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

We just began a large new study on
Autism, ADHD, Anxiety & Depression in 12-17 year-olds.
Read more and learn how you can help!

TitleAuditory Evoked M100 Response Latency is Delayed in Children with 16p11.2 Deletion but not 16p11.2 Duplication.
Publication TypeJournal Article
Year of Publication2016
AuthorsJenkins, J, Chow, V, Blaskey, L, Kuschner, E, Qasmieh, S, Gaetz, L, J Edgar, C, Mukherjee, P, Buckner, R, Nagarajan, SS, Chung, WK, Spiro, JE, Sherr, EH, Berman, JI, Roberts, TPL
JournalCereb Cortex
Date Published2016 May
KeywordsAcoustic Stimulation, Adolescent, Auditory Cortex, Autistic Disorder, Child, Chromosome Deletion, Chromosome Disorders, Chromosome Duplication, Chromosomes, Human, Pair 16, Evoked Potentials, Auditory, Female, Genotype, Humans, Intellectual Disability, Magnetoencephalography, Male, Neuropsychological Tests

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.

Alternate JournalCereb. Cortex
PubMed ID25678630
PubMed Central IDPMC6276914
Grant ListU54 HD086984 / HD / NICHD NIH HHS / United States
Leave a Comment