Related Experiment Video
Updated: Apr 17, 2026
Quantitative Assessment of Cortical Auditory-tactile Processing in Children with Disabilities
Published on: January 29, 2014
Auditory Evoked M100 Response Latency is Delayed in Children with 16p11.2 Deletion but not 16p11.2 Duplication
Julian Jenkins1, Vivian Chow1, Lisa Blaskey1
1Lurie Family Foundations MEG Imaging Center, Department of Radiology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
Insights
Children with a 16p11.2 deletion show significantly delayed auditory M100 responses, indicating impaired auditory processing. This finding is more pronounced than in idiopathic autism spectrum disorder (ASD).
Area of Science:
- Neuroscience
- Genetics
- Developmental Pediatrics
Background:
- The 16p11.2 BP4-BP5 copy number variant (CNV) is linked to behavioral phenotypes, including autism spectrum disorder (ASD) and cognitive impairments.
- Auditory processing deficits are common in ASD, but their specific relationship with 16p11.2 CNVs requires further investigation.
Purpose of the Study:
- To investigate auditory processing differences in children with 16p11.2 deletion and 16p11.2 duplication CNVs compared to controls.
- To determine if auditory evoked response latency is affected by the 16p11.2 CNV and cognitive ability.
Main Methods:
- Magnetoencephalography (MEG) was used to record auditory evoked responses (M100 latency) in children with 16p11.2 deletion, 16p11.2 duplication, and age-matched controls.
- Participants passively listened to binaural tones during MEG recordings.
- M100 latency was analyzed, controlling for age and cognitive ability.
Main Results:
- Children with the 16p11.2 deletion exhibited significantly delayed M100 latencies compared to controls, indicating impaired auditory processing.
- No significant M100 latency differences were found between 16p11.2 duplication carriers and controls.
- Auditory processing delays in 16p11.2 deletion carriers were more pronounced than those typically seen in idiopathic ASD.
Conclusions:
- The 16p11.2 deletion is strongly associated with significant auditory processing delays.
- These delays are a distinct neurophysiological marker linked to the 16p11.2 deletion.
- The findings suggest a specific auditory processing phenotype in 16p11.2 deletion carriers, distinct from idiopathic ASD.
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.
