CHRONIC TINNITUS AFFECTS TONOTOPIC ORGANIZATION IN HUMAN AUDITORY CORTEX.

A.M. Leaver1, M.A. Chevillet1, L. Renier1,4, S. Morgan2, H.J. Kim3, J.PRauschecker1
Laboratory of Integrative Neuroscience and Cognition1, Department ofAudiology2,
Department of Otolaryngology3, Georgetown University MedicalCenter,
Washington DC; Neural Rehabilitation Engineering Laboratory4, Université
Catholique de Louvain, Belgium.

Despite the pervasiveness of tinnitus, little is known about its mechanisms of origin. Three factors seem to contribute to creating this auditory phantom sensation:

1) damage to the peripheral auditory system;
2) reorganization of central auditory structures; and
3) involvement of non-auditory central gating systems.

In a previous study (Leaver et al., Soc. Neurosci. Abstr. 2006), we provided some of the first direct evidence for cortical involvement, specifically demonstrating functional reorganization of primary auditory cortex in patients with chronic tinnitus. Using highresolution functional magnetic resonance imaging (fMRI), we monitored changes in cerebral blood oxygenation levels while tinnitus patients and control participants
with normal hearing listened to narrow band-passed noise bursts. A broad range of stimulus frequencies was tested. Stimuli were either matched to the patients’ tinnitus frequency, or were one-half, one, and two octaves above or below the middle/tinnitus frequency. Each tinnitus patient was matched with one control subject that heard the same range of stimulus frequencies. Results indicated a significant hyperactivity in the hemodynamic response to auditory stimulation in the auditory cortices of tinnitus patients, as compared to controls. We also observed distortion
within the tonotopic map of primary auditory cortex in tinnitus patients.

The distance between the tinnitus frequency and non-tinnitus frequencies was increased in patients as compared to inter-frequency spacing in controls. Thus, tinnitus results not only in hypersensitivity of primary auditory cortex, it induces plastic changes in the tonotopic organization of this area as well. With the present results, we corroborate the previous data in a larger number of patients and offer a more refined analysis of the distortions found in the tonotopic maps of tinnitus patients. Since hearing loss does not automatically result in tinnitus, we also discuss
the degree to which hearing loss affects auditory cortical reorganization and to what extent thalamic gating mechanisms play a role. Taken together, our data provide strong evidence for reorganization of auditory cortex as one important factor in the origin of chronic tinnitus.