Abstract

Subjective tinnitus is characterised by the conscious perception of a phantom sound. Previous studies have shown that individuals with chronic tinnitus have disrupted sound-evoked cortical tonotopic maps, time-shifted evoked auditory responses, and altered oscillatory cortical activity. The main objectives of this study were to: (i) compare sound-evoked brain responses and cortical tonotopic maps in individuals with bilateral tinnitus and those without tinnitus; and (ii) investigate whether changes in these sound-evoked responses occur with amelioration of the tinnitus percept during a 30-week tinnitus treatment program. Magnetoencephalography (MEG) recordings of 12 bilateral tinnitus participants and 10 control normal-hearing subjects reporting no tinnitus were recorded at baseline, using 500 Hz, 1000 Hz, 2000 Hz, and 4000 Hz tones presented monaurally at 70 dBSPL through insert tube phones. For the tinnitus participants, MEG recordings were obtained at 5-, 10-, 20- and 30- week time points during tinnitus treatment. Results for the 500 Hz and 1000 Hz sources (where hearing thresholds were within normal limits for all participants) showed that the tinnitus participants had a significantly larger and more anteriorly located source strengths when compared to the non-tinnitus participants. During the 30-week tinnitus treatment, the participants’ 500 Hz and 1000 Hz source strengths remained higher than the non-tinnitus participants; however, the source locations shifted towards the direction recorded from the non-tinnitus control group. Further, in the left hemisphere, there was a time-shifted association between the trajectory of change of the individual’s objective (source strength and anterior-posterior source location) and subjective measures (using tinnitus reaction questionnaire, TRQ). The differences in source strength between the two groups suggest that individuals with tinnitus have enhanced central gain which is not significantly influenced by the tinnitus treatment, and may result from the hearing loss per se. On the other hand, the shifts in the tonotopic map towards the non-tinnitus participants’ source location suggests that the tinnitus treatment might reduce the disruptions in the map, presumably produced by the tinnitus percept directly or indirectly. Further, the similarity in the trajectory of change across the objective and subjective parameters after time-shifting the perceptual changes by 5 weeks suggests that during or following treatment, perceptual changes in the tinnitus percept may precede neurophysiological changes. Subgroup analyses conducted by magnitude of hearing loss suggest that there were no differences in the 500 Hz and 1000 Hz source strength amplitudes for the mild-moderate compared with the mild-severe hearing loss subgroup, although the mean source strength was consistently higher for the mild-severe subgroup. Further, the mild-severe subgroup had 500 Hz and 1000 Hz source locations located more anteriorly (i.e., more disrupted compared to the control group) compared to the mild-moderate group, although this was trending towards significance only for the 500Hz left hemisphere source. While the small numbers of participants within the subgroup analyses reduce the statistical power, this study suggests that those with greater magnitudes of hearing loss show greater cortical disruptions with tinnitus and that tinnitus treatment appears to reduce the tonotopic map disruptions but not the source strength (or central gain).

Highlights

  • Subjective tinnitus is the perception of sound which does not arise from a detectable external physical source

  • We compared mean sound-evoked MEG source amplitudes recorded in response to pure tones at octave-intervals between 500–4000 Hz, and 500 Hz cortical source locations in participants with significant tinnitus before, during, and following a 30-week tinnitus treatment program and compared this with a nontinnitus group

  • The results demonstrate that significant differences in the mean source strength of 500 Hz and 1000 Hz sound-evoked responses in the left hemisphere exist between individuals with tinnitus compared to those without, which did not change significantly throughout treatment

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Summary

Introduction

Subjective tinnitus is the perception of sound which does not arise from a detectable external physical source. In spite of growing neurophysiological research in humans and animals, the pathophysiological mechanisms that cause tinnitus remain unclear [3,4,5]. Animal models of tinnitus have shown that increases in spontaneous and sound-evoked responses occur in the cochlear nucleus [13, 14], inferior colliculus [15], and auditory cortex [16,17,18], despite reductions in spontaneous and evoked activity in the primary afferent neurons of the cochlea. In hamsters exposed to loud noise, Kaltenbach and colleagues [14] showed that moderate correlations exist between the peak level of dorsal cochlear nucleus hyperactivity and behavioural correlates of tinnitus, further supporting a more central mechanism of tinnitus

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