Discrimination of Speech in Children with History of Conductive Hearing Loss

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 infectionis 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 (SanesWooley, 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 efferentsmay 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 fromefferent neurons initiating in the superior oliveafter vocal stimulation.Distortion product otoacoustic emissions would not be expected to be inhibited and adapt as rapidlyafter 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 wouldshow 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 lifemay have prevented important auditory experience.

References

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Syka, J. (2002). Plastic changes in the central auditory system after hearing loss, restoration of function and during learning. Pysiological Reviews, 82(3), p. 601-636.