Tinnitus and Normal Hearing: A Study of 175 Cases

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Introduction: Due to our actual knowledge tinnitus in most cases results from abnormal neural activity elicited at any level of auditory pathways and is interpreted in auditory cortex as a perception of sound, which is not accompanied by any mechanic activity within the cochlea. Tinnitus patients usually present various degrees of cochlear dysfunction, which can be manifested as sensorineural hearing loss, loudness intolerance, a distinct decrease of the DPOAE amplitude, recruitment or abnormal efferent reduction of OAEs through contralateral acoustic stimulation. But 8-15% of tinnitus patients present normal audiometric profiles. In these patients the mechanism of tinnitus generation remains unclear.

Aim of the study: The aim of the study was to assess DPOAE levels and EHF thresholds in tinnitus subjects with normal hearing and compare the data with those from a normally hearing control group without tinnitus, in order to evaluate if any detectable high frequency cochlear dysfunction might be responsible for the tinnitus generation.

Material and methods: 175 tinnitus patients (group 1 – tinnitus in left ear - 47 patients, group 2 – tinnitus in right ear – 23 patients, group 3 – bilateral tinnitus – 105 patients) and 60 controls (group 4). Inclusion criteria: age up to 40, normal otoscopic examination, type A tympanometry, normal hearing (up to 20 dB) in PTA (250-8000 Hz), no loudness intolerance, constant tinnitus for at least 6 months of stable localization (site of tinnitus has not changed from the previous localization). In each patient high frequency audiometry (at 10, 12.5, 14 and 16 kHz) and DPOAE registration (L1=65 dB SPL, L2=55 dB SPL, f2/f1= 1.2, S/N≥3 dB) were performed. Then statistical analysis was applied for comparison between left and right ears in the same group and also across different group of patients. Results: statistically significant differences were observed mainly in unilateral tinnitus group. These differences were more evident in audiometric data than DPOAE data. Leftsided tinnitus was twice more frequent than right-sided tinnitus. Few statistically significant differences were found between bilateral tinnitus group and controls. Conclusions: Unilateral tinnitus in normally hearing individuals may be caused by the damage of the basal region of the cochlea. There is greater incidence of high frequency hearing loss (above 8 kHz) in the ear with tinnitus in comparison to control group. In unilateral tinnitus group, the organ of Corti at the site of tinnitus is more seriously damaged than in the opposite ear. The asymmetry of cochlear damage may be crucial for tinnitus lateralization. Bilateral tinnitus, more frequently than unilateral one, can result from other pathologies, not connected with the organ of Corti.


Antwerp, Germany

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