February 7, 2006 Feature

Vestibular Disorders and Audiology

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The sensitivity of the vestibular system to acoustic stimulation is well established. Sound-evoked vestibular symptoms in humans were first described by Tullio in 1929. In some lower vertebrates such as amphibians and fish, the saccule is the organ of hearing (Popper, Platt, & Saidal, 1982; Moffat & Capranica, 1976). Although the cochlea has replaced the saccule as the primary organ of hearing in mammals, there is evidence that the mammalian saccule remains responsive to sound. Vestibular afferent nerve fibers have been found to be acoustically responsive in the squirrel monkey (Young, Fernandez, & Goldberg, 1977), in the guinea pig (Murofushi, et al., 1995), and in the cat (McCue & Guinan, 1995).

Vestibular evoked myogenic potentials (VEMPs) are short latency electromyograms (EMG) that are evoked by high-level acoustic stimuli and are recorded from surface electrodes over the tonically contracted sternocleidomastoid (SCM) muscle. Studies using human subjects with well-documented peripheral audiovestibular lesions have confirmed the vestibular origin of the response (Colebatch & Halmagyi, 1992). Colebatch and Halmagyi demonstrated that the VEMP is abolished following unilateral vestibular neurectomy. These studies also demonstrated that there is no correlation between the VEMP and the degree of sensorineural hearing loss suggesting that the VEMP is not mediated by the cochlear afferents (Colebatch et al., 1994). The saccule has been implicated as the origin of the VEMP and a response pathway has been suggested from the vestibular saccule to the inferior vestibular nerve, the lateral vestibular nucleus, and the lateral vestibulospinal tract to motoneurons in the SCM muscle.

The presence of a VEMP is dependent upon adequate acoustic stimulation and ipsilateral activation of the SCM muscle. In our laboratory, VEMPs are recorded with patients seated upright and heads turned to one side to activate unilaterally the SCM muscle. Since VEMP amplitude is proportional to the SCM muscle EMG level, patients are instructed to maintain the rectified EMG rms amplitude at 50 mV during the recording of each evoked potential waveform to control for the effect of tonic EMG level on the VEMP (Akin & Murnane, 2001). A two-channel recording of the vestibular evoked myogenic potential (VEMP) is obtained using a commercially-available evoked potential unit. Click or low-frequency tone burst stimuli are presented monaurally at 100 dB nHL and 120 dB peakSPL, respectively. The VEMP waveform is characterized by a positive peak (P1) at ~11 ms, and a negative peak (N1) at ~18 ms.

In our laboratory, click-evoked VEMP thresholds in normals ranged from 80-100 dB nHL, and the average threshold was 91 dB nHL (Akin et al., 2003). The VEMP amplitude is influenced by the stimulus level, stimulus frequency, and tonic EMG level, whereas VEMP latency is independent of these variables. We examined the response characteristics and thresholds of tone burst-evoked VEMPs, and observed that the largest P1-N1 amplitudes were obtained at 500 Hz and 750 Hz (Akin, Murnane, & Medley, 2003). In a group of subjects with normal audiovestibular function, VEMP thresholds ranged from 100-120 dB peakSPL across frequency with the lowest thresholds obtained at 500 Hz and 750 Hz and the highest thresholds obtained at 2000 Hz. The results of this study were consistent with the neurophysiological findings that acoustically responsive afferent fibers in the mammalian inferior vestibular nerve have broad, V-shaped tuning curves with best frequencies between 500 Hz and 1000 Hz (McCue & Guinan, 1995).

VEMP abnormalities vary with vestibular pathology. Abnormally increased amplitude and reduced thresholds have been reported in patients with superior canal dehiscence. In contrast, reduced amplitude or absent VEMPs have been reported in some patients with vestibular schwannoma, Meniere's disease, and acoustic neuroma. An attenuated or absent VEMP suggests saccular and/or inferior nerve involvement. Patients with reduced amplitude VEMPs may be candidates for vestibular rehabilitation therapy (VRT), however, the efficacy of VRT for patients with otolithic disturbances has not been determined.

Conventional vestibular assessment has been limited to the evaluation of one of the five peripheral vestibular end organs, the horizontal semicircular canal. Thus, the VEMP may supplement the current test battery by providing diagnostic information about saccular and/or inferior vestibular nerve function.

[This work is funded by the Rehabilitation Research & Development Service, Department of Veterans Affairs through a Merit Review, an Advanced Career Development Award, and the Research Enhancement Award Program.]

Editor's note: The authors presented a keynote on vestibular disorders and audiology at the 2005 ASHA Convention in San Diego. This is a summary of their talks.

Faith W. Akin, is the director of the Vestibular/Balance Laboratory at the James H. Quillen VA Medical Center, Mountain Home, TN and associate professor, Department of Communicative Disorders, East Tennessee State University, Johnson City, TN.

Owen D. Murnane, is the director of the Auditory Electrophysiology Laboratory at the James H. Quillen VA Medical Center, Mountain Home, TN and associate professor, Department of Communicative Disorders, East Tennessee State University, Johnson City, TN.

cite as: Akin, F. W.  & Murnane, O. D. (2006, February 07). Vestibular Disorders and Audiology. The ASHA Leader.

References

Akin, F.W. and Murnane O.D. (2001). Vestibular evoked myogenic potentials: preliminary report. Journal of the American Academy of Audiology, 12, 445-452.

Akin, F.W., Murnane O.D., and Medley T.M. (2003). The effects of click and tone burst stimulus parameters on the vestibular evoked myogenic potential (VEMP). Journal of the American Academy of Audiology, 14(9): 500-508.

Akin , F.W., Murnane, O.D., Panus, P.C., Caruthers, S.K., Wilkinson, A.E., and Medley, T.M. (in press). The influence of voluntary tonic EMG level on the vestibular evoked myogenic potential. Journal of Rehabilitation Research & Development.

Colebatch, J.C., and Halmagyi, G.M. (1992). Vestibular evoked potentials in human neck muscles before and after unilateral vestibular deafferentation. Neurology 42: 1635-1636.

Colebatch, J.C., Halmagyi, G.M., and Skuse, N.F. (1994). Myogenic potentials generated by a click-evoked vestibulocollic reflex. Journal of Neurology, Neurosurgery, and Psychiatry, 57:190-197.

Moffat, A., and Capranica, R. (1976). Auditory sensitivity of the saccule in the American toad (Bufo americanus). J Comp. Physiol. 105: 1.

Murofushi, T., Curthoys, I.S., Topple, A.N., Colebatch, J.G., Halmagyi, G.M. (1995). Response of guinea pig primary vestibular neurons to clicks. Experimental Brain Research, 103: 174-178.

McCue, M.P., and Guinan, J.J. (1994). Acoustically responsive fibers in the vestibular nerve of the cat. Journal of Neuroscience, 14(10): 6058-6070.

Popper, A., Platt, C., and Saidal, W. (1982). Acoustic functions in the fish ear. Trends in Neuroscience, 5: 276-280.

Young, E., Fernandez, C., and Goldberg, J. (1977). Responses of squirrel monkey vestibular neurons to audio-frequency sound and head vibration, Acta Oto-Laryngologica, 84: 352-360.

Tullio, P. (1929). Das Ohr und die Entstehung der Sprache und Schrift. Urban and Scharzenberg; M√ľnchen, Germany.



  

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