Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital, Goethe University Frankfurt am Main, Deutschordenstraße 50, 60528, Frankfurt am Main, Germany.
Department of Child and Adolescent Psychiatry and Psychotherapy, Medical Faculty Mannheim, Central Institute of Mental Health, Heidelberg University, Heidelberg, Germany.
Eur J Neurosci. 2018 Jan;47(2):115-125. doi: 10.1111/ejn.13795. Epub 2018 Jan 10.
Children with autism spectrum disorder (ASD) exhibit diminished visual engagement to environmental stimuli. Aberrant attentional function provides an explanation by reduced phasic alerting and orienting to exogenous stimuli. We review aberrant attentional function (alerting, orienting and attentional control) in children with ASD as studied by neurocognitive and neurophysiological tasks as well as magnetic resonance imaging studies. The locus coeruleus-norepinephrine (LC-NE) system is outlined as a pacemaker of attentional function. The LC-NE system regulates adaptive gain in synaptic signal transmission, which moderates phasic alerting ('promoting') and the activation of the ventral frontoparietal attention network within orienting ('permitting'). In children with ASD, atypical LC-NE activity is proposed as underlying mechanism of aberrant attentional function. It may manifest as (i) increased tonic activity with reduced phasic reactivity to exogenous stimuli, (ii) attenuated bottom-up signalling mitigating salience and predictive reward attribution during phasic alerting, and (iii) reduced activation of the ventral frontoparietal attention system attenuating orienting to exogenous stimuli. Increased tonic pupil dilation and aberrant pupil reactivity are discussed as indicators of atypical LC-NE activity. Pupillometry is outlined as feasible method to assess alerting, orienting and attentional control that can be dissected from the pupil dilation time course. In children with ASD, aberrant attentional function through atypical LC-NE activity is proposed as developmental mechanism leading to reduced social attention as well as social interaction and communication impairments.
自闭症谱系障碍（ASD）儿童对外界环境刺激的视觉参与度降低。注意力功能异常可以通过对外源性刺激的相位警觉和定向反应减少来解释。我们回顾了自闭症谱系障碍儿童的异常注意力功能（警觉、定向和注意力控制），这些功能是通过神经认知和神经生理学任务以及磁共振成像研究来研究的。蓝斑-去甲肾上腺素（LC-NE）系统被描述为注意力功能的起搏器。LC-NE 系统调节突触信号传递的适应性增益，从而调节相位警觉（“促进”）和定向过程中腹侧额顶注意网络的激活（“允许”）。在自闭症谱系障碍儿童中，异常的 LC-NE 活动被认为是异常注意力功能的潜在机制。它可能表现为（i）对外源性刺激的相位反应性降低而紧张性活动增加，（ii）减弱的下行信号减轻了相位警觉时的显著性和预测奖励归因，以及（iii）减少了腹侧额顶注意系统的激活，从而降低了对外源性刺激的定向。我们讨论了增加的紧张性瞳孔扩张和异常的瞳孔反应作为异常 LC-NE 活动的指标。瞳孔测量学被概述为评估警觉、定向和注意力控制的可行方法，它可以从瞳孔扩张时间过程中分离出来。在自闭症谱系障碍儿童中，通过异常 LC-NE 活动导致的异常注意力功能被认为是导致社交注意力以及社交互动和沟通障碍的发展机制。
