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Sensory-First Dissection of ASD with and without Epilepsy Using Combined Analysis of Auditory Event Related Potentials.
Sensory processing is increasingly regarded as a critical cornerstone for understanding ASD. So far, mechanistic understanding of sensory processing alterations in ASD is limited. A leading theory is that these alterations are closely related to an imbalance of excitation and inhibition. This theory is supported by the frequent occurrence of seizures or epileptiform changes in patients with ASD. It is yet unknown how this comorbidity affects sensory processing and sensory behavioral reactivity. As part of the Sensory Processing Program in Utrecht, we tested how sensory processing of auditory stimuli might predict behavioral outcome in ASD with and without epilepsy comorbidity.
Objectives:
The objective of this study was to investigate the relationship between neurophysiological measures of sensory processing and sensory behavioral reactivity, such as irritability, and assess the influence of comorbid epilepsy.
Methods:
90 children with ASD (with and without comorbid epilepsy) and 30 typically developing (TD) children aged 7-12 were assessed with an extensive neurophysiological battery. Using EEG, measured mismatch negativity (MMN), an automatic orienting reflex occurring after deviation of stimuli in the environment without requiring conscious perception. On a more conscious level, we measured selective attention (SA) which demands the focus on stimuli while ignoring irrelevant information in the environment, captured in the P3b component. In addition, multiple behavioral parental questionnaires (ABC, SP-NL and SRS) were included in the analyses.
Results:
Children with ASD (with and without epilepsy) showed less selective attention, as indicated by lower P3b amplitude to attended auditory stimuli. Autonomous discrimination as measured with MMN was not significantly different between ASD and TD children on the ASD group level, but a discrepancy between ASD with and without epilepsy was found: children with ASD and comorbid epilepsy showed increased MMN compared to TD, whereas children with ASD without seizures showed decreased MMN. Furthermore, reduced selective attention was associated with increased irritability and sensory hyper-reactivity. Finally, concurrent problems in MMN and SA had additive effects on behavioral outcome as indicated by increased irritability.
Conclusions:
This sensory-first approach raises new possibilities for rational diagnostics and treatment on a neurophysiological basis. Results show that crucial sensory contrasts may be lost when ASD is analyzed without stratification. Epilepsy comorbidity has a profound impact on sensory processing as indicated by the MMN, suggesting the presence of opposing neural phenotypes within the autism spectrum. In addition, the integration of multiple sensory processing (ERP) components into the diagnostic equation might further disentangle the variability in clinical manifestations.