Visual feedback and motor memory contributions to sustained motor control deficits in autism spectrum disorder across childhood and into adulthood.

IF 4.1 2区 医学 Q1 CLINICAL NEUROLOGY
Robin L Shafer, James Bartolotti, Abigail Driggers, Erin Bojanek, Zheng Wang, Matthew W Mosconi
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引用次数: 0

Abstract

Background: Autistic individuals show deficits in sustained fine motor control which are associated with an over-reliance on visual feedback. Motor memory deficits also have been reported during sustained fine motor control in autism spectrum disorders (ASD). The development of motor memory and visuomotor feedback processes contributing to sustained motor control issues in ASD are not known. The present study aimed to characterize age-related changes in visual feedback and motor memory processes contributing to sustained fine motor control issues in ASD.

Methods: Fifty-four autistic participants and 31 neurotypical (NT) controls ages 10-25 years completed visually guided and memory guided sustained precision gripping tests by pressing on force sensors with their dominant hand index finger and thumb. For visually guided trials, participants viewed a stationary target bar and a force bar that moved upwards with increased force for 15s. During memory guided trials, the force bar was visible for 3s, after which participants attempted to maintain their force output without visual feedback for another 12s. To assess visual feedback processing, force accuracy, variability (standard deviation), and regularity (sample entropy) were examined. To assess motor memory, force decay latency, slope, and magnitude were examined during epochs without visual feedback.

Results: Relative to NT controls, autistic individuals showed a greater magnitude and a trend for a steeper slope of force decay during memory guided trials. Across conditions, the ASD group showed reduced force accuracy (β = 0.41, R2 = 0.043, t79.3=2.36, p = .021) and greater force variability (β=-2.16, R2 = 0.143, t77.1=-4.04, p = .0001) and regularity (β=-0.52, R2 = 0.021, t77.4=-2.21, p = .030) relative to NT controls at younger ages, but these differences normalized by adolescence (age x group interactions). Lower force accuracy and greater force variability during visually guided trials and steeper decay slope during memory guided trials were associated with overall autism severity.

Conclusions: Our findings that autistic individuals show a greater magnitude and tendency for a greater rate of force decay than NT individuals following the removal of visual feedback indicate that motor memory deficits contribute to fine motor control issues in ASD. Findings that sensorimotor differences in ASD were specific to younger ages suggest delayed development across multiple motor control processes.

视觉反馈和运动记忆有助于自闭症谱系障碍在儿童期和成年期持续的运动控制缺陷。
背景:自闭症个体表现出持续精细运动控制的缺陷,这与过度依赖视觉反馈有关。在自闭症谱系障碍(ASD)的持续精细运动控制中也有运动记忆缺陷的报道。运动记忆和视觉运动反馈过程的发展对ASD中持续的运动控制问题的贡献尚不清楚。本研究旨在描述视觉反馈和运动记忆过程的年龄相关变化,这些变化有助于ASD患者持续的精细运动控制问题。方法:54名年龄在10 ~ 25岁的自闭症患者和31名神经正常(NT)对照组分别用左手食指和拇指按压力传感器完成视觉引导和记忆引导下的持续精确抓握测试。在视觉引导试验中,参与者观看一个静止的目标杆和一个向上移动的力杆,时间为15秒。在记忆引导试验中,力杆在3秒内可见,之后参与者试图在没有视觉反馈的情况下保持他们的力输出,再持续12秒。为了评估视觉反馈处理,检查了力的准确性、可变性(标准差)和规律性(样本熵)。为了评估运动记忆,在没有视觉反馈的情况下,测试了力衰减潜伏期、斜率和大小。结果:与NT对照组相比,自闭症个体在记忆引导试验中表现出更大的力衰减幅度和更陡的斜率趋势。在不同的条件下,与NT对照组相比,ASD组在更年轻的时候表现出更低的力量准确性(β= 0.41, R2 = 0.043, t79.3=2.36, p = 0.021)和更大的力量变异性(β=-2.16, R2 = 0.143, t77.1=-4.04, p = 0.0001)和规律性(β=-0.52, R2 = 0.021, t77.4=-2.21, p = 0.030),但这些差异在青春期(年龄x组相互作用)被标准化。在视觉引导试验中较低的力准确性和较大的力变异性以及在记忆引导试验中较陡的衰减斜率与整体自闭症严重程度相关。结论:我们的研究结果表明,在移除视觉反馈后,自闭症个体比NT个体表现出更大程度和更大速度的力衰减趋势,这表明运动记忆缺陷有助于ASD精细运动控制问题。发现ASD的感觉运动差异是年轻人特有的,这表明多个运动控制过程的发育延迟。
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来源期刊
CiteScore
7.60
自引率
4.10%
发文量
58
审稿时长
>12 weeks
期刊介绍: Journal of Neurodevelopmental Disorders is an open access journal that integrates current, cutting-edge research across a number of disciplines, including neurobiology, genetics, cognitive neuroscience, psychiatry and psychology. The journal’s primary focus is on the pathogenesis of neurodevelopmental disorders including autism, fragile X syndrome, tuberous sclerosis, Turner Syndrome, 22q Deletion Syndrome, Prader-Willi and Angelman Syndrome, Williams syndrome, lysosomal storage diseases, dyslexia, specific language impairment and fetal alcohol syndrome. With the discovery of specific genes underlying neurodevelopmental syndromes, the emergence of powerful tools for studying neural circuitry, and the development of new approaches for exploring molecular mechanisms, interdisciplinary research on the pathogenesis of neurodevelopmental disorders is now increasingly common. Journal of Neurodevelopmental Disorders provides a unique venue for researchers interested in comparing and contrasting mechanisms and characteristics related to the pathogenesis of the full range of neurodevelopmental disorders, sharpening our understanding of the etiology and relevant phenotypes of each condition.
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