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Brain's Central Auditory System Could Compensate for Some of Limbaugh's Hearing Loss, Research at UB Suggests


BUFFALO, N.Y. -- Rush Limbaugh's loss of sensory inner-ear hair cells, a condition that likely contributed to his hearing loss, could lead to changes in his brain that would allow him optimize use of his remaining hearing, research being done at the University at Buffalo indicates.

The popular radio talk-show host announced last week that he has lost all hearing in his left ear and 80 percent of the hearing in his right ear. Limbaugh's physicians confirmed that his deafness is the result of autoimmune damage to hair cells.

Researchers at UB's Center for Hearing and Deafness, one of the nation's foremost hearing research groups, have found that the central auditory system in the brain reorganizes itself to compensate for the partial loss of hearing.

The phenomenon is called 'plasticity.' Robert Burkard, Ph.D. and Richard Salvi, Ph.D., both UB professors of communicative disorders and sciences, have found evidence of this ability while working with chinchillas as an animal model. The animals had experienced significant inner-ear damage, but had surprising little hearing loss.

'When the brain's usual pathways are no longer adequately stimulated, the brain will try to compensate,' Burkard said. 'We think that somewhere in the brain, the normal inhibition mechanism is lowered to compensation for less activity coming in via the ear.

'This might explain why when people try a hearing aid, they frequently don't like it at first. Maybe this is because the brain already has compensated for a lower input signal and the new signals are unsettling. But if they give it a month or so, the brain has a chance to reorganize itself again, and it can adapt to the renewed stimulation provided by the hearing aid.'

In addition to studying auditory plasticity, scientists at the Center for Hearing and Deafness are engaged in research that includes drug therapy and ototoxic drugs that causing hearing loss, various mechanisms involved in noise-induced hearing loss, regeneration of hair cells, mechanical transduction, age-related hearing loss and the role of free radicals in hearing loss.

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