Neurophysiologic Mechanisms of Tinnitus

Abstract

AbstractResearch over the past decade has provided new insights into the neural mechanisms likely to produce the false percepts of sound associated with tinnitus. These insights have emerged mainly as a result of electrophysiologic studies, examining changes in brain activity, and behavioral studies, examining changes in perception, in animals that have been treated with well-known tinnitus inducers such as salicylates, quinine, and intense sound. The available evidence, based on electrophysiologic studies, suggests that tinnitus is associated with disturbances in spontaneous neural activity in the auditory system. These abnormalities include increases in spontaneous activity (hyperactivity), changes in the timing of neural discharges (i.e., the temporal firing properties of neurons), and an increase in bursting activity of neurons. Parallel studies using behavioral testing methods have demonstrated that agents, which produce these neural changes, also cause tinnitus in animals. This article reviews the literature concerned with both behavioral evidence for tinnitus in animal models and the associated changes that occur at peripheral and central levels of the auditory system. Abbreviations: Al = primary auditory cortex, All = secondary auditory cortex, AFF = anterior auditory field, CF = characteristic frequency, C02 = carbon dioxide, DCN = dorsal cochlear nucleus, EEG = electroencephalogram, FMRI = functional magnetic resonance imaging, IC = inferior colliculus, OAEs = otoacoustic emissions, PET = positron emission tomography, SA = spontaneous activity, SOAEs = spontaneous otoacoustic emissions