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Objective: To investigate how tinnitus affects the processing of speech and non-speech stimuli at the subcortical level., Study Design: Cross-sectional analytical study., Setting: Academic, tertiary referral center., Patients: Eighteen individuals with tinnitus and 20 controls without tinnitus matched based on their age and sex. All subjects had normal hearing sensitivity., Intervention: Diagnostic., Main Outcome Measures: The effect of tinnitus on the parameters of auditory brainstem responses (ABR) to non-speech (click-ABR), and speech (sABR) stimuli was investigated., Results: Latencies of click ABR in waves III, V, and Vn, as well as inter-peak latency (IPL) of I to V were significantly longer in individuals with tinnitus compared with the controls. Individuals with tinnitus demonstrated significantly longer latencies of all sABR waves than the control group. The tinnitus patients also exhibited a significant decrease in the slope of the V-A complex and reduced encoding of the first and higher formants. A significant difference was observed between the two groups in the spectral magnitudes, the first formant frequency range (F1) and a higher frequency region (HF)., Conclusions: Our findings suggest that maladaptive neural plasticity resulting from tinnitus can be subcortically measured and affects timing processing of both speech and non-speech stimuli. The findings have been discussed based on models of maladaptive plasticity and the interference of tinnitus as an internal noise in synthesizing speech auditory stimuli.

The possible role of cochlear function in tinnitus generation is still a matter of debate. To assess the role of outer hair cell dysfunction in tinnitus and its possible relationship with ultra-high frequency (UHF) hearing sensitivity, transient evoked otoacoustic emissions (TEOAE) and UHF hearing thresholds were investigated in normal hearing individuals with and without tinnitus. Eighteen individuals with tinnitus and 22 without tinnitus participated in this study. TEOAE was recorded with click stimulus at 80 dBpeSPL. UHF pure tone audiometry was performed at 10, 12.5, 16, and 18 k Hz. The individuals with tinnitus had significantly poorer UHF hearing sensitivity compared to the control group at 12.5 and 18 k Hz (p<0.048). TEOAE was significantly abnormal in 72.2% of the tinnitus, and 18.2% of the control groups (p=0.001). 'There was a stronger correlation between increasing UHFs hearing threshold and decreasing SNRs of TEOAEs in the tinnitus group compared to the controls. The results support the deafferentation hypothesis, which suggests that the cochlear damage triggers tinnitus incidence, even in patients with normal hearing sensitivity on conventional audiometry, and considers a deafferentation as the underlying cause that elicits central reorganization and eventually leads to tinnitus. The deafferentation hypothesis provides a rationale for performing UHF threshold and OAE assessments in subjectively normal hearing patients with tinnitus. Our study revealed poorer UHF hearing thresholds and more TEOAE abnormalities in normal hearing individuals with tinnitus compared to the controls. Perhaps the alterations in the basal cochlea, following a decrease in UHF hearing sensitivity, affect OAEs that are originated from more apical cochlear parts in tinnitus ears more than non-tinnitus ears. [ABSTRACT FROM AUTHOR]

Tinnitus can cause functional or even structural changes at cortical regions. Given the possible role of the inferior colliculus (IC) in tinnitus due to the distribution of lateral inhibition and receiving input from top-down pathways, we investigated whether tinnitus can also affect subcortical regions, mainly the IC. Auditory brainstem responses to click (cABR) and speech stimuli (sABR) were recorded in 18 individuals with tinnitus and 22 controls without tinnitus matched based on their ages and genders. All subjects had normal hearing sensitivity. Latencies of cABR in waves V and Vn, as well as interpeak latencies (IPLs) of III-V and I-V were significantly longer in individuals with tinnitus compared to the controls. Individuals with tinnitus presented significantly longer latencies of all sABR waves than the control group. The tinnitus patients also presented significant decrease in the amplitude and slope of the V-A complex and declined encoding of the first and higher formants. A combination of bottom-up and top-down processes were involved in the impaired timing in the individuals with tinnitus. The deficits in the auditory processing at the subcortical level (presumably the mi dBrain) could be caused by abnormal bottom-up inputs (i.e. those from more peripheral auditory structures) or abnormal top-down inputs (i.e. abnormal modulations from more central structures through efferent pathways. As a main possible generator of late waves of cABR and all waves of sABR is the IC, these findings indicate that the subcortical regions, particularly the IC, may undergo maladaptive plasticity following tinnitus. The consistency between the results of cABR and sABR indicated that tinnitus might affect the processing of simple and complex stimuli in the same manner. [ABSTRACT FROM AUTHOR]