Abstract
Objective: To describe the quantitative treatment outcomes of patients undergoing acoustic coordinated reset (CR) neuromodulation at a single independent audiology practice over a 22- to 26-week period as part of an open label, non-randomized, non-controlled observational study.Methods: Sixty-six patients with subjective tonal tinnitus were treated with acoustic CR neuromodulation with a retrospective review of patient records being performed in order to identify changes of visual analog scale (VAS, n = 66) and in the score of the tinnitus handicap questionnaire (THQ, n = 51). Patients had their tinnitus severity recorded prior to the initiation of therapy using the tinnitus handicap inventory in order to categorize patients into slight up to catastrophic impact categories. THQ and VAS for tinnitus loudness/annoyance were obtained at the patient’s initial visit, at 10–14 and 22–26 weeks.Results: Visual analog scale scores were significantly improved, demonstrating a 25.8% mean reduction in tinnitus loudness and a 32% mean reduction in tinnitus annoyance with a clinically significant reduction in percept loudness and annoyance being recorded in 59.1 and 72.7% of the patient group. THQ scores were significantly improved by 19.4% after 22–26 weeks of therapy compared to baseline.Conclusion: Acoustic CR neuromodulation therapy appears to be a practical and promising treatment for subjective tonal tinnitus. However, due to the lack of a control group it is difficult to reach an absolute conclusion regarding to what extent the observed effects are related directly to the acoustic CR neuromodulation therapy. Also, as the observed patient group was made up of paying clients it is unknown as to whether this could have caused any additional placebo like effects to influence the final results.
Highlights
Tinnitus is the involuntary perception of sound, in the absence of corresponding auditory stimuli, which is perceived as originating within an individual’s ears or head
EEG recordings for this study demonstrated a change in pathologically altered power spectra, for α, γ, and δ bandwidths, to a more normative level within a network of brain areas [19, 23] along with a significant reduction of abnormal effective connectivity [15] and cross-frequency coupling [24] within a tinnitus-related network of brain areas
The results obtained in the randomized proof-of-concept trial [19] were confirmed in a real life study in 200 patients suffering from chronic tonal tinnitus [25]
Summary
Tinnitus is the involuntary perception of sound, in the absence of corresponding auditory stimuli, which is perceived as originating within an individual’s ears or head. Even subjects who have normal audiometric thresholds have been shown to have outer hair cell damage [3] and dead cochlea regions [4]. This peripheral damage is thought to result in central neural plastic changes that affect the balance between excitatory and inhibitory processes leading to a potential promotion of increased afferent activity [5] and neural synchronicity [6]. It has been noted that cochlea pathology causes a reduction in spontaneous firing rates in mammalian auditory nerve fibers [8] These observations serve to implicate activity changes in central structures as being the causal factor for the phantom percept generation. MEG data demonstrating altered spectral power, in subjects experiencing tinnitus, suggest that this does not adequately explain the emergence of the percept in a satisfactory manner [4]
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