Researchers at UB and the U.S. Department of Veterans Affairs Medical Center in Buffalo, using positron emission tomography (PET), have pinpointed for the first time the specific brain regions responsible for tinnitus, a constant and debilitating ringing in the ears experienced by millions of Americans.
The findings are a major breakthrough in the study of these "phantom sounds," for which there is no known cause or effective treatment. Results of the study appear in the January issue of Neurology.
Based on the results of the study, the lead researchers have received a $1.5 million grant from the National Institutes of Health to conduct a major investigation of tinnitus and hearing loss using PET scanning.
"People with severe tinnitus, which is about 10 percent of elderly Americans, often suffer depression, anxiety, sleep disruption and other symptoms that have a major impact on their quality of life," said Alan H. Lockwood, lead author of the study. "Without objective information on how and where the condition originates, developing effective treatments has been difficult. By identifying the sites in the brain that mediate tinnitus, we have taken a critical step down the road toward a cure for this disabling condition."
Lockwood, a neurologist, directs the Center for Positron Emission Tomography at the Buffalo VA Medical Center, a joint venture with UB, where the research was conducted. He holds appointments as a professor of neurology, nuclear medicine and communicative disorders and sciences at UB.
Lockwood and Richard Salvi, co-director of the Center for Hearing and Deafness, studied tinnitus patients who have the unusual ability to control the loudness of the ringing by clenching their jaws. They 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.
In addition, they reported significant findings never before observed:
The study involved four tinnitus patients and six persons with normal hearing and no tinnitus, who served as controls. All participants took standard hearing tests before PET scanning. The tinnitus patients had mild-to-severe high-frequency hearing loss.
The researchers were able to pinpoint the origin of tinnitus activity to sites in the temporal lobe opposite the affected ear by comparing PET scans of tinnitus patients while they manipulated their loudness with their scans at rest and with scans of normal controls as they performed the same jaw movements.
"Identifying sites in the brain that mediate tinnitus is a critical first step in the difficult task of defining the factors that create these phantom sensations and developing rational treatments for this chronic and disabling condition," Lockwood said.
The researchers also found, unexpectedly, that the hippocampus, part of the brain responsible for emotions, was activated in tinnitus patients, but not in normal controls, indicating one possible pathway for the adverse psychological effects often experienced with the condition.
In addition, they observed that external sounds activated a more extensive network of nerves in tinnitus patients with hearing loss (nearly all tinnitus patients have impaired hearing) than in normal subjects. Lockwood said this finding indicated that the auditory system in tinnitus patients reorganizes as a result of the reduction in auditory stimuli.
"Changes in the brain occur following many forms of neural injury or changes in the sensory input to the brain," Lockwood said. "These changes may be responsible for symptoms such as phantom limb pain, a syndrome in which amputees feel excruciating pain that seems to originate in the missing limb. We believe that tinnitus may be the auditory counterpart to phantom limb pain.
"We still have a lot of work to do."
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