Auditory Training in Tinnitus

Abstract

1. We reviewed sensory training studies from the point of view that tinnitus is caused by synchronous neural activity that develops in tonotopic regions of primary auditory cortex deafferented by hearing loss. Studies were classified according to whether training was conducted within the tinnitus frequency region or outside of it, and whether training was active (requiring behavioral responses) or passive (sounds were presented as background signals). Effects of training on the psychoacoustic properties of tinnitus were distinguished from those on the distress behavior that accompanies tinnitus. 2. Studies in all four categories have reported significant reductions compared to untreated controls in tinnitus distress, measured by standardized questionnaires and visual analogue scales at the first compared to untreated controls in-course assessment, with little further change thereafter. Because the particular details of sensory training do not appear to matter, these gains could reflect important nonspecific effects of the treatment procedures. 3. Psychoacoustic measures may more directly assess tinnitus sensations. Reductions in minimum masking level (MML) on the order of 5–10 dB have been reported by several studies, implying that tinnitus has become weaker. Improvements in loudness discomfort levels (LDL) have also been reported, as have changes in the frequency content of tinnitus. Improvements in MML and LDL are more gradual than those on distress behavior assessed by ­questionnaires, suggesting that neural plasticity may be at work. 4. Several studies reporting improvements in psychoacoustic measures and questionnaire data used passive sound presentation procedures. Hence, active sensory training requiring discriminated behavioral responses is not needed for these changes. 5. Systematic manipulation of the frequency content of trained sounds has been attempted in only a few studies. This step is needed to determine whether sound training induces specific changes in tinnitus. Alternatively, sound therapy may amplify the nonspecific effect of elements common to all tinnitus therapies. 6. Future studies should continue the practice of specifying how many participants of the total recruited contributed to a data analysis, and why and when exclusions occurred. Substantial sample sizes will be needed to establish treatment effects. Neural ­correlates offer the advantage of comparative immunity to patient expectations and self-report bias. When sounds are used to evoke neural responses, changes in loudness recruitment consequent on ­rescaling of loudness growth functions by sound exposure are a potential contributing factor.