Introduction: Encoding of CE-chirp and click stimuli in auditory system was studied using auditory brainstem responses (ABRs) among individuals with and without noise exposure. Materials and Methods: The study consisted of two groups. Group 1 (experimental group) consisted of 20 (40 ears) individuals exposed to occupational noise with hearing thresholds within 25 dB HL. They were further divided into three subgroups based on duration of noise exposure (0–5 years of exposure-T1, 5–10 years of exposure-T2, and >10 years of exposure-T3). Group 2 (control group) consisted of 20 individuals (40 ears). Absolute latency and amplitude of waves I, III, and V were compared between the two groups for both click and CE-chirp stimuli. T1, T2, and T3 groups were compared for the same parameters to see the effect of noise exposure duration on CE-chirp and click ABR. Result: In Click ABR, while both the parameters for wave III were significantly poorer for the experimental group, wave V showed a significant decline in terms of amplitude only. There was no significant difference obtained for any of the parameters for wave I. In CE-Chirp ABR, the latencies for all three waves were significantly prolonged in the experimental group. However, there was a significant decrease in terms of amplitude in only wave V for the same group. Discussion: Compared to click evoked ABR, CE-Chirp ABR was found to be more sensitive in comparison of latency parameters in individuals with occupational noise exposure. Monitoring of early pathological changes at the brainstem level can be studied effectively by using CE-Chirp stimulus in comparison to click stimulus. Conclusion: This study indicates that ABR’s obtained with CE-chirp stimuli serves as an effective tool to identify the early pathological changes due to occupational noise exposure when compared to click evoked ABR.
Keywords: ABR, ce-chirp stimulus, click stimulus, NIHL, occupational noise exposure
|How to cite this article:|
Pushpalatha ZV, Konadath S. Auditory brainstem responses for click and CE-chirp stimuli in individuals with and without occupational noise exposure. Noise Health 2016;18:260-5
|How to cite this URL:|
Pushpalatha ZV, Konadath S. Auditory brainstem responses for click and CE-chirp stimuli in individuals with and without occupational noise exposure. Noise Health [serial online] 2016 [cited 2022 Jul 3];18:260-5. Available from: https://www.noiseandhealth.org/text.asp?2016/18/84/260/192477
| Introduction|| |
Noise-induced hearing loss (NIHL) is one of the major health issues, as there has been an increase in opportunities to noise exposure in recent days which might lead to damage of hearing. Noise exposure can cause two kinds of health effects, namely non-auditory and auditory effects. Non-auditory effects include disturbance with sleep, stress, anxiety reaction, etc., whereas auditory effects include temporary threshold shift (TTS) and permanent threshold shift (PTS) which are primarily seen due to the damage of cochlear hair cells. This damage may be seen within minutes or it might continue for days. These early cochlear changes might take a long time (days to years) to express as hearing loss on a standard pure tone audiometry. However, normal hearing thresholds might not necessarily indicate normal cochlear function across the audible frequency regions. Kujawa and Liberman revisited the issue of neural degeneration in ears with noise-induced threshold shifts in mice subjected to mild acoustic trauma. A temporary shift in hearing thresholds was noted along with 50–60% permanent deafferentation of auditory nerve fibers in the high frequency region of cochlea. Results of this study suggest that normal hearing thresholds can be accompanied by impaired function of efferent fibers that project from the brainstem to the cochlea.,,, Electrophysiological research has shown that after exposure to noise, spontaneous neuronal activity and compound action potentials in the auditory nerve are decreased., Similar findings have been reported within the first-day postexposure of intense noise in the central structure of the dorsal cochlear nucleus of cats. Further, clinical sequel of noise exposures like tinnitus and hyperacusis are usually present after hearing has been recovered. This cannot be explained with cochlear pathology satisfactorily. These discrepancies might possibly be related to additional, central mechanisms involved in the generation of NIHL.
Auditory brainstem response (ABR), being one of the electrophysiological measures, is a test to measure the functional integrity of brainstem auditory structures. ABR has become widely recognized as a sensitive and cost-effective screening modality in neuro-otologic diagnosis. ABR can be recorded using various kinds of stimuli like click, tone burst, speech, etc. A study done by Attias and Pratt showed that there are latency changes in click ABR with individuals exposed to noise. Recently, chirp stimulus compensating for basilar membrane traveling wave delay has come into existence. It yields better amplitude and early latency of peaks compared to click-evoked ABR. The CE-chirp is designed using a delay model based on derived band ABRs to overcome cochlear traveling wave delay and to increase synchronicity. Broadband CE-chirp has been included in Interacoustics EP-25 equipment which has a flat spectrum in five octave bands from 350 to 11,300 Hz. Hence, chirp ABR might result in giving better information when compared to click-evoked ABR. This might help in monitoring the early pathological changes seen in auditory brainstem in industrial workers. The present study was conducted with the aim to compare the efficacy of CE-chirp vs. click stimuli in ABR elicited in industrial workers exposed to occupational noise.
- To study the encoding of CE-chirp and click stimuli in auditory system using ABR among individuals with and without noise exposure.
- To find the effect of duration of noise exposure on ABR elicited using click and CE-chirp stimuli in individuals exposed to occupational noise.
| Materials and Methods|| |
Gender-matched 40 male individuals participated in the study. They were divided into two groups. Group 1 (experimental group) consisted of 20 industrial workers (40 ears) exposed to continuous occupational noise [>85 dB(A)] for a minimum duration of 8 h per day. They were in the age range of 20–45 years (mean age 31.8). All the subjects had hearing sensitivity less than or equal to 25 dB HL (from 250 Hz to 8 kHz). The participants of Group 2 served as controls. The group consisted of 20 individuals (40 ears) in the age range of 18–45 years (mean age 26.33) and had hearing sensitivity less than or equal to 15 dB HL (from 250 Hz to 8 kHz).
To examine the effect of duration of noise exposure, Group 1 was further divided into three Subgroups, namely T1, T2, and T3 (T1: 0–5 years of noise exposure, T2: 5–10 years of noise exposure, T3: >10 years of noise exposure). A detailed case history was taken for all the individuals to rule out any history or complaint of otological and neurological problems, hereditary hearing loss, or any other major illness. Consent for willingness to participate in the study was also taken from each individual.
The participants were seated in a reclining chair and the skin surface was cleaned using skin abrasive at the mastoid (M1 and M2) and forehead (Fz and Fpz). Impedance obtained was less than 5 kΩ for all the electrodes. Electrodes were placed in their respective places using skin conduction gel and were secured with surgical plaster. Click-evoked ABR and CE-chirp ABR were recorded using Inter-acoustics Eclipse EP-25. Both the stimuli were presented at an intensity of 80 dB nHL and 11.1/s repetition rate.
| Results|| |
Data from 80 ears (40 normal hearing and 40 ears exposed to occupational noise) were analyzed using the statistical package for social sciences (SPSS) software version 17. Shapiro–Wilk’s test, was done to check the normality. As the data for between-group comparisons did not follow the normal distribution, nonparametric tests were selected to check the significant differences. The variability is attributed to heterogeneity in the participants of the study. But parametric tests were conducted for within-group comparison as the data followed normal distribution. Absolute latency and amplitude of waves I, III, and V were compared between group and within group.
Comparison of absolute latency and amplitude of waves I, III, and V between Group 1 and Group 2 for click and CE-chirp ABR
Descriptive statistics of waves I, III, and V are shown in [Table 1]. Mean latency of waves I, III, and V for click-evoked and CE-chirp ABR for both groups are given in [Figure 1],[Figure 2],[Figure 3] respectively. Mean amplitude of waves I, III, and V for click-evoked and CE-chirp ABR for both groups are given in [Figure 4],[Figure 5],[Figure 6] respectively.
|Table 1: Mean (SD) latency and amplitude of waves I, III, and V of click and CE-chirp ABR|
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|Figure 1: Mean and SD of wave I latency for click-evoked and CE-chirp ABR|
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|Figure 2: Mean and SD of wave III latency for click-evoked and CE-chirp ABR|
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|Figure 3: Mean and SD of wave V latency for click-evoked and CE-chirp ABR|
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|Figure 4: Mean and SD of wave I amplitude for click-evoked and CE-chirp ABR|
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|Figure 5: Mean and SD of wave III amplitude for click-evoked and CE-chirp ABR|
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|Figure 6: Mean and SD of wave V amplitude for click-evoked and CE-chirp ABR|
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When CE-chirp-evoked ABR was done in Group 1, 30 ears had absent wave I, 29 ears had absent wave III, and 11 ears had absent wave V. Further, Mann–Whitney U test was performed to check for any significant difference between the two groups in terms of latency and amplitude. In click ABR, while both the parameters for wave III were significantly poorer for the experimental group, wave V showed a significant decline in terms of amplitude only. There was no significant difference obtained for any of the parameters for wave I. In CE-chirp ABR, the latencies for all three waves were significantly prolonged in the experimental group. However, there was a significant decrease in terms of amplitude in only wave V for the same group. The Z values obtained for the same are shown in [Table 2].
Comparison of absolute latency and amplitude of wave V within Group 1 (subgroups) for click and CE-chirp ABR
Only the comparison of wave V was considered due to lack of data, as more than 70% of the participants in Group 1 had absent waves I and III in CE-chirp ABR. Descriptive statistics was done for all the three subgroups (T1, T2, and T3) of Group 1 and the same is represented in [Table 3]. Mean latency and amplitude of wave V for click-evoked and CE-chirp ABR for T1, T2, and T3 are shown in [Figure 7] and [Figure 8] respectively.
|Table 3: Mean (SD) latency and amplitude of wave V of click and CE-chirp ABR in Group 1|
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|Figure 7: Mean and SD of wave V latency for click-evoked and CE-chirp ABR in three subgroups of Group 1|
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|Figure 8: Mean and SD of wave V amplitude for click-evoked and CE-chirp ABR in three subgroups of Group 1|
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Multivariate analysis of variance (MANOVA) was done to compare the two parameters for Group 1. A significant difference in wave V was obtained for latency [F(2,29) = 5.636, P < 0.05] and amplitude [F(2,29) = 4.847, P < 0.05] of click-evoked ABR and CE-chirp ABR respectively. Hence, post hoc least significant difference (LSD) was done to look for pair-wise comparisons for the same parameters. It revealed a progressive increase in terms of latency and decrease in terms of amplitude from T1 to T3.
| Discussion|| |
ABR, being one of the electrophysiological measures, is a test to measure the functional integrity of brainstem auditory structures. Basically, two parameters are usually considered while interpreting ABR waveforms, namely latency and amplitude. The goal of the present study was to observe encoding of CE-chirp and click stimuli in auditory system using ABR among individuals with and without noise exposure. In addition, it was aimed at finding the effect of duration of noise exposure on ABR elicited using click and CE-chirp stimuli in individuals exposed to occupational noise. The study compared absolute latencies and amplitude of peaks I, III, and V between experimental group and control group for both the stimuli.
A CE-chirp stimulus is designed in such a way that it compensates for basilar membrane delay and hence, results in enhanced synchrony in nerve fibers. As a result, we found earlier latencies in CE-chirp-evoked ABR in control group. When CE-chirp-evoked ABR was done for the experimental group, 30 ears had absent wave I, 29 ears had absent wave III, and 11 ears had absent wave V. These changes can be attributed to damage in auditory nerve fibers at some particular frequency region, especially at basal region affecting the overall firing rate of auditory nerve fibers leading to prolonged conduction time and also affecting the efficiency of nerve fibers. This finding can take support from a study done by Kujawa and Liberman, where they found 50–60% permanent deafferentation of the auditory nerve fibers in the high frequency region of the cochlea in mice subjected to acoustic trauma even when acoustic thresholds returned to normal. Hence, synchronous activity could be adversely affected in some of the individuals exposed to occupational noise resulting in absence of CE-chirp ABR. However, when present, the latencies of all the three peaks were significantly prolonged and wave V amplitude was significantly decreased when compared to control group. This finding also suggests that there might be a lesion or deafferentation of the auditory neurons at the level of synapse. As observed clinically, latency is a more reliable measure as compared to amplitude, as amplitude tends to vary in both inter and intrasubject recordings. There was significant variability in latency measures of all the peaks under observation between the two groups when CE-chirp stimulus was used for recording ABR.
When comparison was made for the above parameters in click ABR, latency parameter did not differ from control group for waves I and V. However, both the parameters for wave III were significantly poorer for the experimental group [Table 2] and wave V showed a significant reduction in terms of amplitude only [Table 2]. As the peak III originates at the level of cochlear nucleus, we can presume that there could be subtle damage to the cells in the structure which might indicate that cochlear nucleus in central auditory pathway could be slightly sensitive to noise-induced changes.
While studying the effect of duration of noise exposure on ABR, there was a small, but significant prolongation of click-evoked wave V latency. The duration of exposure to noise increased from T1 to T3 but the value was within normal range (5–6 ms). This may be attributed to slow pathological changes, further leading to slow manifestation of NIHL which might be difficult to monitor at early stages. A small, but significant decrease in CE-chirp amplitude was also found from T1 to T3 without significant shift in the latency parameter. This indicates that the damage to auditory nerve fibers is directly proportional to the noise exposure duration. From this study, we can conclude that CE-chirp ABR can be used as an effective tool to identify the early neural changes in the auditory system in individuals exposed to occupational noise. Compared to click-evoked ABR, CE-chirp ABR was found to be more sensitive in comparison of latency parameters in individuals with occupational noise exposure. Monitoring of early pathological changes at the brainstem level can be studied effectively by using CE-chirp stimulus.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
DHHS. Healthy People 2010: Understanding and Improving Health. Washington, DC: U.S. Department of Health and Human Services 2009.
Cohen S, Weinstein N. Nonauditory effects of noise on behavior and health. J Soc Issues 1981;37:36-70.
Wang Y, Hirose K, Liberman MC. Dynamics of noise-induced cellular injury and repair in the mouse cochlea. J Assoc Res Otolaryngol 2002;3:248-68.
Kujawa SG, Liberman MC. Adding insult to injury: Cochlear nerve degeneration after “temporary” noise-induced hearing loss. J Neurosci 2009;29:14077-85.
Kim S, Frisina DR, Frisina RD. Effects of age on contralateral suppression of distortion product otoacoustic emissions in human listeners with normal hearing. Audiol Neurootol 2002;7:348-57.
Jacobson M, Kim S, Romney J, Zhu X, Frisina RD. Contralateral suppression of distortion-product otoacoustic emissions declines with age: A comparison of findings in CBA mice with human listeners. Laryngoscope 2003;113:1707-13.
Zettel ML, Zhu X, O’Neill WE, Frisina RD. Age-related decline in Kv3.1b expression in the mouse auditory brainstem correlates with functional deficits in the medial olivocochlear efferent system. J Assoc Res Otolaryngol 2007;8:280-93.
Zhu X, Vasilyeva ON, Kim S, Jacobson M, Romney J, Waterman MS et al.
Auditory efferent feedback system deficits precede age-related hearing loss: Contralateral suppression of otoacoustic emissions in mice. J Comp Neurol 2007;503:593-604.
Dallos P, Harris D, Ozdamar O, Ryan A. Behavioral, compound action potential and single unit thresholds: Relationship in normal and abnormal ears. J Acoust Soc Am 1978;64:151-7.
Salvi RJ, Ding D, Wang J, Jiang HY. A review of the effects of selective inner hair cell lesions on distortion product otoacoustic emissions, cochlear function and auditory evoked potentials. Noise Health 2000;2:9-25.
Liberman MC, Kiang NY. Acoustic trauma in cats. Cochlear pathology and auditory-nerve activity. Acta Otolaryngol Suppl 1978;358:1-63.
House JW, Brackmann DE. Tinnitus: Surgical treatment. Ciba Found Symp 1981;85:204-16.
Telian SA, Kileny PR, Niparko JK, Kemink JL, Graham MD. Normal auditory brainstem response in patients with acoustic neuroma. Laryngoscope 1989;99:10-4.
Attias J, Pratt H. Auditory-evoked potential correlates of susceptibility to noise-induced hearing loss. Audiology 1985;24:149-56.
Elberling C, Don M. A direct approach for the design of chirp stimuli used for the recording of auditory brainstem responses. J Acoust Soc Am 2010;128:2955-64.
Zeena Venkatacheluvaiah Pushpalatha
All India Institute of Speech and Hearing, Mysuru 570 006, Karnataka
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
[Table 1], [Table 2], [Table 3]