Tinnitus with a Normal Audiogram: Physiological Evidence for Hidden Hearing Loss and Computational Model

Abstract

Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

“…They are in agreement with previous reports of the following in tinnitus subjects: elevated V/I amplitude ratio (Kehrle et al 2008;Schaette and McAlpine 2011), elevated wave III amplitude (Attias et al 1996), and reduced wave I amplitude (Attias et al 1993;Schaette and McAlpine 2011). An absence of reduction in wave III of tinnitus subjects (Attias et al 1993) or wave V (Attias et al 1993; Schaette and McAlpine 2011), despite reduced wave I, has also been reported, which is tantamount to enhanced activity given the reduction in wave I (as discussed above).…”

“…Kehrle et al (2008), comparing tinnitus and non-tinnitus subjects with clinically normal thresholds, reported an enhanced V/I amplitude ratio in tinnitus subjects. While they did not report whether the enhanced amplitude ratio arose from a reduction in wave I, an elevation in wave V or, a combination of both, the earlier data of Attias et al (1993) and recent report of Schaette and McAlpine (2011) indicate that reduced wave I was a factor. Although the study of Barnea et al (1990) reported normal ABR amplitudes in tinnitus subjects with clinically normal audiograms, it compared the tinnitus data with clinical norms, not with a closely matched control group, an approach suitable for detecting gross ABR abnormalities but not subtler ones.…”

“…Notably, previous studies that examined ABR wave amplitudes (as opposed to only latencies) and also controlled for hearing sensitivity already provide indications that wave I may be reduced and subsequent waves elevated in human subjects with tinnitus (Attias et al 1993;Attias et al 1996;Kehrle et al 2008;Schaette and McAlpine 2011). Attias et al (1996) reported greater wave III amplitude in tinnitus subjects with high-frequency hearing loss compared with threshold-, sex-, and age-matched control subjects without tinnitus.…”

Mobile Apps for Management of Tinnitus: Users’ Survey, Quality Assessment, and Content Analysis (Preprint)

“…The majority of respondents reported some degree of hearing loss (494, 76.8%), consistent with the association between tinnitus and hearing loss [15]; [16]. The largest group of respondents reported mild hearing loss (n=261, 40.6%), with 149 respondents reporting no hearing loss (23.2%), 172 -moderate (26.8%) and 61 severe/profound hearing loss (9.5%).…”

Rapid Increase in Neural Conduction Time in the Adult Human Auditory Brainstem Following Sudden Unilateral Deafness

“…Nevertheless, increases in ABR amplitude, assumed to be triggered by deafferentation, have been reported elsewhere (e.g. Schaette and McAlpine 2011;Gu et al 2012).…”