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ORIGINAL ARTICLE
Year : 2014  |  Volume : 1  |  Issue : 2  |  Page : 71-79

Chronic noise exposure: impact on the vestibular function


Audiology Unit, Tanta University Hospitals, Tanta, Egypt

Date of Submission22-Sep-2014
Date of Acceptance10-Oct-2014
Date of Web Publication9-Jan-2015

Correspondence Address:
Takwa A Gabr
Audiology Unit, ENT Department, Tanta University Hospitals, El-Geesh street, Tanta 31527
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2314-8667.149015

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  Abstract 

Background
Noise exposure causes permanent or temporary hearing loss. High levels of noise may stimulate the vestibular system and thereby cause disturbances in the balancing mechanism.
Objectives
This work was designed to investigate the effect of chronic noise exposure on the vestibular system.
Participants and methods
Two groups were included in this study: control group: 20 healthy individuals with normal hearing and vestibular function and study group: 40 patients with a history of prolonged noise exposure at work. This group was further divided into two subgroups: 20 patients with noise-induced hearing loss and 20 individuals with normal hearing sensitivity. All participants in this study were subjected to combined vestibular evoked myogenic potentials (VEMPs) and videonystagmography (VNG).
Results
cVEMPs were absent in 5 and 20% of participants of subgroup IIa and IIb, respectively, with significantly delayed P13 and N23 latencies in the rest of participants in subgroup IIb. In terms of P13 and N23 amplitudes, there was no statistically significant difference between the control and the study subgroups. oVEMPs were absent in 40% of participants of subgroup IIb, with normal latencies and amplitudes in the rest of the participants. For VNG, only saccades latency was significantly delayed in subgroup IIb compared with subgroup IIa. A correlation was found between the participants' complaints and the results of the vestibular function tests.
Conclusion
Chronic noise exposure is hazardous to the inner ear structures and enhances vestibular damage, especially the sacculocollic reflex pathway. Vestibular insult is higher among patients with noise-induced hearing loss than in those with normal hearing.

Keywords: cervical vestibular evoked myogenic potentials, noise-induced hearing loss, ocular vestibular evoked myogenic potentials, videonystagmography


How to cite this article:
Emara AA, Gabr TA. Chronic noise exposure: impact on the vestibular function. Adv Arab Acad Audio-Vestibul J 2014;1:71-9

How to cite this URL:
Emara AA, Gabr TA. Chronic noise exposure: impact on the vestibular function. Adv Arab Acad Audio-Vestibul J [serial online] 2014 [cited 2017 Aug 16];1:71-9. Available from: http://www.aaj.eg.net/text.asp?2014/1/2/71/149015


  Introduction Top


The human vestibular system is extremely sensitive to low-frequency sounds. Vestibular damage is a potential problem with cochlear-damaging factors because vestibular receptors are coupled physically with the auditory receptors and both receptors share the membranous labyrinth and the common arterial blood supply [1],[2] . Evidence from primates indicates that afferent projections from the saccule reach the medial vestibular nucleus or the inferior vestibular nucleus, which then projects bilaterally to the spinal cord. In humans, this pathway mediates vestibular evoked myogenic potentials (VEMPs) [3] . The conventional method for recording the VEMP involves measuring electromyographic activity from surface electrodes placed over the tonically activated sternocleidomastoid muscles (SCM). The 'cervical vestibular evoked myogenic potential' (cVEMP) is thus a manifestation of the sacculocollic reflex and they assess the descending vestibular pathway as an ipsilateral sacculocollic reflex that originates mainly from the saccule. However, recent research has shown that VEMPs can also be recorded from the extraocular muscles using surface electrodes placed near the eyes. These 'ocular vestibular evoked myogenic potentials' (oVEMPs) are a manifestation of the vestibulo-ocular reflex, which is responsible for stabilizing vision on the retina during head and body movements. Information from the utricle stimulates the six ocular muscles (the superior oblique, superior rectus, and medial rectus eye muscles ipsilaterally and the inferior oblique and inferior rectus eye muscles on the contralateral side). The connections between the saccule and the ocular system are less extensive compared with those related to the utricle [4],[5] . Iwasaki et al. [6] reported that oVEMPs evaluate the ascending vestibular pathway as a crossed vestibulo-ocular reflex.

Noise is not usually considered a common etiology of dizziness, vertigo, or other vestibular disturbances. Although temporary or permanent threshold shifts in hearing following loud noise exposure are well known to occur in both humans and animals, relatively few studies have examined similar phenomena in the vestibular system. This may be related to the lower sensitivity of the semicircular canals to noise, even at very high intensities [7] . However, studies on VEMPs have shown that the saccule can be stimulated with sound levels at or above 100 dB SPL [8],[9] . Considering this, the levels of noise that can cause damage to the cochlea could also stimulate the balance system as the saccule has been reported to withstand much lesser force than the Reissner's membrane. Therefore, with similar stimulations, there is a probability of the balance system being affected because of noise exposure [10] .

However, in view of the few number of researches focused on the vestibular system in this area, the present study is designed to study the effect of chronic noise exposure on the vestibular system.


  Aims of the work Top


This work was designed to assess the effect of prolonged noise exposure on the cervical and ocular VEMPs using the combined procedure. This might provide a new tool for evaluating the vestibular system because of the different origins and pathways of the cervical and ocular VEMPs. The assessment was further extended to evaluate the effect of noise on videonystagmography (VNG).


  Participants and methods Top


This study included 60 adults. Their age ranged from 23 to 55 years. They were divided into two groups:

  1. The control group (GI) included 20 healthy adults with bilateral normal peripheral hearing and bilateral normal middle ear function. None of the participants had vestibular complaints, neurological problems, general health problems (e.g.: hypertension and diabetes mellitus), neck, or visual problems. All participants were relatives of patients or volunteers attending our Audiology Unit.
  2. The study group (GII) included 40 patients with a history of prolonged noise exposure at work ( > 10 years). The inclusion criteria were as follows: age range from 19 to 55 years, with a history of prolonged machinery noise exposure at work. Patients with vestibular complaints, a history of ear infections, head trauma, neurological or general health problems, a family history of hearing impairment, and patients with acute acoustic trauma or blast injury were excluded. All patients in this group were volunteers from Spinning and Weaving Companies. This research was approved by the Research Ethics Committee at our University Hospitals. Approval Code is 933/01/12. Consents were obtained from all participants after an explanation of the test procedures was provided.


All participants were evaluated in terms of the following:



  1. Full audiological history.
  2. Otological examination.
  3. Basic audiological evaluation including pure tone audiometry (PTA), speech audiometry, and immittancemetry.
  4. Office tests, including the following tests:


  1. Ocular motor examination: ocular alignment and range of movement; vergence, saccades, and smooth pursuit eye movements.
  2. Vestibulo-ocular reflex: head thrust test, head shake test.
  3. Posture and gait tests: tandom gait, Romberg's test, tandem Romberg test, and Fukuda tests


[5]Combined cervical and ocular VEMPs According to Chou et al. [11] , nine electrodes were used as follows:

For recording cVEMPs: two active electrodes were placed on the middle third of the contracted SCM of the neck on each side and two reference electrodes were placed on the middle third of both clavicles. For recoding oVEMPs: two active electrodes were placed just inferior to each eye, about 1 cm below the center of the lower eyelid, two reference electrodes were placed about 1-2 cm below the corresponding active electrodes below each eye, and one ground electrode was placed over the forehead.

Participants were asked to rotate their heads to the opposite side of recording by flexing the head ~30° degrees forward to contract the SCM and to look upward at a distant target in the midline from the eyes. The eye position was measured as a vertical visual angle of ~30-35° above horizontal.

The stimulating parameters for combined VEMPs were a click stimulus presented at 95 dBnHL at a 5/s repetition rate and the total number of sweeps was 128, delivered through ER3A insert earphones. The filter setting was 3-3000 Hz, with a time window of 0-100 ms and a gain factor of 50 000. At least two consecutive averages were recorded from each side to verify reproducibility.

(6) VNG: infrared glasses of VNG was done using GN Otometric ICS-CHARTR (version 5.3, USA) were placed on the patient's eye and adjusted to fit him/her firmly, but comfortably. Calibration was performed by asking the participant to follow a target on the light bar moving in the horizontal plane at 0.25 Hz. After calibration, the following tests were performed:



Observation for the spontaneous nystagmus test: the participant's eyes were observed under infrared goggles for spontaneous nystagmus for 30 s with visual fixation and 30 s without visual fixation.

(b) Oculomotor tests: including:

  1. Tracking: participants were asked to follow a target on the light bar moving in the horizontal plane at a frequency range of 0.2-0.7 Hz. At the end of the test, the gain (eye velocity/stimulus velocity) was calculated. Gain of less than 70% was considered to be abnormal.
  2. Saccade: participants were asked to fixate upon a visual target on the light bar. The target jumped randomly to the right and to the left with amplitudes ranging from 5 to 25°. At the end of the test, saccadic latency, accuracy, and peak velocity were calculated. Latency of more than 280 ms, accuracy of less than 80%, and peak velocity of less than 300°/s were considered to be abnormal.
  3. Optokinetic: participants were asked to follow a series of targets moving in rightward and leftward directions at a speed of 30°/s. The optokinetic nystagmus was assessed for its presence or absence and when present, it was assessed for symmetry in both eyes in the rightward and leftward directions.


(c)

Positioning test: Dix-Hallpike maneuver, where the participant was seated with the head rotated 45° to the right or left and then was pulled quickly to the head-hanging position over the end of the examining table. Eye movements were observed for at least 30 s. Then, the participant was returned to the sitting position with further observation of eye movement. If nystagmus was elicited in the head-hanging position, the test was repeated to observe nystagmus fatigability.

(d)

Positional tests: in positional tests, the eye movements of the participant were recorded for 30 s in each of supine, head right, head left, right ear down, and left ear down positions for the presence of nystagmus.

(e)

Caloric test: cool (30°C) and warm (44°C) irrigations were performed while the participants were engaged in a mental task during delivery of the stimulus. After the end of the irrigation, recording of the eye movement was continued while the participant was being mentally tasked, followed by fixation suppression testing [12] .

Statistical analysis

Using the SPSS statistical package version 20, two types of statistical analyses were carried out: for quantitative data, the range, mean, and SD were calculated. For comparison between means of two groups of parametric data, the student t-test was used. For comparison between more than two means of parametric data, the F-value of analysis of variance (ANOVA) was calculated. Significance was considered at P less than 0.05 for interpretation of results of tests of significance.


  Results Top


This study included two groups of adults.

The control group (group I) included 20 men. Their mean age was 38.02 ± 11.9 years. Their PTA mean and SD was 10.03 ± 3.2 dBHL [Table 1].
Table 1 Comparison of mean and SD of age, pure tone audiometry, speech recognition threshold, and acoustic reflex among the groups studied


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The study group (group II) included 40 patients with a history of noise exposure. Their mean age was 40.15 ± 5.2 years. This group was further subdivided into two subgroups according to their hearing thresholds.

  1. Subgroup IIa included 20 male patients with a history of prolonged noise exposure at work and normal hearing. Their mean PTA was 15.7 ± 4.53 dBHL and the mean duration of noise exposure was 16.0 ± 7.72 years. Five patients had dizziness (25%), six patients had tinnitus (30%), and two patients had a sense of aural fullness (10%) [Table 1] and [Table 2].
    Table 2 Clinical manifestations of the two study subgroups


    Click here to view
  2. (Subgroup IIb included 20 male patients with a history of prolonged noise exposure at work and noise-induced bilateral and symmetrical sensorineural hearing loss (NIHL). Their mean PTA was 32.68 ± 12.9 dBHL, whereas that of the speech recognition threshold was 24.5 ± 14.5 dB. The mean duration of noise exposure was 26.25 ± 7.9 years. All patients had hearing loss, nine patients had dizziness (45%), and 12 patients had tinnitus (60%) [Table 1] and [Table 2].{Table 1}{Table 2}


  1. Basic audiologic evaluation:
  2. Comparison of the pure tone threshold between the control and the study subgroups showed a statistically significant increased average pure tone threshold in subgroup IIb compared with the control group or subgroup IIa. The elevated PTA threshold was observed along the entire frequency range (250-8000 Hz), especially at 4 and 8 kHz. Subgroup IIa also showed a significant elevated threshold at 2, 4, and 8 kHz compared with the control group. Speech recognition thresholds were significantly elevated in the study subgroup IIb. Acoustic reflex thresholds were significantly elevated in the study subgroups, especially in subgroup IIb, and were proportional to PTA in each subgroup (P < 0.5). There was a positive correlation between pure tone threshold and duration of noise exposure in group II [Table 2] and [Table 3]; [Figure 1] and [Figure 2].
    Figure 1Average pure tone audiometry from all participants of the control (GI) and the study subgroups (GIIa, GIIb).

    Click here to view
    Figure 2: Correlation between pure tone audiometry (PTA) thresholds and duration of noise exposure in years in group II.

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    Table 3 Comparison of pure tone threshold at each frequency among the control and study subgroups


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  3. Office test: results of the office test for the two subgroups were within the normal range and not significantly different from the control group (P > 0.05).
  4. Combined VEMPs:


Comparison of cVEMPs and oVEMPs latencies and amplitudes of the waves was performed between the right and the left side. There was no statistically significant difference. Thus, a statistical analysis was carried out by adding right and left sides in each group.

(a) cVEMPs:

Control group: P13 and N23 of cVEMPs were recorded successfully from all participants. The mean and SD of P13 and N23 latencies were 11.8 ± 1.46 and 17.5 ± 3.8 ms, respectively. P13 and N23 amplitudes of the waves were 3.2 ± 3.3 and 3.01 ± 2.8 μV, respectively [Table 4]; [Figure 3].
Figure 3: Normal cVEMPs, (a) and oVEMPs (b) of the combined VEMPs in normal participants and absent cVEMPs, (c) and oVEMPs (d) of the combined VEMPs in patients with a history of noise exposure. cVEMPs, cervical vestibular evoked myogenic potentials; oVEMPs, ocular vestibular evoked myogenic potentials.

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Table 4 Comparison of the cervical vestibular evoked myogenic potentials wave latencies (ms) and amplitudes (μ V) among the control and study subgroups using the analysis of variance test


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  1. Subgroup IIa: cVEMPs were absent in two ears (5%). The mean latencies of P13 and N23 were 12.58 ± 4.1 and 18.9 ± 6.1 ms, respectively. P13 and N23 amplitudes were 2.08 ± 3.0 and 2.2 ± 2.49 μV, respectively [Table 4]; [Figure 3].
  2. Subgroup IIb: cVEMPs were absent in eight ears (20%). The mean latencies of P13 and N23 were 14.45 ± 1.83 and 22.04 ± 2.9 ms, respectively. P13 and N23 amplitudes were 2.5 ± 2.9 and 2.95.41 μV, respectively [Table 4]; [Figure 3).


The ANOVA test was performed to compare P13 and N23 latencies and amplitudes between the control and the study subgroups and results showed a significant difference only in latency (F = 9.89 and P<0.005; F = 11.3 and P<0.005 for P13 and N23, respectively). P13 and N23 latencies were significantly delayed in the subgroup IIb than the control group or subgroup IIa. For P13 and N23 amplitudes, there was no statistically significant difference (F = 1.33 and P = 0.268; F = 0.745 and P = 0.47 for P13 and N23, respectively) [Table 4].

No correlation was found between the duration of noise exposure and cVEMPs latencies or amplitudes.

(b) oVEMPs:

  1. Control group: nI and pI of oVEMPs were recorded successfully from all participants. The mean and SD of nI and pI latencies were 8.9 ± 4.02 and 13.2 ± 7.4 ms, respectively. The amplitudes of nI and pI were 1.2 ± 1.6 and 0.86 ± 1.1 μV, respectively [Table 5]; [Figure 3].
    Table 5 Comparison of the mean ocular vestibular evoked myogenic potentials wave latencies (ms) and amplitudes (μ V) among the studied groups using the analysis of variance test


    Click here to view
  2. Subgroup IIa: nI and pI of oVEMPs were recorded from all patients. The mean latencies of nI and pI were 9.6 ± 4.2 and 14.5 ± 6.1 ms, respectively. nI and pI amplitudes were 1.9 ± 3.38 and 1.3 ± 1.6 μV, respectively [Table 5].
  3. Subgroup IIb: oVEMPs were absent in 16/40 ears (40%). The mean nI and pI latencies were 10.8 ± 4.7 and 15.5 ± 2.6 ms, respectively. nI and pI amplitudes were 2.6 ± 4.5 and 1.5 ± 1.9 μV, respectively [Table 5]; [Figure 3].
  4. The ANOVA test was performed to compare nI and pI latencies and amplitudes among the control and study subgroups, and the results showed no significant difference (P > 0.05)


[Table 5].

No correlation was found between oVEMPs latencies or amplitudes and duration of noise exposure in subgroup IIa. In subgroup IIb, the correlation was not examined as oVEMPs were not recorded in 40% of the ears.

(4) VNG:

In subgroup IIa: occulomotor tests, positioning, and positional testing were normal; however, two out of twenty participants (10%) showed bilateral caloric weakness.

(a) In subgroup IIb: one patient showed gazed evoked left-beating nystagmus and bilateral down-beating nystagmus with right and left positions (11 and 6°/s, respectively) and three patients (10%) showed bilateral caloric weakness.

Comparison between the two subgroups: the smooth pursuit test showed no significant difference between both subgroups (P > 0.05). For saccades, subgroup IIb showed significantly delayed saccade latency compared with subgroup IIa (P < 0.05). However, comparison of optokinetic and caloric tests results showed similar results in the two subgroups.


  Discussion Top


Exposure to noise can have adverse effects on hearing and balance mechanisms. Damage to the vestibular system, especially the saccule, is a potential problem with a cochlear-damaging effect of loud sound [13],[14],[15],[16] . Industrial workers chronically exposed to various kinds of occupational noise, especially those with NIHL, often suffer from balance disorders such as dizziness, vertigo, and even spontaneous nystagmus. Saccular stimulation by loud sounds appears to be the underlying cause of the vestibular symptoms following loud sound exposure. Saccular macula is preferentially activated by sound, and neurons originating from the saccular striola are particularly affected [17],[18] . On the basis of this fact and on the intercommunications between the fluid spaces in the cochlea, the vestibule, and in the SCCs, the possibility that sound stimuli can activate the vestibular end organs has been studied using several approaches [19] .

In this study, patients with a history of noise exposure at work showed elevated hearing threshold, especially in the high-frequency region of the audiogram, with a characteristic notch at 4 kHz even in those with normal hearing (subgroup IIa). Similar findings were reported by Henderson et al. [20] . Several explanations have been proposed for this notch: first, the effect of broadband industrial noise, which is enhanced by the fundamental resonance of the external auditory canal to a 3 kHz noise. Noise has its greatest effect approximately half octave above the peak frequency of the noise spectrum. Thus, the greatest loss will be in the 4000-6000 Hz region, with the characteristic 4 kHz notch seen on the audiogram in noise-exposed individuals [21],[22] . The second reason may be the degenerative changes in the auditory sense organ, most severely in the 9-13 mm region of the cochlea, which responds maximally to the 4 kHz frequency range [23],[24] . The third reason may be poor cochlear blood supply to the 3000-6000 Hz region and the greater susceptibility for damage of the supporting structures of hair cells in this region. The fourth reason may be orientation of the stapes footplate with its constant hydromechanical action toward those hair cells, causing eventual damage at the corresponding frequency region [25] .

There was a positive correlation between hearing thresholds and duration of noise exposure in group II. This could be because of direct mechanical injury or metabolic damage to the organ of Corti. The latter includes ischemia, metabolic exhaustion, and ionic imbalance. In addition, prolonged noise exposure leads to a prolonged set of biochemical processes including the production of reactive oxygen species and reactive nitrogen species with corresponding hair cell loss [26] . Moreover, noise has an effect on cochlear blood flow and this effect depends on the duration and intensity of the noise exposure [27],[28] .

In the study group (GII), 25% of patients with noise exposure and normal hearing had complaints of vertigo and again this percentage increased to 45% in patients with NIHL. Individuals with noise-induced vestibular disease will not have subjective balance disturbances as there is a gradually developing vestibulopathy as a result of chronic noise exposure. Shupak et al. [29] and Manabe et al. [30] found that there is a symmetrical decrease in the vestibular end organ response that was associated with symmetrical hearing loss. They suggested that the low incidence of clinical symptoms in individuals with NIHL might be explained by the ability of the central nervous system to compensate for peripheral vestibular malfunction as the visual and somatosensory input compensates for the vestibular deficit. Juntunen et al. [31] and Ylikoski et al. [16] reported that as the duration and intensity of the noise exposure increased, reduced blood flow may have led to permanent hearing threshold shifts and subclinical disturbance of the vestibular system, resulting in vestibular acoustic trauma.

Other otological complaints encountered in this study such as aural fullness were also reported in other studies [24],[32] , suggesting that these symptoms can be found in patients with a history of prolonged noise exposure.

VEMPs were recorded in this study using the combined procedure. Generally, cVEMPs were absent in two ears (5%) in participants with a history of noise exposure and normal hearing (IIa). This percentage increased to 20% (eight ears) in participants with NIHL with significantly delayed P13 and N23 latencies among the rest of the participants with NIHL. cVEMPs amplitudes were not significantly different from those of the control participants [Table 4]. Similar results were reported by Wang and Young [24] , who found abnormal cVEMPs in 50% of their participants. The ANOVA test was used for comparison of P13 and N23 latencies and amplitudes between the control and the study subgroups. There were significantly delayed latencies in patients with NIHL compared with participants exposed to noise with normal hearing or controls [Table 4]. Wang and Young [24] reported that patients with a bilateral 4-kHz notched audiogram and a hearing threshold of 4 kHz more than 40 dB may show abnormal (absent or delayed) VEMPs. This indicated that the vestibular part, especially the sacculocollic reflex pathway, has also been damaged. There are also clinical findings indicating that permanent saccular functional loss following noise exposure may reflect permanent threshold shifts in hearing [33] .

There was no correlation between the duration of noise exposure and cVEMPs latency or amplitude. This was in agreement with the findings of Oosterveld et al. [17] and Golz et al. [32] .

oVEMPs were recorded from all ears of the participants in subgroups IIa with no significant difference from controls in latency or amplitude. In subgroup IIb (participants with NIHL), oVEMPs were absent in 16 ears (40%); however, the rest of the ears showed a nonsignificant difference compared with the control group or subgroup IIa. oVEMPs abnormalities in patients with occupational noise exposure have not been investigated before. Results in patients with NIHL (subgroup IIb) showed that otolith organs are affected by noise. No correlation was found between duration of noise exposure and the oVEMPs latency and amplitude (P > 0.05). Although 20% of patients with NIHL showed absent oVEMPs, the rest of the patients showed a normal response, suggesting the possibility of spontaneous recovery of vestibular dysfunction by central compensation [16] .

The results of combined VEMPs showed that the saccule, utricle, ascending, and descending vestibular pathway are affected by noise exposure. This effect is more obvious in patients with NIHL. Wang et al. [33] showed that the VEMP test may provide another clue for assessment of the hearing outcome in patients with a history of loud sound exposure. In other words, absent or delayed VEMPs in patients after acute acoustic trauma may indicate a poor prognosis with respect to hearing improvement. Thus, permanent saccular functional loss following noise exposure may reflect permanent threshold shifts in hearing [33] .

This result was not in agreement with that of Wang and Young [24] , who reported that the saccule rather than the utricle is the locus of predilection for noise damage. However, these authors used only cVEMPs to examine their patients with a history of noise exposure.

VNG was performed in the two study subgroups. VNG was started by observation of spontaneous nystagmus. None of the 40 patients showed spontaneous nystagmus. One patient showed bilateral down-beating nystagmus with right and left positions (11 and 6°/s, respectively). However, this was not significant as positional nystagmus was considered abnormal when it was persistent in three or more of five head positions and the slow phase eye speed exceeded 6°/s in any head position [32] . However, Oosterveld et al. [17] reported that 62% of their patients with a history of prolonged noise exposure had spontaneous nystagmus and 28% showed positional nystagmus. This discrepancy could be related to the selection criteria of their participants as they had complaints of occasional spells of dizziness and the sensation of being off balance. Tracking test results showed no significant difference between the two subgroups. There was a reduced gain at high frequencies (0.6-0.7 Hz) in two subgroups that did not reach significance. For saccade, the two subgroups showed within normal accuracy, velocity, and latency. The results of oculomotor tests in the current study appeared to be within normal in patients with a history of noise exposure, whether they had normal hearing sensitivity or had NIHL. These results might indicate a symmetrical centrally compensated decrease in the vestibular end organ response that is associated with a history of noise exposure [29],[32] .

For the caloric test result, abnormalities were found in 15 and 10% of the participants in subgroup IIb and IIa, respectively. These abnormalities appeared in the form of a bilateral weak caloric response. This could be related to the tendency toward a bilateral reduction in the horizontal semicircular canal function in patients with symmetrical hearing loss [29] . Similar results were obtained by Wang and Young [24] who reported 45% abnormalities of the caloric test in twenty patients with NIHL, and also, Golz et al. [32] who reported caloric hypofunction in patients with NIHL, especially if their hearing loss was asymmetrical. Manabe et al. [30] performed caloric tests in patients with NIHL with a complaint of vertigo. The authors reported a reduced response in 47.1% of ears. It is important to report that all patients with vestibular complaints in the study subgroups (IIa and IIb) had abnormal vestibular results either in the caloric test or the VEMPs test or both. This was in agreement with Golz et al. [32] . Shupak et al. [29] suggested that there may be a single mechanism for both cochlear and vestibular noise-induced injury with the possibility of reduction of central compensation in the vestibular end organ in patients with a history of noise exposure, especially if they have NIHL.

In this study, we have shown objective evidence of vestibular involvement in combination with cochlear damage in individuals exposed to occupational noise. The mechanism of noise-induced vestibular dysfunction can be explained by both mechanical and acoustic trauma, which may cause contusion of the labyrinth. Mechanical trauma can directly damage the vestibulum, whereas acoustic energy can damage the vestibular system through the round window of the cochlea [34] .


  Conclusion Top


Chronic noise exposure is a hazard to the inner ear structures and enhances the damage of the vestibular part. Both the saccule and the utricle are affected by noise exposure, especially the sacculocollic reflex pathway. Vestibular insult is more likely to occur in patients with NIHL (as they probably have more prolonged duration of noise exposure) than those who have normal hearing. However, central compensation should be considered in such cases. The combined oVEMP and cVEMP test is a convenient and noninvasive procedure that can be used in noise-exposed individuals as a screening tool for the assessment of contralateral vestibulo-ocular reflex and ipsilateral sacculocollic reflex functions, with definite rapid and accurate test results. The caloric test is also a valuable test for assessment of peripheral vestibular function in noise-exposed individuals.


  Acknowledgements Top


The authors of this work thank Dr Sara Nabil Abd EL-Latif El-Banna for her participation in data acquisition in this research.

Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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