Timothy C. Hain, MD Page last modified: October 26, 2016
Unlike the situation with hearing, noise is not generally recognized as a common cause of dizziness or vestibular disturbances. This likely results 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 about 20 and 20,000 hz, while vestibular hair cells are "tuned" to respond to input between 0 and 10 hz. Nevertheless, there are several contexts in which noise can cause vestibular damage.
Goltz and associates (2001) reported on 258 military subjects who had been heavily exposed to noise. They found that vestibular damage caused by intense noise exposure might be expressed clinically in subjects with asymmetrical hearing loss. There was a strong correlation between the subjects' complaints and the results of the vestibular function tests. There was no correlation between the severity of the hearing loss and the vestibular symptomatology and pathology. They concluded that subjects exposed to intense noise may have evidence of vestibular pathology only when there is an asymmetrical hearing loss. Whenever hearing loss is symmetrical, an equal damage to the vestibular system of both ears is most probably responsible for the absence of abnormal findings on the vestibular function tests The results of this study have important medicolegal implications for individuals exposed to intense noises.
Oosterveld and others (1982) carried out an extensive vestibular examination in a group of 29 noise-exposed technicians. A spontaneous nystagmus was found in 18 persons, and 24 had a positional nystagmus exceeding a velocity of the slow phase of 5 degrees/s in three or more positions. In 17 subjects a cervical nystagmus could be provoked, while a nystagmus preponderance of more than 20% in the rotation test was found in seven persons. A difference in excitability between the labyrinths of more than 20% was shown by seven subjects. None of the subjects showed pathology in the tests for central vestibular disorders. s. No correlation was found between the grade of the hearing loss and the vestibular function disturbance. This can be explained in terms of the adaptive properties of the vestibular system. All subjects showed pathology in one or more of the vestibular tests. The medico-legal aspects of vestibular involvement in noise-induced hearing loss can be of some importance. Hearing loss itself does not affect work capability directly; however, a vestibular disorder might well do so. In consequence, noise-exposed individuals could be disabled because of vertigo or balance disorder--an important and perhaps neglected aspect of noise-induced hearing damage.
Manabe and others (1995) reported results in Thirty-six NIHL patients were divided into two groups according to the presence (vertigo group) or absence (non-vertigo group) of vestibular complaints. Electrocochleograms were recorded from all subjects after pure tone audiometry. A higher incidence of increased -summating potential (SP)/action potential (AP) ratio was observed in the vertigo group than in the non-vertigo group. Caloric tests were performed in the vertigo group, and a reduced response was observed in 47.1% of ears. It is generally considered that the -SP/AP ratio is a useful indicator of endolymphatic hydrops. Therefore, episodic vertigo in NIHL patients may result from a pathophysiological mechanism similar to that of Meniere's disease.
Shupak and others (1994) evaluated vestibular function in a group of subjects with documented NIHL, employing electronystagmography (ENG) and the smooth harmonic acceleration (SHA) test. Subjects were 22 men suffering from NIHL and 21 matched controls. Significantly lower vestibulo-ocular reflex gain (p = 0.05), and a tendency towards decreased caloric responses were found in the study group. No differences in the incidence of vertigo symptoms, spontaneous, positional and positioning nystagmus, directional preponderance and canal paresis in the ENG, or the SHA test phase and asymmetry parameters were observed between the groups. These results demonstrated a symmetrical centrally compensated decrease in the vestibular end organ response which is associated with the symmetrical hearing loss measured in the study group. Statistically significant correlations were found between the average hearing loss, the decrement in the average vestibulo-ocular reflex gain (p = 0.01), and ENG caloric lateralization (p = 0.02). These correlations might indicate a single mechanism for both cochlear and vestibular noise-induced injury. The results imply subclinical, well compensated malfunction of the vestibular system associated with NIHL.
Likoski et al (1988) reported results in sixty patients with varying degrees of noise-induced hearing loss (NIHL) after long-term exposure to intense impulse noise from firearms, but without manifest clinical symptoms of vestibular pathology, were tested for body sway using a stable platform. The results were compared with those from 115 healthy referents examined in the same way. Subjects with NIHL showed significantly more body sway, estimated as movement of the centre of gravity in the horizontal plane, than did the referents. Subjects with more severe NIHL showed more sway than subjects with milder acoustic trauma. The results show that body sway is increased in patients with NIHL from exposure to impulse noise of high intensity in a way suggesting an exposure-effect relationship. This suggests subclinical disturbances of the vestibular system in these patients.
Aantaa et al (1977) reported findings in 49 male workers, mean age 30 years, who had been working in conditions of extreme noise and vibration for between 6 months and 10 years. Vestibular disturbances could be shown (in the form of spontaneous nystagmus, lowered caloric excitability, or pathology in rotatory tests) in as high as 44.9%. The lesions were believed to have arisen in the peripheral vestibular organ as a consequence of the low frequency vibration.