Chapter 20 - Auditory Neuronal Networks and Chronic Tinnitus

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Tinnitus, or ringing in the ears, is a chronic auditory disorder that negatively impacts 2–10% of the adult population. With contributions from laboratory animal models, the neuronal basis of this heterogeneous disorder is unfolding. The most common cause of tinnitus is loss of peripheral sensitivity. Homeostatic compensation, or overcompensation, in the central auditory system produces the sensation of sound in the absence of acoustic input. Current knowledge indicates that even in animal models, where causal factors are singular, a distributed network of neural alterations underpins tinnitus. These alterations begin with a partial loss of cochlear neurons, and downregulation of inhibition in the auditory brainstem. Excitatory glutamatergic interneurons also upregulate. Downstream from the cochlear nuclei, alterations in neural discharge patterns are evident in the inferior colliculus, and tonotopic reorganization may occur in the auditory cortex. In animals, gamma-aminobutyric acid agonists and glutamatergic antagonists have been used successfully as therapeutics. In humans, therapeutic success has been more limited.