PubMed · 6551425
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P R Weldon, T J Murray, D B Quine. 1983. Hearing changes in multiple sclerosis.. https://doi.org/10.1097/01376517-198304000-00009
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The ability to lateralize dichotic clicks with either interaural time delays (ITD) or interaural level differences (ILD) was tested in seven multiple sclerosis (MS) subjects who had normal audiograms. Along with the psychoacoustical tests, magnetic resonance images (MRI) of the subjects' brainstem were obtained. After matching each MRI section with the corresponding section of a computerized atlas of the brainstem, the parts of the auditory pathway affected by each MS lesion were determined. Of the seven subjects two performed normally with both types of interaural asymmetry and had no brainstem lesions involving the auditory pathway. Two subjects performed normally only with level differences, but perceived all the dichotic clicks with different ITDs in the center of the head; both had lesions involving the trapezoid body. Three subjects could not perform normally with either task, perceiving the clicks to the sides and never in the center for both ITDs and ILDs; all three had unilateral lesions of the lateral lemniscus. A multi-level decision making model is proposed to account for these results.
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Evoked otoacoustic emissions (OAEs) are assumed to reflect healthy outer hair cell function. Over the past few years, evoked OAEs have been shown to be useful as indicators of cochlear hearing loss. Because basic studies have shown that OAEs are extremely sensitive to cochlear anoxia and hypoxia, as well as to the adverse effects of many inner ear diseases, it is possible that these objective tests can provide some insight into the fundamental basis of the hearing loss exhibited by patients with acoustic neuromas. The primary aim of the present study was to examine the effects of acoustic neuromas on the amplitudes of evoked OAEs and to compare these findings with tumor-induced hearing levels. To this end, tests of behavioral audiometry, distortion-product otoacoustic emissions and transiently evoked otoacoustic emissions were performed on 44 patients with verified acoustic neuromas. The results demonstrated that the majority of ears with acoustic neuromas displayed one of two distinct patterns of evoked OAEs: a cochlear pattern or a noncochlear pattern. Although behavioral hearing thresholds were higher with larger tumors, OAE levels exhibited no clear relationship to tumor size. The present findings support the notion that acoustic neuromas may cause hearing impairment according to two types of influence that act at different levels of the peripheral auditory system. The tumor's cochlear effect on evoked OAE activity is most likely caused by an indirectly mediated compromise of the organ of Corti's vascular supply. It is probable that the direct pressure of the tumor on the eighth cranial nerve is responsible for the observed noncochlear effects.