Mostofsky Stewart H, Powell Stephanie K, Simmonds Daniel J, Goldberg Melissa C, Caffo Brian, Pekar James J
Kennedy Krieger Institute, Baltimore, MD 21205, USA.
Brain. 2009 Sep;132(Pt 9):2413-25. doi: 10.1093/brain/awp088. Epub 2009 Apr 23.
Although motor deficits are common in autism, the neural correlates underlying the disruption of even basic motor execution are unknown. Motor deficits may be some of the earliest identifiable signs of abnormal development and increased understanding of their neural underpinnings may provide insight into autism-associated differences in parallel systems critical for control of more complex behaviour necessary for social and communicative development. Functional magnetic resonance imaging was used to examine neural activation and connectivity during sequential, appositional finger tapping in 13 children, ages 8-12 years, with high-functioning autism (HFA) and 13 typically developing (TD), age- and sex-matched peers. Both groups showed expected primary activations in cortical and subcortical regions associated with motor execution [contralateral primary sensorimotor cortex, contralateral thalamus, ipsilateral cerebellum, supplementary motor area (SMA)]; however, the TD group showed greater activation in the ipsilateral anterior cerebellum, while the HFA group showed greater activation in the SMA. Although activation differences were limited to a subset of regions, children with HFA demonstrated diffusely decreased connectivity across the motor execution network relative to control children. The between-group dissociation of cerebral and cerebellar motor activation represents the first neuroimaging data of motor dysfunction in children with autism, providing insight into potentially abnormal circuits impacting development. Decreased cerebellar activation in the HFA group may reflect difficulty shifting motor execution from cortical regions associated with effortful control to regions associated with habitual execution. Additionally, diffusely decreased connectivity may reflect poor coordination within the circuit necessary for automating patterned motor behaviour. The findings might explain impairments in motor development in autism, as well as abnormal and delayed acquisition of gestures important for socialization and communication.
尽管运动缺陷在自闭症中很常见,但即使是基本运动执行功能紊乱背后的神经关联仍不清楚。运动缺陷可能是最早可识别的异常发育迹象之一,对其神经基础的深入了解可能有助于洞察自闭症在平行系统中与社交和沟通发展所需的更复杂行为控制相关的差异。功能性磁共振成像被用于检查13名8至12岁的高功能自闭症(HFA)儿童和13名年龄及性别匹配的典型发育(TD)同龄人在顺序性、并列性手指敲击过程中的神经激活和连接情况。两组在与运动执行相关的皮质和皮质下区域均显示出预期的初级激活[对侧初级感觉运动皮层、对侧丘脑、同侧小脑、辅助运动区(SMA)];然而,TD组在同侧前小脑显示出更大激活,而HFA组在SMA显示出更大激活。尽管激活差异仅限于部分区域,但与对照组儿童相比,HFA儿童在整个运动执行网络中的连接性普遍降低。大脑和小脑运动激活的组间差异代表了自闭症儿童运动功能障碍的首个神经影像学数据,为影响发育的潜在异常回路提供了见解。HFA组小脑激活减少可能反映出将运动执行从与费力控制相关的皮质区域转移到与习惯性执行相关区域存在困难。此外,连接性普遍降低可能反映出在自动化模式化运动行为所需的回路内协调不良。这些发现可能解释了自闭症中运动发育的损害,以及对社交和沟通很重要的手势异常和延迟习得。