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Tinnitus is a phantom auditory sensation that reduces quality of life for millions of people worldwide, and for which there is no medical cure. Most cases of tinnitus are associated with hearing loss caused by ageing or noise exposure. Exposure to loud recreational sound is common among the young, and this group are at increasing risk of developing tinnitus. Head or neck injuries can also trigger the development of tinnitus, as altered somatosensory input can affect auditory pathways and lead to tinnitus or modulate its intensity. Emotional and attentional state could be involved in the development and maintenance of tinnitus via top-down mechanisms. Thus, military personnel in combat are particularly at risk owing to combined risk factors (hearing loss, somatosensory system disturbances and emotional stress). Animal model studies have identified tinnitus-associated neural changes that commence at the cochlear nucleus and extend to the auditory cortex and other brain regions. Maladaptive neural plasticity seems to underlie these changes: it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures, possibly generating the phantom percept. This Review highlights the links between animal and human studies, and discusses several therapeutic approaches that have been developed to target the neuroplastic changes underlying tinnitus.

A neural connection between the trigeminal ganglion and the auditory brainstem was investigated by using retrograde and anterograde tract tracing methods: iontophoretic injections of biocytin or biotinylated dextran‐amine (BDA) were made into the guinea pig trigeminal ganglion, and anterograde labeling was examined in the cochlear nucleus and superior olivary complex. Terminal labeling after biocytin and BDA injections into the ganglion was found to be most dense in the marginal cell area and secondarily in the magnocellular area of the ventral cochlear nucleus (VCN). Anterograde and retrograde labeling was also seen in the shell regions of the lateral superior olivary complex and in periolivary regions. The labeling was seen in the neuropil, on neuronal somata, and in regions surrounding blood vessels. Retrograde labeling was investigated using either wheatgerm agglutinin‐horseradish peroxidase (WGA‐HRP), BDA, or a fluorescent tracer, iontophoretically injected into the VCN. Cells filled by retrograde labeling were found in the ophthalmic and mandibular divisions of the trigeminal ganglion. We have previously shown that these divisions project to the cochlea and middle ear, respectively. This study provides the first evidence that the trigeminal ganglion innervates the cochlear nucleus and superior olivary complex. This projection from a predominantly somatosensory ganglion may be related to integration mechanisms involving the auditory end organ and its central targets. J. Comp. Neurol. 419:271–285, 2000. © 2000 Wiley‐Liss, Inc.

This paper reports that endolymphatic hydrops causes a significant reduction of retrogradely labeled cell bodies of the ipsilateral trigeminal ganglion following application of horseradish peroxidase in the cochlea. We previously showed that the trigeminal ganglion is a source of primary sensory innervation to the cochlear blood vessels. The innervation of the cochlea from the trigeminal ganglion may provide the basis of an alternative mechanism for Ménière's syndrome (imbalance, hearing loss, tinnitus, and a sensation of fullness in the ear) for which a central neural basis has been speculated. Innervation patterns of sensory nerves from the trigeminal ganglion to the cochlear blood vessels were studied using retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). Healthy and hydropic guinea pigs were unilaterally implanted with an osmotic pump and a cannula for cochlear delivery of 2% WGA-HRP or vehicle alone. In other guinea pigs the cochlea was pretreated with 100 μmol capsaicin before administering 2% WGA-HRP. Histological sections of the ipsi- and contralateral trigeminal ganglia were obtained 48 h after WGA-HRP infusion. In the hydropic guinea pig, the number of labeled nerve cell bodies observed in the anteriomedial portion of the trigeminal ganglion at the origin of the ophthalmic nerve was reduced by 70% relative to normal animals. Capsaicin pretreatment nearly eliminated the labeled sensory fibers as expected. These data indicate that the trigeminal innervation to the cochlea could be involved in inner ear homeostatic disturbances, including the hydrops that is symptomatic of Ménière's disease.

Noninvasive bimodal auditory stimulation targets the dorsal cochlear nucleus and reduces tinnitus in guinea pigs and humans.