Tinnitus and Hyperacusis (TH)
Adam Sheppard, Center for Hearing and Deafness
Assistant Professor
University at Buffalo
Buffalo, New York, United States
Background: Hyperacusis is an intolerance to moderately-loud sounds with a prevalence of ~9% in the adult population (Paulin et al., 2016). Animal studies suggest that hyperacusis may result from enhanced sound-evoked neural activity due to an imbalance in excitatory/inhibitory network control along the auditory neuroaxis (Sheppard et al., 2019). In animals, prolonged exposure to low-level noise (LLN) can reduce sound-evoked activity in sub-cortical and cortical auditory nuclei (Pienkowski, 2018; Sheppard et al., 2018). In humans, using LLN therapy for several weeks has shown to elevate the intensity at which sounds become intolerably loud (Formby et al., 2015), this conceivably would reverse reduced loudness tolerance in patients with hyperacusis. However, there remains little evidence that links LLN-induced elevated loudness discomfort levels to reduced sound-evoked neural activity in humans. This project objectively assessed sub-cortical and cortical auditory regions before and during LLN noise therapy. The goal was to (1) determine if self-reported change in loudness was linked to reduced sound-evoked activity and (2) evaluate the utility of clinically available objective tools to assess noise therapy effectiveness at treating abnormal loudness symptoms.
Methods: Seven adults that self-reported abnormal loudness tolerance (hyperacusis questionnaire score) used ear-level noise therapy for a minimum of 12 h/day for 3 weeks. Noise therapy consisted of a 1-4 kHz band-passed noise; the spectrum of noise was confirmed using on-ear probe-mic measures. Consistent usage of noise therapy was monitored by data logging the average hours/day from the device on a weekly basis. A test battery that included subjective questionnaires, auditory brainstem response (ABR), cortical auditory evoked potentials (CAEPs), acoustic reflex thresholds (ARTs) and auditory reaction-time intensity (RT-I) functions were collected before noise therapy began and on a weekly basis for three consecutive weeks.
Results: Participants adhered to the consistent use of noise-therapy (mean ~12h/day). After two weeks of noise therapy participants self-reported a significant decline in the functional impact of their loudness intolerance, this remained declined after three-weeks (repeated one-way ANOVA, p< .05). There was no significant change in ARTs evoked with .5 or 1 kHz tones, but there was a significant increase in ARTs evoked with a 2 kHz tone after three weeks of noise therapy (repeated one-way ANOVA, p< .01). There was no significant change in ABR amplitude or latency (wave V), or CAEP (P1) amplitude input/output functions. However, CAEP latencies were significantly longer after 3 weeks of noise therapy (repeated two-way ANOVA, p< .05), primarily those evoked with moderately-high intensities. There was no significant change in RT-I at any time point compared to baseline.
Conclusions: These preliminary findings suggest that noise therapy may improve (increase) loudness tolerance by reducing sound-evoked neural activity in both sub-cortical (ARTs) and Cortical (CAEPs) auditory regions of the brain. With further characterization, these objective tests may serve as a method of evaluating treatment efficacy for patients with hyperacusis.
Funding: This project was funded by the American Academy of Audiology Foundation New Investigator AwardLearning Objectives: