Objective: The most probable place generating tinnitus in the auditory pathway is the outer hair cells (OHCs) inside the cochlea. Otoacoustic emissions are used to assess their activity. The objective of the investigation was to measure the features of distortion product otoacoustic emissions (DPOAE) in a group of tinnitus patients without hearing loss, estimate the diagnostic value of the parameters for the analysis of cochlear function in the patients, emphasizing those most useful in localizing tinnitus generators, and determine the hypothetical influence of hyperacusis and misophony on DPOAE parameters in tinnitus patients.
Patients and methods: The material consisted of 44 patients with tinnitus and without hearing loss. In the control group were 33 patients without tinnitus with the same state of hearing. The tinnitus patients were divided into three subgroups: those with hyperacusis, those with misophonia, and those with neither. After collecting medical history and performing clinical examination of all the patients, tonal and impedance audiometry, ABR, and discomfort level were evaluated. Then DPOAE were measured using three procedures. First the amplitudes of two points per octave were assessed, second the "fine structure" method with 16-20 points per octave (f2/f1=1.22, L1=L2=70 dB), and the third procedure included recording the growth function in three series for input tones of f2=2002, 4004, and 6006Hz (f2/f1=1.22) and L1=L2 levels increasing by increments of 5 dB in each series.
Results and conclusions: Hyperacusis was found in 63% and misophonia in 10% of the tinnitus patients with no hearing loss. DPOAE amplitudes in recordings with two points per octave and the fine structure method are very valuable parameters for estimating cochlear function in tinnitus patients with normal hearing. Function growth rate cannot be the only parameter in measuring DPOAE in tinnitus patients, including subjects with hyperacusis and misophonia. The markedly higher DPOAE amplitudes in the group of tinnitus patients without hearing loss suggest that tinnitus may be caused by increased motility of the OHCs induced by decreasing efferent fiber activity, and not by OHC failure. Hyperacusis significantly increases the amplitude of DPOAE in tinnitus patients with no hearing loss.
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