Summary of evidence pointing to a role of the dorsal cochlear nucleus in the etiology of tinnitus.
Evidence has accumulated in the last decade that the dorsal cochlear nucleus (DCN) may be an important site in the etiology of tinnitus. This evidence comes from a combination of studies conducted in animals and humans. This paper will review the key findings, as follows. 1) Direct electrical stimulation of the DCN leads to changes in the loudness of tinnitus. This suggests that the loudness of tinnitus may be linked to changes in the level of neural activity in the DCN. 2) Exposure to tinnitus inducers, such as intense sound or cisplatin, causes neural activity in the DCN to become chronically elevated, a condition known as neuronal hyperactivity. 3) This hyperactivity is very similar to the activity that is evoked in the DCN by sound stimulation, suggesting that the hyperactivity represents a code that signals the presence of sound, even when there is no longer any sound stimulus. 4) Noise-induced hyperactivity in the DCN is correlated with tinnitus. Behavioral studies have demonstrated that animals exposed to the same intense sound that causes hyperactivity in the DCN develop tinnitus-like percepts. The correlation between the level of hyperactivity and the behavioral index of tinnitus was found to be statistically significant. 5) The DCN is a polysensory integration center, and electrophysiological studies have shown that both spontaneous activity and hyperactivity of neurons in the DCN can be modulated by stimulation of certain ipsilateral cranial nerves, such as the sensory branch of the trigeminal nerve. This ipsilateral modulation of DCN activity offers a plausible explanation of how tinnitus, when perceived on one side, can be modulated by certain manipulations of the head and neck on the side ipsilateral to the tinnitus, but rarely on the contralateral side. 6) The DCN exhibits various forms of neuronal plasticity that parallel the various forms of plasticity that characterize tinnitus. These findings collectively strengthen the view that the DCN may be a key structure that should be included as a target of anti-tinnitus treatment.
Kaltenbach
James A
JA
Auditory Neurobiology Laboratory, Department of Otolaryngology-Head and Neck Surgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. jkalten@med.wayne.edu
D000161:Acoustic Stimulation / Q000009:adverse effects; D000818:Animals; D017626:Cochlear Nucleus / Q000503:physiopathology*; D006224:Cricetinae; D004558:Electric Stimulation / Q000295:instrumentation; D004567:Electrodes, Implanted; D005072:Evoked Potentials, Auditory / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D012720:Severity of Illness Index; D013997:Time Factors; D014012:Tinnitus / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology*