Application of Inter-Trial-Coherence Methods to Investigate Early Visual Processing in Infants at Familial Risk for ASD or ADHD

Background: Atypicalities in sensory perception are observed in individuals diagnosed with Autism Spectrum Disorders (ASD) and Attention Deficit Hyperactivity Disorders (ADHD) but have rarely been contrasted in experimental studies. In the visual domain, superior performance on visual search tasks in ASD individuals and hypersensitivity to flickering lights in both ASD and ADHD populations have been cited as evidence of unusual sensory profiles. Investigating similarities and differences in early sensory symptomatology may help in unraveling common or distinct developmental pathways.

Objectives: To measure a reliable visual response, black-and-white checkerboards were presented under free-viewing conditions to three groups of 10-month-olds: infants at familial risk for ASD (HR-ASD, N=47), ADHD (HR-ADHD, N=21) and low risk controls with no family history of ASD or ADHD (LR-CT, N=18).

Methods: 138 checkerboards were presented during two blocks lasting 4 minutes each. Continuous EEG was recorded and three indices time-locked to checkerboards presentation computed: 1) early visual-evoked potentials (VEPs); 2) alpha band (6Hz-10Hz) inter-trial phase coherence (ITC); 3) neural habituation of early VEPs (i.e., change in amplitude/latency of VEP components between first vs. second half of the first block presentation).

Results: Analysis of VEPs amplitude and latency revealed statistically significant group differences in the first 200ms post-stimulus onset. The P100 component was enhanced in amplitude and delayed in latency in infants at familial risk for ASD or ADHD compared to controls (ps<.05) (Fig.1). Analysis of ITC revealed a statistically significant increase in alpha band phase alignment (p<.05) occurring in HR-ASD and HR-ADHD infants compared to controls. Furthermore, in line with research describing VEPs as resulting from a phase alignment of the ongoing EEG, a positive correlation between P1 peak amplitude and ITC was found in the whole sample (p<.05) (Fig.2). Finally, analysis of neural habituation of VEPs indicated that reduction in the peak-to-peak amplitude of the N1-P2 complex with repeated stimulus presentation was absent in infants at familial risk for ASD, whereas an overall sensitization to repeated visual stimulation was observed in infants at familial risk for ADHD (ps<.05).

Conclusions: Neural hypersensitivity to low-level visual information might represent a common pathway to later behavioral atypicality in both infants at familial risk for ASD or ADHD. Despite this similarity, distinct profiles of neural tuning to repeated low-level visual stimulation were observed in HR-ASD and HR-ADHD infants. While absence of habituation to repeated visual stimulation in HR-ASD infants might result from consistent cortical hyperexcitability, sensitization to repeated visual stimulation in HR-ADHD infants might result from reduced cortical inhibition. In turn, these atypicalities might contribute to aberrant top-down sampling of visual information. The nature of these atypicalities will be further characterized by investigating alpha band pre-stimulus phase properties and by relating EEG indices to parent report measures of infants’ sensory processing.