Auditory evoked M100 latency in children with 16p11.2 deletions and duplications

Contains the data, scripts and statistical analyses for published manuscript investigating the latency of the auditory evoked M100 response in children with 16p11.2 deletions and duplications. Main finding is that individuals with 16p11.2 deletions exhibit delayed latencies relative to controls and 16p11.2 duplications; no statistically significant difference between controls and 16p11.2 duplications is observed. Results are mainly analyzed via Linear Mixed Effects Models (LMMs) in conjunction with multiple comparison procedures (i.e., Tukey HSD) with other tests (e.g., Brown-Forsythe test) used as needed.

Abstract

Individuals with the 16p11.2 BP4–BP5 copy number variant (CNV) exhibit a range of behavioral phenotypes that may include mild impairment in cognition and clinical diagnoses of autism spectrum disorder (ASD). To better understand auditory processing impairments in populations with this chromosomal variation, auditory evoked responses were examined in children with the 16p11.2 deletion, 16p11.2 duplication, and age-matched controls. Stimuli consisted of sinusoidal binaural tones presented passively while children underwent recording with magnetoencephalography (MEG). The primary indicator of auditory processing impairment was the latency of the ∼100-ms “M100” auditory response detected by MEG, with the 16p11.2 deletion population exhibiting profoundly delayed M100 latencies relative to controls. This delay remained even after controlling for potential confounds such as age and cognitive ability. No significant difference in M100 latency was observed between 16p11.2 duplication carriers and controls. Additionally, children meeting diagnostic criteria for ASD (16p11.2 deletion carriers) exhibited nonsignificant latency delays when compared with the corresponding CNV carriers not meeting criteria for ASD. Present results indicate that 16p11.2 deletion is associated with auditory processing delays analogous to (but substantially more pronounced than) those previously reported in “idiopathic” ASD.