VOLUME 32, NUMBER 22 THURSDAY, March 1, 2001
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Ringing found in brain, not ears

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By LOIS BAKER
Contributing Editor

Tinnitus, the disruptive ringing in the ears that affects millions of people, originates not in the ear but in the brain, and not even exclusively in the brain's auditory centers, a new study has shown.

In research published Monday in Neurology, scientists at UB and the Buffalo VA Medical Center show that some people with tinnitus can change the ear-ringing by specific eye movements, evidence that one sensory system can affect another.

"These findings show us that in many cases, tinnitus is not caused by a simple disturbance of brain function, but by a combination of things, including an abnormal interaction between the visual and auditory systems," said Alan H. Lockwood, first author on the study. Lockwood is professor of neurology, nuclear medicine, and communicative disorders and sciences and directs the Center for Positron Emission tomography (PET), a joint UB/VA venture.

"This additional level of complexity helps to explain why there hasn't been a simple solution to this problem," he said. "There is no drug that is effective for the relief of tinnitus. Maybe the system is so complex that no one drug can do the job."

Lockwood and colleagues were the first to show that tinnitus sounds originate in the brain, not the cochlea, as previously thought. Lockwood and Richard Salvi, co-director of the Center for Hearing and Deafness, previously studied tinnitus patients who have the unusual ability to control the loudness of the ringing by clenching their jaws. The researchers were able to track fluctuations in cerebral blood flow through PET scans taken while these patients manipulated their symptoms, creating a map of the brain site responsible for tinnitus activity.

Their current research involved a small group people with tinnitus who can modulate their tinnitus by looking to the far right or left of center, an unusual condition called gaze-evoked tinnitus, or GET.

"About 70 percent of tinnitus sufferers have some 'trick' they've learned that changes the loudness of tinnitus," Lockwood said. "In this research we concentrated on one small group of these 'tricksters.' If these findings generalize to much larger groups, we will show that tinnitus is caused by abnormalities in the major brain systems."

The study focused on eight patients with GET, a condition that may develop after surgical removal of auditory-nerve tumors. As researchers mapped the patients' brains using PET, they found an unexpected imbalance between the auditory and visual parts of the brain.

Lateral gaze suppresses auditory brain activity in normal subjects, Lockwood noted.

"This so-called 'cross-modal inhibition' is a mechanism that enables the brain to suppress unwanted sensations. By suppressing hearing during lateral gaze, the brain is telling us to pay attention with our eyes. This cross-modal inhibition was absent in GET patients, indicating a disruption in normal brain circuitry that may be at the core of the tinnitus phenomenon," he said.

Lockwood's next step in his continuing investigation of the mystery of tinnitus is to look at other "tricks" known to influence the condition and at how they influence brain circuitry.

One such mechanism, called residual inhibition, involves brief suppression of tinnitus by overwhelming the auditory system with a very loud noise-a power saw, for example, which one of Lockwood's patients finds effective in temporarily stopping tinnitus sounds.

Additional researchers on the study were Davis S. Wack, Robert F. Burkard, Mary Lou Coad, Samuel A. Reyes, Sally A. Arnold and Salvi, all affiliated with UB.

The study was supported by grants form the National Institute of Deafness and Communicative Disorders and the James H. Cummings Foundation in Buffalo.

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