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.