Public Release: 

Research reveals that temporary hearing deprivation can lead to 'lazy ear'

Massachusetts Eye and Ear Infirmary

Hearing scientist Daniel Polley, Ph.D., an investigator at Massachusetts Eye and Ear Infirmary's Eaton-Peabody Laboratories of Auditory Physiology, has gained new insight into why a relatively short-term hearing deprivation during childhood may lead to persistent hearing deficits, long after hearing is restored to normal. The research, featured on the cover on the March 11 issue of the journal Neuron, reveals that, much like the visual cortex, development of the auditory cortex is quite vulnerable if it does not receive appropriate stimulation at just the right time.

It is well established that degraded sensory experience during critical periods of childhood development can have detrimental effects on the brain and behavior. In the classic example, a condition called amblyopia (also known as lazy eye) can arise when balanced visual signals are not transmitted from each eye to the brain during a critical period for visual cortex development.

"An analogous problem may exist in the realm of hearing, in that children commonly experience a buildup of viscous fluid in the middle ear cavity which can degrade the quality of acoustic signals reaching the brain, which has been associated with a long-lasting loss of auditory perceptual acuity," explains senior study author, Dr. Polley.

Dr. Polley and his colleague Dr. Maria Popescu from Vanderbilt University implemented a method to reversibly block hearing in one ear in infant, juvenile and adult rats then looked at how the parts of the brain involved in hearing were impacted by the temporary hearing loss.

They observed that the temporary hearing loss in one ear distorted auditory patterning in the brain, weakened the deprived ear's representation and strengthened the open ear's representation. The scope of reorganization was most striking in the cortex (and not "lower" parts of the central auditory pathways) and was more pronounced when hearing deprivation began in infancy than in later life. Therefore, it appears that maladaptive plasticity in the developing auditory cortex might underlie "amblyaudio," in a similar fashion to the contributions of visual cortex plasticity to amblyopia.

"The good news about amblyaudio is that it is unlikely to be a permanent problem for most people," concludes Dr. Polley. "Even if the acoustic signal isn't corrected within the critical period, the mature auditory cortex still expresses a remarkable degree of plasticity. We know that properly designed visual training can improve visual acuity in adult amblyopia patients. We are gearing up now to study whether auditory perceptual training may also be a promising approach to accelerate recovery in individuals with unresolved auditory processing deficits stemming from childhood hearing loss."

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About Dr. Daniel Polley

Dr. Daniel Polley is a principal investigator at the Eaton-Peabody Laboratories of Auditory Physiology at the Massachusetts Eye and Ear Infirmary in Boston, Mass., where the focus of his research is auditory cortex development and plasticity. Dr. Polley received a B.A. in Psychology from the University of Richmond (1996), a Ph.D. in Biological Sciences from the University of California, Irvine (2001) and completed a Postdoctoral Fellowship at the University of California, San Francisco (2005). He was formerly an Assistant Professor at Vanderbilt University.

About Mass. Eye and Ear

Founded in 1824, Massachusetts Eye and Ear Infirmary is an independent specialty hospital providing patient care for disorders of the eye, ear, nose, throat, head and neck. Mass. Eye and Ear is an international leader in Ophthalmology and Otolaryngology research and a teaching partner of Harvard Medical School. For more information, call 617-523-7900 or visit http://www.masseyeandear.org/.

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