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|Year : 2012
: 14 | Issue : 56 | Page
|Audiological and electrophysiological assessment of professional pop/rock musicians
Alessandra G Samelli, Carla G Matas, Renata M. M. Carvallo, Raquel F Gomes, Carolina S de Beija, Fernanda C. L. Magliaro, Camila M Rabelo
Departments of Physical Therapy, Speech language Pathology and Audiology, and Occupational Therapy, School of Medicine, University of São Paulo, SP, Brazil
Click here for correspondence address
|Date of Web Publication||29-Feb-2012|
In the present study, we evaluated peripheral and central auditory pathways in professional musicians (with and without hearing loss) compared to non-musicians. The goal was to verify if music exposure could affect auditory pathways as a whole. This is a prospective study that compared the results obtained between three groups (musicians with and without hearing loss and non-musicians). Thirty-two male individuals participated and they were assessed by: Immittance measurements, pure-tone air conduction thresholds at all frequencies from 0.25 to 20 kHz, Transient Evoked Otoacoustic Emissions, Auditory Brainstem Response (ABR), and Cognitive Potential. The musicians showed worse hearing thresholds in both conventional and high frequency audiometry when compared to the non-musicians; the mean amplitude of Transient Evoked Otoacoustic Emissions was smaller in the musicians group, but the mean latencies of Auditory Brainstem Response and Cognitive Potential were diminished in the musicians when compared to the non-musicians. Our findings suggest that the population of musicians is at risk for developing music-induced hearing loss. However, the electrophysiological evaluation showed that latency waves of ABR and P300 were diminished in musicians, which may suggest that the auditory training to which these musicians are exposed acts as a facilitator of the acoustic signal transmission to the cortex.
Keywords: Auditory evoked potentials, auditory pathways, auditory stimulation, auditory threshold, evoked otoacoustic emissions, music
|How to cite this article:|
Samelli AG, Matas CG, Carvallo RM, Gomes RF, de Beija CS, Magliaro FC, Rabelo CM. Audiological and electrophysiological assessment of professional pop/rock musicians. Noise Health 2012;14:6-12
|How to cite this URL:|
Samelli AG, Matas CG, Carvallo RM, Gomes RF, de Beija CS, Magliaro FC, Rabelo CM. Audiological and electrophysiological assessment of professional pop/rock musicians. Noise Health [serial online] 2012 [cited 2021 Oct 16];14:6-12. Available from: https://www.noiseandhealth.org/text.asp?2012/14/56/6/93314
| Introduction|| |
Exposure to noise of high intensity and for a long period increases the risk of permanent hearing damage. The degree of hearing loss it may cause depends on the frequency and intermittency of the exposure. ,
Even as the controversy over whether or not music causes permanent hearing loss remains,  many studies have presented evidence of a potential risk for hearing damage from music exposure. ,, This hearing loss has been referred to as a music-induced hearing loss. 
It is well known that the pathophysiological effects of noise act mainly on the cochlea, ,,, but some previous investigations have shown that the central components of the auditory pathways can also be affected by acoustic overstimulation. ,,,
Exposure to noise tends to cause structural and metabolic changes in the hair cells, which can subsequently degenerate. ,,,,, Additionally, it has been shown that noise exposure alters mitochondrial activity, leading to increased production of free radicals that cause changes in blood flow and neural activity that induce the death of hair cells by both necrosis and apoptosis. 
Once the cochlea is damaged, a sequence of events occurs in a pathophysiological cascade. In summary, decreasing cochlear input into the central auditory pathway may induce apoptosis in the neurons, which reduces cell density in the ventral cochlear nucleus. Next, the cell density and important structures of the central auditory pathway (central nucleus of the inferior colliculus, medial geniculate body, and primary auditory cortex) are also affected by overstimulation of the neurons and intense calcium influx.  These changes lead to toxic neurodegenerative processes and an enhanced neurotransmitter release that can induce glutamate excitotoxicity due to ionic homeostasis changes. ,
Despite the injuries that exposure to music may cause to the peripheral and central auditory pathway, clinical practice and even the research done on the subject in humans have been limited to audiological assessment.  However, audiological assessment is a poor indicator of the degree of damage caused to the auditory pathways. Hence, recent studies on music-induced hearing loss have adopted advanced audiological measurements (high frequency audiometry and otoacoustic emission) for the early identification of these damages, even before the changes can be detected by conventional audiometry.  Our study is the first in which a battery of assessments that include electrophysiological, eletroacoustic, and audiological assessments have been used to investigate the impact that exposure to music may have on whole auditory pathways.
The present study
In the present study, we evaluated peripheral and central auditory pathways in professional musicians (with and without hearing loss) compared to non-musicians. The goal was to verify if music exposure could affect auditory pathways as a whole.
- Professional Pop/Rock Musician Groups: The inclusion criteria adopted in this study were (a) being a professional musician, (b) being a member of a pop/rock band for more than five years, (c) having had exposure to intense sound levels from electrically amplified music for at least two hours weekly, (d) being male, (e) being between 18 and 45 years old, and (f) having an audiological threshold from 250 to 8000 Hz ≤40 dBNA. The exclusion criteria were (a) existing acoustic trauma, (b) exposure to noise (≥80 dBA) during occupational activities from sources other than music, (c) a history of recurrent otitis media, (d) previous ear surgery, (e) conductive hearing loss and excessive ear cerumen, and (f) use of potentially ototoxic drugs.
- Non-musicians Group: The inclusion and exclusion criteria for the control subjects were the same, except for exposure to music considered at a professional level according to the criteria adopted for the musicians group.
Our study group of professional musicians contained 16 subjects with ages ranging between 21 and 41 years (mean, 27.10 years; SD, 6.02 years) and the control group contained 16 subjects with ages ranging between 20 to 43 years (mean, 26.87 years; SD, 7.40 years) (P value=0.936). The instruments considered in the musicians group were guitar (n=4) and drums (n=12). The mean average of weekly noise exposure to intense sound levels in the musicians group was approximately 23.1 hours over a mean period of approximately 16.3 years.
The musicians group, in turn, was classified in two subgroups: HLG - hearing loss musician group (0.25 kHz - 20 kHz), according to analysis criteria of British Society of Audiology  and Burguetti et al.,  and MG - musicians without hearing loss in any frequencies (0.25 kHz - 20 kHz).
| Procedures and Measures|| |
Informed consent was obtained from each individual who participated in this study. The study was approved by the Ethics Committee of the University of São Paulo, Brazil.
All subjects were requested to complete a detailed questionnaire concerning their age, gender, education, medical history, occupational history, and the circumstances surrounding their musical activities, such as how long the subject played per day, how loud, how often, and what instruments, as well as whether or not they had used ear protection.
An audiometric assessment was conducted on all participants. Screening acoustic immittance measurements (GSI 38 Auto Tymp, Grason-Stadler, Inc., Madison, WI) and otoscopy were performed.
Pure-tone air conduction thresholds at all frequencies from 0.25 to 8 kHz and in the extended high frequencies of 9, 10, 12.5, 14, 16, 18, and 20 kHz were carried out with a GSI 61 Clinical Audiometer (Grason-Stadler, Inc., Madison, WI) using standard audiometric techniques in a sound-attenuated testing room.
Transient Evoked Otoacoustic Emissions (TEOAE) were recorded using an ILO 292 Plus OAE analyzer, v 6 (Otodynamics Ltd., Hatfield, UK), using ILO insert phones. The TEOAEs were recorded in a nonlinear mode. Under all conditions, the mean intensity of the clicks was 78 - 83 peSPL, and 200 sweeps were recorded for each ear. The response level was determined by measuring the signal-to-noise ratio with an analysis time window of 4 - 20 ms. The nonlinear transient click of 80-μ s duration was presented at a rate of 50 Hz, in alternating blocks. The individuals were tested in a sound booth, in a quiet room.
The electrophysiological tests (Auditory Brainstem Response - ABR, and Cognitive Potential - P300) were carried out in an electric- and sound-attenuated testing room. The electrophysiological assessment was done using a two-channel electroneuromyograph equipment (Biologic Traveler Electrodiagnostic Testing System; Biological Systems Corp., Mundelein, IL, USA). The individual was asked to remain with his eyes fixed on a figure positioned about five feet away during the recording of potentials, in order to control eye movement artifacts.
For the ABR, a rate of 19 clicks per second, with 0.1 μ s duration, were used with a filter slope of 12 db/octave, with the band pass filter 100-1500 Hz, and 2000 sweeps. The stimulus was 80 dBnHL. The ABR measurements were duplicated to ensure fidelity.
The oddball paradigm was used in the P300 recordings. This paradigm was based on distinguishing between a target stimulus repeated randomly (20% of the time) and the non-target stimuli, with frequent repetition (80% of the time). The subjects were asked to count the stimuli when they discriminated the target stimulus. A monaural auditory stimulus was presented. Frequencies were 1000 Hz for the frequent stimuli (non-target) and 1500 Hz for the rare (target) stimulus. The stimulus was 75 dBnHL. A rate of 1.1 tone-burst per second was used with the low filter setup in 30 Hz and the high filter in 1 Hz, and 300 sweeps.
The electrodes were positioned according to an international electrode system (IES), 10 - 20.  Electrode impedances were always less than 5 kΩ. Standard Bio-logic TDH49 headphones were used to deliver the sound stimuli for the electrophysiological tests.
Latency and amplitude of the waves were analyzed. The P300 were analyzed after subtracting the curves resulting from the rare and frequent stimulus (of the same ear), and were measured at the most positive point (amplitude), from 250 to 600 ms.
For the statistical analyses, the Kolmogorov-Smirnov test was applied to determine normality of the variable distribution. We used the Analysis of Variance (ANOVA) and Tukey's test for quantitative analysis and Chi-square (Fisher's exact test and Mantel-Haenszel) for qualitative analysis. The level of significance was set at 0.05. Significant values were designated with an asterisk (*).
| Results|| |
There was no statistically significant difference between the right and left ears (P>0.05; ANOVA) for conventional and high frequency pure-tone audiometry, amplitudes of OAE, or the wave latencies of electrophysiological tests, for all individuals in all groups. Thus, both ears of the individuals in each group were grouped and 16 musician subject responses (32 ears) were compared with 16 non-musician subject responses (32 ears). The HLG was composed of 14 ears and the MG was composed of 18 ears.
Hearing thresholds in both conventional and high frequency audiometry
A statistical analysis performed for pure-tone thresholds revealed that values significantly differed between the three groups for 2 and 3 kHz, and for 12.5 to 18 kHz [Table 1]. The musicians groups (HLG and MG) exhibited higher thresholds than the controls, in general.
For pairwise comparison (Tukey's test), we observed the statistical significant difference for: 2 kHz NG×HLG (P=0.013); 3 kHz NG×HLG (P=0.049); 12.5 kHz NG×HLG (P=0.007); MG×HLG (P=0.001); 14 kHz NG×HLG (P=0.004); MG×HLG (P=0.001); 16 kHz NG×MG (P=0.017); NG×HLG (P=0.009); MG×HLG (P=0.001); 18 kHz NG×HLG (P=0.001); MG×HLG (P=0.001)
|Table1: Mean, standard deviation (in dB), and P value of hearing thresholds of the musicians group with hearing loss (HLG), musicians group without hearing loss (MG), and non-musicians group (NG), to frequencies from 250 Hz to 20 kHz as indicated by ANOVA|
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On audiometry, 7.15% of the HLG ears had hearing loss in at least one frequency (significant difference between groups). In the high-frequency audiometry, 100% of the HLG ears had hearing loss in at least one frequency (significant difference between groups) [Table 2].
|Table2: Percentage of ears with sensorineural hearing loss in conventional and high frequency pure tone thresholds|
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Amplitudes of otoacoustic emissions
In transient evoked otoacoustic emissions, a statistically significant difference between the mean response (amplitude) of the three groups for all frequencies was observed [Table 3]. The HLG and MG had smaller TEOAE amplitudes when compared with the NG. For this comparison, we excluded the subjects with absent OEA.
|Table 3: Mean, standard deviation (in dB), and P value of the amplitude of otoacoustic emissions for frequencies from 1 kHz to 4 kHz and response (dB) as indicated by ANOVA|
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For pairwise comparison (Tukey's test), we observed statistical significant difference for: 1 kHz NG×MG ( P≤0.001); NG×HLG ( P≤0.001); 1.5 kHz NG×MG ( P≤0.001); NG×HLG ( P≤0.001); 2 kHz NG×MG ( P≤0.001); NG×HLG ( P≤0.001); 3 kHz NG×MG ( P≤0.001); NG×HLG ( P≤0.001); 4 kHz NG×MG ( P≤0.001); NG×HLG ( P≤0.001); Response NG×MG ( P≤0.001); NG×HLG ( P≤0.001).
In HLG, 14.28% of the ears had absent TEOAE and 85.71% had TEOAE partially present, although a statistically significant difference between the groups was observed only for TEOAE, which was partially present [Table 4].
Short and late latency responses
We compared the waves and interpeak latencies of ABR between the three groups [Table 5]. There was statistically no significant difference in any waves or interpeaks comparison between the groups.
|Table 5: Comparative study of the waves and interpeak latencies of ABR between musician and non- usician groups as indicated by ANOVA|
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For pairwise comparison (Tukey's test), we observed a statistically significant difference for: NG×MG (P=0.041).
There was a statistically significant difference between the groups [Table 6]; the MG had smaller mean latency of P300 when compared to NG and HLG.
There was a statistically significant difference for ABR alterations between groups, with more alterations in NG than in MG and HLG [Table 7]. There was statistically no significant difference between groups for the P300 (data not shown), because no P300 alterations (according to McPherson  normality) were observed in both groups.
|Table 6: Comparative study of P300latencies between musician and non-musician groups as indicated by ANOVA|
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|Table 7: Comparative study of abnormal results between the musicians and non-musicians groups for ABR|
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| Discussion|| |
We found that musicians (HLG) had 7.15% of their ears with sensorineural hearing loss (as shown by conventional audiometry) and 100% of their ears with hearing loss in high frequencies. The values significantly differed between the three groups for 2 and 3 kHz, and for 12.5 to 18 kHz. Nevertheless, the mean values in the musicians group (MG and HLG) were worse than in the control group. This fact showed that the musicians already had some degree of peripheral damage, even though these individuals were still young.
These results agreed with other studies that found worse hearing thresholds when comparing pop/rock musicians with a control group  or those that found different prevalence of hearing loss among musicians from different musical genres (58% of the musicians;  52.5% of the musicians;  37% of the musicians;  33 to 52% of the musicians, depending on the criteria of hearing loss used;  49% of the musicians;  more than 50% of the musicians had a hearing loss of 15 dB(A) and more;  42.9% of the musicians  ). Previously, our group showed that depending on the hearing loss criteria used (different thresholds of cut off, averages of thresholds, uni-or bilateral hearing loss, etc.),  the prevalence of hearing loss could change, which might explain the differences observed in the previous studies.
Concerning TEOAE, the musician groups (MG and HLG) presented significantly smaller mean amplitudes for all frequencies compared to the non-musician groups. Moreover, if we considered the absent emissions and the partly present emissions together, the HLG showed 100% alteration, the MG showed 44.44% alteration, whereas, the NG showed no absent or partially present emissions.
Among the studies in which TEOAE were used to draw the audiological profile of musicians, the results varied considerably. A previous study  found 38% sensorineural hearing loss in high frequencies and 69% absent otoacoustic emissions in orchestral musicians. Another study  found 100% normal hearing, but 60% absent responses of TEOAE in rock musicians. A third study  observed that TEOAE was present in all evaluated singers, but with less robust responses when compared to the control group. A recent investigation  found nearly 21% hearing loss and 45.8% absent TEOAE in pop/rock musicians.
These values were higher than those observed in this study (12.5%, if were consider HLG and MG together). It should be noted that these studies evaluated parameters different from those evaluated in our study and did not consider the 'partially present' values, which in our study showed a high prevalence (100%). Despite these differences, our findings suggested worse function of outer hair cells (OHC) in MG and HLG, when compared with NG, suggesting cochlear damage in most of the musicians, even though this damage had not yet been seen in conventional and/or high frequency audiometry.
For the electrophysiological evaluation, we have found early responses to ABR and P300 waves in musicians. These professionals, with musical training and practice, increase the spontaneous attention to the sound and their sound discrimination abilities.  This fact suggests that musical training provides a better processing of acoustic information by the central auditory nervous system. Some authors  have evaluated the ABR and cortical evoked responses of musicians and non-musicians and shown that musicians have earlier responses when compared to non-musicians, indicating rapid identification and perception of sound by musicians. The auditory training through the musical experience provides a neural synchrony to the auditory system as well as faster responses to the presence of sound, as has been concluded in another study,  which has analyzed the ABR of musicians to speech sounds.
Our results agree with those of the previous studies, although no significant differences for ABR waves were found between groups. Also, for qualitative analysis, we found that the MG and HLG had fewer individuals with alterations in ABR than the NG, a result that suggests a good integrity of the auditory brainstem response in this population.
With regard to the P300 results, although three groups showed mean values within normal limits, the MG and HLG showed a shorter latency than the NG. Some authors  assessed how musicians responded to pure tones, harmonics, and speech, by analyzing the components in N1, and P300 auditory evoked potentials of long latency, and compared these results with those obtained in the control group (non-musicians). They concluded that musicians regularly exposed to music showed shorter latencies for harmonic and speech stimuli, and for pure tone results they found no difference between the groups, although the musicians group had shorter latencies of the P300 wave, similar to what we found.
Thus, our findings do not support the hypothesis that the central components of the auditory pathways can also be affected by acoustic overstimulation. ,,, However, previous studies have dealt with the damage caused by noise and not the music itself. Thus, it is possible that music and noise do not act in the same way about the central auditory pathways, although both stimuli cause damage to the peripheral auditory pathways, as previously mentioned.
Therefore, alterations in otoacoustic emissions and high frequency audiometry presented by musicians with and without hearing loss showed that despite the fact that the central portion was not clearly affected by noise exposure, the peripheral portion showed that it was already affected, and these two tools could be used to predict the possible damage caused by exposure to very intense pressure levels sounds.
Musicians are different from factory workers in several areas that make the former slightly less susceptible to hearing loss. Music tends to be intermittent, with loud passages and quiet passages intermixed, while industrial noise tends to be continuous. Perhaps this intermittency makes the music slightly less damaging than an equal intensity of noise for a similar length of time. 
A study  showed that musicians who had played for less than 10 years did not develop hearing loss, whereas, 40% who had played between 10 and 19 years, and 66% who had played for more than 20 years, had developed hearing loss. However, another study  documented a measurable loss in the hearing function of workers in 328 construction industries in their first three years of work. Also, it is possible that a change in the circulation in the auditory pathway on a hormonal basis, if music is perceived as pleasant, makes music less damaging than noise.  It is well known that the impact of the perception of pleasant and unpleasant sounds may result in endocrine changes, including the production of stress hormones such as cortisol and ACTH, catecholamines, and others.  On account of these physiological reactions, the noise becomes detrimental to health in many ways, leading to sleep disturbance, cardiovascular disease, psychiatric symptoms, and psychosocial effects, including the discomfort with noise, reduction in performance/attention, and increased aggressive behavior. 
Thus, it is possible that compared to noise, music causes less harmful effects to the central auditory pathways, due to its spectral and temporal (intermittence) characteristics, as a function of hormonal changes. This function may be caused by sounds rated as pleasant or unpleasant, which may trigger negative reactions in the entire system that results in a cascade of adverse events.
Future studies with animals comparing different acoustic stimuli that resemble the characteristics of music (spectral and temporal) are important for this hypothesis to be tested. A comparison with the effects of noise can be made by checking the effects on the peripheral and central pathways of different types of stimuli.
A limitation of our study is our small sample of musicians, which included guitarists and drummers only. This was done in an attempt to minimize the variety of different instruments and music exposure of professional musicians, as they may carry different audiological features.
An analysis of musicians showed that drummers had worse hearing thresholds and smaller TEOAE amplitudes when compared to guitar players. Drummer players present a bigger damage most likely because of the impact noise produced by the instrument. This finding has also been observed by others. 
Our study is the first to assess both the central and peripheral auditory pathway of professional musicians. This approach allowed us to find that music can cause damage to the peripheral auditory pathways. Additionally, music may act as a training tool for central auditory pathways, improving the processing of acoustic information to the cortex. Future studies in which more musicians playing different instruments are included will be enlightening.
However, we cannot rule out that central damage can also be caused by the music itself, when exposure occurs for long times. Thus, longitudinal studies of this kind are also needed to clarify these issues. As indicated by others, ,, hearing protection measures should always be taken with this group of professionals, including engineering control measures (acoustically, the sound source distance, decreased amplification, etc.), personal protection (use of protective earplugs for musicians, with uniform attenuation of frequencies), training in placement and cleaning earplugs, educational programs, audiological monitoring, and others. ,,
| Conclusion|| |
Our findings suggest that the population of musicians is at risk for developing music-induced hearing loss. However, the electrophysiological evaluation showed that latency waves of ABR and P300 diminished in musicians, which may suggest that the auditory training of musicians, who are exposed to sound in the profession, acts as a facilitator of the acoustic signal transmission to the cortex, that is, provides a better processing of acoustic information by the central auditory nervous system.
| Acknowledgments|| |
This study was funded by FAPESP (The State of São Paulo Research Foundation).
| References|| |
|1.||Zhao F, Manchaiah VK, French D, Price SM. Music exposure and hearing disorders: An overview . Int J Audiol 2010;49:54-64. |
|2.||Levey S, Levey T, Fligor B. Noise exposure estimates of urban MP3 player users. J Speech Lang Hear Res 2011;54:263-77. |
|3.||Schmuziger N, Patscheke J, Probst R. Hearing in nonprofessional pop/rock musicians. Ear Hear 2006;27:321-30. |
|4.||Potier M, Hoquet C, Lloyd R, Nicolas-Puel C, Uziel A, Puel JL. The risks of amplified music for disc-jockeys working in nightclubs. Ear Hear 2009;30:291-3. |
|5.||Morata TC. Young people: Their noise and music exposures and the risk of hearing loss. Int J Audiol 2007;46:111-2. |
|6.||Lim DJ, Melnick W. Acoustic damage of the cochlea. A scanning and transmission electron microscopic observation. Arch Otolaryngol 1971;94:294-305. |
|7.||Axelsson A, Dengerink H. The effects of noise on histological measures of the cochlear vasculature and red blood cells: A review. Hear Res 1987;31:183-91. |
|8.||Mulroy MJ, Henry WR, McNeil PL. Noise-induced transient microlesions in the cell membranes of auditory hair cells. Hear Res 1998;115:93-100. |
|9.||Henderson D, Bielefeld EC, Harris KC, Hu BH. The role of oxidative stress in noise-induced hearing loss. Ear Hear 2006;27:1-19. |
|10.||Kujala T, Shtyrov Y, Winkler I, Saher M, Tervaniemi M, Sallinen M, et al. Long-term exposure to noise impairs cortical sound processing and attention control. Psychophysiology 2004;41:875-81. |
|11.||Brattico E, Kujala T, Tervaniemia M, Alku P, Ambrosie L, Monitilloe V. Long-term exposure to occupational noise alters the cortical organization of sound processing. Clin Neurophysiol 2005;116:190-203. |
|12.||Kujala T, Brattico E. Detrimental noise effects on brain's speech functions. Biol Psychol 2009;81:135-43. |
|13.||Gröchel M, Götze R, Ernst A, Basta D. Differential impact of temporary and permanent noise-induced hearing loss on neuronal cell density in the mouse central auditory pathway. J Neurotrauma 2010;27:1499-507. |
|14.||British Society of Audiology. Recommendation. Descriptors for pure-tone audiograms. Br J Audiol 1988;22:123. |
|15.||Burguetti FA, Pelogia AG, Carvallo RM. High Frequency Thresholds in Subjects with Tinnitus Complaint. Int Arch Otorhinolaryngol 2004;8:277-83. |
|16.||Klem GH, Lüders HO, Jasper HH, Elger C. The ten-twenty electrode system of the International Federation. The International Federation of Clinical Neurophysiology. Electroencephalogr Clin Neurophysiol Suppl 1999;52:3-6. |
|17.||Linares AE, Carvallo RM. Acoustic immittance in children without otoacoustic emissions. Braz J Otorhinolaryngol 2008;74: 410-6. |
|18.||McPherson DL. Late potentials of the auditory system. San Diego: Singular Publishing Group; 1996. |
|19.||Hall III JW. New handbook of auditory evoked responses. Boston: Allyn and Bacon; 2007. |
|20.||Ostri B, Eller N, Dahlin E, Skylv G. Hearing impairment in orchestral musicians. Scand Audiol 1989;18:243-9. |
|21.||Royster JD, Royster LH, Killion MC. Sound exposure and hearing thresholds of symphony orchestra musicians. J Acoust Soc Am 1991;89:2793-803. |
|22.||Axelsson A, Eliasson A, Israelsson B. Hearing in pop/rock musicians: A follow-up study. Ear Hear 1995;16:245-53. |
|23.||Samelli AG, Schochat E. Hearing loss induced by high sound pressure level in a professional rock-and-roll musicians. Acta AWHO 2000;19:136-43. |
|24.||Kähäri K, Zachau G, Eklöf M, Möller C. The influence of music and stress on musicians' hearing. J Sound Vib 2004;277:627-31. |
|25.||Emmerich E, Rudel L, Richter F. Is the audiologic status of professional musicians a reflection of the noise exposure in classical orchestral music? Eur Arch Otorhinolaryngol 2008;265:753-8. |
|26.||Martins JP, Magalhães MC, Sakae TM, Magajewski FC. Evaluation of noise-induced hearing loss in musicians from Tubarão-SC. Arq Cat Med 2009;37:69-74. |
|27.||Nammur FA, Fukuda Y, Onishi ET, Toledo RN. Hearing Evaluation in Musicians of the Municipal Symphony Orchestra - São Paulo. Braz J Otorhinolaryngol 1999;64:390-5. |
|28.||Maia JR, Russo IC. Study of the hearing of rock and roll musicians. Pro Fono. 2008;20:49-54. |
|29.||Hamdan AL, Abouchacra KS, Zeki AL Hazzouri AG, Zaytoun G. Transient-evoked otoacoustic emissions in a group of professional singers who have normal pure-tone hearing thresholds. Ear Hear 2008;29:360-77. |
|30.||Santoni CB, Fiorini AC. Pop-rock musicians: Assessment of their satisfaction provided by hearing protectors. Braz J Otorhinolaryngol 2010;76:454-61. |
|31.||Musacchia G, Strait D, Kraus N. Relationships between behavior, brainstem and cortical encoding of seen and heard speech in musicians and non-musicians. Hear Res 2008;241:34-42. |
|32.||Parbery-Clark A, Skoe E, Kraus N. Musical experience limits the degradative effects of background noise on the neural processing of sound. J Neurosci 2009;29:14100-7. |
|33.||Nikjeh DA, Lister JJ, Frisch SA. Preattentive cortical-evoked responses to pure tones, harmonic tones, and speech: Influence of music training. Ear Hear 2009;30:432-46. |
|34.||Chasin M. Hearing loss prevention for musicians and introduction to the problem. In: Chasin M, editor. Hearing loss in musicians: Prevention and management. San Diego: Plural Publishing; 2009. p. 1-10. |
|35.||Juman S, Karmody CS, Simeon D. Hearing loss in steelband musicians. Otolaryngol Head Neck Surg 2004;131:461-5. |
|36.||Seixas NS, Goldman B, Sheppard L, Neitzel R, Norton S, Kujawa SG. Prospective noise induced changes to hearing among construction industry apprentices. Occup Environ Med 2005;62:309-17. |
|37.||Evers S, Suhr B. Changes of the neurotransmitter serotonin but not of hormones during short time music perception. Eur Arch Psychiatry Clin Neurosci 2000;250:144-7. |
|38.||WHO. Burden of disease from environmental noise: Quantification of healthy life years lost in Europe. WHO - JCR European Commission. Geneva: World Health Organization; 2011. |
|39.||Mendes MH, Morata TC, Marques JM. Acceptance of hearing protection aids in members of an instrumental and voice music band. Braz J Otorhinolaryngol 2007;73:785-92. |
Alessandra G Samelli
Department of Physical Therapy, Speech language Pathology and Audiology, and Occupational Therapy, School of Medicine, University of São Paulo, Rua Cipotânea, 51, Cidade Universitária, SP Brasil 05360 160
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]
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