n veits ceap dissertation

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This dissertation is submitted in part fulfilment of the BSc Honours degree programme regulations in the Department of Vision and Hearing, Anglia Ruskin University.Word count 6000Author: Nauris VeitsMay 2015


I would like to thank all Anglia Ruskin University staff who have been with us last nine months. You have been fantastic! Thanks to Phil, Eldre, Sri, Clare, Leah, Victoria and Fei.I would like to thank my employer Jane Taylor for understanding and support.Finally, I would like to thank my dear wife Anda for support.I do apologise if I have forgotten someone and do greatly appreciate everyone's support through my time at university!

..We choose to go to the moon in this decade and do the other things, not because they are easy, but because they are hard... JFK


Cortical auditory evoked potential (CAEP) wave P1 is a biomarker of maturity of the auditory cortex. Delayed auditory stimulus in hearing impaired children presents longer and abnormal P1 latency. Early intervention with cochlear implant(s), where hearing aids have failed, could lead to successful maturation of auditory cortex.Objective: Aim of major project is to review researches on Cortical Auditory Evoked Potentials.Aim 1: Age of implantation; early and late interventions affect on maturity of the auditory cortex and P1 wave.Aim 2: Factors that influence morphology of P1 wave.Design: Reviewed four studies on CAEP published from 2002 to 2013.Results: Children, fitted with CI up to age of 3 to 4 years demonstrate rapid change and shift towards normal normative data in P1 latency over first 6 to 12 months after in-sound experience. Reduction of amplitude of P1 wave is consistent as brain matures however, it has broad variation across studies as different types of stimuli and test set-ups are used.Conclusion: Resent studies consistently shows that P1 can be used as biomarker of maturity of the auditory cortex and could be used as diagnostic tool in evaluation of efficiency of cochlear implant(s) in children with hearing loss, particularly in difficult to test individuals. However, further research in universal diagnostic test protocol would be required.Key words: P1-N1-P2, plasticity of auditory cortex, children with hearing loss, cochlear implants, morphology of P1 wave

Table of contents

Introduction1P1-N1-P2 complex6Morphology of P1-N1 complex6Stimulus types6Delivery of stimuli7Analysis of studies9Literature review - methodology9Subjects10Stimulus presentations and recordings10Results11Discussion20Conclusion24References25


Prevalence of congenital deafness in the UK is 1 in 1000 live births. Most common cause of congenital deafness is syndrome, neo- or perinatal infection, trauma at birth, prematurity and genetic predisposition. Incidence of hearing loss doubles in first 10 years of age. Postnatal infections and health problems, time spent in intensive care (noise induced hearing loss for not-well babies), syndromes, traumas and many other can be accounted for cause of acquired hearing loss later on in life (NSC, 2006). Unaided hearing loss will delay child's development of speech and language. In long term, it has broader impact on social interaction, child's self-esteem, education and employability (Parfect, 2015). Since introduction of newborn hearing screening in the UK in 2006, hearing impairment can be detected few hours after birth and very young infants can be fitted with hearing aids as early as few weeks old. Cochlear implants (CI) become beneficial in children with severe to profound hearing loss where hearing aids have failed to provide efficient improvement. Evaluation can be done with subjective and objective tests, additionally parents or carers can monitor effectiveness of hearing aid or CI. Subjective testing, Visual Reinforcement Audiometry provides information on benefit of the device. However, because it involves conditioning and observing child, it does become more difficult and unreliable if child is not cooperating or is not providing valid response. Although objectively, Auditory Brainstem Response can measure performance of the hearing aid or CI, it will not provide access to more detailed information on how the auditory cortex has responded to the sound and how the sound is processed, and how it develops (Burkard, et.al. 2007).Short latency potentials demonstrate function of cochlea or auditory nerve, and middle latency demonstrates function of auditory. If short and mid latencies, require short stimulus to elicit potential then Cortical Auditory Evoked Potential (CAEP) can be evoked either with short stimulus or with longer, speech-like sounds (Burkard, et.al. 2007). In the last two decades, CAEP has been used to evaluate impact of the cochlear implants on auditory cortex as well as hearing aids and/or frequency transposition/compression. Late latency P1-N1-P2 complex can be used as a biomarker of maturity of the brain (Sharma, et.al. 2005; Dorman, et.al. 2007). In newborns, the latency of P1 is considerably greater, around 300ms, and in adults it is much shorter - 60ms (Nash, et.al. 2007).Some of the researches of the past decade have noted that use of the cochlear implants has impact on latency of wave of P1. If hearing impaired infants and young children are left unaided, maturation of P1-N1-P2 and later on negative,N2 wave, complex will be delayed. Researches noticed if children get early cochlear implant, then 6-8 months after hook-up P1 latency shortens and is closer to the individual of same age and normal hearing (Sharma, et.al. 2002; Nash, et.al. 2007; Jiwani, et.al. 2013; Alvarenga, et.al 2013).As a diagnostic tool evaluation of CAEP can be used to investigate disorders affecting central processing of sound, estimate threshold sensitivity, monitor changes in hearing system with the hearing loss and evaluate outcome of rehabilitation of hearing aids and CI (Burkard, et.al. 2007; Glista, et.al. 2012).

Figure 1 (reprinted from Burkard, et.al. 2007) Auditory Evoked Potentials in relation of the auditory pathway.

Figure 2 (reprinted from ASHA, n.d.) Short, middle and late latencies and average wave peak times.Evidence from animal experiments proposes that sound deprivation affects dendritic development (McMullen and Glaser, 1988). The P1-N1-P2 complex in infants starts with P1 wave at 200-250 msec after onset of stimulus. Up to age of ten, N1 wave is not very prominent. Over the years, P1 latency becomes shorter until it stabilises; N1 and P2 waves emerge. It is suggested, that sound deprivation in early childhood leads to subnormal myelination (Moore and Linthicum, 2007). Hypomyleination affects velocity of conduction therefore prolonged P1 can be observed (Sharma, et.al., 2002). Later in life, N1 and P2 latencies show changes in aging adults (Burkard, et.al., 2007).

Figure 3 (reprinted from Sharma, et.al, 2001) P1 latencies in normal hearing individuals. Shortening of latency as auditory cortex matures.P1 latency in normal hearing individuals (average values): Infants = 300ms 3 years = 125ms 15 years = 95ms Middle-aged = 60ms (Nash, et.al., 2007)Ponton and Eggermont (2001) suggest the P1 matures at age of 12 and changes very little after that. In congenitally deaf children development of P1 latency is delayed and auditory brain is vulnerable to be taken over by non-auditory networks, e.g. by visual cortex (Moore and Shannon, 2009). Negative wave, N1 latency's, absence in CI users who have been deaf for period of 3 years below of age of 6 could have potentially poor performance in perception of degraded speech later in life (Eggermont and Ponton, 2003).

The aim and outline of the dissertationFor the major project, literature review was conducted. In total four researches by Sharma, et.al. 2002; Sharma, et.al. 2005; Hossain, et.al. 2013; and Alvarenga, et.al. 2013 were chosen and reviewed.The key words used for search: cortical auditory evoked potential; cochlear implant; hearing impaired children; maturity of the brain; plasticity; P1 latency; P1-N1-P2; late latency.Databases used: sciencedirect.com (Elsevier); journals.lww.com (LWW); ncbi.nlm.nih.gov (PubMed); ovidsp.ovid.com (Ovid). Access, for some publications, via Anglia Library was used. Databases gave access to e-journal publications, e.g. Ear and Hearing; American Academy of Audiology; International Journal of Audiology.Although CAEP has been known for decades, only in recent years it has been researched in more details. There is very little data on hearing aid amplification and congenital hearing loss, and CAEP. Therefore, cochlear implants in children, congenital hearing loss and CAEP were chosen as it provided sufficient and reliable data for literature review.Main interest is how the age of subject and length of auditory deprivation when CI is implanted affects maturity of the auditory cortex, especially P1 latency from P1-N1-N2 complex.Studies use various types of stimulus: speech like sounds or tone bursts. Therefore, additional interest is in morphology, latency and amplitude, of the P1 wave and how it changes depending on various types of stimulus used. Hopefully, there could be drawn conclusion on what test set-up are most reliable for repeatability of P1 latency recordings and could be used in further studies about CAEP.Chapter 2 describes in more details morphology of P1-N1-P2 latency complex and different types of stimulus that can be used to elicit P1 wave. Chapter 3 analyses four studies; subjects, procedures and their results. Discussion summarise finding on plasticity of auditory cortex and advantages/disadvantages of different types of stimulus. Finally, conclusion draws summary on findings and proposes future study.P1-N1-P2

Morphology of P1-N1 complex Cortical Auditory Evoked Potentials (CAEP) can be recorded from very early age. Firstly, late evoked potential changes as brain matures demonstrating plasticity of young auditory cortex; other changes of latency depends on hearing threshold, and integrity of auditory cortex, e.g. auditory processing disorders. Secondly, morphology of P1-N1-P2 latency complex depends to characteristics of stimulus (Brown, et.al. 2008).

P1-N1-P2 complex late cortical responses are obligatory responses that depend on the physical properties of the stimulus, its intensity and frequency (Purdy, et.al. 2002). Adults have small P1 amplitude