Long-term hearing
loss from loud explosions, such as blasts from roadside bombs, may not be as
irreversible as previously thought, according to a new study by researchers at
the Stanford University School of Medicine.
Using a mouse
model, the study found that loud blasts actually cause hair-cell and nerve-cell
damage, rather than structural damage, to the cochlea, which is the auditory
portion of the inner ear. This could be good news for the millions of soldiers
and civilians who, after surviving these often devastating bombs, suffer
long-term hearing damage.
"It means we
could potentially try to reduce this damage," said John Oghalai, MD,
associate professor of otolaryngology and senior author of the study, published
July 1 in PLOS ONE. If the cochlea, an extremely delicate structure, had been
shredded and ripped apart by a large blast, as earlier studies have asserted,
the damage would be irreversible. (Researchers presume that the damage seen in
these previous studies may have been due to the use of older, less
sophisticated imaging techniques.)
"The most
common issue we see veterans for is hearing loss," said Oghalai, a
scientist and clinician who treats patients at Stanford Hospital & Clinics
and directs the hearing center at Lucile Packard Children's Hospital.
The increasingly
common use of improvised explosive devices, or IEDs, around the world provided
the impetus for the new study, which was primarily funded by the U.S.
Department of Defense. Among veterans with service-connected disabilities,
tinnitus -- a constant ringing in the ears -- is the most prevalent condition.
Hearing loss is the second-most-prevalent condition. But the results of the
study would prove true for anyone who is exposed to loud blasts from other
sources, such as jet engines, air bags or gunfire.
More than 60
percent of wounded-in-action service members have eardrum injuries, tinnitus or
hearing loss, or some combination of these, the study says. Twenty-eight
percent of all military personnel experience some degree of hearing loss
post-deployment. The most devastating effect of blast injury to the ear is
permanent hearing loss due to trauma to the cochlea. But exactly how this
damage is caused has not been well understood.
The ears are
extremely fragile instruments. Sound waves enter the ear, causing the eardrums
to vibrate. These vibrations get sent to the cochlea in the inner ear, where
fluid carries them to rows of hair cells, which in turn stimulate auditory
nerve fibers. These impulses are then sent to the brain via the auditory nerve,
where they get interpreted as sounds.
Permanent hearing
loss from loud noise begins at about 85 decibels, typical of a hair dryer or a
food blender. IEDs have noise levels approaching 170 decibels.
Damage to the
eardrum is known to be common after large blasts, but this is easily detected
during a clinical exam and usually can heal itself -- or is surgically
repairable -- and is thus not typically the cause of long-term hearing loss.
In order to
determine exactly what is causing the permanent hearing loss, Stanford
researchers created a mouse model to study the effects of noise blasts on the
ear.
After exposing
anesthetized mice to loud blasts, researchers examined the inner workings of
the mouse ear from the eardrum to the cochlea. The ears were examined from day
one through three months. A micro-CT scanner was used to image the workings of
the ear after dissection.
"When we
looked inside the cochlea, we saw the hair-cell loss and auditory-nerve-cell
loss," Oghalai said.
"With one
loud blast, you lose a huge number of these cells. What's nice is that the hair
cells and nerve cells are not immediately gone. The theory now is that if the
ear could be treated with certain medications right after the blast, that might
limit the damage."
Previous studies
on larger animals had found that the cochlea was torn apart and shredded after
exposure to a loud blast. Stanford scientists did not find this in the mouse
model and speculate that the use of older research techniques may have caused
the damage.
"We found
that the blast trauma is similar to what we see from more lower noise exposure
over time," said Oghalai. "We lose the sensory hair cells that
convert sound vibrations into electrical signals, and also the auditory nerve
cells."
Much of the
resulting hearing loss after such blast damage to the ear is actually caused by
the body's immune response to the injured cells, Oghalai said. The creation of
scar tissue to help heal the injury is a particular problem in the ear because
the organ needs to vibrate to allow the hearing mechanism to work. Scar tissue
damages that ability.
"There is
going to be a window where we could stop whatever the body's inflammatory
response would be right after the blast," Oghalai said. "We might be
able to stop the damage. This will determine future research."
In addition to
the Department of Defense, the study was funded by the National Institutes of
Health (grants K08DC006671 and P30DC010363) and Chosun University in South
Korea.
The first author
of the study, Sung-Il Cho, MD, assistant professor at Chosun University, was
working at Stanford during the study. Other Stanford authors were graduate
students Simon Gao, Jongmin Baek and David Jacobs; senior research scientist
Anping Xia, MD, PhD; research technician Rosalie Wang; research associate
Felipe Salles, PhD; computer programmer Patrick Raphael; and research
coordinator Homer Abaya.
Source sciencedaily :
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