hearing impairment. Our brain adapts in different ways to hearing loss: by generating internal noise to compensate for lost frequencies, by decreasing the threshold for internal noise perception, by decreasing lateral inhibition, and by altering correlated or synchronous activity between different regions in the brain. All these neuroplastic changes contribute to the perception of tinnitus.
Neuron: A nerve cell that transmits sensory data throughout the brain via electrical and chemical signals. There are nearly 100 billion neurons in the human brain. Neurons specialize to serve different general functions (ex: hearing) and to process specific stimuli (ex: sound).
Lateral Inhibition: Within the brain, excess excitability in one sensory neuron will often inhibit activity in neighboring neurons, effec- tively isolating neural hyperactivity. When this lateral inhibition is decreased, the excitability of one neuron can spread to others. This tends to make sensory perception (including tinnitus) a more acute sensation.
BF: So hearing loss can cause neuroplastic changes that produce tinnitus. But why do some people with hearing loss develop tinnitus and others not?
FH: This is the question that drives my research. As of today, we don’t have a definite answer. However, the research is advancing rapidly and the data hints at a couple of possibilities. From my own lab’s work, we know that the brain networks that control atten- tion and emotion differ in patients with hearing loss and tinnitus versus those with hearing loss alone. This suggests that the brains of tinnitus patients may be particularly susceptible both to focus on the perception of tinnitus and to ascribe a negative emotional component to tinnitus.
BF: So can we predict who will develop burdensome tinnitus?
FH: At the moment, no. This is a ‘chicken-and-egg’ problem. We study patients only after they have developed tinnitus. We can measure how their brains have changed after the onset of tinnitus, but don’t know if some of these changes were in place prior to developing tinnitus or if they occurred afterwards. Therefore, we can’t predict, ahead of time, whose brains are more or less susceptible to the condition. Longitudinal patient studies, that track both people who do develop tinnitus over the course of their lives and those who don’t, are needed to identify indicators that would suggest a brain predisposition to tinnitus.
Dr. Husain has served on ATA’s Scientific Advisory Committee since 2012.
BF: It sounds like the brain’s auditory system and the emotional networks are closely connected.
FH: There is a very close relationship between the auditory system, which regulates hearing, and the limbic system, which regulates emotion, behavior, and motivation. Anatomically, there are neural con- nections between the auditory cortex, the thalamus (a brain structure that relays sensory information), and the amygdala (one of the key processors of emo- tion.) Thus the auditory cortex not only receives and processes sound stimuli, but also feeds information into the brain’s emotional structures.
This makes sense when you consider your own emotional reaction to sound. Think for a moment about how certain sounds evoke unique emotions: some sounds make you joyful while others make you scared or angry. Likewise, the same sound can be pleasant for some individuals and unpleasant for others. The limbic system is what controls the emotional reaction to sound—including tinnitus. In other words, it regulates whether the tinnitus signal is perceived as bothersome or non-affective, deeply upsetting or no-big-deal.
Summer 2014 | Tinnitus Today 19
SCIENCE & RESEARCH
GLOSSARY
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