Evidence for differential modulation of primary and nonprimary auditory cortex by forward masking in tinnitus.

It has been proposed that tinnitus is generated by aberrant neural activity that develops among neurons in tonotopic of regions of primary auditory cortex (A1) affected by hearing loss, which is also the frequency region where tinnitus percepts localize (Eggermont and Roberts 2004; Roberts et al., 2010, 2013). These models suggest (1) that differences between tinnitus and control groups of similar age and audiometric function should depend on whether A1 is probed in tinnitus frequency region (TFR) or below it, and (2) that brain responses evoked from A1 should track changes in the tinnitus percept when residual inhibition (RI) is induced by forward masking.

Modulation of electrocortical brain activity by attention in individuals with and without tinnitus.

Age and hearing-level matched tinnitus and control groups were presented with a 40 Hz AM sound using a carrier frequency of either 5 kHz (in the tinnitus frequency region of the tinnitus subjects) or 500 Hz (below this region). On attended blocks subjects pressed a button after each sound indicating whether a single 40 Hz AM pulse of variable increased amplitude (target, probability 0.67) had or had not occurred.

Neural plasticity expressed in central auditory structures with and without tinnitus.

Sensory training therapies for tinnitus are based on the assumption that, notwithstanding neural changes related to tinnitus, auditory training can alter the response properties of neurons in auditory pathways. To assess this assumption, we investigated whether brain changes induced by sensory training in tinnitus sufferers and measured by electroencephalography (EEG) are similar to those induced in age and hearing loss matched individuals without tinnitus trained on the same auditory task. Auditory training was given using a 5 kHz 40-Hz amplitude-modulated (AM) sound that was in the tinnitus frequency region of the tinnitus subjects and enabled extraction of the 40-Hz auditory steady-state response (ASSR) and P2 transient response known to localize to primary and non-primary auditory cortex, respectively.

Re-examining the relationship between audiometric profile and tinnitus pitch.

Objective: We explored the relationship between audiogram shape and tinnitus pitch to answer questions arising from neurophysiological models of tinnitus: 'Is the dominant tinnitus pitch associated with the edge of hearing loss?' and 'Is such a relationship more robust in people with narrow tinnitus bandwidth or steep sloping hearing loss?'

Design: A broken-stick fitting objectively quantified slope, degree and edge of hearing loss up to 16 kHz. Tinnitus pitch was characterized up to 12 kHz. We used correlation and multiple regression analyses for examining relationships with many potentially predictive audiometric variables.

Residual inhibition functions overlap tinnitus spectra and the region of auditory threshold shift.

Animals exposed to noise trauma show augmented synchronous neural activity in tonotopically reorganized primary auditory cortex consequent on hearing loss. Diminished intracortical inhibition in the reorganized region appears to enable synchronous network activity that develops when deafferented neurons begin to respond to input via their lateral connections. In humans with tinnitus accompanied by hearing loss, this process may generate a phantom sound that is perceived in accordance with the location of the affected neurons in the cortical place map.

Residual inhibition functions in relation to tinnitus spectra and auditory threshold shift.

Conclusions: Psychoacoustic functions relating the depth and duration of tinnitus suppression ('residual inhibition') to the center frequency of band-passed noise masking sounds appear to span the region of hearing loss, as do psychoacoustic measurements of the tinnitus spectrum. The results (1) suggest that cortical map reorganization induced by hearing loss is not the principal source of the tinnitus sensation and (2) provide a necessary baseline for optimizing residual inhibition in individual cases.

Objective: To measure residual inhibition functions and tinnitus spectra using sounds spanning the region of hearing loss.

Distributed auditory cortical representations are modified when non-musicians are trained at pitch discrimination with 40 Hz amplitude modulated tones.

Several functional brain attributes reflecting neocortical activity have been found to be enhanced in musicians compared to non-musicians. Included are the N1m evoked magnetic field, P2 and right-hemispheric N1c auditory evoked potentials, and the source waveform of the magnetically recorded 40 Hz auditory steady state response (SSR). We investigated whether these functional brain attributes measured by EEG are sensitive to neuroplastic remodeling in non-musician subjects.

Enhancement of neuroplastic P2 and N1c auditory evoked potentials in musicians.

P2 and N1c components of the auditory evoked potential (AEP) have been shown to be sensitive to remodeling of the auditory cortex by training at pitch discrimination in nonmusician subjects. Here, we investigated whether these neuroplastic components of the AEP are enhanced in musicians in accordance with their musical training histories. Highly skilled violinists and pianists and nonmusician controls listened under conditions of passive attention to violin tones, piano tones, and pure tones matched in fundamental frequency to the musical tones.