Assessing Human Medial Olivocochlear Reflex Function with Complementary Pre-Neural and Neural Assays

Abstract

The auditory nervous system contains an extensive and distributed network of efferent pathways connecting auditory cortices to cochleae. At the most caudal level of the efferent auditory system, cochlear outer hair cells (OHCs) receive direct innervation from the auditory brainstem via the medial olivocochlear (MOC) bundle. Through the MOC bundle, the brainstem modulates cochlear amplifier gain – an effect termed the MOC reflex. One putative role of the MOC reflex is improving the signal-to-noise ratio by reducing cochlear gain for noise (i.e., "unmasking"). The human MOC reflex has been studied using pre-neural assays of OHC function, such as otoacoustic emissions. A limitation of this approach is that it is insensitive to subsequent “downstream” MOC reflex effects on the neural ensembles that mediate hearing. To elucidate the functional role of the MOC reflex, it is imperative to understand relationships between the pre-neural OAE assays of MOC reflex function and their downstream neural complements: compound nerve action potentials and auditory brainstem responses. The specific aims of this dissertation were to 1) examine predictive relationships between complementary pre-neural and neural assays of MOC reflex function, and 2) test the hypothesis that the human MOC reflex is advantageous in speech-in-noise processing. Three experiments were undertaken to address these aims. In the first experiment, click-evoked otoacoustic emissions and click- and chirp- evoked auditory nerve compound action potentials were measured with and without activation of the MOC reflex using contralateral noise. We hypothesized that MOC reflex amplitude inhibition of compound action potentials would be larger than otoacoustic emission amplitude inhibition and that compound action potential inhibition would be predicted by otoacoustic emissions inhibition. In the second experiment, distortion product otoacoustic emissions and distortion product frequency following responses were measured with and without activation of the MOC reflex using contralateral noise. We hypothesized than MOC reflex inhibition of distortion product frequency following responses would be larger than distortion product otoacoustic emissions and that distortion product frequency following response inhibition would be predicted by distortion product otoacoustic emission inhibition. In the third experiment, we measured MOC reflex strength using otoacoustic emissions as well as brainstem speech-in-noise processing with and without activation of the MOC reflex. We hypothesized that otoacoustic emission inhibition would predict brainstem speech-in-noise unmasking. The results of Experiment 1 suggested that compound action potential amplitude inhibition was larger than otoacoustic emission amplitude inhibition when results were reported on the same scale. Further, chirp-evoked compound action potential inhibition was larger than click-evoked compound action potential inhibition, suggesting that chirps may be a better tool for measuring MOC reflex inhibition of auditory nerve responses. The results of Experiment 2 revealed that distortion product frequency following response inhibition was largest for the component measured at 2f1-f2 than for f1 or f2. Further, distortion product otoacoustic emission inhibition was mildly predictive of distortion product frequency following response inhibition at 2f1-f2 and f2. The results of Experiment 3 revealed that otoacoustic emission inhibition was not predictive of speech-in-noise "unmasking" at the level of the brainstem. Taken together, the experiments suggest that pre-neural inhibition measurements likely underestimate MOC reflex strength and that neural assays may be more beneficial in understanding the functional significance of the MOC reflex in humans.