Download 5 - Neurobiology of Hearing

MEDS 5377 Paper 1:
26 May 2012
Discrimination of Speech in Children with History of Conductive Hearing Loss
Background: It is not unusual for children to acquire ear problems early in life that can cause a
buildup of fluid or mucous. One variety that is not actually an infection is called otitis media
with effusion, and is prevalent in about 20% of 2 year olds (Bennett et. al, 2001). It can be
recurrent and sometimes without noticeable symptoms. Babies often are affected more than
other ages because the Eustachian tube is shorter and easier to block (Bennett et. al, 2001).
This can lead to conductive hearing loss by raising the threshold of sound intensity needed to
elicit a response from the middle ear because of the mass of the fluid inside. Some parts of the
auditory system are near fully developed at the time of birth, such as the inner ear, its basic
tuning curves and tonotopic maps, and intensity coding (Werner, 2007). On the other hand,
much of human hearing ability depends on experience of specific auditory features, especially
in the first year of life. This allows complex sounds and vocalizations to be properly coded and
organized. Children become more sensitive to the meaningful sounds of the language they are
surrounded by at around 9 months, while losing detection ability for other language sounds
(Sanes & Wooley, 2011). In children with repeated OME, the (at least partial) deafness may
cause synaptic connections to develop in a different way due to abnormal hearing experience.
This has the potential to lead to delays in speech and learning deficits throughout childhood
after hearing is restored. It has been shown that children with hearing loss can have difficulty
placing attention on speech sounds over background noise, and discriminating voice onset time
(Yoshinaga, 1998). These normal abilities result in part from medial efferent inhibition of
cochlear neurons in order to disregard meaningless sounds (Smith, et. al, 2004). Efferent
neurons which release acetylcholine have also been proposed to influence plasticity and
learning in the auditory cortex. De-efferentation has been shown to cause more threshold shifts
as well as less cochlear sensitivity and adaptation (Syka, 2002). Lack of efferents may make it
harder to focus attention specifically on vocal sounds when masked by other sounds. The
question is, are the efferent neurons fully active or present when there is little auditory
experience in the first years of life?
Hypothesis: I hypothesize that children who experience serious recurrent OME in the critical
period of development are likely to have weakened or postponed auditory medial efferent
nerve mechanisms that are necessary for selective listening and efficient language modulation.
Supporting evidence would include lower output from efferent neurons initiating in the
superior olive after vocal stimulation. Distortion product otoacoustic emissions would not be
expected to be inhibited and adapt as rapidly after sound onset - different from the normal
process for sound discrimination.
Method: In order to measure and compare the activity of efferent neurons, we will have two
groups of children at age 3. One group will have had significant hearing problems in the first
two years of life due to recurrent otitis media with effusion, with later surgery to restore
hearing ability; the second group will have had no history of any ear problems as a control. A
sound stimulus will be used that incorporates a spoken conversation in the native language of
the child (English) among distracting broadband noise. The complex sound stimulus will be
played to both ears. Simultaneously, an ILO92 Otoacoustic Distortion Product Analyser for
distortion product otoacoustic emissions will record what the ear itself is producing in response
to the complex sound (Topolska, et. al, 2000). These emissions are produced due to feedback
vibrations of outer hair cells, and normally they would show rapid adaptation and decrease in
amplitude due to cholinergic medial efferent neurons inhibiting them in order to isolate the
meaningful sound parts. We will be looking for relative differences in the change over time in
the amplitude of the OAEs between the two subject groups. The sound stimulus will be played
for 10 seconds so as to allow time for recognition of the presence of speech but not more than
necessary to measure initial adaptation if any. We can also use an fMRI to measure relative
superior olivary brain activity, which sends descending output to efferent neurons acting on the
cochlea. It is likely that this will not be as efficacious in showing only efferent neuron activity
since this brain region is activated as part of the ascending auditory pathway as well.
Expected Results: If the hypothesis is supported, we would expect to see little change or
adaptation in the amplitude of otoacoustic emissions produced in young children who have
lived a large portion of their lives without normal hearing ability. We would also expect to see
somewhat less activity in the superior olive, although this difference may be too difficult to
detect. This is a way of indirectly measuring a decrease in medial efferent activity present in the
olivo-cochlear system that is thought to normally act as a way of detecting and discriminating
sounds among background noise. The hypothesis would not be supported if we saw the same
pattern of otoacoustic emissions and fMRI images from both subject groups (healthy and with
past hearing loss).This would indicate that efferent connections developed normally even
though hearing loss in the critical period of life may have prevented important auditory
experience.
References
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