Approximately 12% of adults experience tinnitus, but about 1% experience severe tinnitus that is in some cases disabling. Tinnitus is often accompanied by hyperacusis, a debilitating condition in which moderate intensity sounds are perceived as extremely loud. Tinnitus and hyperacusis were originally thought to originate in the cochlea as a consequence of hearing loss; however, over the past two decades, there has been a growing recognition that tinnitus and hyperacusis originate from aberrant neuroplastic changes in the central nervous system caused or triggered by cochlear hearing loss.
Recent brain imaging studies using multichannel quantitative EEG, positron emission tomography (PET) and functional MRI have revealed a plethora of functional and structural changes in the central nervous system associated with tinnitus and hyperacusis. From these studies, a number of key concepts have emerged linking tinnitus and/or hyperacusis to enhanced central gain, altered functional connectivity in neural network, aberrant rhythmic activity in cortical networks, spontaneous hyperactivity, and aberrant activity in regions of the brain associated with anxiety, attention, emotion, and memory.
In this Research Topic, we invite some of the world's leading brain imaging experts to produce a series of state of the art reviews and groundbreaking research dealing with tinnitus and hyperacusis in humans and animal models.
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