While difficulties in communication are characteristic of autism spectrum disorders (ASD), it remains unclear whether the observed language delays are intrinsic to language processing abilities or develop secondary to social deficits. Non-syndromic craniosynostosis (NCS) and deformational plagiocephaly are craniofacial conditions resulting in abnormal head shape that have also been associated with atypical language development. NCS occurs as the result of premature fusion at one or more skull growth sites and affects roughly 1 in 2000 live births. Deformational plagiocephaly, which affects as many as 48% of infants, is caused by mechanical forces acting on the head in utero or by postnatal positioning. Despite shared difficulties, there has been no study to date comparing atypical neural development in ASD and conditions of cranial asymmetry.
Given recent evidence that infants at high risk for ASD demonstrate atypical perceptual narrowing (Seery et al., 2010), this study aimed to examine language processing in infants at high risk for ASD relative to those with NCS or deformational plagiocephaly. Our goals were to elucidate the underlying processes behind language delay in ASD through comparison to (a) other conditions of atypical cognitive development and (b) normal-risk infants.
Three groups of infants under 12 months participated in the study: 15 infants at high risk for ASD by virtue of having a sibling diagnosed with the disorder, 15 normal-risk controls, and 40 infants previously diagnosed with NCS or deformational plagiocephaly. ERPs were recorded with a 128 channel HydroCel Geodesic Sensor Net during auditory presentations of native (English) and non-native (Hindi) phonemes. ERP analysis focused on the mismatch negativity (MMN) recorded over the midline scalp.
Consistent with predictions, control infants displayed a robust MMN between 6 and 9 months, indicating differentiation of native and non-native phonemes (mean difference= 3.56 microvolts). Analyses in progress contrast MMN amplitude between these normal-risk controls, infants at high risk for ASD, and non-ASD risk infants. We predict that subjects from ASD and non-ASD risk conditions will demonstrate persistent discrimination of the non-native phoneme at later ages relative to normal-risk subjects, indicating deviant or delayed language processing.
Results will provide insight into the contributory mechanisms of language impairment in ASD. By examining the degree of deficient intrinsic language processing, our study will help to clarify the development of communicative delay in ASD. Because prior research in the neural development of infants at risk for ASD has lacked non-ASD clinical groups, this study will provide critical information regarding the specificity of atypical developmental patterns in ASD.