Trends in Neurosciences
Volume 27, Issue 11, November 2004, Pages 676-682
Journal home page for Trends in Neurosciences

The neuroscience of tinnitus

https://doi.org/10.1016/j.tins.2004.08.010Get rights and content

Tinnitus is an auditory phantom sensation (ringing of the ears) experienced when no external sound is present. Most but not all cases are associated with hearing loss induced by noise exposure or aging. Neuroscience research has begun to reveal how tinnitus is generated by the brain when hearing loss occurs, and to suggest new avenues for management and prevention of tinnitus following hearing injuries. Downregulation of intracortical inhibition induced by damage to the cochlea or to auditory projection pathways highlights neural processes that underlie the sensation of phantom sound.

Section snippets

Is tinnitus in the ear or the brain?

Tinnitus sensations associated with hearing loss are usually localized towards the affected ear(s). Does this mean that tinnitus is generated in the ear? This contentious issue, which has great implications for which types of treatment should be developed, can only be resolved in animal models that are conditioned to signal the presence of tinnitus following application of ototoxic drugs 4, 5 or excessive noise [6]. There is limited support for the assumption that tinnitus is the result of

Cortical reorganization in tinnitus

The animal research reviewed here investigated the response properties of neurons following hearing injuries or application of ototoxic drugs, and points to changes in the balance of excitation and inhibition at multiple levels of the projection pathway [5]. It is reasonable to assume that expression of these effects in the cortex contributes in some way to the perception of tinnitus. One change that has been well documented is alteration of tonotopic maps in AI following cochlear damage

Listening to tinnitus

Changes in cortical organization and in neural dynamics that occur after exposure to noise or tinnitus-inducing drugs should relate to what the tinnitus subject hears. But which changes correlate with the perception of tinnitus?

One possibility is that over-representation in the cortical tonotopic map of edge frequencies (i.e. those frequencies at the low-frequency and/or high-frequency borders of the hearing loss that have near normal thresholds) is itself responsible for the tinnitus sensation

Plasticity gone wrong?

It is unlikely that changes in neural activity (response properties of neurons and cortical organization) that are induced in auditory pathways by noise exposure and other tinnitus-inducing events occur in isolation. In particular, synchronous activity among neurons in the cortex reflects the number of shared axon collaterals (thalamocortical and corticocortical), the strength of their synapses, and their firing rates. Decreases in intracortical inhibition and increases in spontaneous activity

Alleviating tinnitus

At present, evidence for a contribution of neuroplastic processes to tinnitus is indirect, relying on documented properties of neural plasticity, including rapid remodeling of synaptic strengths by temporally coincident inputs, as revealed in physiological studies. Recent evoked potential studies of human subjects confirm that acoustic behavioral training modifies neural dynamics in the auditory cortex [61] with changes occurring in AII and AI [62], although more readily in AII, in agreement

Acknowledgements

We acknowledge the support of the Canadian Institutes of Health Research (CIHR) New Emerging Team grant on ‘Understanding, treating and preventing tinnitus’.

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