAF升高的病因，我们在15名CP儿童[中位（IQR）年龄：8.9（2.2）]、15名DMD男孩[8.7（3.1）]和15名发育正常（TD）儿童[8.6（2.7）]中，以自选步行速度测量了臀中肌、股直肌、腘绳肌内侧、腓肠肌内侧头和胫骨前肌的肌肉活动数据，并分析了膝伸肌、膝屈肌、背屈肌和跖屈肌的力量数据。我们使用非负矩阵分解从10个连续步幅中计算tVAF，并通过Mann-Whiney检验比较三组之间的tVAF。使用Spearman等级相关系数来确定特定肌肉群的无力是否导致tVAF改变。在DMD儿童[tVAF：0.60（0.07）]和TD儿童[0.65（0.07）]之间未发现tVAF有显著差异，而CP儿童的tVAF[（0.74（0.09）]显著高于其他组（均P<0.005）。在CP中，跖屈肌无力与较高的tVAF相关（r = -0.72）。在DMD中，膝伸肌无力与tVAF升高相关（r = -0.50）。这些结果表明，DMD中的非神经无力对步态期间运动控制的复杂性影响有限，且CP儿童中较高的tVAF主要与脑损伤引起的神经损伤有关。
