Efforts are under way to figure out how to dampen the neural hyperactivity that leads to tinnitus.
Tinnitus is widely believed to stem from abnormal spontaneous activity of neurons in the central auditory system. Damage to the inner ear hair cells reduces input to the auditory pathways of the brain, causing “plasticity” or alterations in their synaptic connections. This leads them to become hyperactive, which includes changes in the frequency and timing of neural impulses that signal the presence of sound.
Presently, efforts to bring comfort to tinnitus sufferers are focused on finding ways to reduce or abolish this abnormal activity. Most studies testing drug therapies have focused on agents that are known to quiet the nervous system.
For example, benzodiazepines, antidepressants, and antiepileptic drugs have been tested in numerous studies. Historically, such drugs have not been found to be hugely successful in tinnitus treatment in human subjects (see “Drugs on Trial
A more experimental category of tinnitus treatment that has attracted much attention recently is electrical stimulation of pathways in the nervous system that modulate neural activity in the auditory system. A number of studies have reported that cochlear stimulation can sometimes be effective in reducing tinnitus.
For example, some patients with cochlear implants (CIs), used to restore hearing in the deaf, experience a reduction in their tinnitus when their implants are turned on, and the effect can sometimes endure for hours even after the implants are turned off.
However, it is not always clear what is the primary mechanism of the diminished tinnitus that accompanies cochlear stimulation. While in some cases it seems tinnitus is suppressed by the CI, in others the benefit may simply be the result of the covering up or masking of tinnitus by the sounds that are made audible by CI stimulation. More research is needed to clarify which mechanism is more predominant.
It has been known for some time that a large proportion of tinnitus sufferers can modulate the loudness of their tinnitus by contracting certain muscles of the head or neck region. Recent studies in animals have shown that the activity of neurons in the auditory system that play a role in the generation of tinnitus can be modulated by stimulating specific cranial nerves that control the contractions of head and neck muscles.
For instance, the activation of the trigeminal or cervical nerves can reduce neural activity. Other recent research conducted in animals shows that stimulation of the vagus nerve can be effective in abolishing tinnitus. Clinical trials will determine whether some of these effects can be reproduced in human tinnitus sufferers.
Still other research has found that tinnitus can sometimes be suppressed by stimulating pathways that descend from the auditory cortex to the brainstem nuclei, where tinnitus is first generated. Activation of these pathways can be accomplished by placing electrodes directly in the auditory cortex or by stimulating auditory areas of the cortex using repetitive transcranial magnetic stimulation (rTMS).
As with CIs, these approaches only benefit a small subset of tinnitus patients, and the effects vary greatly from one person to another. But as knowledge continues to grow about these experimental approaches, insights into how best to suppress tinnitus may emerge.
The increasing efforts of researchers to understand the biology of tinnitus and develop new anti-tinnitus strategies should result in more—and better—treatment options.
James A. Kaltenbach, Ph.D., is the director of Otology Research at the Head and Neck Institute and the Department of Neurosciences at the Cleveland Clinic in Ohio. He has served on numerous national committees including the Scientific Advisory Board for the American Tinnitus Association, the Editorial Board for the journal Hearing Research, and numerous review panels for the National Institute of Health and the National Science Foundation.