Modulation of hyperacusis and tinnitus loudness in tinnitus patients with and without hearing loss following 3 weeks of acoustic stimulation: A proof-of-concept study

Tinnitus and hyperacusis are two debilitating conditions that are highly comorbid. It has been postulated that they may originate from similar pathophysiological mechanisms such as an increase in central gain. Interestingly, sound stimulation has been shown to reduce central gain and is currently used for the treatment of both conditions. This study investigates the effect of sound stimulation on both tinnitus and hyperacusis in the same patients. Two distinct series of tinnitus participants were tested: one with normal or near-normal hearing (n = 16) and one with hearing loss (n = 14). A broadband noise shaped to cover most of the tinnitus frequency spectrum was delivered through hearing aids using the noise generator feature (no amplification) and verified through real-ear measurements. Participants received sound stimulation for 3 weeks and were tested before (at baseline), then after 1 week and at the end of the 3 weeks of sound stimulation. There was also a 1-month follow-up after the end of the stimulation protocol. The measurements included self-reported measures of tinnitus and hyperacusis (VAS), validated questionnaires (THI, HQ) and psychoacoustic measurements (tinnitus battery and loudness functions). On both self-assessment (VAS of sound tolerance and tinnitus loudness) and psychoacoustic measures (loudness function and tinnitus loudness in dB), about 50% of tinnitus participants had a synchronous (either a decrease or an increase) modulation of hyperacusis and tinnitus loudness after 1 week and 3 weeks of acoustic stimulation and up to about 70% of participants at 1-M follow-up. The decrease of hyperacusis and tinnitus loudness was more prevalent in normal-hearing participants. There was a significant increase in tinnitus loudness during and following the stimulation in the group with hearing loss. Hyperacusis improvement as assessed by loudness function was significantly correlated with the intensity level of the acoustic stimulation (dB level of the noise produced by the noise generator) in tinnitus participants with normal/near-normal hearing thresholds. Our study partly supports the central gain hypothesis by showing synchronous modulation of hyperacusis and tinnitus loudness. It also shows beneficial effects of acoustic stimulation in some tinnitus individuals, in particular those with normal or near-normal hearing, while highlighting the importance of a careful fitting of sound generators to prevent increase. Since the amplification feature was not turned on in our study, future work should determine whether amplification alone, or in addition to acoustic stimulation (sound generators), would benefit to those with hearing loss.