Publications (26) View all
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Article: Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus.
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ABSTRACT: Numerous studies have demonstrated elevated spontaneous and sound-evoked brainstem activity in animal models of tinnitus, but data on brainstem function in people with this common clinical condition are sparse. Here, auditory nerve and brainstem function in response to sound was assessed via auditory brainstem responses (ABR) in humans with tinnitus and without. Tinnitus subjects showed reduced wave I amplitude (indicating reduced auditory nerve activity) but enhanced wave V (reflecting elevated input to the inferior colliculi) compared with non-tinnitus subjects matched in age, sex, and pure-tone threshold. The transformation from reduced peripheral activity to central hyperactivity in the tinnitus group was especially apparent in the V/I and III/I amplitude ratios. Compared with a third cohort of younger, non-tinnitus subjects, both tinnitus, and matched, non-tinnitus groups showed elevated thresholds above 4 kHz and reduced wave I amplitude, indicating that the differences between tinnitus and matched non-tinnitus subjects occurred against a backdrop of shared peripheral dysfunction that, while not tinnitus specific, cannot be discounted as a factor in tinnitus development. Animal lesion and human neuroanatomical data combine to indicate that waves III and V in humans reflect activity in a pathway originating in the ventral cochlear nucleus (VCN) and with spherical bushy cells (SBC) in particular. We conclude that the elevated III/I and V/I amplitude ratios in tinnitus subjects reflect disproportionately high activity in the SBC pathway for a given amount of peripheral input. The results imply a role for the VCN in tinnitus and suggest the SBC pathway as a target for tinnitus treatment.Journal of the Association for Research in Otolaryngology 08/2012; · 2.84 Impact Factor -
Article: Subcallosal brain structure: Correlation with hearing threshold at supra-clinical frequencies (>8 kHz), but not with tinnitus.
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ABSTRACT: This study tested for differences in brain structure between tinnitus and control subjects, focusing on a subcallosal brain region where striking differences have been inconsistently found previously. Voxel-based morphometry (VBM) was used to compare structural MRIs of tinnitus subjects and non-tinnitus controls. Audiograms of all subjects were normal or near-normal at standard clinical frequencies (≤8 kHz). Mean threshold through 14 kHz, age, sex and handedness were matched between groups. There were no definitive differences between tinnitus and control groups in modulated or unmodulated maps of gray matter (GM) probability (i.e., GM volume and concentration, respectively). However, when the image data were tested for correlations with parameters that were either not measured or not matched between the tinnitus and control groups of previous studies, a notable correlation was found: Threshold at supra-clinical frequencies (above 8 kHz) was negatively correlated with modulated GM probability in ventral posterior cingulate cortex, dorsomedial prefrontal cortex, and a subcallosal region that included ventromedial prefrontal cortex and coincided with previously-reported differences between tinnitus and control subjects. The results suggest an explanation for the discrepant findings in subcallosal brain: threshold at supra-clinical frequencies may have differed systematically between tinnitus and control groups in some studies but not others. The observed correlation between (1) brain structure in regions engaged in cognitive and attentional processes and (2) hearing sensitivity at frequencies generally considered unnecessary for normal human auditory behavior is surprising and worthy of follow up.Hearing research 04/2012; · 2.18 Impact Factor -
Article: Hearing without listening: functional connectivity reveals the engagement of multiple nonauditory networks during basic sound processing.
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ABSTRACT: The present functional magnetic resonance imaging (fMRI) study presents data challenging the traditional view that sound is processed almost exclusively in the classical auditory pathway unless imbued with behavioral significance. In a first experiment, subjects were presented with broadband noise in on/off fashion as they performed an unrelated visual task. A conventional analysis assuming predictable sound-evoked responses demonstrated a typical activation pattern that was confined to classical auditory centers. In contrast, spatial independent component analysis (sICA) disclosed multiple networks of acoustically responsive brain centers. One network comprised classical auditory centers, but four others included nominally "nonauditory" areas: cingulo-insular cortex, mediotemporal limbic lobe, basal ganglia, and posterior orbitofrontal cortex, respectively. Functional connectivity analyses confirmed the sICA results by demonstrating coordinated activity between the involved brain structures. In a second experiment, fMRI data obtained from unstimulated (i.e., resting) subjects revealed largely similar networks. Together, these two experiments suggest the existence of a coordinated system of multiple acoustically responsive intrinsic brain networks, comprising classical auditory centers but also other brain areas. Our results suggest that nonauditory centers play a role in sound processing at a very basic level, even when the sound is not intertwined with behaviors requiring the well-known functionality of these regions.Brain connectivity. 01/2011; 1(3):233-44. -
Article: Ringing ears: the neuroscience of tinnitus.
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ABSTRACT: Tinnitus is a phantom sound (ringing of the ears) that affects quality of life for millions around the world and is associated in most cases with hearing impairment. This symposium will consider evidence that deafferentation of tonotopically organized central auditory structures leads to increased neuron spontaneous firing rates and neural synchrony in the hearing loss region. This region covers the frequency spectrum of tinnitus sounds, which are optimally suppressed following exposure to band-limited noise covering the same frequencies. Cross-modal compensations in subcortical structures may contribute to tinnitus and its modulation by jaw-clenching and eye movements. Yet many older individuals with impaired hearing do not have tinnitus, possibly because age-related changes in inhibitory circuits are better preserved. A brain network involving limbic and other nonauditory regions is active in tinnitus and may be driven when spectrotemporal information conveyed by the damaged ear does not match that predicted by central auditory processing.Journal of Neuroscience 11/2010; 30(45):14972-9. · 7.11 Impact Factor -
Article: Tinnitus, diminished sound-level tolerance, and elevated auditory activity in humans with clinically normal hearing sensitivity.
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ABSTRACT: Phantom sensations and sensory hypersensitivity are disordered perceptions that characterize a variety of intractable conditions involving the somatosensory, visual, and auditory modalities. We report physiological correlates of two perceptual abnormalities in the auditory domain: tinnitus, the phantom perception of sound, and hyperacusis, a decreased tolerance of sound based on loudness. Here, subjects with and without tinnitus, all with clinically normal hearing thresholds, underwent 1) behavioral testing to assess sound-level tolerance and 2) functional MRI to measure sound-evoked activation of central auditory centers. Despite receiving identical sound stimulation levels, subjects with diminished sound-level tolerance (i.e., hyperacusis) showed elevated activation in the auditory midbrain, thalamus, and primary auditory cortex compared with subjects with normal tolerance. Primary auditory cortex, but not subcortical centers, showed elevated activation specifically related to tinnitus. The results directly link hyperacusis and tinnitus to hyperactivity within the central auditory system. We hypothesize that the tinnitus-related elevations in cortical activation may reflect undue attention drawn to the auditory domain, an interpretation consistent with the lack of tinnitus-related effects subcortically where activation is less potently modulated by attentional state. The data strengthen, at a mechanistic level, analogies drawn previously between tinnitus/hyperacusis and other, nonauditory disordered perceptions thought to arise from neural hyperactivity such as chronic neuropathic pain and photophobia.Journal of Neurophysiology 09/2010; 104(6):3361-70. · 3.32 Impact Factor
