• tinnitus
• hearing
• otology
• audiology

Tinnitus in adults has received much scientific and clinical attention of late. Traditional theories about the pathogenesis of tinnitus concentrated on the cochlea, but this model had some serious shortcomings and could not explain some clinical findings. A purely cochlear model of tinnitus fails to explain those patients who have tinnitus in the presence of normal hearing and conversely why many patients with cochlear hearing loss do not have tinnitus. In addition, symptoms of tinnitus related anxiety, insomnia, and general agitation are very common in adults troubled with tinnitus¹ and cannot be ascribed to cochlear dysfunction alone.

To explain these seeming paradoxes it is necessary to look at what happens to auditory information in the brain as well as in the ear. Information is sent from the cochlea to the brain stem and then to the primary and associative auditory cortices in the temporal lobes to give the conscious sensation of hearing. However, information is also sent from brain stem auditory nuclei to the reticular formation and to the sympathetic autonomic nervous system. These systems are involved with reaction to alerting or challenging stimuli. In addition information is sent to the limbic system, specifically the amygdalae, which are involved in emotional responses. These connections are vital for the role of hearing as the major alerting and warning sense, and a consensus view that the mammalian auditory system evolved to allow the perception of sounds with survival value is now held.² If there is an audible threat in the environment the brain filters that threat from other auditory information and instigates an appropriate limbic and reticular reaction with a sympathetically mediated fight or flight response. Tinnitus distress arises when this response is generated not to an outside stimulus but to internal neural …