Summary of Study: The emergence of tinnitus has been thought to depend on damage to the inner ear. The idea is that this damage prevents sound information from the outside world from being received by the inner ear and retransmitted to the central nervous system. In this way, a gap is formed between the auditory information that the central nervous system expects to receive and what actually makes its way there. In response, the brain tries to fill in this gap, creating a phantom sound, or tinnitus. But what happens when that gap – between what is expected and what is received – is varied? Is the brain’s response to the gap different depending on the gap’s breadth? A recent investigation by Sven Vanneste, Ph.D., at the University of Texas at Dallas and Dirk De Ridder, M.D., Ph.D., at the University of Otago addresses these questions with the help of 129 tinnitus patients some who had little or no hearing loss (i.e., equal to or under 20 decibel hearing, averaged across a range of frequencies) and others with severe hearing loss (hearing loss of greater than 20 decibels). The little or no hearing loss group represented those whose brains had to deal with a small gap between the sound information it expected and the sound information it received and the patients with severe hearing loss represented those whose brains had to overcome large gaps. The investigators recorded brain activity with electroencephalogram (EEG) from these patients while these patients were at rest, idle. They found that activity in the auditory cortex, the region of the brain that processes basic sounds, is hyperactive in tinnitus patients with little or no hearing loss when compared both to controls and tinnitus patients with severe hearing loss. Meanwhile the parahippocampal area, an area more related to memory processing, was found to be more active in tinnitus patients with severe hearing loss when compared to controls. The study went on to assess possible communication between auditory cortex and parahippocampal areas by comparing the degree to which their activities were synchronized over time. Interestingly, they found that activity in these brain areas was more synchronized in tinnitus patients with severe hearing loss when compared to healthy controls and tinnitus patients with little or no hearing loss.
Key Outcomes: This study suggests the underlying brain areas contributing to the experience may be different for tinnitus patients depending upon their degree of hearing loss. The brains of those with tinnitus may have different ways of overcoming gaps between expected and actual sound information depending on the breadth of the gap.
Relevance to tinnitus/hyperacusis: Tinnitus patients share the experience of a phantom sound, but the features of the sound (e.g., its pitch, volume) can vary quite considerably from patient to patient. Similarly, the underlying cause of the tinnitus seems to vary, with some people reporting noise-induced trauma and others reporting stress. This study parallels this line of thinking, showing that tinnitus subtypes do indeed exist.
Study authors: Sven Vanneste, Ph.D., and Dirk De Ridder, M.D., Ph.D., NeuroImage.