Vestibular evoked myogenic potential in noise-induced hearing loss :<b>Kaushlendra Kumar, Christina Jean Vivarthini, Jayashree S Bhat</b>, Noise Health

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Year : 2010 \| Volume : 12 \| Issue : 48 \| Page : 191--194

Vestibular evoked myogenic potential in noise-induced hearing loss

Kaushlendra Kumar, Christina Jean Vivarthini, Jayashree S Bhat
Department of Audiology and Speech Language Pathology, KMC (Unit of Manipal University) Mangalore - 575 001, Karnataka, India

Correspondence Address:
Kaushlendra Kumar
Kasturba Medical College, Mangalore, Karnataka
India

Abstract

Noise affects one's hearing as well as balance mechanism. The hearing mechanism of the noise-exposed individuals has been extensively studied. However, in view of the poor research focus on the sacculo-collic reflexes, especially in this study area, the present study was undertaken to examine the vestibular evoked myogenic potentials (VEMP) in subjects with noise-induced hearing loss (NIHL). A total of 30 subjects (55 ears) with NIHL participated in the present study within the age range of 30-40 years. VEMP recordings were done at 99 dBnHL using IHS instrument. The results indicated that as the average pure tone hearing threshold increased, the VEMP latencies were prolonged and peak to peak amplitude was reduced in NIHL subjects. Out of the 55 ears, VEMP was absent in 16 (29.0%) ears. The latency was prolonged and the peak to peak amplitude was reduced in 19 (34.6%) ears. VEMP results were normal in 20 (36.4%) ears. Therefore, VEMP was abnormal or absent in 67% of NIHL subjects in the present study. Hence it can be concluded that the possibility of vestibular dysfunction, specially the saccular pathway, is high in individuals with NIHL. VEMP, a non-invasive and user friendly procedure, can be employed in these individuals to assess sacculo-collic reflex.

How to cite this article:
Kumar K, Vivarthini CJ, Bhat JS. Vestibular evoked myogenic potential in noise-induced hearing loss.Noise Health 2010;12:191-194

How to cite this URL:
Kumar K, Vivarthini CJ, Bhat JS. Vestibular evoked myogenic potential in noise-induced hearing loss. Noise Health [serial online] 2010 [cited 2023 Dec 9 ];12:191-194
Available from: https://www.noiseandhealth.org/text.asp?2010/12/48/191/64973

Full Text

Introduction

Unlike the situation with hearing, noise is not generally recognized as a common cause of vestibular disturbances. This is likely a result from the difference in "tuning" between the hair cells of the cochlea and the vestibular labyrinth. Cochlear hair cells are "tuned" to respond to frequencies between 20 and 20 000 Hz, while vestibular hair cells are "tuned" to respond for inputs between 0 and 10 Hz. [1]

It is known that noise affects hearing as well as vestibular system. There are numerous studies indicating noise as a cause of vestibular damage. Golz et al. had reported that noise results in asymmetrical or symmetrical hearing loss with abnormal vestibular functions. [2],[3],[4] Exposure to industrial solvents and noise can have an adverse effect on hearing and balance mechanisms in humans and animals. [5],[6] Body sway increases in patients with noise-induced hearing loss (NIHL) suggesting sub-clinical disturbances of the vestibular system. [7] On the contrary, Sohmer et al. [8] reported that at higher intensity levels (113dB SPL), there was a clear effect on cochlea but not on vestibular end organs. Although loud noise clearly shifts temporary and permanent hearing thresholds, vestibular changes are less clearly understood, possibly because the vestibulo-occular reflex is less sensitive to impulse noise even at maximum intensities unless the labyrinth is opened (eg., Superior semicircular canal dehiscence). In this case, the so-called Tullio phenomenon occurs. [9],[10]

The neurophysiological and clinical data indicate that the vestibular evoked myogenic potentials (VEMPs) are mediated by a pathway that includes the saccular macula, the inferior vestibular nerve, the lateral vestibular nucleus, the lateral vestibulospinal tract, and the motorneurons of the ipsilateral sternocleidomastoid (SCM) muscle. [11] VEMP is a reliable clinical test of saccular or inferior vestibular nerve function. [12] There is initially a positive peak P1 at 13 ms, followed by a negative peak N1 at 23 ms recorded from the averaged surface electromyography (EMG) which occurs at short latency and ipsilateral to the stimulated ear. [13] Wang et al. [14] reported abnormal Caloric and VEMP responses in 45 and 50%, respectively, in individuals exposed to chronic noise.

Need of the study

The vestibular functioning, especially sacculo-collic reflexes, on the noise-exposed individuals are not well understood especially in this area of study. Hence the present study was taken up with an aim of assessing the VEMP in noise-induced hearing loss subjects. It was also aimed to check the correlation between the hearing thresholds and the VEMP responses in NIHL subjects.

Materials and Methods

Subjects

A total of 30 NIHL subjects (28 males and two females) were involved in the present study within the age range of 30 to 40 years in the experimental group (55 ears). Five ears were excluded from the test due to middle ear pathology. Control group comprised of age and sex matched 30 normal hearing subjects (60 ears). The following subject selection criteria were adopted for the study.

Control group: (Normal subjects)

All the ears with hearing sensitivity within 15 dBHL for frequencies from 250 to 8000 Hz, having 'A' type tympanogram with normal acoustic reflexes. None of the subjects had recent history or presence of any otological problem (like ear discharge, ear ache etc) or any neurological symptoms.Uncomfortable levels (UCL) for speech were greater than 105 dBHL in all the subjects.

Experimental group (NIHL subjects)

All the ears were having sensory neural hearing loss ranging from mild to moderately severe degree (pure tone average ranging from 25dB to 70dB). Subjects were having exposure to noise greater than 90dBA daily for 8 hours. Subjects were working in an industrial setup for 10 years or more. None of the subjects had recent history or presence of any otologic problem (like ear discharge, ear ache etc.) or neurological symptoms.

Instrumentation

GSI 61 Diagnostic Audiometer was used to obtain pure tone audiometry and UCL. GSI-Tympstar was used for middle ear analysis. IHS Smart EP version: 3140 (Intelligent hearing systems, Florida, USA) was utilized for VEMP recording.

Procedure

Initially each subject was subjected to pure tone audiometry across octave frequencies from 250 to 8000 Hz for air conduction and from 250 to 4000 Hz for bone conduction. Using the same instrument, uncomfortable level for speech was obtained using ascending method in 5dB steps. Subjects were asked to indicate when the loudness of the speech was not tolerable. Subsequently tympanogram and acoustic reflexes were established using 226 Hz probe tone. Finally for the VEMP recording, the subjects were seated in an upright position and were instructed to turn their head to opposite side of the test ear to activate the ipsilateral SCM muscle. Surface EMG was monitored between 50 and 100 ΅v using VEMP software. The electrode montage that was used was Non-inverting electrode (+) to mid point of the SCM muscle of the side being stimulated, Inverting electrode (-) to sternoclavicular junction and ground electrode to the forehead. Inverting and non-inverting electrodes record the VEMP response with reference to ground. All the electrodes were connected with an amplifier box. VEMP was recorded at 99 dBnHL. Total of 250 sweeps were taken for the recording. Rarefaction click stimulus was used with repetition rate of 5/s. It was ensured that the electrode impedance at each electrode site was less than 5 KΩ and the inter electrode impedance was within 3 KΩ.

The positive/negative polarity of biphasic waveforms were termed as waves P1 and N1 on the basis of their respective latencies. Consecutive runs were performed to confirm reproducibility of peaks P1 and N1 and thus VEMP responses were considered to be present. Conversely, VEMP responses were absent, when reproducibility of biphasic P1-N1 waveform was lacking. A VEMP response was considered as normal if it was within mean+ 2SD. VEMP latency (P1-N1) and amplitude were noted. Independent t test was employed to measure the statistical difference between control group and clinical group. Pearson correlation test was applied to see the correlation between four frequency pure tone average thresholds (average of 500 Hz, 1000 Hz, 2000 Hz and 4000 Hz) and VEMP responses. The study was approved by the institutional ethical board and consent was obtained from all the subjects.

Results

The data was obtained from only 55 ears (30 subjects) who met the inclusion criteria. The mean and standard deviation of P1, N1 and peak to peak amplitude obtained at the 99 dBnHL are shown in [Table 1].

The mean latency of P1 and N1 was prolonged and peak to peak amplitude was reduced in experimental group when compared to control group. An independent sample t-test was done to find if the VEMP parameters are significantly different between the control group and the experimental group. An independent t-test demonstrated that there was a significant difference in VEMP responses between control group and clinical group subjects for latencies P1 and N1. The peak-to-peak amplitude was also significantly different between control group and NIHL group [Table 2].

Obtained normative was compared with experimental group and the table below details the VEMP responses [Table 3].

The results from the current study indicate that out of the 55 ears, VEMP was absent in 16 (29.0%) ears. The latency was prolonged and the peak to peak amplitude was reduced in 19 (34.6%) ears. VEMP responses were obtained with normal latency (P1 and N1) and normal amplitude in 20 (36.4%) ears. The Pearson correlation test indicated significant correlation between pure tone average and different VEMP parameters tested (r = 0.67, Pr = 0.56, Pr = -0.40, Pet al. [14] reported an increasingly damaged saccule results in abnormal VEMPs (eg, absent or delayed VEMPs) in subjects with bilateral 4 kHz notched audiogram with hearing threshold of > 40dB at 4 kHz. An animal study in which guinea pigs were exposed to 136 to 150 dB sound pressure level for 20 min also demonstrated that the saccule and cochlea (pars inferior) are most readily damaged structures, where the utricle and semicircular canals (pars superior) remain free of structural changes. [15] The mechanism of noise-induced hearing loss can be classified as direct mechanical injury or metabolic damage to the organ of Corti. The latter includes ischemia, generation of reactive oxygen species (ROS), toxic free radicals, metabolic exhaustion, and ionic imbalance in the inner ear fluid. The extent of noise effect on cochlear blood flow appears to be heavily influenced by the duration and intensity of the noise exposure. [16] Although the cochlea receives its blood supply mainly from the common cochlear artery and the saccule is supplied by anterior and posterior vestibular arteries, all these arteries originate from the labyrinthine artery. Therefore, as Wang et al. [14] mentions, as the duration and intensity of the noise exposure increased, reduced blood flow may have led to permanent hearing threshold shifts and abnormal VEMP responses.

The current study indicated that the VEMP responses were abnormal or absent in 64% of the subjects in the experimental group. Wang et al. [14] reported abnormal VEMP in 50% NIHL subjects. Higher abnormal VEMP in this study may be due to the differences in the exposure duration and intensity of noise. Moreover, the subject inclusion from different occupation environment may be also contributing toward this difference. Another supporting study indicated bilateral sensory neural hearing impairment associated with symptoms of vestibular function dysfunction after chronic exposure to carbon di sulfide and noise. [4],[6]

The present findings suggest that malfunction of vestibular system is associated with NIHL. The results imply a strong possibility of vestibular system disturbances in subjects with chronic noise exposure, which can be identified by VEMP responses indicating saccular pathway abnormality. Therefore, metabolic damage to the sacculocollic reflex pathway may be, at least in part, responsible for the abnormal VEMPs in NIHL individuals.

Conclusion

The present study demonstrated VEMP abnormalities in NIHL subjects reflecting the deviation in sacculo-collic function. Moreover, with an increase in the pure tone average hearing threshold, a VEMP abnormality also increases. It can also be concluded that VEMP, a noninvasive and user-friendly procedure, can be employed in noise-exposed individuals to assess sacculo-collic function.

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