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Cereb Cortex. 2016 May;26(5):1957-64. doi: 10.1093/cercor/bhv008. Epub 2015 Feb 11.

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

Author information

1
Lurie Family Foundations MEG Imaging Center, Department of Radiology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
2
Department of Radiology.
3
Department of Psychology, Harvard University, Cambridge, MA 02138, USA.
4
Department of Pediatrics, Columbia University Medical Center, New York, NY 10032, USA.
5
Simons Foundation, New York, NY 10010, USA.
6
Department of Neurology, University of California, San Francisco School of Medicine, San Francisco, CA 94143, USA.

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.

KEYWORDS:

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

PMID:
25678630
DOI:
10.1093/cercor/bhv008
[Indexed for MEDLINE]

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