ArticlebioRxiv : the preprint server for biology2025
Disrupted Top-Down Modulation as a Mechanism of Impaired Multisensory Processing in Children with an Autism Spectrum Diagnosis.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Atypical sensory processing is a core feature of autism, particularly when integration across sensory modalities is required. The neural mechanisms underlying these multisensory differences remain unclear. We recorded high-density EEG while autistic children aged 8-13 (AU; n=40), unaffected siblings of autistic children (SIB; n=26), and non-autistic controls (NA; n=36) performed a simple reaction-time task to auditory (A), visual (V), and audiovisual (AV) stimuli. Analyses targeted event-related potentials (ERPs; P1/N1/P2), alpha-band event-related desynchronization (α-ERD), and long-range theta-band functional connectivity (weighted phase-lag index, wPLI). Across all unisensory measures (ERPs, α-ERD, and connectivity), groups did not differ, indicating broadly comparable unisensory processing. By contrast, multisensory integration (MSI; operationalized for ERPs and α-ERD as AV - (A+V)) differed across groups: NA children showed significant ERP MSI over parieto-central sites that was absent in AU and SIB; and α-ERD MSI was present in all groups but significantly reduced in AU, with SIB showing an intermediate profile. Connectivity analyses revealed that AV theta-band fronto-parieto-occipital coupling was reduced in autistic relative to non-autistic children, consistent with weaker large-scale coordination during multisensory processing. Together, these results point to a multisensory-specific deficit in autism spanning early sensory encoding, posterior α-ERD, and fronto-posterior coupling. The convergence of results supports a mechanistic account of disrupted multisensory influences on sensory processing due to reduced multisensory attentional orientation. Intermediate SIB profiles suggest inherited liability for these neural phenotypes. These results help explain well-documented behavioral MSI differences in autism by linking impaired early enhancement with attenuated top-down control of sensory cortex.
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