ASA PRESSROOM

ASA 75th Anniversary Meeting, New York, NY


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Hearing Loss

Sandra Gordon-Salant - sgordon@hesp.umd.edu
University of Maryland at College Park
College Park, MD

Marjorie R. Leek - LeekMar@aol.com
Walter Reed Army Medical Center
Washington, DC


Special Lay-Language Paper for
ASA's 75th Anniversary Meeting
May 2004


Remember that Grateful Dead concert you attended in 1976? Ever wonder if that quiet hush after the concert is connected to the difficulty you have hearing today? You're not alone. Approximately 34 million U.S. citizens report hearing difficulty. Hearing impairment is the second most common chronic health condition experienced by senior citizens, affecting 1/3 of the population between 65-74 years of age. Baby Boomers aren't far behind, with 21% of adults between 45-64 years old reporting hearing loss. Hearing impairment affects an estimated 1-5% of children, too. Fortunately, we live in an era where scientists have discovered many of the causes of hearing impairment, and have developed accurate methods for assessing and treating most forms of hearing loss. This was not the case a century ago. At that time, hearing was evaluated with tuning fork tests that lacked precision about the nature of hearing impairment, and there were few treatment options. However, developments over the last 75 years in auditory science have revolutionized our understanding of hearing loss and our ability to treat it.

Hearing loss is classified by its severity across the frequency range (does hearing loss affect detection of low frequency sounds, i.e., low pitches, high frequency sounds, or sounds across the acoustic spectrum?) and the location of damage in the auditory system. Auditory damage may occur due to disease of the ear, overexposure to noise, some medications, hereditary factors, or the aging process. "Conductive" hearing loss results from damage to the outer and/or middle ears, while "sensorineural" hearing loss reflects damage to the inner ear (cochlea) or auditory nerve.

The two most common forms of hearing loss occur at different ends of the life cycle. Many children under the age of 5 years suffer from middle ear disease (called otitis media), which usually causes ear pain and a loss of hearing sensitivity. The middle ear also may become infected, threatening other structures in close proximity.

Presbycusis is hearing loss due to age-related damage to auditory structures. Although we begin to lose our hearing at about 20 years of age, typically it is not until age 50-60 years thatloss of hearing becomes troublesome. Initially, the loss is restricted to the high frequencies, but, with time, the loss progresses to lower frequencies as well. Presbycusis involves difficulty understanding speech, particularly in noisy environments. It is this additional hearing difficulty that is most problematic to elderly people.

A third common source of hearing loss is overexposure to loud sounds. Hearing can be lost with one exposure to intense noise (for example, a firecracker going off near a person's ear) or the loss can progress over many years of exposure to high levels of sound (industrial noise, for example). There is increasing concern about the noise damage that is occurring in young people who attend loud concerts or who listen to loud music over earphones. The damage may not be apparent until these people reach middle age, when the combined effects of aging and of their youthful noise exposure begin to interfere with speech communication.

The systematic evaluation and diagnosis of hearing impairment has its origins post-World War II, when many veterans returned from combat with noise-induced hearing loss [see Bergman (2002) for an historical review]. Scientists standardized methods to assess hearing thresholds (Bekesy, 1947; Carhart and Jerger, 1959) using an electronic device, the audiometer, that precisely controls the frequency and intensity of sounds presented to the listener. The resulting audiogram has become the "gold standard" for defining hearing loss. At about the same time, the first sets of speech materials were developed for assessing a listener's accuracy in receiving speech (Hudgins et al., 1949; Hirsh et al. 1952). Both the audiogram and speech recognition results aid in diagnosis of an auditory disorder and are used to determine candidacy for a hearing aid or cochlear (inner-ear) implant.

Over the last 35 years, sophisticated electrophysiologic techniques of measuring auditory function have been developed. With the introduction of acoustic "immittance" measures (Jerger, 1970), clinicians have a noninvasive view of the health of the middle ear. Drawing upon earlier studies (e.g., Davis et al., 1950), Jewett et al. (1970) developed the "Auditory Brainstem Response" (ABR), a noninvasive technique to evaluate hearing status by recording electrical activity from the auditory nerve and brainstem in response to acoustic signals. The integrity of the sensory hair cells in the cochlea may now be assessed by recording otoacoustic emissions (OAEs), which are very soft sounds that are present in the ear canal immediately after delivery of a test sound (Kemp, 1978). OAEs are generated by a healthy inner ear, but they are absent when there is cochlear damage, and therefore provide a powerful tool for diagnosis.

What can be done for people with hearing loss? If the problem is localized in the outer or middle ears, then medication or surgical intervention is usually successful. Hearing aids are recommended for individuals with problems in the inner ear or auditory nerve. Some people with severe or profound hearing loss may benefit from cochlear implants - surgically implanted devices that deliver electrical pulses representing speech and other sounds directly to the nerve of hearing.

Current research on hearing loss is entering an exciting phase that emphasizes new knowledge about the molecular biology of hearing and gene-based interventions. Perhaps the most tantalizing is the possibility of regenerating cochlear sensory cells. Some animal species spontaneously replace damaged cochlear hair cells, but this does not occur in mammals (Corwin & Cotanche, 1988; Ryals & Rubel, 1988). However, progress has been made in understanding the mechanisms of this process, and in developing therapies for regeneration or repair of damaged hair cells in mammals (Kawamoto et al., 2003). Scientists have also reported success from antioxidant therapies used prior to noise exposure that may reduce noise-induced hearing loss (Kopke et al., 2000). These emerging clinical approaches reflect the application of groundbreaking basic research on hearing and the ear, with great promise for the treatment and prevention of hearing loss. And just in time, too, as the Baby Boomers approach a time of escalating hearing difficulties in their lives.

For further information on the topics of hearing and hearing loss, please consult the web sites of the National Institute on Deafness and Other Communication Disorders and the Association for Research in Otolaryngology. The latter site has a number of links to other hearing institutes and organizations as well.

REFERENCES
Bekesy, G. v. (1947). A new audiometer. Acta Oto-laryngologica Stockholm 35, 411-422.

Bergman, M. (2002). On the origins of Audiology: American wartime military Audiology. Audiology Today, Monograph 1, 1-28.

Carhart, R. & Jerger, J. (1959). Preferred method for clinical determination of pure-tone thresholds. Journal of Speech and Hearing Disorders, 24, 330-345

Corwin, J. T. and Cotanche, D.A. (1988). Regeneration of sensory hair cells after acoustic trauma. Science 240, 1772-1774.

Davis, H., Fernandez, C., & McAuliffe, D.R. (1950). The excitatory process in the cochlea. Proceedings of the National Academy of Science U.S., 36, 580-587.

Hirsh, I.J., Davis, H., Silverman, S.R., Reynolds, E.G., Eldert, E., & Benson, R.W. (1952). Development of materials for speech audiometry. Journal of Speech and Hearing Disorders 17, 321-337.

Hudgins, C.V., Hawkins, J.E., Jr., Karlin, J.E., & Stevens, S.S. (1947). The development of recorded auditory tests for measuring hearing loss for speech. The Laryngoscope, 57, 57-89.

Jerger, J. (1970). Clinical experience with impedance audiometry. Archives of Otolaryngology, 92, 311-324.

Jewett, D.L., Romano, M.N., & Williston, J.S. (1970). Human auditory evoked potentials: Possible brain-stem components detected on the scalp. Science, 167, 1517-1518.

Kawamoto, Kohei, Ishimoto, Shin-Ichi, Minoda, Ryosei, Brough, Douglas E., and Raphael, Yehoash. (2003). Math1 gene transfer generates new cochlear hair cells in mature guinea pigs In Vivo. The Journal of Neuroscience, 23(11), 4395-4400.

Kopke, Richard D., Weisskopf, Peter A., Boone, John L., Jackson, Ronald L., Wester, Derin C., Hoffer, Michael E., Lambert, David C., Charon, Christopher C., Ding, D.,-L., and McBride, Dennis. (2000). Reduction of noise-induced hearing loss using L-NAC and salicylate in the chinchilla. Hearing Research 149, 138-146.

Ryals, B. M. and Rubel, E. W. (1988). Hair cell regeneration after acoustic trauma in adult Coturnix quail. Science 240, 1774-1776.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.


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