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ORIGINAL ARTICLE
Year : 2015  |  Volume : 28  |  Issue : 1  |  Page : 213-218

Validity of P1 testing as an objective tool for hearing aid verification in children


1 Department of Otorhinolaryngology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Otorhinolaryngology, Faculty of Medicine, Al Azhar University, Egypt

Date of Submission06-Nov-2013
Date of Acceptance11-Mar-2014
Date of Web Publication29-Apr-2015

Correspondence Address:
Ahmed Mahmoud Zein El-Abedein
MSc, Shebein Elkom, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.155997

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  Abstract 

Objective
The aim of this study was to determine the efficiency of P1 as an objective tool for verification of hearing aids in children.
Background
Hearing loss in childhood interferes with the normal development of speech. The use of hearing aids improves speech perception. Cortical auditory-evoked potentials (CAEPs) (dominated by a large P1 response) may be a good tool for assessment of hearing aids.
Patients and methods
In this study, 200 children ranging in age from 3 to 6 years were divided into two groups: the control group (50 volunteers), which included children with normal hearing sensitivity, matched for age and sex with the study group, and the study group, which included 150 children with sensorineural hearing loss. This group was subdivided as follows: subgroup a (group with well-fitted hearing aids), subgroup b (poorly fitted group), and subgroup c (not wearing hearing aids). All were subjected to a full assessment of history, psychosocial evaluation, otological examination, basic audiological evaluation, and the CAEPs test, which was performed serially each month for subgroup a for 15 months.
Results
The P1 wave dominates the CAEPs as it appeared in 100% of the normal children. The N1 wave, in contrast, did not appear in all individuals. In the study subgroup a, P1 appeared with longer latency, which led to a decrease in hearing aid usage to normal after 15 months. Children of subgroup b showed less improvement in P1 latency. In subgroup c, only very few children gave for P1 with delayed latency.
Conclusion
P1 is reliable for the evaluation of hearing aids. It appears in all children and usually improves to normal values after 15 months of using suitable hearing aids. The N1 wave, in contrast, is not a reliable wave.

Keywords: Assessment of hearing aids, cortical auditory-evoked potentials, hearing-aided children, N1 wave, P1 development, sensorineural hearing loss, speech development


How to cite this article:
El-Sharnouby MK, El-Mousely MM, Ragab AA, El-Abedein AM. Validity of P1 testing as an objective tool for hearing aid verification in children. Menoufia Med J 2015;28:213-8

How to cite this URL:
El-Sharnouby MK, El-Mousely MM, Ragab AA, El-Abedein AM. Validity of P1 testing as an objective tool for hearing aid verification in children. Menoufia Med J [serial online] 2015 [cited 2019 Sep 20];28:213-8. Available from: http://www.mmj.eg.net/text.asp?2015/28/1/213/155997


  Introduction Top


There is no doubt that moderate to severe hearing loss will have a serious impact on the child's development. Permanent hearing loss in childhood interferes with the normal development of speech perception, production, language literacy skills, and social-emotional development [1]. The consequences of peripheral hearing loss can be observed throughout the central auditory system including portions of the cochlear nucleus, the inferior colliculus, and the primary auditory cortex [2]. Cortical auditory-evoked potentials (CAEPs) are noninvasive measures used to quantify the central auditory system in humans [3]. From birth up to 7 years of age, the CAEP response is dominated by a large, late P1 response [4].

P1 response yields a robust positivity at a latency of 100-300 ms in young children. It reflects the maturation of the auditory system over time. In children with normal hearing, the latency of the P1 decreases consistently with age [5]. The latency of P1 reflects the accumulated sum of delays in synaptic propagation through the peripheral and central auditory pathways [6]. P1 latency is considered a measure of central auditory development in patients using hearing aids. P1 latency may be an objective tool for the clinician to evaluate whether amplification in hearing-impaired children provides sufficient stimulation for normal development of the central auditory pathway [7]. This study aimed to determine the validity of the P1 response as an objective tool to assess hearing aids by providing information on maturation of the central auditory pathway and thus provide an objective assessment of central auditory development in children with sensorineural hearing loss after wearing hearing aids.


  Patients and methods Top


This study included 200 children ranging in age from 3 to 6 years. They were recruited from among children attending the Audiology Unit of Menoufia University in the period between January 2010 and July 2012. Consent was obtained from the parents of the all the children who participated in this study. The children were divided into two groups. The control group included 50 volunteers with normal hearing sensitivity, matched to the study group for age and sex [Table 1]. Children of the control group were selected according to the following criteria: no history of hearing loss, ear disease, trauma, ototoxic drug intake, or ear operation, no neurological disorders, normal hearing sensitivity, pure tone average not exceeding 15 dBHL in the frequencies from 250 to 8000 Hz by air conduction [8], normal middle ear functions as evidenced by otological examination, tympanometry, and an acoustic immittance test, and normal psychointellectual ability. The study group included 150 children ranging in age from 3 to 6 years with severe to profound sensorineural hearing loss. They were divided into three groups: subgroup a, which included 50 children well-fitted hearing aids (26 with 360 essential, 17 with Beltone force, and seven with Davinci), with onset of fitting at 3 years of age; subgroup b, which included 50 children fitted poorly with hearing aids (32 fitted with 360 essential, 11 Viking, five force, two Davinci); and subgroup c, which included 50 children with hearing loss who did not wear hearing aid.
Table 1: Mean and SD of the pure tone threshold of the control group in the right and left ears versus pure tone thresholds (for each of the study subgroups)

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All children were subjected to the following:

Assessment of history, otological examination, and basic audiological evaluation including play audiometry and aided warble tone response thresholds in the sound field assessed using a two-channel audiometer (Madsen Orbiter 922 and Sound Treated Room Amplisilence Model S.P.A. 10070), immittance testing using GSI tempstar, neurological examination to exclude children with CNS disorders, psychometric evaluation (IQ above 90), and the P1 CAEP test, which was performed using the Intelligent Hearing System (Model Smart EP 2 Channel).

Cortical auditory-evoked potential measurement

Children were seated comfortably in a chair placed in a sound booth. They watched a videotaped movie or cartoon of their choice on a laptop placed in front of them in the sound booth. Videotape audio levels were maintained below a 45-dB sound pressure level.

Stimuli

CAEPs were recorded in response to a synthesized speech syllable /ba/. The stimulus was presented through a loudspeaker with an intensity of 90 dBNHL placed at an angle of 45° to the hearing aid side. Processors were set to the children's usual processor settings.

Electrode montage

Evoked potentials were collected using Cz as the active electrode (Cz refers to the vertex midline placement). The reference electrode was placed on the mastoid and the ground electrode was placed on the forehead. The recording window included a 100-ms prestimulus time and a 600-ms poststimulus time. Incoming evoked responses were analog filtered from 0.1 to 30 Hz. Approximately 300 response sweeps were collected for each child. The test session, including electrode application and evoked response recording, lasted for about 30 min. Sweeps were averaged to compute a grand average waveform for the each child.

We defined P1 as the first robust positivity in the auditory-evoked potential waveform in the 50-175-ms range. The P1 latency was labeled at the peak of the response or, if the peak was broad, at the midpoint. The P1 response latencies were plotted against the 95% confidence interval for normal development of the P1 response. The test was performed serially each month for 15 months for children wearing hearing aids.

Statistical analysis

Data were analyzed using the SPSS (version 16.0; SPSS Inc., Chicago, Illinois, USA) statistical package. Quantitative data were expressed as mean and SD and were analyzed using the analysis of variance test for comparison between more than two groups of normally distributed variables. The Student t-test was used to assess whether there was a significant difference between two variables. The Pearson correlation coefficient was used to calculate the correlation between the variables. The level of significance was set at P-value less than 0.05.


  Results Top


Both the study and the control groups had the same age range, with no statistically significant difference. The IQ of the children in both the study and the control groups were average and above average (90-110), with no statistically significant difference between the two groups. Pure tone thresholds of the children in the control group were equal to or better than 20 dBHL at all test frequencies from 250 to 8000 Hz [Table 2]. This indicated normal peripheral hearing according to American National Standard Institute specifications [8]. All children had a type A tympanogram, indicating normal middle ear pressure, and the acoustic reflex thresholds were within the normal range. However, the children in the study group had severe sensorineural hearing loss (pure tone average; 86.92 dBHL), with no statistically significant difference between the study subgroups a, b, and c. The control group and each of the study subgroups showed statistically significant differences in the hearing thresholds. Aided thresholds of the study subgroups a and b showed statistically significant differences.
Table 2: Aided thresholds between study subgroups a and b

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Slow cortical potential results (P1-N1 wave measurements)

The control group

The P1 wave dominated the CAEPs in 100% of the normal children. It appeared as a large positive peak at a latency of 105.8 ms and an amplitude of 2.6 mV (arithmetic mean of the control group results) [Table 3].
Table 3: Comparison of the control group with study subgroup a in P1 latency

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The N1 wave, in contrast, appeared only in 48% of the children. It appeared as the first negative wave after the P1 wave. The value of N1 latency was 139.33 ms and the amplitude was 0.97 mV [Table 4].
Table 4: Comparison of the control group with the study subgroup a in the N1 values

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The study group

The children of the study group had sensorineural hearing loss and were subdivided as follows:

Study subgroup a:

These children, who had hearing aids with satisfactory aided response, were examined serially to follow up and monitor the development of the P1-N1 waves as a result of wearing the hearing aids.

At the onset of wearing the hearing aid, not all children had P1-N1 waves. The P1 wave appeared in 72% of children at onset of fitting and this percent increased to 100% after 1 week of wearing a hearing aid and by the follow-up of children after 1, 3, 6, 9, 12, and 15 months. The development of the P1 wave was monitored and the appearance of the N1 wave was also monitored. As in the control group, it appeared as large positivity, but with longer latency average (443.4 ms), with a higher statistically significant prolonged latency than that of the children in the control group.

This latency decreased with hearing aid usage, but it there was a statistically significant difference from the average latency of the normal children. After 15 months of wearing the hearing aid, the latency of the P1 showed no statistically significant difference from the P1 latency in the control group. This indicates that maturation of the auditory system by sufficient amplification requires regular wearing of a hearing aid for 15 months [Figure 1].
Figure 1: Development of the P1 wave using hearing aids over 15 months.

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The amplitude showed huge variability among the children. The mean amplitude at onset was 3.8 mV, with a reduction in amplitude with the use of hearing aids. This value of amplitude is significantly larger than that of the normal group over the entire follow-up period of the children of study subgroup a.

The N1 wave only started to appear at 9 months after fitting of the hearing aid in 32% of the children; then, it appeared in 44% of the children at 12 months and finally in 48% of the children at 15 months of wearing hearing aids. By 9 months after fitting, N1 appeared with a latency of 190.5 ms, which was highly significantly delayed than that found in the control group. However, latency reduced significantly with wearing of hearing aids. After 15 months of using the hearing aid, the latency of N1 was not statistically significantly different from that of the normal group.

However, amplitude at 9 months was 0.72 mV, which did not change significantly with the regular use of the hearing aid.

Study subgroup b:

In this subgroup, which included children with hearing loss who wore hearing aids with unsatisfactory amplifications, the P1-N1 waves were followed up at the onset and after 3 months of amplification. P1 appeared only in 50% of the children with average latency (451 ms), which is statistically significantly different from the latency in the previous subgroup a at onset. However, after 3 months of using the same hearing aids, it was found that there was a statistically significant difference in P1 latency (443.6 ms). On comparing these results with the previous group, there were greater differences in the latency after the use of the hearing aids for three months as in the children of subgroup a. These children did not show the N1 wave. So these children referred to change their hearing aids to better ones, if no improvement after another 3 months they were referred to the cochlear implantation.

Study subgroup c:

The P1-N1 waves were measured in children with no hearing aids. Only very few children yielded results (8%) for P1 with delayed latency, but the N1 did not appear at all. After performing this step in the study, we referred them for hearing aid fitting [Table 5].
Table 5:Comparison between the latency and amplitude of P1 in subgroups a and b at onset of fitting and after 3 months
of fitting


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  Discussion Top


In the control group, the P1 wave dominated the CAEPs and this was in agreement with the findings of Gilley et al. [9]. The N1 wave, in contrast, did not appear in all normal children. These findings were in agreement with those of Sharma et al. [10]. This indicated that P1 is more reliable and its measures are more dependable.

In the children well fitted with hearing aids (subgroup a, the development of the P1 wave was monitored; it appeared as a large positivity, but with longer latency than that found in normal children. Prolonged CAEPs' latencies with SNHL provide a sensitive index of increased neural processing time associated with hearing loss, and discriminative processing is more adversely affected by hearing loss compared with speech detection processes [11]. This indicated that hearing loss and cochlear damage disrupt the response properties of cortical neurons [12]. This latency decreased with hearing aid usage, but still showed a statistically significant difference from that of normal children, except after 15 months of fitting, at which point, the latency of the P1 showed no statistically significant difference from P1 latency in the normal control group. This indicated the development of the neuro-otological pathway with the use of hearing aids and that it takes time (15 months) with the use of a hearing aid to achieve normal development of the central auditory system.

The P1 amplitude was significantly larger than that of the normal group over the entire follow-up period of the children of study subgroup a. The explanation for this difference could be a recruitment phenomenon that occurs in children with sensorineural hearing loss at a high stimulus intensity [11]. Amplitude decreased with the use of hearing aids as a part of the development of P1-N1 waves. No conclusive data were obtained for amplitude, especially because of the huge variability observed among the children.

The N1 wave was not only often absent in young normal children [13] but was also affected by reduced audibility [11]. The N1 wave started to appear at 9 vmonths after fitting of the hearing aid in 32% of the children with delayed latency than that of the control group; then, latency reduced significantly with wearing of hearing aids until normal values were achieved after 15 months. These results were in agreement with those of Muccllagh [14], who found that with increasing duration of HA use, N1 latency decreased, but amplitude did not change significantly with the regular use of the hearing aid.

Eggermont [15] suggested that changes in N1 latency were related to increases in myelin and synaptic efficiency of the neurons contributing toward the N1 potential. Similarly, Kaas [16] explained that plasticity that occurred as a result of changes in the existing connections occurred soon after the alteration in stimulation. The effectiveness of synapses in the dense core of activated neurons spread to the areas of deprived input to increase neuronal activity to the stimulus. This is in agreement with Rapin et al. [17], Martin and Boothroyd [18], and Purdy and Kelly [19]. They found that, with the use of hearing aids, neural response patterns were shorter in latency (neural conduction travel-time) when compared with individuals not using hearing aids.

In the study subgroup b, P1 appeared only in 50% of the children with delayed latency than that in the previous study subgroup a. This may be because of either the delayed maturation of the auditory pathway or insufficient amplification, which caused a weak stimulus that could not induce CAEP.

However, after 3 months of use of the same hearing aids (as a trial to enhance the amplification, but with no change), it was found that there were statistically significant improvements in P1 wave latency, but significantly latent compared with the study subgroup a, indicating that children with hearing aids fitted well gained more benefit in terms of the development of the neuro-otological pathway. This showed that although the development of the neuro-otological pathway had started, it did not progress in the same manner as amplification. Also, this shows that even if the hearing aid has unsatisfactory amplification, the patient should wear it until readjustment occurs or until the hearing aid is changed or even switch to the use of a cochlear implant. The N1 wave did not appear in the children in this group, which could have been because of the delay in the maturation of the auditory pathway as a result of insufficient amplification of the stimulus.

In study subgroup c, the CAEPs were measured in children with no hearing aids.

Results for P1 with delayed latency were obtained in very few children. The N1 did not appear at all. This could have been because the stimulus could not be amplified because of the lack of a hearing aid (in addition to the delayed maturation of the neuro-otological pathway). These children ware referred for immediate fitting after the test.

From the data obtained in the previous control group and the study subgroups, we found that P1 is affected in terms of latency and amplitude in the presence of hearing loss, it appears in 100% of the normal population, changes regularly with hearing compensation, the degree of amplification affects the degree of wave development, and satisfactory amplification can be achieved with the development of P1 to match that of the normal values of the P1 wave (latency).

However, the N1 wave appeared only in older children, not appearing in all children in this study (3-6 years of age). It showed significant differences even with good amplification (in the latency and intensity values within the same group) and have many shapes and that may lead to misunderstanding.

Hearing loss has a significant impact on the timing, strength, and location of the cortical brain processes underlying the detection and discrimination of speech [11]. Many studies have shown that hearing loss can induce changes in the auditory nervous system. This effect depends on the degree of hearing loss (or sound deprivation) and its duration [20].


  Conclusion Top


P1 CAEP is a reliable method for assessment of hearing aids or any amplification device. Also, it can be used as a tool for the diagnosis of central auditory disorders in children with hearing impairment fitted with hearing aids. The N1 wave, in contrast, is not a reliable wave for assessment in the age group of children in this study (3-6 years of age). This, this study found results that are in agreement with many studies reported in the literature that had shown that CAEPs can be used to show the benefits of amplification in children and infants.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.[21]

 
  References Top

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Sharma A, Tobey E, Dorman M, Bharadwaj S, Martin K, Gilley P, Kunkel F. Central auditory maturation and babblingdevelopment in infants with cochlear implants. Arch Otolaryngol Head Neck Surg 2004; 130 :511-516.  Back to cited text no. 10
    
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Muccllagh J. An investigation of central auditory nervous system plasticity following amplification [dissertation for MD degree]. USA: University of Connecticut; 2009.  Back to cited text no. 14
    
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Eggermont J. Neural interactions in cat primary auditory cortex. Dependence on recording depth, electrode separation and age. J Neurophysiol 1992; 68: 1216-1220.  Back to cited text no. 15
    
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Kaas J. Plasticity of sensory and motor maps in adult mammals. Ann. Rev Neurosci 1991; 14: 137-167.  Back to cited text no. 16
    
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Rapin I, Schimmel H, Tourk L, Krasnegor N, Pollak C. Evoked responses to clicks and tones of varying intensity in waking adults. Electroenceph Clin Neurophysiol 1966; 21 :335-344.  Back to cited text no. 17
    
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Martin B, Boothroyd A. Cortical auditory evoked potentials in response to changes of spectrum and amplitude. J Acoust Soc Am 2000; 107: 2155-2161.  Back to cited text no. 18
    
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Purdy S, Kelly A. Cortical auditory evoked potential testing in infants and young children. N Z Audiol Soc Bull 2001; 11 :16-24.  Back to cited text no. 19
    
20.
Krall A, Tillein J. Moller AR, editors. Brain plasticity under cochlear implant stimulation. Cochlear and brainstem implants. Adv Otorhino laryngol 2006; 64 :89-108.  Back to cited text no. 20
    
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Rapin I, Graziani L. Auditory-evoked responses in normal, brain-damaged, and deaf infants. Neurology 1967; 17 :881-894.  Back to cited text no. 21
    


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