Auditory Evoked M100 Response Latency is Delayed in Children with 16p11.2 Deletion but not 16p11.2 Duplication

作者：Jenkins Julian III; Chow Vivian; Blaskey Lisa; Kuschner Emily; Qasmieh Saba; Gaetz Leah; Edgar J Christopher; Mukherjee Pratik; Buckner Randall; Nagarajan Srikantan S; Chung Wendy K; Spiro John E; Sherr Elliott H; Berman Jeffrey I; Roberts Timothy P L^*

来源：Cerebral Cortex, 2016, 26(5): 1957-1964.

DOI：10.1093/cercor/bhv008

• autism spectrum disorder
• 16p112 deletion
• 16p112 duplication
• M100
• magnetoencephalography

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 similar to 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.

• 出版日期2016-5