Atypical Electrophysiological Response and Lateralization to Speech Stimuli in Infants at Risk for Autism Spectrum Disorder

Background: Converging research suggests that individuals with autism spectrum disorder (ASD) often show atypical neural language lateralization including reversed asymmetry of frontal language areas.  This atypical lateralization has been shown in individuals with ASD as young as 24 months (Coffey-Corina, Padden, and Kuhl, 2008); however, it remains unclear at what age this atypical pattern manifests.  Additionally, while language delays and abnormalities are common in young children with ASD, it is unknown the extent to which these impairments may be due to early atypicalities in acquiring basic underlying building blocks necessary for language development, such as the ability to selectively perceive the phonemes relevant to one’s native language.

Objectives: Here, we employ an electrophysiological method to look developmentally at the perceptual narrowing of native language phonemic contrasts in infants at risk for ASD.  This firstly allows us to determine whether phonemic perceptual narrowing occurs atypically, and secondly whether auditory stimuli evoke an atypical neural response in these at-risk infants.

Methods: As part of a larger longitudinal study, we compared high-density event related potentials (ERPs) of infants at risk for ASD (HRA) against low risk control infants (LRC) at 6 months (19 HRA, 18 LRC), 9 months (28 HRA, 22 LRC), and 12 months (30 HRA, 17 LRC).  In a double-oddball paradigm, we presented infants with consonant-vowel syllable stimuli that were either phonemic or non-phonemic in the infants’ native language (English).

Results: Over the frontal and temporal/central regions, we found an initial positive inflection (150-300ms) that was sensitive to the type of syllable heard and which revealed a significant atypical developmental trajectory of responses in HRA infants.  Analysis of a later slow wave (300-700ms) revealed that LRC infants showed lateralization beginning at 9 months but that HRA infants failed to develop this lateralization even by 12 months.  These atypical patterns remained even when excluding infants who met preliminary diagnostic criteria for ASD at 18 months.

Conclusions: Our data suggest that by 9 months, the development of HRA infants begins to diverge from that of typically developing infants regarding response to auditory stimuli. The HRA infants show an atypical trajectory of perceptual narrowing in addition to a failure to develop a lateralized response to auditory stimuli.  Consideration of preliminary outcome data suggests that these differences are indicative of the overall autism endophenotype rather than the clinical-level disorder itself.