Delayed Auditory Evoked Responses in Autism Spectrum Disorder across the Life Span

Abstract

The M50 and M100 auditory evoked responses reflect early auditory processes in the primary/secondary auditory cortex. Although previous M50 and M100 studies have been conducted on individuals with autism spectrum disorder (ASD) and indicate disruption of encoding simple sensory information, analogous investigations of the neural correlates of auditory processing through development from children into adults are very limited. Magnetoencephalography was used to record signals arising from the left and right superior temporal gyrus during auditory presentation of tones to children/adolescents and adults with ASD as well as typically developing (TD) controls. One hundred and thirty-two participants (aged 6-42 years) were included into the final analyses (children/adolescents: TD, n = 36, 9.21 ± 1.6 years; ASD, n = 58, 10.07 ± 2.38 years; adults: TD, n = 19, 26.97 ± 1.29 years; ASD, n = 19, 23.80 ± 6.26 years). There were main effects of group on M50 and M100 latency (p < 0.001) over hemisphere and frequency. Delayed M50 and M100 latencies were found in participants with ASD compared to the TD group, and earlier M50 and M100 latencies were associated with increased age. Furthermore, there was a statistically significant association between language ability and both M50 and M100 latencies. Importantly, differences in M50 and M100 latencies between TD and ASD cohorts, often reported in children, persisted into adulthood, with no evidence supporting latency convergence.

Keywords: Autism spectrum disorder; Language ability; Life span; M100; M50; Magnetoencephalography; Tones.

Figure 1.

Source modeled activity waveform from right superior temporal gyrus for a representative participant in each group. Black vertical lines on the waveform and arrow indicate stimulus onset (zero ms). Gray lines indicate M50 peaks for the representative TD adult marked at 59 ms and for the representative ASD adult marked at 79 ms and TD child marked at 101 ms, for the representative ASD child marked at 117 ms. A clear prolongation of latency is observed in ASD in both child and adult.

Figure 2.

Estimated marginal means latencies by group across hemisphere for M50 and M100 latency. Error bars represent one standard error of the marginal means. There is a significant main effect of group on M50 and M100 latency (p < 0.05) across hemispheres. ASD showed significantly delayed M50 and M100 latency compared to TD across frequency and hemisphere in both children and adults (p < 0.05).

Figure 3.

A scatter plot of M50 and M100 latency (Figure 3, averaged across Hemisphere and Frequency) vs log₁₀(age) shows a statistically significant negative association across groups (M50: R² = 0.384, p < 0.001, M100: R² = 0.086, p = 0.002). Figure 3 also reports the within group M50 and M100 vs log₁₀(age) associations and their respective R² (M50: TD: R² = 0.578, p < 0.001, ASD: R² = 0.239, p < 0.001; M100: TD: R² = 0.191, p = 0.005, ASD: R² = 0.011, p = 0.398).