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|Year : 2000 | Volume
| Issue : 9 | Page : 45--48
Noise-induced vestibular dysfunction
Ben I Nageris, Joseph Attias, Raphael Feinmesser
Department of Otolaryngology, Petah Tiqva, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Ben I Nageris
Department of Otolaryngology, Head & Neck Surgery,Rabin Medical Center, Beilinson Campus, Petah Tiqva, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv
An association between noise exposure and vestibular function has long been suspected. Our wide experience in a major otologic outpatient clinic yielded six patients within the last seven years who presented with Meniere's disease and a history of long-term exposure to noise. Two of the cases are described in detail. Our evaluation in light of the data in the literature suggests that the relationship between vestibular dysfunction and exposure to hazardous noise may be more than coincidental.
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Nageris BI, Attias J, Feinmesser R. Noise-induced vestibular dysfunction.Noise Health 2000;3:45-48
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Nageris BI, Attias J, Feinmesser R. Noise-induced vestibular dysfunction. Noise Health [serial online] 2000 [cited 2023 Jan 26 ];3:45-48
Available from: https://www.noiseandhealth.org/text.asp?2000/3/9/45/31771
Noise has long been recognized as a cause of cochlear damage resulting in tinnitus and hearing loss. However, its role in vestibular dysfunction remains unclear, and a cause-effect relationship has not been accepted.
The first study on the effect of occupational noise hazard was published in 1886. Barr pointed out that 15 of the 100 individuals studied had "some sensation of giddiness" but little importance was attached to the finding at the time. By 1915, vestibular stimulation with noise was recognized by Rodger, who found that 10% of patients with nose induced hearing loss (NIHL) complained of giddiness. In 1966, Chadwick reported that of 1800 patients with NIHL, eight had the fluctuant hearing loss, tinnitus and attacks of vestibular dysfunction characteristics of Meniere's disease. Thereafter both Pulec (1972) and Paparella and Mancini (1983) noted that some patients with Meniere's disease had a history of exposure to hazardous noise, and they speculated that the noise exposure may in fact have caused the disease.
The present study describes six individuals with NIHL and Meniere-like symptomatology. The relevant literature is reviewed and a possible explanation for vestibular dysfunction secondary to noise exposure is presented.
During the last seven years, thousands of patients with NIHL have been treated in our Otologic Outpatient Clinic. Six of them had a clear presentation of full-blown Meniere's disease. Their clinical data are shown in [Table 1]. Complete physical and laboratory work-up and brain magnetic resonance imaging (MRI) study revealed no abnormalities. In all cases, the Meniere's disease developed after prolonged exposure to noise. Two representative cases are described in detail.
This 65-year-old man with an unremarkable past medical history had been employed as a turbine mechanic at a local electric company. In the course of his job he had been exposed to loud noise (up to 118dB SPL) at least 5 hours a day, five days a week for 38 years, during 20 of which he did not use ear protection. At the age of 45 years, bilateral NIHL and tinnitus were diagnosed. Five years later, he presented with vertiginous attacks accompanied by a sensation of ear fullness and fluctuations in hearing that lasted for hours; the otologic symptoms disappeared at termination of the attacks. Repeated audiograms demonstrated fluctuating hearing loss.
Results of complete blood work-up, including VDRL, and neurologic and ophthalmologic examinations were unremarkable. Brain MRI was negative for cerebropontine angle tumor or other brain disease. Electronystagmography, including water and caloric tests, showed bilateral vestibular hypofunction, and dynamic posturography showed vestibular dysfunction.
A 53-year-old man had been exposed to intense explosive noise since his recruitment to the army at age 18 years. At age 35 years still serving in the army, he began to complain of hearing loss and tinnitus. An audiogram showed a NIHL pattern on the left side. Now, 18 years later, he presented with repeated episodes of vertigo, ear fullness, hearing fluctuation and increased tinnitus in the left ear. There was a progressive deterioration in hearing, especially at the low-tone range (0.25-0.5-1.0 kHz), and the speech reception threshold was 70 dB. Complete blood count, brain MRI and relevant consultations were noncontributory.
NIHL has been linked to Meniere's disease in several epidemiological and clinical studies. Pulec (1972) found that in 3% of their 120 patients with Meniere's disease, the cause could be traced to acoustic or physical trauma. Paparella and Mancini (1983) investigated 37 cases of Meniere's disease which occurred following acoustic trauma, and Liard et al. (1991) reported on 93 patients presenting with classic unilateral Meniere's disease, four of whom (5%) had acquired the disorder after significant acoustic trauma. Both Ylikoski (1988) and Okuno et al (1996) studied military personnel, among whom noise exposure is common. Ylikoski (1988) reported on 18 army officers with NIHL, balance disturbances and a history of long exposure to hazardous noise. Okuno et al. (1996) found that of 475 soldiers tested, 1.4% had Meniere's disease and 32.5% had experienced dizzy spells.
Manabe et al (1995) divided 36 patients with NIHL into two groups according to the presence or absence of vestibular complaints. Results of electrocochleograms, performed in all participants, and electronystagmograms, performed in the group with vestibular complaints showed that episodic vertigo in NIHL may result from a pathophysiological mechanism similar to that of Meniere's disease. In the present study, we describe six patients who complained of hearing loss, tinnitus and vertigo after prolonged exposure to hazardous noise levels.
The repeated observations of vestibular dysfunction and a history of exposure in the same individuals have raised the possibility of a cause-effect relationship. Authors have been unable to confirm it statistically because of the high incidence of vestibular abnormalities in the otherwise healthy population, reaching to 60% according to some studies (Hinchcliffe 1961; DHEW 1968; Coles and Sinclair 1988; Roitman 1989), the low incidence of Meniere's disease, and the long time interval between noise exposure and disease symptomatology. Nevertheless, the clinical findings have been supported by experimental studies, using a guinea pig model. Kimura (1982) showed that acoustic trauma produced endolymphatic hydrops in 38% of the exposed animals; these results re-emphasized the fact that histological damage could occur secondary to noise exposure, as was first described by Wittmaack in 1907. This prompted Paparella (1991), in his textbook to list trauma, specifically acoustic trauma, as a cause of Meniere's disease.
We suggest that the mechanism of noise-induced vestibular dysfunction can be explained physiologically. Both mechanical and acoustic trauma may cause contusion of the labyrinth. Mechanical trauma can directly damage the vestibulum, and acoustic energy can deliver a damaging effect to the vestibular system by way of the round window of the cochlea.
A possible alternation to the cause-and-effect notion was provided by the work of Nakai et al (1991). These authors induced one-sided endolymphatic hydrops in guinea pigs by endolymphatic sac obliteration. Two months later, the animals were subjected to noise for 2 hours and their inner ears were examined histologically. Changes were noted in the ears with endolymphatic hydrops but not in the normal, contralateral ones. The authors concluded that ears with endolymphatic hydrops are highly sensitive to noise exposure. Thus, Meniere's disease may not be secondary to noise exposure, but its presence may make affected patients who are exposed to high noise levels more susceptible to inner ear damage.
During our 20-year experience with NIHL, we encountered six patients in whom Meniere's disease developed after long-term exposure to high noise levels. The noise exposure type could be either continuous or periodic. The cumulative clinical, epidemiological and laboratory data over the last decade indicate that there may be a direct link between NIHL and vestibular disorders. However, because it still is difficult to reach a definite conclusion, each case must be evaluated on an individual basis.
The authors thank Mrs. Charlotte Sachs and Mrs. Gloria Ginzach of the Editorial Board, Rabin Medical Center, Beilinson Campus, for their assistance.
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