Tactile Sensory Gating in Infant Siblings of Children with ASD or ADHD and Age-Matched Controls

Saturday, May 13, 2017: 12:00 PM-1:40 PM
Golden Gate Ballroom (Marriott Marquis Hotel)
E. S. Piccardi, M. H. Johnson and T. Gliga, Centre for Brain and Cognitive Development, Birkbeck University of London, London, United Kingdom
Background: Atypical responses to sensory stimuli, in the forms of hypersensitivity and hyposensitivity, are commonly observed in individuals diagnosed with ASD and ADHD (Schauder & Bennetto, 2016) but have rarely been contrasted in experimental studies. Given the genetic overlap between the two diagnoses, investigating similarities and differences in early sensory symptomatology may help in unraveling shared/unshared developmental pathways (Johnson & al., 2015). Inefficient filtering of environmental stimulation (“sensory gating”) has been proposed as a cause of the sensory abnormalities observed in children with ASD/ADHD, and previously measured by employing ERP auditory gating paradigms (Orekhova et al., 2008; Orekhova & Stroganova, 2014).

Objectives: This study investigated behavioral and neural mechanisms mediating tactile sensory gating in three groups of 10-month-olds: infants at familial risk of ASD (N=49), infants at familial risk of ADHD (N=17) and age-matched controls (N=22). We expected to observe greater variability in contingent behavioral responses and reduced habituation to tactile stimulation in at-risk infants. These results would support research indicating that both hypersensitivity and hyposensitivity occur in individuals diagnosed with ASD and ADHD. Additionally, they would point to impairments in habituation mechanisms occurring in these disorders. From a neural perspective, we predicted to observe sensory gating deficits in at-risk infants. These results would extend previous research employing ERP auditory paradigms indicating that sensory gating abnormalities are indexed by neural aberrations in atypical cohorts.

Methods: 10-month-old infants were tested with a paired-stimulus paradigm: 100 ms pairs of vibro-tactile stimuli (S1-S2) with 700 ms ISI within the pair and 8 seconds ISI between the pairs. Stimuli were delivered through headphones placed to the infants’ feet: 38 pairs were administered during 2 blocks lasting 4 minutes each. Infants’ behavior (looking, moving) was scored during the “anticipation phase” (4 seconds before S1) and the “reactive phase” (4 seconds after S2). Continuous scalp EEG was recorded, the mean amplitude of ERPs time-locked to vibrotactile stimulation was extracted from four electrode pools.

Results: Analysis of behavioral data revealed a main effect of stimulation time (p<.0001) in all groups, indicating that infants’ mean behavioral reactivity was higher during the “reactive phase” as compared to the “anticipation phase”. Moreover, all groups exhibited habituation effects (1st half vs. 2nd half, p<.001). Analysis of ERPs mean amplitude revealed a main effect of stimulus (S1 vs. S2, p<.05) in the central and inferior parietal pools, indicating that efficient sensory gating occurred in the three groups.

Conclusions: Our findings suggest that behavioral and neural mechanisms mediating tactile sensory gating in infants at familial risk of ASD and ADHD are not significantly different from those observed in age-matched controls. In spite of typical behavioral reactivity and decrease amplitude of ERPs with stimulus repetition, other neural indexes may be atypical in at-risk cohorts (i.e., lateralization of responses, ongoing EEG power). Future analyses will be implemented to compare these indexes and characterize possible risk markers across the three groups.