Wang Zheng, Kwon Minhyuk, Mohanty Suman, Schmitt Lauren M, White Stormi P, Christou Evangelos A, Mosconi Matthew W
Schiefelbusch Institute for Life Span Studies, University of Kansas, 1000 Sunnyside Ave., Lawrence, KS 66045, USA.
Clinical Child Psychology Program, University of Kansas, 1000 Sunnyside Ave., Lawrence, KS 66045, USA.
Int J Mol Sci. 2017 Mar 25;18(4):698. doi: 10.3390/ijms18040698.
Force control deficits have been repeatedly documented in autism spectrum disorder (ASD). They are associated with worse social and daily living skill impairments in patients suggesting that developing a more mechanistic understanding of the central and peripheral processes that cause them may help guide the development of treatments that improve multiple outcomes in ASD. The neuromuscular mechanisms underlying force control deficits are not yet understood. Seventeen individuals with ASD and 14 matched healthy controls completed an isometric index finger abduction test at 60% of their maximum voluntary contraction (MVC) during recording of the first dorsal interosseous (FDI) muscle to determine the neuromuscular processes associated with sustained force variability. Central modulation of the motorneuron pool activation of the FDI muscle was evaluated at delta (0-4 Hz), alpha (4-10 Hz), beta (10-35 Hz) and gamma (35-60 Hz) frequency bands. ASD patients showed greater force variability than controls when attempting to maintain a constant force. Relative to controls, patients also showed increased central modulation of the motorneuron pool at beta and gamma bands. For controls, reduced force variability was associated with reduced delta frequency modulation of the motorneuron pool activity of the FDI muscle and increased modulation at beta and gamma bands. In contrast, delta, beta, and gamma frequency oscillations were not associated with force variability in ASD. These findings suggest that alterations of central mechanisms that control motorneuron pool firing may underlie the common and often impairing symptoms of ASD.
在自闭症谱系障碍(ASD)中,力量控制缺陷已被多次记录。它们与患者更严重的社交和日常生活技能损害相关,这表明对导致这些缺陷的中枢和外周过程形成更具机械性的理解,可能有助于指导开发能够改善ASD多种症状的治疗方法。力量控制缺陷背后的神经肌肉机制尚不清楚。17名患有ASD的个体和14名匹配的健康对照在记录第一背侧骨间肌(FDI)时,以其最大自主收缩(MVC)的60%完成了等长食指外展测试,以确定与持续力量变异性相关的神经肌肉过程。在δ(0 - 4Hz)、α(4 - 10Hz)、β(10 - 35Hz)和γ(35 - 60Hz)频段评估FDI肌肉运动神经元池激活的中枢调制。在试图保持恒定力量时,ASD患者表现出比对照组更大的力量变异性。相对于对照组,患者在β和γ频段也表现出运动神经元池的中枢调制增加。对于对照组,力量变异性降低与FDI肌肉运动神经元池活动的δ频率调制降低以及β和γ频段调制增加有关。相比之下,δ、β和γ频率振荡与ASD中的力量变异性无关。这些发现表明,控制运动神经元池放电的中枢机制改变可能是ASD常见且往往具有损害性症状的基础。