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, 9 (4), 417-35

Residual Inhibition Functions Overlap Tinnitus Spectra and the Region of Auditory Threshold Shift

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Residual Inhibition Functions Overlap Tinnitus Spectra and the Region of Auditory Threshold Shift

Larry E Roberts et al. J Assoc Res Otolaryngol.

Abstract

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. The neural synchrony hypothesis predicts that tinnitus spectra, and heretofore unmeasured "residual inhibition functions" that relate residual tinnitus suppression to the center frequency of masking sounds, should cover the region of hearing loss in the audiogram. We confirmed these predictions in two independent cohorts totaling 90 tinnitus subjects, using computer-based tools designed to assess the psychoacoustic properties of tinnitus. Tinnitus spectra and residual inhibition functions for depth and duration increased with the amount of threshold shift over the region of hearing impairment. Residual inhibition depth was shallower when the masking sounds that were used to induce residual inhibition showed decreased correspondence with the frequency spectrum and bandwidth of the tinnitus. These findings suggest that tinnitus and its suppression in residual inhibition depend on processes that span the region of hearing impairment and not on mechanisms that enhance cortical representations for sound frequencies at the audiometric edge. Hearing thresholds measured in age-matched control subjects without tinnitus implicated hearing loss as a factor in tinnitus, although elevated thresholds alone were not sufficient to cause tinnitus.

Figures

FIG. 1
FIG. 1
Summary of steps in the Tinnitus Tester and residual inhibition tester. A The Tinnitus Tester. A familiarization program was administered before the Tinnitus Tester to acquaint subjects with the user interface and to illustrate the dimensions of pitch and loudness (see text for details). B Spectra of the BPN5 and BPN15 sounds at a CF of 0.5 kHz (top) and 5.0 kHz (bottom). The spectra for BPN5 and BPN15 sounds at other CFs were similarly shaped. C Residual inhibition tester. WN white noise masker.
FIG. 2
FIG. 2
RI functions and tinnitus spectra inversely track the region of threshold shift in bilateral tinnitus. A Hamilton and Vancouver cohorts are shown separately. B Grand averaged results. The data point to the left in each panel gives RI depth induced by white noise (WN). The arrow denotes the “audiometric edge” of normal hearing (the stimulus frequency adjoining the frequency at which the hearing threshold falls above 25 dB HL on the audiometrically reversed dB axis). Error bars denote 1 standard error in this and subsequent figures.
FIG. 3
FIG. 3
Tinnitus spectra and loudness. A Tinnitus spectra vary with tinnitus bandwidth (tonal, ringing, and hissing tinnitus). The broken line denotes a rating of 40 on a Borg CR100 scale, indicating that the sound is beginning to resemble the tinnitus. B The tinnitus spectrum peaks at 6 kHz in poorer hearing tinnitus subjects but continues to rise to higher frequencies in better hearing tinnitus subjects (tinnitus bandwidths combined). Better hearing subjects had hearing thresholds ≤35 dB HL at 8 kHz (poorer hearing subjects had hearing thresholds >35 dB HL at 8 kHz). C The tinnitus spectrum covered higher frequencies when the audiometric edge was above 4 kHz. The three tinnitus bandwidths are combined. D Tinnitus loudness is greater when matched using sound frequencies outside of the region of hearing loss. Tinnitus loudness matches are shown separately for the Hamilton and Vancouver cohorts (averaged over tinnitus bandwidth). Loudness matches for tonal cases and their audiogram converted to SPL are also given for the Hamilton sample only. The inset contrasts the difference between the latter two functions at 1 and 6 kHz (tinnitus loudness).
FIG. 4
FIG. 4
RI functions for depth and duration reach their maxima in and cover the region of hearing loss (2–10 kHz). A Mean RI depth (left panel) and RI duration (right panel) for the three tinnitus bandwidths. Sample size is n = 12, 13, and 34 subjects in the hissing, ringing, and tonal subgroups, respectively. B Subjects are distributed according to peak RI depth and peak RI duration (n = 59 bilateral cases).
FIG. 5
FIG. 5
RI depth increases with masking level. A Contrast of subgroups with good RI (RI depth ≤−2.0) and poor RI, for RI depth and RI duration. The poor RI group does not show significant RI depth (mean rating is zero across CFs). B RI masker loudness (ML) and tinnitus loudness (TL) in SPL, in the good RI and poor RI subgroups. C Mean masking level is higher in the good compared to the poor RI subgroup. Masking level is the difference between RI masker loudness and tinnitus loudness in B.
FIG. 6
FIG. 6
RI functions and tinnitus spectra inversely track the region of threshold shift in unilateral tinnitus. The format is the same as in Figure 2.
FIG. 7
FIG. 7
Hearing thresholds are elevated between 2–8 kHz in tinnitus subjects compared to age-matched controls. This is true for younger subjects (age ≤50 years) as well as older subjects (age >50 years), even though the mean audiogram for younger subjects is in the normal range up to 10 kHz.

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