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What is the Physiology Behind Non-Suppression of OAEs in Auditory Neuropathy?

Gerald Popelka, PhD

March 10, 2008

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Question

What is the physiology behind non-suppression of OAE by ipsi/contra noise in cases of auditory neuropathy?

Answer

In the normal ear, evoked otoacoustic emissions (OAE) (either distortion product or click evoked) can be suppressed (reduced in level) by another acoustic signal (suppressor) applied ipsilaterally or contralaterally. The pathway for an evoked OAE is from the external ear canal to the cochlea and back to the ear canal. An evoked OAE is primarily an ipsilateral process that represents ipsilateral cochlear function and not neural activity beyond the cochlea, nor cochlear function in the contralateral ear. Efferent function is not required to maintain normal OAE levels. Neither is efferent function required for more complex cochlear functions such as frequency tuning, as the data from Abdala et al (2000) suggests. Typical DPOAE ipsilateral indicators of cochlear function are normal in patients with auditory neuropathy.

The pathway for the contralateral suppression process is the external ear canal, to the cochlea, to afferent neural fibers, to the brain stem and then to efferent neural fibers back down to both cochleae to suppress the evoked OAE, and finally back to the ear canal. The suppression process can be ipsilateral or contralateral.

In auditory neuropathy (I prefer term dys-synchrony) the cochlea is functioning well enough to elicit an OAE (normal OAE) but the neural pathways beyond the cochlea are not functioning normally (no auditory brain stem response, that is, no ABR). The presence of the OAE implies that the cochlea is functioning normally and the abnormal ABR implies that the afferent nerves are not functioning normally. Auditory neuropathy always affects the afferent fibers on the involved side but may or may not affect the efferent fibers on the involved side. It would be highly unlikely that an ipsilateral suppression signal would suppress the ipsilateral evoked OAE through the efferent system because the ipsilateral afferent fibers are not functioning normally (no ABR). Suppression signals presented to the ipsilateral ear provide no information concerning the efferent fibers back down to the ipsilateral cochlea. Suppression signals presented to the contralateral ear can add to the picture.

Case 1: Ipsilateral auditory neuropathy, normal contralateral ear. If the contralateral suppression signal suppresses the ipsilateral OAE, the efferent fibers on the ipsilateral side are functioning normally. If the contralateral suppression signal does not suppress the ipsilateral OAE, then the efferent fibers on the ipsilateral side are not functioning normally. In cases of unilateral auditory neuropathy, the integrity of the efferent fibers back down to the cochlea on the involved side can be determined.

Case 2: Bilateral auditory neuropathy. It would be highly unlikely that a contralateral suppression signal would suppress an ipsilateral OAE because the afferent fibers on the contralateral side are not functioning normally (no ABR on contralateral side). In cases of bilateral auditory neuropathy no information can be obtained for either side concerning the integrity of the efferent fibers back down to the cochlea.

This is just the basic picture. In the real word, there are degrees of cochlear involvement, degrees of auditory neuropathy and even other factors such as degrees of conductive pathology. There are other factors to consider for spontaneous emissions.

Abdala, C., Y. S. Sininger, et al. (2000). "Distortion product otoacoustic emission suppression in subjects with auditory neuropathy." Ear Hear 21(6): 542-53.

Gerald Popelka holds a PhD degree from the University of Wisconsin in Madison with an emphasis in neuroscience, and a two year post doctoral research fellowship in otolaryngology from UCLA. Prior to these he earned a masters degree in audiology from Kent State University. He was a faculty member for 24 years at Washington University in St. Louis and joined the faculty at Stanford in 2004.

Dr. Popelka's research has been funded continuously with grants from a wide variety of agencies. He has initiated and completed successful collaborative research projects among diverse academic divisions including medicine and engineering.

Dr. Popelka is a co-inventor of the world's first all digital hearing aid. The resulting patent formed the basis of all current programmable and digital hearing aids or ~90% of all hearing aids currently sold. In 1996 he conceived and lead the development of JARO, the Journal of the Association for Research in Otolaryngology, now recognized as a premier, international auditory scientific research journal that was launched in 2000.

With over 90 research articles, many research presentations, two college textbooks, and various achievement awards, he has developed an international reputation for creating and using leading-edge technology that addresses both basic science and clinical applications. He remains in the forefront of developing innovative technology for biomedical applications, currently focusing on noninvasive measures of neonatal auditory function and hyperbilirubinemia and real-time MRI imaging for speech and swallowing.


Gerald Popelka, PhD

VP of R&D, Everest Biomedical Instruments, Professor of Otolaryngology – Washington University


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