Bethesda, Md – Researchers from the National Institute on Deafness and Other Communication Disorders (NIDCD) have theorized that the human limbic system can make some people more vulnerable to tinnitus than others and perhaps cause depression.
The researchers’ theory is that the limbic system—a linked network of brain structures involved in emotion, behavior, and long-term memory—acts as a gatekeeper to keep the tinnitus signal from reaching the auditory cortex, the part of the brain that mediates our conscious perception of sounds. In people with tinnitus, they suggest, the gate has “broken.”
In previous studies, Josef Rauschecker, PhD, DSc, and his colleagues in the Department of Neuroscience, the Division of Audiology, and the Department of Otolaryngology at Georgetown University had noted a significant loss of volume in the medial prefrontal cortex (mPFC), an area located in the frontal lobe of the brain, of people with tinnitus. The finding was intriguing because although this isn’t an area of the brain that processes sound, it is an area that has the potential to modulate sensory information—such as sound—because of its intimate connections with key structures in the limbic system.
The fact that tissue loss in this particular area was a prominent feature was puzzling, but changes had been noted before in other structures associated with the limbic system in people with tinnitus. Previous researchers had tended to interpret the involvement of the limbic system as a reflection of the emotional reaction to the sound. The depression that often accompanies tinnitus (and that has deep roots in the limbic system) was seen as a normal reaction to an upsetting condition that wouldn’t go away.
However, Rauschecker’s team wondered if the damage they saw in the mPFC wasn’t a consequence of tinnitus, but instead a part of its cause.
Most researchers agree that tinnitus begins as a result of the brain trying to regain the ability to hear the sound frequencies it has lost by turning up the signals of neighboring frequencies. In the model proposed by Rauschecker and his colleagues, the critical place for determining whether these new hyperactive signals—the tinnitus—will eventually be perceived is where the auditory and limbic systems interact.
Sensory information enters both the auditory and the limbic systems through the medial geniculate nucleus (MGN), a small oval mass that protrudes slightly from the underside of the thalamus, a large double-lobed structure buried beneath the cerebral cortex. Before the signal can travel on, however, it travels through another nearby structure called the thalamic reticular nucleus (TRN), which evaluates whether the signal should be passed on.
This is how, in a healthy limbic system, a tinnitus signal is stopped in its tracks. The question remains, then, what is happening in people who end up hearing the tinnitus signal? Rauschecker and his researchers think there is a clue in the loss of volume in the mPFCs of the people with tinnitus. This is a structure that projects into and activates the TRN. If the volume loss can be interpreted as a loss of neurons, then the mPFC won’t be doing its job effectively and neither will the TRN. This means it will be much less successful at suppressing unwanted signals and people will begin to hear ringing in their ears.
Additional imaging research has shown that another limbic structure—the nucleus accumbens—appears to be trying to make up for the loss of activity in other parts of the limbic system. It is one more piece of evidence to support the model that Dr Rauschecker and his colleagues propose.
Although these findings still aren’t able to definitively tell us how and why tinnitus happens to some people rather than others, they do give researchers a new set of places to explore where the tinnitus signal is processed in the brain and could potentially be stopped.
The findings might also explain why the incidence of depression in people with tinnitus is more than twice the national average.
The study "Dysregulation of Limbic and Auditory Networks in Tinnitus" was published in the January 13, 2011, issue of Neuron.