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dc.contributor.advisorJennifer R. Melcher.en_US
dc.contributor.authorGu, Jianwen Wendy, 1981-en_US
dc.contributor.otherHarvard University--MIT Division of Health Sciences and Technology.en_US
dc.date.accessioned2011-08-30T15:44:49Z
dc.date.available2011-08-30T15:44:49Z
dc.date.copyright2011en_US
dc.date.issued2011en_US
dc.identifier.urihttp://hdl.handle.net/1721.1/65515
dc.descriptionThesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2011.en_US
dc.descriptionCataloged from PDF version of thesis.en_US
dc.descriptionIncludes bibliographical references (p. 83-90).en_US
dc.description.abstractTinnitus, the ongoing perception of sound in the absence of a physical stimulus, and hyperacusis, the intolerance of sound intensities considered comfortable by most people, are two often co-occurring clinical conditions lacking effective treatments. This thesis identified neural correlates of these poorly understood disorders using functional magnetic resonance imaging (fMRI) and auditory brainstem responses (ABRs) to measure sound-evoked activity in the auditory pathway. Subjects with clinically normal hearing thresholds, with and without tinnitus, underwent fMRI or ABR testing and behavioral assessment of sound-level tolerance (SLT). The auditory midbrain, thalamus, and primary auditory cortex (PAC) showed elevated fMRI activation related to reduced SLT (i.e. hyperacusis). PAC, but not midbrain or thalamus, showed elevated fMRI activation related to tinnitus, perhaps reflecting undue attention to the auditory domain. In contrast to fMRI activation, ABRs showed relationships only to tinnitus, not SLT. Wave I of the ABR, which reflects auditory nerve activity, was reduced in tinnitus subjects, while wave V, reflecting input activity to the midbrain, was elevated. Wave I reduction in tinnitus subjects suggests that auditory nerve dysfunction apparent only above threshold is a factor in tinnitus. Because ABRs reflect activity in only one of multiple pathways from cochlear nucleus to midbrain, the wave V elevation implicates this particular pathway in tinnitus. The results directly link tinnitus and hyperacusis to hyperactivity within the central auditory system. Because fMRI and ABRs reflect different aspects of neural activity, the dependence of fMRI activation on SLT and ABR activity on tinnitus in the midbrain raises the possibility that tinnitus and hyperacusis arise in parallel from abnormal activity in separate brainstem pathways.en_US
dc.description.statementofresponsibilityby Jianwen Wendy Gu.en_US
dc.format.extent90 p.en_US
dc.language.isoengen_US
dc.publisherMassachusetts Institute of Technologyen_US
dc.rightsM.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.en_US
dc.rights.urihttp://dspace.mit.edu/handle/1721.1/7582en_US
dc.subjectHarvard University--MIT Division of Health Sciences and Technology.en_US
dc.titleNeural abnormalities underlying tinnitus and hyperacusisen_US
dc.typeThesisen_US
dc.description.degreePh.D.en_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technology.en_US
dc.identifier.oclc746792840en_US


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