A school aged sample of children with congenital disorders o

A school-aged sample of children with congenital disorders of the peripheral visual system (CDPVS), aged 8–13 years of normal verbal intelligence, were recruited for the investigation with matched controls of typical sight. Parent-reported questionnaires that are validated on children with typical sight for social communication difficulties, pragmatic language disorder, autism risk, and behavioural strengths and difficulties were included to assess the level of difficulties in the social domain. It was hypothesised further that individual differences between children with VI on the questionnaire measures (Sonksen and Dale 2002; Tadic et al., 2009) would be associated with differences in the ERP response to SON.
Materials and methods
Results
Discussion In a first step, the current study investigated the neurophysiological response to basic auditory social stimuli in children with VI in order to elucidate any differences in the neural processing of social signals. Differences between the own-name and control condition in the N1 and P2 time window indicated that own-name stimuli were preferentially processed. Higher amplitudes to self-relevant stimuli in early time windows are generally interpreted to reflect automatic capture of attention that does not require conscious awareness of the stimuli (Perrin et al., 1999; Perrin et al., 2006). Similar responses in both children with VI and typically sighted controls suggests that automatic attentional processing of self-relevant stimuli was not affected by congenital VI. In NMS-873 to the current findings that indicated no differences in latency or amplitude of early ERP components, some studies reported enhanced auditory processing in congenitally blind adults characterised by larger amplitudes and early latencies of N1 (Roder et al., 1999; Roder et al., 2000). Differences in early-latency auditory processing in children with VI may only emerge later in development, may only be present in individuals with the most severe forms of VI, or may be more apparent with non-social stimuli. The current study used complex auditory stimuli and a low number of trails, which is not optimal to resolve subtle differences in early ERP components. Differences in auditory processing in children with VI should be addressed in future experiments. While no differences in early components related to auditory processing and responses to control names between children with VI and typically-sighted controls were detected, group differences emerged in a later time window with less negative amplitudes to own-name stimuli in the VI group compared to controls. Similarly reduced amplitude of the ERP in response to own-name stimuli has also been reported for adults with ASD (Cygan et al., 2014). Responses to own name stimuli as presented in Acceptor splicing site study are thought to engage more social cognitive processing such as Theory of Mind (ToM) processing. Differences in the responsiveness to own name stimuli have been associated with deficits in Theory of Mind in ASD across several paradigms (Cygan et al., 2014, Lombardo et al., 2009; Carmody and Lewis, 2011). Reduced behavioural responsiveness to self-related information, e.g lack of response to name calling in situ, are now even part of clinical diagnostic observational schedules for autism e.g. the Autism Diagnostic Observation Schedule (ADOS, Lord et al., 2008). The current study found reduced amplitudes in response to own name stimuli over central and right frontal channels. Central channel regions also show the largest own-name specific effects in typically-sighted adults (Eichenlaub et al., 2012; Muller and Kutas, 1996). The topography of the SON response in the VI group deviates from the topography in the typically-sighted control group and from the published results for typical adults. This may indicate that different neural substrates are engaged in own-name processing in children with VI. This could be associated with deficits in social processing or may indicate compensatory engagement of additional neural substrates in the VI group.