THE EFFECT OF SOMATIC MODULATION ON AUDITORY BRAINSTEM-EVOKED RESPONSES IN NORMA

[Emiliano]

THE EFFECT OF SOMATIC MODULATION ON AUDITORY BRAINSTEM-EVOKED RESPONSES IN NORMAL SUBJECTS AND TINNITUS PATIENTS

Eui-Cheol Nam1,2, Robert A. Levine2, Jennifer R. Melcher2,3
1 Department of Otolaryngology, College of Medicine, Kangwon National
University, Chunchon, Korea
2 Massachusetts Eye & Ear Infirmary, Massachusetts General Hospital, Eaton-Peabody Laboratory, Affiliated to the Harvard Medical School, Boston, MA, USA
3 Speech and Hearing Sciences Program, Massachusetts Institute of Technology-
Harvard Division of Health Sciences and Technology, Cambridge, MA, USA.


Background: Several lines of evidence support the principle that auditory function can be modified by somatosensory input. In particular tinnitus can (a) be caused by disorders involving the somatosensory system and (b) be modulated by somatosensory activation.

Aims: To further our understanding of how the somatosensory system modulates the auditory system, we examined how the human auditory brainstem-evoked response (ABR) is modulated by changes in jaw position in both subjects with and without tinnitus.

Subjects & Methods: Seventy non-tinnitus subjects with normal hearing (28 M, 42 F; ages 20-29) and 29 tinnitus subjects (13 M, 16 F; ages 43-72) with mild hearing loss (average pure-tone threshold <40 dB) participated. Before measuring the ABR, we determined how maximal clenching and jaw opening modulated their tinnitus.

The ABR to 90 dB HL, 11.3/sec, monaural rarefaction clicks was recorded with contralateral masking in a soundproof audio booth from forehead and ipsilateral mastoid electrodes under three jaw conditions: (a) at rest, (b) clenched, and (c) widely opened. The order of testing was randomized.
Results: Clenching increased wave II amplitude of all subjects (p= 0.008), likewise for the control (p=0.028) and tinnitus (p=0.046) subjects when considered separately.

Clenching suppressed wave III amplitude (p=0.031) and prolonged its latency only for the group whose tinnitus was suppressed by clenching. Clenching enhanced wave III amplitude for the group whose tinnitus was unchanged by clenching For the group whose tinnitus was enhanced with jaw opening, I-III interpeak latency was prolonged with jaw opening.

When comparing jaw opening to the resting state of the nine subjects with unilateral tinnitus, the ABR ipsilateral to the tinnitus had greater (a) wave III amplitude suppression (p=0.020) and (b) II-III interpeak latency prolongation (p=0.041), as compared to the ABR contralateral to the tinnitus.

Conclusions: Jaw position modulates the ABR, likely through the somatosensory system. In some cases how the ABR is modulated is related to how the tinnitus is modulated. Modulation of wave III is more prominent on the side with unilateral tinnitus. When taken together with our prior studies of the ABR generators, the findings in unilateral tinnitus subjects suggests that jaw opening is modulating the output of the spherical cells of the ipsilateral ventral cochlear nucleus.