OTOLOGY

Sequence of vestibular deficits in patients with noise-inducedhearing loss

Chia-Chen Tseng • Yi-Ho Young

Received: 3 March 2012 / Accepted: 2 November 2012 / Published online: 10 November 2012

� Springer-Verlag Berlin Heidelberg 2012

Abstract This study utilized audiometry, and cervical

vestibular-evoked myogenic potential (cVEMP), ocular

VEMP (oVEMP) and caloric tests to investigate the

sequence of vestibular deficits in patients with noise-induced

hearing loss (NIHL). Thirty patients with NIHL underwent

an inner ear test battery. Another 30 normal controls with

age- and sex-matched were included for comparison. The

abnormal percentages of the audiometry, and cVEMP,

oVEMP and caloric tests were 100, 70, 57 and 33 % in NIHL

patients, which showed significant differences from 13, 13, 7

and 3 % in normal controls, respectively. A significantly

decreasing trend among the four tests, with the sequence of

damage from the cochlea, followed by the saccule, utricle,

and semicircular canals was noted in NIHL patients, but not

in normal controls. In conclusion, the decreasing order of

abnormal percentages in the function of the cochlea, saccule,

utricle and semicircular canals after chronic noise exposure

further supports that the pars inferior (cochlea and saccule) is

more vulnerable to noise exposure than the pars superior

(utricle and semicircular canals).

Keywords Cervical vestibular-evoked myogenic

potential � Inner ear monitoring system � Noise-induced

hearing loss � Ocular vestibular-evoked myogenic potential

Introduction

Extreme noise is a well known cause of cochlear damage

leading to temporary or permanent hearing loss [1].

Conversely, vestibular damage by noise has less been

investigated [2], possibly because vestibular deficits often

subside via central compensation. Occasionally, some

individuals experience vertigo or imbalance when exposed

to intense impulse noise. This condition, known as the

Tullio phenomenon, arises from vestibular activation in

response to acoustic stimulation, especially when the lab-

yrinth is opened, such as in the case of superior canal

dehiscence [3]. In addition to semicircular canal damage,

transmission of impulse noise from a gunshot may cause

the otoconia to detach from the otolithic organs, resulting

in paroxysmal vertigo after repeated exposure [4].

Acoustic trauma such as saccular damage from chronic

exposure to very high intensity noise can cause abnormal

vestibular-evoked myogenic potentials (VEMPs) [5]. In

guinea pigs, the recovery of VEMP from damage by short-

term noise exposure occurs before the hearing threshold is

restored [6]. Thus, noise exposure can cause the saccule to

exhibit temporary or permanent functional loss resembling

hearing threshold shifts. However, whether noise affects

the utricular macula remains unexplored.

Recently, VEMP can also be recorded from extraocular

muscles, termed ‘‘ocular’’ VEMP (oVEMP), which is

thought to arise from the otolithic macula, via superior

vestibular nerve, along the crossed vestibulo-ocular reflex

(VOR), and recorded on the extraocular muscles [7, 8].

Therefore, VEMPs recorded from the neck muscles via

sacculo-collic reflex are now termed ‘‘cervical’’ VEMPs

(cVEMPs). Through bone-conducted vibration (BCV)

stimuli, Yang et al. [9] have recently established an animal

model of oVEMP in guinea pigs, which sets the stage for

investigating the pathophysiology of utricular disorders.

Thus, the inner ear function can be completely evaluated

via an inner ear test battery including audiometry, and

cVEMP, oVEMP, and caloric tests. This study used the

C.-C. Tseng � Y.-H. Young (&)

Department of Otolaryngology, National Taiwan University

Hospital, 1, Chang-Te St., Taipei, Taiwan

e-mail: youngyh@ntu.edu.tw

123

Eur Arch Otorhinolaryngol (2013) 270:2021–2026

DOI 10.1007/s00405-012-2270-6

inner ear test battery to investigate the vestibular deficits in

patients with noise-induced hearing loss (NIHL).

Subjects and methods

Subjects

A total of 30 patients with NIHL (26 males and 4 females,

aged 22–64 years, mean 48 years) were enrolled in this

study. The diagnostic criteria of NIHL were based on

American College of Occupational and Environmental

Medicine (ACOEM) guidelines [10]. Briefly, the principal

characteristics of NIHL are as follows:

1. Sensorineural hearing loss affects hair cells in the inner

ear.

2. Usually, symmetrical bilateral hearing loss.

3. Initially, ‘‘notching’’ of the audiogram at 3, 4 or 6 kHz,

with recovery at 8 kHz.

4. Usually, low-tone limits are approximately 40 dBHL,

and high-tone limits are approximately 75 dBHL.

5. Hearing loss reaches maximal after approximately

10–15 years of exposure.

6. No significant further progression of hearing loss

occurs after termination of noise exposure.

7. Continuous noise exposure is more damaging than

interrupted noise exposure.

Excluding criteria consisted of subjects with previous ear

disorders, systemic diseases, aged [65 years, receiving

ototoxic reagents, and lacking notched audiogram. The

occupational environments for the participants included steel

factory in seven, construction in six, electronics plant in four,

telecom industry in three, textile factory in two, commercial

ship in two, railway in two, wood shop in two and others in

two. The years of work history in these 30 NIHL patients

were 1–19 years in 10 patients, 20–29 years in 9 patients, and

[30 years in 11 patients. All patients received otoscopy first,

followed by audiometry, caloric, oVEMP and cVEMP tests.

Another 30 normal controls (26 males and 4 females,

aged 24–64 years, mean 48 years) without noise exposure

were tested in the same paradigm for comparison.

Caloric test

Bithermal caloric test was conducted with electronystag-

mographic (ENG) recordings (Nagashima, OK-5, Tokyo,

Japan). Canal paresis was defined as a greater than 25 %

difference between maximum slow phase velocity mea-

surements for each ear, when compared with the sum of

slow phase velocities from each ear. If cold water failed to

elicit caloric response, the subject underwent ice water

(0 �C, 10 mL) caloric test.

oVEMP test

The subject was in a sitting position. Surface potentials,

predominantly electromyographic (EMG) activities, were

recorded (Smart EP 3.90, Intelligent Hearing Systems,

Miami, FL, USA). Two active electrodes were placed around

1 cm below the center of the two lower eyelids. The other

two reference electrodes were positioned about 1–2 cm

below the active ones, and one ground electrode was placed

on the sternum. During recording, the subject was instructed

to look upward at a small fixed target[2 m from the eyes,

with a vertical visual angle of approximately 30� above

horizontal. The EMG signals were amplified and bandpass

filtered between 1 and 1,000 Hz. The input signal was a half

cycle 500 Hz sine wave, driven by a custom amplifier. The

drive voltage was adjusted and fixed to produce a peak force

of 15 N, about 128 dB force level (FL) from the vibrator, as

measured by an artificial mastoid (model 4930, Bruel &

Kjaer P/L, Denmark). Notably, the reference levels for air

and bone-conducted sound (0 dB) are defined differently.

For sound in air, 0 dB sound pressure level (SPL) is defined

as a pressure (20 lP), for bone conduction 0 dB SPL is

defined as a force (1 lN) [11]. The operator held the vibrator

by hand and delivered a repeatable tap with little pressure on

the subject’s skull at Fz, with the stimulation rate of 5/s. The

duration of analysis of each response was 50 ms, and 30

responses were averaged for each run [12].

The initial negative-positive biphasic waveform com-

prised peaks nI and pI. Consecutive runs were performed to

confirm the reproducibility of peaks nI and pI, and oVEMPs

were then deemed to be present. Conversely, oVEMPs were

deemed to be absent when the biphasic waveform was not

reproducible. At our laboratory, the norm for the latency of

peak nI was 11.4 ± 0.8 ms. Those with the nI latency

[13.0 ms were defined as delayed response. The asymmetry

ratio (%) was defined as the difference of the amplitude

nI–pI on each ear divided by the sum of amplitude nI–pI of

both ears, that is, (larger amplitude-smaller amplitude/larger

amplitude ? smaller amplitude) 9 100. Those with asym-

metry ratio[40 % were interpreted as reduced responses.

cVEMP test

Each subject was in a supine position. Two active elec-

trodes were placed on the upper half of the sternocleido-

mastoid (SCM) muscles; one reference electrode was

positioned on the suprasternal notch, and a ground elec-

trode was situated on the forehead. The acquisition settings

were similar to oVEMP test, except that the vibrator

delivered a repeatable tap on the subject’s head at inion.

The reason for using BCV tapping to elicit cVEMPs is that

the BCV stimuli evoke neural responses similar to those

evoked by ACS stimuli. Most, but not all, otolithic

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irregular neurons activated by ACS stimulation can also be

activated by BCV stimulation [13]. Thus, substituting BCV

mode for ACS mode to elicit both oVEMPs and cVEMPs,

especially in ‘‘mass detection’’, may increase the simplic-

ity, speed and convenience of VEMP testing.

To measure background muscle activity, subjects were

given feedback of the level of EMG activity in their SCM

muscles during data collection and were required to keep a

background muscle activity of at least [50 lV. The sub-

jects elevated their heads during testing. A total of 50

responses were averaged and recorded bilaterally.

The first positive and second negative polarities of

biphasic waveform were termed waves p13 and n23,

respectively. Consecutive runs were performed to confirm

the reproducibility of peaks p13 and n23, and cVEMP

responses were termed present. The latencies of p13, n23,

and amplitude p13–n23 were measured. At our laboratory,

the norm for the latency of p13 was 14.4 ± 1.3 ms, and we

defined when the latency of peak p13 exceeding 17.0 ms as

delayed cVEMPs. In addition, those with asymmetry ratio

[33 % were defined as reduced response.

Statistical methods

Comparison of the mean hearing levels of each frequency

between the two groups was conducted by unpaired t test.

The abnormal rates of each test between two groups were

compared by Fisher’s exact test. The abnormal percentages

in the inner ear test battery were compared with Cochrane

Q test. A difference of p \ 0.05 is considered significant.

This study was approved by the institutional review board,

and each subject signed the informed consent to participate.

Results

NIHL group

Clinical manifestation consisted of hearing loss in all

30 NIHL patients, followed by tinnitus in 19 (63 %),

rotational vertigo in 14 (47 %), nausea/vomiting in 13

(43 %), headache in 10 (33 %) and aural fullness in four

patients (13 %).

Audiometry revealed bilateral sensorineural hearing loss

in all patients (100 %). The mean hearing thresholds of

each frequency from 250 to 8,000 Hz are shown on

Table 1. There were no significant side-differences in

terms of mean hearing threshold of each frequency

(p [ 0.05, paired t test). The mean hearing threshold of

4,000 Hz revealed the worst hearing threshold compared

with that of other frequencies regardless of whether the

right or left ear was analyzed (p \ 0.01, paired t test),

leading to a 4-kHz-notched audiogram (Fig. 1). The latter

may help to exclude the possibility of Meniere’s disease,

although Meniere’s disease has its diagnostic criteria pro-

posed by American Academy of Otolaryngology, Head and

Neck Surgery in 1995 [14].

The cVEMP test displayed normal responses in 30 ears

and abnormal responses in 30 ears (50 %), consisting of

reduced responses in 2 ears, delayed responses in 6 ears,

and absent response in 22 ears (Fig. 2). The oVEMP test

showed normal responses in 40 ears and abnormal

responses in 20 ears (33 %), including reduced and absent

responses in 9 and 11 ears, respectively (Fig. 2). The

caloric test demonstrated normal responses in 45 ears and

abnormal responses in 15 ears (25 %), including absent

response in 1 ear and canal paresis in 14 ears.

To compare the inner ear deficits, a damaged ear on

either side was considered abnormal. Thus, the percentages

of abnormalities observed in the audiometry, cVEMP,

oVEMP, and caloric tests of the 30 NIHL patients were

100, 70, 57 and 33 %, respectively, revealing a signifi-

cantly decreasing trend among the four tests (p \ 0.001,

Cochrane Q test, Table 2).

Control group

The mean hearing thresholds of each frequency from 250 to

8,000 Hz in the control group were demonstrated in Table 1.

Compared with NIHL group, significant differences existed

Table 1 Comparison of mean hearing thresholds in noise-induced hearing loss (NIHL) patients versus normal controls

Group n 250 Hz 500 Hz 1,000 Hz 2,000 Hz 4,000 Hz 8,000 Hz

R ear

NIHL 30 12 ± 9 15 ± 10 20 ± 13 22 ± 15 44 ± 18 33 ± 20

Control 30 14 ± 6 14 ± 6 15 ± 8 14 ± 8 17 ± 8 20 ± 12

p value NS NS NS \0.05 \0.01 \0.01

L ear

NIHL 30 12 ± 7 16 ± 7 18 ± 9 19 ± 12 42 ± 15 29 ± 14

Control 30 13 ± 6 14 ± 7 15 ± 8 15 ± 8 16 ± 8 21 ± 14

p value NS NS NS \0.05 \0.01 \0.01

Data are expressed as mean ± SD dBHL, p value: unpaired t test

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in the mean hearing thresholds at the frequencies of 2,000,

4,000 and 8,000 Hz regardless of right or left ear was ana-

lyzed (p \ 0.05, unpaired t test, Table 1; Fig. 1).

Hearing loss is defined positive when the hearing

threshold of any frequency is [25 dBHL. Accordingly, 4

(13 %) of the 30 normal controls had hearing loss. The

percentages of abnormalities in audiometry, and cVEMP,

oVEMP and caloric tests in 30 normal controls were 13,

13, 7 and 3 %, respectively, which differed significantly

when compared with those of the NIHL group (p \ 0.001,

Table 2). Unlike NIHL group, no significantly decreasing

trend among the four tests was observed in the control

group (p [ 0.05, Cochrane Q test, Table 2).

Discussion

The mechanism of NIHL can be classified into two major

categories: direct mechanical trauma and metabolic change

to the cochlea [1]. When the noise intensity is [140 dB,

e.g., the noise produced by an explosion, NIHL results

from mechanical trauma alone. In contrast, workplace

noise damaging the cochlea is mainly due to metabolic

stress [15], leading to the production of reactive oxygen

species (ROS), reactive nitrogen species (RNS) and other

free radical molecules in the cochlea. These ROS are quite

capable of inducing cochlear damage as well as loss of

function by destroying DNA and cell membranes, which

Fig. 1 The mean hearing thresholds from 30 NIHL patients (solid circle) versus 30 normal controls (hollow circle). A 4-kHz-notched audiogram

is observed in NIHL patients, but not in normal controls

Fig. 2 Clear oVEMPs and cVEMPs are observed in a normal control (male, 38 years), while clear oVEMPs but absent cVEMPs are noted in a

NIHL patient (male, 48 years)

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up-regulates apoptotic cell death genes [16]. For the ves-

tibular part, the saccule in lower species such as amphib-

ians and fish acts as an acoustic receptor. Hence, loud noise

damaging the hair cells of cochlea may also affect the

saccular macula [6]. Animal studies of guinea pigs exposed

to high level noise shows that the pars inferior (cochlea and

saccule) is the most susceptible to damage whereas the pars

superior (semicircular canals and utricle) remains intact

[17].

The saccular neurons have a strong projection to neck

muscles and a weak projection to the oculomotor system,

while neural connections in the sacculo-ocular system are

relatively weak compared with neural connections in the

utriculo-ocular and sacculo-collic reflexes [13]. Thus,

based on the hypothesis of ‘‘efferent specificity’’ proposed

by Curthoys [8], oVEMPs by bone-conducted vibration

primarily originate from the utricular macula, whereas

cVEMPs originate from the saccular macula. Thereby, all

the inner ear end organs can be completely evaluated via

audiometry, and cVEMP, oVEMP, and caloric tests. In this

study, high abnormal rates in hearing (100 %) and cVEMP

(70 %) tests, and low abnormal rates in oVEMP (57 %)

and caloric (33 %) tests in NIHL patients, further support

that the pars inferior (cochlea and saccule) is more vul-

nerable to noise exposure than the pars superior (utricle and

semicircular canals), compatible with the animal experi-

ment [17].

As the superior vestibular nerve innervates the lateral

and superior semicircular canals, utricular macula, and the

‘‘hook’’ region of the saccular macula; while the inferior

vestibular nerve supplies the posterior semicircular canal

and the elongated ‘‘shank’’ region of the saccular macula,

one may argue that saccular lesion may cause abnormal

responses in both oVEMP and cVEMP tests. Likewise, the

BCV mode may activate the utricular afferents leading to

increased cVEMP amplitude. Nevertheless, this possibility

can be neglected since the contribution of utricular affer-

ents to the SCM muscles and that of saccular afferents to

the extraocular muscles are limited [13].

Morphologically, the cochlear and vestibular receptors

have a similar embryologic origin and share a common

basic structure, namely, a hair cell synapsing with a pri-

mary sensory neuron. However, the vulnerability of the

pars superior differs from that of the pars inferior, probably

due to the existence of membrane limitans.

The membrane limitans, first described by De Burlet

[18] in 1920, serves as a barrier between the pars superior

and pars inferior, protecting the pars superior against

mechanical trauma from fluid pressure. In addition, this

membrane may also prevent or delay toxic substances from

pars inferior to pars superior [19].

In addition to noise effect, aging process may play

another role for causing vestibular deficit, since the ves-

tibular system deteriorates with age. Thus, comparison of

NIHL patients from normal controls was conducted. The

percentages of abnormalities in audiometry, cVEMP,

oVEMP and caloric tests in normal controls were 13, 13, 7

and 3 %, which were significantly less than 100, 70, 57 and

33 % in NIHL group, respectively (Table 2), indicating

that aging effect does not provide a major role in causing

vestibular deficits in NIHL patients.

Further, loss of the hair cell population in the crista

ampullaris (40 %), saccular macula (24 %) and utricular

macula (21 %) were noted in subjects with increasing age

after 40 years [20]. Restated, the cristae showed a more

pronounced degeneration than the maculae, while both

utricular and saccular maculae exhibited the same degree

of degeneration. In contrast, the declining sequence of the

saccule, utricle and semicircular canals in NIHL patients is

opposed from that in aging process, further indicates that

vestibular deficit in NIHL patients is mostly due to chronic

noise exposure. Moreover, aging process is usually a

bilateral phenomenon, while some cases of NIHL showed

asymmetrical audiovestibular deficits, probably because of

the asymmetric sources of noise related to the victim’s

position in a factory [10].

Okuno and Sando [21] studied 22 temporal bones of

Meniere’s disease and reported that next to the cochlea

(100 %), the saccule (77 %) is the second most frequent

site for hydrops formation. Conversely, hydrops are less

common in the utricle (50 %) and semicircular canals

(27 %). Notably, the decreasing order of abnormal per-

centages in the function of the cochlea, saccule, utricle and

semicircular canals after chronic noise exposure mimics

the declining sequence of hydrops formation in the tem-

poral bones and physiological testing [22], which further

suggests that the endolymphatic hydrops can be induced by

noise exposure, as evidenced in animal experiments [23].

Table 2 Comparison of inner ear deficits in noise-induced hearing

loss (NIHL) patients versus normal controls

NIHL patients Normal controls p value

Case no. 30 30

Gender (M/F) 26/4 26/4

Age (Years) 48 ± 10 48 ± 12 0.928a

Abnormal rates in

Audiometry 30/30 (100 %) 4/30 (13 %) \0.001c

cVEMP test 21/30 (70 %) 4/30 (13 %) \0.001c

oVEMP test 17/30 (57 %) 2/30 (7 %) \0.001c

Caloric test 10/30 (33 %) 1/30 (3 %) \0.001c

p value \0.001b [0.05b

a Non-paired t testb Cochrane Q testc Fisher’s exact test

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Based on the clinical and pathological results, Schukn-

echt and Gulya [24] developed a classification of the

endolymphatic hydrops including embryopathic, inflam-

matory, traumatic, and idiopathic types. The pathogenesis

of post-traumatic endolymphatic hydrops is attributable to

the pressure striking force causing direct injury to the

labyrinthine membranous duct [25]. This kind of hydrops

may not progress, and subside or arrest in a short period of

time after injury. Conversely, an idiopathic endolymphatic

hydrops i.e., Meniere’s disease may present repeated pro-

gressive dilatation and rupture of the endolymphatic duct.

Conclusion

The decreasing order of abnormal percentages in the

function of the cochlea, saccule, utricle and semicircular

canals after chronic noise exposure further supports that the

pars inferior (cochlea and saccule) is more vulnerable to

noise exposure than the pars superior (utricle and semi-

circular canals).

Acknowledgments Grant no. NSC 99-2314-B002-049-MY3 from

National Science Council, Taipei, Taiwan.

Conflict of interest The authors declare that they have no conflict

of interest.

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