Abstract:Tinnitus is strongly linked with the presence of damaged hearing. However, it is not known why tinnitus afflicts only some, and not all, hearing-impaired listeners. One possibility is that tinnitus patients have specific inner ear damage that triggers tinnitus. In this study, differences in cochlear function inferred from psychophysical measures were measured between hearing-impaired listeners with tinnitus and hearing-impaired listeners without tinnitus. Despite having similar average hearing loss, tinnitus p… Show more
“…Tan et al [2013] demonstrated that patients with chronic tinnitus tended to experience high-frequency hearing loss, better frequency selectivity and compression. This difference may be caused by the different mechanisms between acute and chronic tinnitus.…”
Objective: We aimed to evaluate the prognostic factors for acute-onset tinnitus associated with unilateral idiopathic sudden sensorineural hearing loss (ISSNHL) and to assess the relationship between these factors and the final recovery. Methods: A total of 770 patients with unilateral ISSNHL were enrolled retrospectively and their medical records reviewed. Patients were classified into two groups according to the presence of acute-onset tinnitus at the initial examination. Patient characteristics and the results of pure-tone audiometry were compared between the two groups initially and 3 months later. Results: A total of 70.9% (n = 546) of patients had tinnitus initially. There was no significant difference in the mean hearing thresholds of the affected ear irrespective of accompanying tinnitus. In contrast, patients with tinnitus in the affected ear tended to have significantly better mean hearing thresholds in the nonaffected ear (p < 0.05). The logistic regression analysis revealed that better mean hearing thresholds in the nonaffected ear were associated with tinnitus occurrence (p < 0.05). Better hearing thresholds in the nonaffected ear, younger age, absence of dizziness, low-tone hearing loss, and combined intratympanic dexamethasone injection were associated with full recovery (p < 0.05). However, tinnitus was not an independent risk factor for full recovery. Conclusion: Better contralateral hearing was associated with both an increased incidence of concurrent tinnitus and a better final recovery. However, tinnitus was not related to full recovery.
“…Tan et al [2013] demonstrated that patients with chronic tinnitus tended to experience high-frequency hearing loss, better frequency selectivity and compression. This difference may be caused by the different mechanisms between acute and chronic tinnitus.…”
Objective: We aimed to evaluate the prognostic factors for acute-onset tinnitus associated with unilateral idiopathic sudden sensorineural hearing loss (ISSNHL) and to assess the relationship between these factors and the final recovery. Methods: A total of 770 patients with unilateral ISSNHL were enrolled retrospectively and their medical records reviewed. Patients were classified into two groups according to the presence of acute-onset tinnitus at the initial examination. Patient characteristics and the results of pure-tone audiometry were compared between the two groups initially and 3 months later. Results: A total of 70.9% (n = 546) of patients had tinnitus initially. There was no significant difference in the mean hearing thresholds of the affected ear irrespective of accompanying tinnitus. In contrast, patients with tinnitus in the affected ear tended to have significantly better mean hearing thresholds in the nonaffected ear (p < 0.05). The logistic regression analysis revealed that better mean hearing thresholds in the nonaffected ear were associated with tinnitus occurrence (p < 0.05). Better hearing thresholds in the nonaffected ear, younger age, absence of dizziness, low-tone hearing loss, and combined intratympanic dexamethasone injection were associated with full recovery (p < 0.05). However, tinnitus was not an independent risk factor for full recovery. Conclusion: Better contralateral hearing was associated with both an increased incidence of concurrent tinnitus and a better final recovery. However, tinnitus was not related to full recovery.
“…Within a run, the masker level was varied to determine the masking threshold for the probe. Between runs, the masker frequency was changed randomly across the following values, 0.5, 0.7, 0.9, 1, 1.1, 1.2, 1.3 and 1.6 times the probe frequency and resulted in an iso-forward masking contour (IFMC; Meddis et al, 2010;Lecluyse et al, 2013;Tan et al, 2013). IFMCs were generated for probe frequencies 0.25, 0.5, 1, 2, 4, and 6 kHz.…”
Section: General Principlesmentioning
confidence: 99%
“…The development and assessment of the measurement procedures have been described elsewhere Tan et al, 2013). Their aim is to generate an auditory profile that summarizes basic aspects of auditory functioning while also being simple enough to be used in the context of computer modelling.…”
The creation of individualized computer models of hearing loss can be used to simulate auditory profiles of impaired listeners and suggest hypotheses concerning the underlying peripheral pathology.
“…The high-threshold ANFs most vulnerable to damage by noise exposure (Furman et al, 2013) or to deterioration with aging (Sergeyenko et al, 2013) are those with high frequency tuning (Kujawa and Liberman, 2009), which is consistent with the percepts reported in audiometrically normal tinnitus (Roberts et al, 2008;Schaette and McAlpine, 2011). Cochlear factors may also explain why not all individuals with high frequency hearing loss detected by the audiogram develop tinnitus (Tan et al, 2013). High threshold ANFs with high frequency tuning could be better preserved in such individuals, although this question has not been extensively studied.…”
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. We tested these predictions by measuring (128-channel EEG) the sound-evoked 40-Hz auditory steady-state response (ASSR) known to localize tonotopically to neural sources in A1. For comparison the N1 transient response localizing to distributed neural sources in nonprimary cortex (A2) was also studied. When tested under baseline conditions where tinnitus subjects would have heard their tinnitus, ASSR responses were larger in a tinnitus group than in controls when evoked by 500 Hz probes while the reverse was true for tinnitus and control groups tested with 5 kHz probes, confirming frequency-dependent group differences in this measure. On subsequent trials where RI was induced by masking (narrow band noise centered at 5 kHz), ASSR amplitude increased in the tinnitus group probed at 5 kHz but not in the tinnitus group probed at 500 Hz. When collapsed into a single sample tinnitus subjects reporting comparatively greater RI depth and duration showed comparatively larger ASSR increases after masking regardless of probe frequency. Effects of masking on ASSR amplitude in the control groups were completely reversed from those in the tinnitus groups, with no change seen to 5 kHz probes but ASSR increases to 500 Hz probes even though the masking sound contained no energy at 500 Hz (an "off-frequency" masking effect). In contrast to these findings for the ASSR, N1 amplitude was larger in tinnitus than control groups at both probe frequencies under baseline conditions, decreased after masking in all conditions, and did not relate to RI. These results suggest that aberrant neural activity occurring in the TFR of A1 underlies tinnitus and its modulation during RI. They indicate further that while neural changes occur in A2 in tinnitus, these changes do not reflect the tinnitus percept. Models for tinnitus and forward masking are described that integrate these findings within a common framework.
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