By Julia Campbell, Au.D., Ph.D.
Tinnitus, or the perception of sound where none is present, has been estimated to affect approximately 15 percent of adults. Unfortunately, there is no cure for tinnitus, nor is there an objective measure of the disorder, with professionals relying instead upon patient report.
There are several theories as to why tinnitus occurs, with one of the more prevalent hypotheses involving what is termed decreased inhibition. Neural inhibition is a normal function throughout the nervous system, and works in tandem with excitatory neural signals for accomplishing tasks ranging from motor output to the processing of sensory input. In sensory processing, such as hearing, both inhibitory and excitatory neural signals depend on external input.
For example, if an auditory signal cannot be relayed through the central auditory pathways due to cochlear damage resulting in hearing loss, both central excitation and inhibition may be reduced. This reduction in auditory-related inhibitory function may result in several changes in the central nervous system, including increased spontaneous neural firing, neural synchrony, and reorganization of cortical regions in the brain. Such changes, or plasticity, could possibly result in the perception of tinnitus, allowing signals that are normally suppressed to be perceived by the affected individual. Indeed, tinnitus has been reported in an estimated 30 percent of those with clinical hearing loss over the frequency range of 0.25 to 8 kilohertz (kHz), suggesting that cochlear damage and tinnitus may be interconnected.
Article republished from hearinghealthfoundation.org/blogs/measuring-brain-signals-leads-to-insights-into-mild-tinnitus