Tinnitus with a Normal Audiogram: Physiological Evidence for Hidden Hearing Loss and Computational Model
By Roland Schaette, David McAlpine. Journal of Neuroscience, 2011
927 citations recorded by the source corpus.
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.
Subfields: Cognitive Neuroscience, Neurology, Sensory Systems
View Paper: https://www.semanticscholar.org/paper/bba7d446e6f95113c85fd6f233f58b0a911af73f
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Citations in the corpus
- Age-Related Cochlear Synaptopathy: An Early-Onset Contributor to Auditory Functional Decline (2013, background): “It may reflect an increase in “central gain” after partial peripheral deafferentation (Schaette and McAlpine, 2011) and has been implicated in the generation of tinnitus, a common affliction in aging (Lockwood et al., 2002).”
- Synaptopathy in the noise-exposed and aging cochlea: primary neural degeneration in acquired sensorineural hearing loss (2015, background): “It has been hypothesized that both these phenomena may arise from a type of homeostatic plasticity, i.e. the upregulation of synaptic gain in central auditory neurons subsequent to the loss of ascending inputs from ANFs to central circuits (Schaette and McAlpine, 2011).”
- Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates. (2013, background): “nontinnitus subjects with matching (normal) audiometric thresholds (Gu et al. 2012; Schaette and McAlpine 2011).”