Rahko Jukka S, Vuontela Virve A, Carlson Synnöve, Nikkinen Juha, Hurtig Tuula M, Kuusikko-Gauffin Sanna, Mattila Marja-Leena, Jussila Katja K, Remes Jukka J, Jansson-Verkasalo Eira M, Aronen Eeva T, Pauls David L, Ebeling Hanna E, Tervonen Osmo, Moilanen Irma K, Kiviniemi Vesa J
PEDEGO Research Unit, Child Psychiatry, University Hospital of Oulu, University of Oulu, P.O. Box 5000, 90014, Oulu, Finland.
Brain Research Unit, O. V. Lounasmaa Laboratory, Department of Neuroscience and Biomedical Engineering, Aalto University School of Science, Espoo, Finland.
Child Psychiatry Hum Dev. 2016 Jun;47(3):503-17. doi: 10.1007/s10578-015-0583-6.
The present study examined attention and memory load-dependent differences in the brain activation and deactivation patterns between adolescents with autism spectrum disorders (ASDs) and typically developing (TD) controls using functional magnetic resonance imaging. Attentional (0-back) and working memory (WM; 2-back) processing and load differences (0 vs. 2-back) were analysed. WM-related areas activated and default mode network deactivated normally in ASDs as a function of task load. ASDs performed the attentional 0-back task similarly to TD controls but showed increased deactivation in cerebellum and right temporal cortical areas and weaker activation in other cerebellar areas. Increasing task load resulted in multiple responses in ASDs compared to TD and in inadequate modulation of brain activity in right insula, primary somatosensory, motor and auditory cortices. The changes during attentional task may reflect compensatory mechanisms enabling normal behavioral performance. The inadequate memory load-dependent modulation of activity suggests diminished compensatory potential in ASD.
本研究使用功能磁共振成像技术,考察了自闭症谱系障碍(ASD)青少年与发育正常(TD)对照组在大脑激活和失活模式上与注意力和记忆负荷相关的差异。分析了注意力(0-back)和工作记忆(WM;2-back)处理及负荷差异(0对2-back)。与工作记忆相关的区域在ASD中随着任务负荷的增加而正常激活,默认模式网络正常失活。ASD在注意力0-back任务中的表现与TD对照组相似,但小脑和右侧颞叶皮质区域的失活增加,其他小脑区域的激活减弱。与TD相比,任务负荷增加导致ASD出现多种反应,且右侧岛叶、初级体感、运动和听觉皮层的大脑活动调节不足。注意力任务期间的变化可能反映了使行为表现正常化的代偿机制。活动的记忆负荷依赖性调节不足表明ASD的代偿潜力降低。