Molholm Sophie, Murphy Jeremy W, Bates Juliana, Ridgway Elizabeth M, Foxe John J
The Cognitive Neurophysiology Laboratory, Department of Pediatrics, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, United States.
Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicin, Bronx, NY, United States.
Front Integr Neurosci. 2020 Feb 11;14:4. doi: 10.3389/fnint.2020.00004. eCollection 2020.
Maladaptive reactivity to sensory inputs is commonly observed in neurodevelopmental disorders (e.g., autism, ADHD). Little is known, however, about the underlying neural mechanisms. For some children, atypical sensory reactivity is the primary complaint, despite absence of another identifiable neurodevelopmental diagnosis. Studying Sensory Processing Disorder (SPD) may well provide a window into the neuropathology of these symptoms. It has been proposed that a deficit in sensory integration underlies the SPD phenotype, but objective quantification of sensory integration is lacking. Here we used neural and behavioral measures of multisensory integration (MSI), which would be affected by impaired sensory integration and for which there are well accepted objective measures, to test whether failure to integrate across the senses is associated with atypical sensory reactivity in SPD. An autism group served to determine if observed differences were unique to SPD.
We tested whether children aged 6-16 years with SPD ( = 14) integrate multisensory inputs differently from age-matched typically developing controls (TD: = 54), or from children with an autism spectrum disorder (ASD: = 44). Participants performed a simple reaction-time task to the occurrence of auditory, visual, and audiovisual stimuli presented in random order, while high-density recordings of electrical brain activity were made.
Children with SPD showed large reductions in the extent to which they benefited from multisensory inputs compared to TDs. The ASD group showed similarly reduced response speeding to multisensory relative to unisensory inputs. Neural evidence for MSI was seen across all three groups, with the multisensory response differing from the sum of the unisensory responses. tests suggested the possibility of enhanced MSI in SPD in timeframes consistent with cortical sensory registration (∼60 ms), followed by reduced MSI during a timeframe consistent with object formation (∼130 ms). The ASD group also showed reduced MSI in the later timeframe.
Children with SPD showed reduction in their ability to benefit from redundant audio-visual inputs, similar to children with ASD. Neurophysiological recordings, on the other hand, showed that major indices of MSI were largely intact, although testing pointed to periods of potential differential processing. While these exploratory electrophysiological observations point to potential sensory-perceptual differences in multisensory processing in SPD, it remains equally plausible at this stage that later attentional processing differences may yet prove responsible for the multisensory behavioral deficits uncovered here.
在神经发育障碍（如自闭症、注意力缺陷多动障碍）中，对感觉输入的适应不良反应很常见。然而，其潜在的神经机制却鲜为人知。对于一些儿童来说，尽管没有其他可识别的神经发育诊断，但非典型的感觉反应是主要问题。研究感觉加工障碍（SPD）很可能为这些症状的神经病理学提供一个窗口。有人提出，感觉统合缺陷是SPD表型的基础，但缺乏对感觉统合的客观量化。在这里，我们使用了多感觉统合（MSI）的神经和行为测量方法，这些方法会受到感觉统合受损的影响，并且有被广泛接受的客观测量方法，以测试跨感觉通道整合失败是否与SPD中的非典型感觉反应相关。一个自闭症组用于确定观察到的差异是否是SPD所特有的。
我们测试了14名6至16岁的SPD儿童与年龄匹配的典型发育对照组（TD：54名）或自闭症谱系障碍（ASD：44名）儿童在整合多感觉输入方面是否存在差异。参与者对随机呈现的听觉、视觉和视听刺激的出现执行简单的反应时任务，同时进行高密度的脑电活动记录。
与TD组相比，SPD儿童从多感觉输入中获益的程度大幅降低。ASD组在多感觉相对于单感觉输入时的反应速度提升也同样降低。在所有三组中都观察到了MSI的神经证据，多感觉反应不同于单感觉反应的总和。检验表明，在与皮层感觉登记一致的时间范围内（约60毫秒），SPD中MSI有增强的可能性，随后在与物体形成一致的时间范围内（约130毫秒）MSI降低。ASD组在较晚的时间范围内也显示出MSI降低。
与ASD儿童相似，SPD儿童从冗余视听输入中获益的能力降低。另一方面，神经生理学记录表明，MSI的主要指标在很大程度上是完整的，尽管检验指出了潜在的差异处理时期。虽然这些探索性的电生理观察结果指出了SPD在多感觉处理方面潜在的感觉-知觉差异，但在现阶段同样合理的是，后期的注意力处理差异可能最终被证明是这里发现的多感觉行为缺陷的原因。
