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dc.contributor.authorAlbouy, Philippe
dc.contributor.authorTillmann, Barbara
dc.contributor.authorCaclin, Anne
dc.contributor.authorNorman-Haignere, Samuel Victor
dc.contributor.authorMcDermott, Joshua H.
dc.contributor.authorKanwisher, Nancy
dc.date.accessioned2017-05-04T14:09:00Z
dc.date.available2017-05-04T14:09:00Z
dc.date.issued2016-03
dc.date.submitted2015-12
dc.identifier.issn2190-8567
dc.identifier.urihttp://hdl.handle.net/1721.1/108659
dc.description.abstractCongenital amusia is a lifelong deficit in music perception thought to reflect an underlying impairment in the perception and memory of pitch. The neural basis of amusic impairments is actively debated. Some prior studies have suggested that amusia stems from impaired connectivity between auditory and frontal cortex. However, it remains possible that impairments in pitch coding within auditory cortex also contribute to the disorder, in part because prior studies have not measured responses from the cortical regions most implicated in pitch perception in normal individuals. We addressed this question by measuring fMRI responses in 11 subjects with amusia and 11 age- and education-matched controls to a stimulus contrast that reliably identifies pitch-responsive regions in normal individuals: harmonic tones versus frequency-matched noise. Our findings demonstrate that amusic individuals with a substantial pitch perception deficit exhibit clusters of pitch-responsive voxels that are comparable in extent, selectivity, and anatomical location to those of control participants. We discuss possible explanations for why amusics might be impaired at perceiving pitch relations despite exhibiting normal fMRI responses to pitch in their auditory cortex: (1) individual neurons within the pitch-responsive region might exhibit abnormal tuning or temporal coding not detectable with fMRI, (2) anatomical tracts that link pitch-responsive regions to other brain areas (e.g., frontal cortex) might be altered, and (3) cortical regions outside of pitch-responsive cortex might be abnormal. The ability to identify pitch-responsive regions in individual amusic subjects will make it possible to ask more precise questions about their role in amusia in future work. SIGNIFICANCE STATEMENT The neural causes of congenital amusia, a lifelong deficit in pitch and music perception, are not fully understood. We tested the hypothesis that amusia is due to abnormalities in brain regions that respond selectively to sounds with a pitch in normal listeners. Surprisingly, amusic individuals exhibited pitch-responsive regions that were similar to normal-hearing controls in extent, selectivity, and anatomical location. We discuss how our results inform current debates on the neural basis of amusia and how the ability to identify pitch-responsive regions in amusic subjects will make it possible to ask more precise questions about their role in amusic deficits.en_US
dc.language.isoen_US
dc.publisherBiomed Central Ltd.en_US
dc.relation.isversionofhttp://dx.doi.org/DOI:10.1523/JNEUROSCI.2705-15.2016en_US
dc.rightsCreative Commons Attribution 4.0 International Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.sourceSociety for Neuroscienceen_US
dc.titlePitch-Responsive Cortical Regions in Congenital Amusiaen_US
dc.typeArticleen_US
dc.identifier.citationNorman-Haignere, S. V. et al. “Pitch-Responsive Cortical Regions in Congenital Amusia.” Journal of Neuroscience 36.10 (2016): 2986–2994.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.departmentMcGovern Institute for Brain Research at MITen_US
dc.contributor.mitauthorNorman-Haignere, Samuel Victor
dc.contributor.mitauthorMcDermott, Joshua H.
dc.contributor.mitauthorKanwisher, Nancy
dc.relation.journalThe Journal of Neuroscienceen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsNorman-Haignere, Sam V.; Albouy, Philippe; Caclin, Anne; McDermott, Josh H.; Kanwisher, Nancy G.; Tillmann, Barbaraen_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-3965-2503
dc.identifier.orcidhttps://orcid.org/0000-0003-3853-7885
mit.licensePUBLISHER_CCen_US


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