Abstract
This study compared magnetoencephalographic (MEG) imaging-derived indices of auditory and somatosensory cortical processing in children aged 8–12 years with autism spectrum disorder (ASD; N = 18), those with sensory processing dysfunction (SPD; N = 13) who do not meet ASD criteria, and typically developing control (TDC; N = 19) participants. The magnitude of responses to both auditory and tactile stimulation was comparable across all three groups; however, the M200 latency response from the left auditory cortex was significantly delayed in the ASD group relative to both the TDC and SPD groups, whereas the somatosensory response of the ASD group was only delayed relative to TDC participants. The SPD group did not significantly differ from either group in terms of somatosensory latency, suggesting that participants with SPD may have an intermediate phenotype between ASD and TDC with regard to somatosensory processing. For the ASD group, correlation analyses indicated that the left M200 latency delay was significantly associated with performance on the WISC-IV Verbal Comprehension Index as well as the DSTP Acoustic-Linguistic index. Further, these cortical auditory response delays were not associated with somatosensory cortical response delays or cognitive processing speed in the ASD group, suggesting that auditory delays in ASD are domain specific rather than associated with generalized processing delays. The specificity of these auditory delays to the ASD group, in addition to their correlation with verbal abilities, suggests that auditory sensory dysfunction may be implicated in communication symptoms in ASD, motivating further research aimed at understanding the impact of sensory dysfunction on the developing brain.
Highlights
A reliable auditory source localization could not be obtained for one typically developing control (TDC) participant, who was not included in analyses of cortical auditory response; somatosensory data was able to be used for this participant
An identifiable M50 auditory response could not be detected in 30% of sensory processing dysfunction (SPD) participants and 38.9% of TDC and autism spectrum disorder (ASD) participants (z = 0.310, p = 0.757)
The ASD group’s left M200 latency was significantly delayed relative to both the TDC and SPD groups, whereas the somatosensory response in the ASD group was only delayed relative to the TDC group and did not significantly differ from the SPD group, who presented with an intermediate somatosensory latency (Figure 3)
Summary
Sensory dysfunction is highly prevalent (≥70%) in Autism Spectrum Disorders (ASD; Greenspan and Wieder, 1997; Mayes and Calhoun, 1999; Adamson et al, 2006; Tomcheck and Dunn, 2007; Al-Heizan et al, 2015), and is associated with autism symptom severity, family stress, and distress, and impairment in communication and socialization (Rogers et al, 2003; Adamson et al, 2006; Brock et al, 2012; Ben-Sasson et al, 2013; Brandwein et al, 2015; Demopoulos et al, 2015a,b; Sanz-Cervera et al, 2015; Corbett et al, 2016). Our understanding of its neuropathology, both in ASD as well as in children who do not meet ASD criteria, is still emerging While this dysfunction can manifest in any sensory domain or as deficits in multimodal integration (Khalfa et al, 2004; Rogers and Ozonoff, 2005; Ben-Sasson et al, 2009; Marco et al, 2011; Stevenson et al, 2014), recent evidence suggests that auditory and tactile processing may be among the most severely impacted (Fernandez-Andres et al, 2015). These sensory modalities are the focus of the present study.
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