Tinnitus: Understanding Malfunctioning Neural Mechanisms

A research team from Georgetown University Medical Center and Germany’s Technische Universität München reports the identification of a shared brain malady that is a causal factor in tinnitus and in chronic pain that persists long after an initial injury. Identification of the neural mechanism is described as a first step in the development of effective therapies for these conditions. The research is detailed in this month’s edition of Trends in Cognitive Sciences.

In both tinnitus and postinjury pain, the brain has been reorganized in response to an injury in its sensory apparatus, according to the authors. The neural mechanisms that normally “gate” or control noise and pain signals can become dysfunctional, leading to a chronic perception of these sensations. The brain regions responsible for these errant sensations are the nucleus accumbens, the reward and learning center, and several areas that serve “executive” or administrative roles—the ventromedial prefrontal cortex and the anterior cingulate cortex. These areas also affect the experience of various comorbidities such as depression and anxiety. But because these systems rely on transmission of dopamine and serotonin between neurons, drugs that modulate dopamine may help restore sensory gating, according to the researchers.

Read a press release from Georgetown University Medical Center on the findings here.

The journal abstract and full article may be read here.


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