Relationship between M100 Auditory Evoked Response and Auditory Radiation Microstructure in 16p11.2 Deletion and Duplication Carriers.

Learn how you can help with a new
Autism, ADHD, Anxiety & Depression study.

CAR stands united with the Black Lives Matter movement
against racism and social injustice.

TitleRelationship between M100 Auditory Evoked Response and Auditory Radiation Microstructure in 16p11.2 Deletion and Duplication Carriers.
Publication TypeJournal Article
Year of Publication2016
AuthorsBerman, JI, Chudnovskaya, D, Blaskey, L, Kuschner, E, Mukherjee, P, Buckner, R, Nagarajan, S, Chung, WK, Sherr, EH, Roberts, TPL
JournalAJNR Am J Neuroradiol
Date Published2016 Jun
KeywordsAuditory Pathways, Child, Chromosome Deletion, Chromosome Duplication, Chromosomes, Human, Pair 16, Developmental Disabilities, Evoked Potentials, Auditory, Female, Humans, Magnetoencephalography, Male

BACKGROUND AND PURPOSE: Deletion and duplication of chromosome 16p11.2 (BP4-BP5) have been associated with developmental disorders such as autism spectrum disorders, and deletion subjects exhibit a large (20-ms) delay of the auditory evoked cortical response as measured by magnetoencephalography (M100 latency). The purpose of this study was to use a multimodal approach to test whether changes in white matter microstructure are associated with delayed M100 latency.MATERIALS AND METHODS: Thirty pediatric deletion carriers, 9 duplication carriers, and 39 control children were studied with both magnetoencephalography and diffusion MR imaging. The M100 latency and auditory system DTI measures were compared between groups and tested for correlation.RESULTS: In controls, white matter diffusivity significantly correlated with the speed of the M100 response. However, the relationship between structure and function appeared uncoupled in 16p11.2 copy number variation carriers. The alterations to auditory system white matter microstructure in the 16p11.2 deletion only partially accounted for the 20-ms M100 delay. Although both duplication and deletion groups exhibit abnormal white matter microstructure, only the deletion group has delayed M100 latency.CONCLUSIONS: These results indicate that gene dosage impacts factors other than white matter microstructure, which modulate conduction velocity.

Alternate JournalAJNR Am J Neuroradiol
PubMed ID26869473
PubMed Central IDPMC4907815
Grant ListK01 MH096091 / MH / NIMH NIH HHS / United States
R01 DC008871 / DC / NIDCD NIH HHS / United States
U54 HD086984 / HD / NICHD NIH HHS / United States
Leave a Comment