Autism spectrum disorder (ASD) is associated with hyper- and/or hypo-sensitivity to sensory input. Spontaneous alpha power, which plays an important role in shaping responsivity to sensory information, is reduced across the lifespan in individuals with ASD. Furthermore, an excitatory/inhibitory imbalance has also been linked to sensory dysfunction in ASD and has been hypothesized to underlie atypical patterns of spontaneous brain activity. The present study examined whether resting-state alpha power differed in children with ASD as compared to TD children, and investigated the relationships between alpha levels, concentrations of excitatory and inhibitory neurotransmitters, and atypical sensory processing in ASD. Participants included thirty-one children and adolescents with ASD and thirty-one age- and IQ-matched typically developing (TD) participants. Resting-state electroencephalography (EEG) was used to obtain measures of alpha power. A subset of participants (ASD = 16; TD = 16) also completed a magnetic resonance spectroscopy (MRS) protocol in order to measure concentrations of excitatory (glutamate + glutamine; Glx) and inhibitory (GABA) neurotransmitters. Children with ASD evidenced significantly decreased resting alpha power compared to their TD peers. MRS estimates of GABA and Glx did not differ between groups with the exception of Glx in the temporal-parietal junction. Inter-individual differences in alpha power within the ASD group were not associated with region-specific concentrations of GABA or Glx, nor were they associated with sensory processing differences. However, atypically decreased Glx was associated with increased sensory impairment in children with ASD. Although we replicated prior reports of decreased alpha power in ASD, atypically reduced alpha was not related to neurochemical differences or sensory symptoms in ASD. Instead, reduced Glx in the temporal-parietal cortex was associated with greater hyper-sensitivity in ASD. Together, these findings may provide insight into the neural underpinnings of sensory processing differences present in ASD.

中文翻译：

---

ASD 儿童感觉处理与电生理和神经化学测量之间的关联：EEG-MRS 研究

自闭症谱系障碍 (ASD) 与对感觉输入的高敏感性和/或低敏感性有关。自发的阿尔法能量在塑造对感觉信息的反应方面起着重要作用，但在 ASD 患者的整个生命周期中都会降低。此外，兴奋性/抑制性失衡也与 ASD 的感觉功能障碍有关，并被假设为自发大脑活动非典型模式的基础。本研究检查了与 TD 儿童相比，ASD 儿童的静息状态阿尔法功率是否不同，并调查了阿尔法水平、兴奋性和抑制性神经递质浓度以及 ASD 中非典型感觉处理之间的关系。参与者包括 31 名患有 ASD 的儿童和青少年以及 31 名年龄和智商匹配的典型发育 (TD) 参与者。静息状态脑电图 (EEG) 用于获得阿尔法功率的测量值。一部分参与者 (ASD = 16; TD = 16) 还完成了磁共振波谱 (MRS) 协议，以测量兴奋性 (谷氨酸 + 谷氨酰胺; Glx) 和抑制性 (GABA) 神经递质的浓度。与 TD 同龄人相比，患有 ASD 的儿童的静息阿尔法功率显着降低。GABA 和 Glx 的 MRS 估计在各组之间没有差异，除了颞顶叶交界处的 Glx。ASD 组内 α 功率的个体间差异与特定区域的 GABA 或 Glx 浓度无关，它们也与感觉处理差异无关。然而，非典型性 Glx 降低与 ASD 儿童感觉障碍增加有关。尽管我们复制了先前关于 ASD 中 alpha 功率降低的报告，但非典型降低的 alpha 与 ASD 中的神经化学差异或感觉症状无关。相反，颞顶叶皮质中 Glx 的减少与 ASD 中更大的超敏反应有关。总之，这些发现可能有助于深入了解 ASD 中存在的感觉处理差异的神经基础。相反，颞顶叶皮质中 Glx 的减少与 ASD 中更大的超敏反应有关。总之，这些发现可能有助于深入了解 ASD 中存在的感觉处理差异的神经基础。相反，颞顶叶皮质中 Glx 的减少与 ASD 中更大的超敏反应有关。总之，这些发现可能有助于深入了解 ASD 中存在的感觉处理差异的神经基础。