Auditory magnetic mismatch field latency: a biomarker for language impairment in autism.

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TitleAuditory magnetic mismatch field latency: a biomarker for language impairment in autism.
Publication TypeJournal Article
Year of Publication2011
AuthorsRoberts, TPL, Cannon, KM, Tavabi, K, Blaskey, L, Khan, SY, Monroe, JF, Qasmieh, S, Levy, SE, J Edgar, C
JournalBiol Psychiatry
Date Published2011 Aug 01
KeywordsAcoustic Stimulation, Adolescent, Auditory Cortex, Autistic Disorder, Child, Evoked Potentials, Auditory, Female, Humans, Language Disorders, Language Tests, Magnetoencephalography, Male, Neuropsychological Tests, Reaction Time

BACKGROUND: Auditory processing abnormalities are frequently observed in autism spectrum disorders (ASD), and these abnormalities may have sequelae in terms of clinical language impairment (LI). The present study assessed associations between language impairment and the amplitude and latency of the superior temporal gyrus magnetic mismatch field (MMF) in response to changes in an auditory stream of tones or vowels.METHODS: Fifty-one children with ASD, and 27 neurotypical control subjects, all aged 6 to 15 years, underwent neuropsychological evaluation, including tests of language function, as well as magnetoencephalographic recording during presentation of tones and vowels. The MMF was identified in the difference waveform obtained from subtraction of responses to standard from deviant stimuli.RESULTS: Magnetic mismatch field latency was significantly prolonged (p < .001) in children with ASD, compared with neurotypical control subjects. Furthermore, this delay was most pronounced (∼50 msec) in children with concomitant LI, with significant differences in latency between children with ASD with LI and those without (p < .01). Receiver operator characteristic analysis indicated a sensitivity of 82.4% and specificity of 71.2% for diagnosing LI based on MMF latency.CONCLUSIONS: Neural correlates of auditory change detection (the MMF) are significantly delayed in children with ASD, and especially those with concomitant LI, suggesting a neurobiological basis as well as a clinical biomarker for LI in ASD.

Alternate JournalBiol. Psychiatry
PubMed ID21392733
PubMed Central IDPMC3134608
Grant ListR01 DC008871 / DC / NIDCD NIH HHS / United States
R01 DC008871-01 / DC / NIDCD NIH HHS / United States
R01DC008871 / DC / NIDCD NIH HHS / United States
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