An Account of Some Relationships Between Otoacoustic Emissions and the Olivocochlear Bundle

Dr. Frank Musiek
September 6, 2017

Aaron Whiteley


The focused examination of otoacoustic emissions began in the 1940s with Georg von Bekesy. Inspired, yet unconvinced by Helmholtz’ idea that the cochlea consisted of resonant structures, Bekesy developed an intricate method of examination that would lead to the place theory and traveling wave theory (Hall, 2000). Bekesy’s experiments built the foundation for a common understanding that cochlear function was a passive process. Though the traveling wave theory led to the Nobel Prize, the notion of the cochlea being a passive system did not stand uncontested for long.


In 1948, physicist Thomas Gold theorized that the cochlea’s function was comprised of active processes. Bekesy, having performed his experiments on cadavers, understandably resisted this theory. The scientific community at the time rallied around Bekesy, and it was not until thirty years later that David Kemp lent credence to Gold’s theory. Kemp first recorded otoacoustic emissions (OAEs) in 1978, using the term “echoes” to describe his findings.


With the idea of an active rather than passive cochlea and the advent of OAEs as a back drop, let us switch gears slightly. We now introduce Robert Galambos and suppression of afferent auditory activity linked to the olivocochlear bundle. Robert Galambos was among the first to examine the effect of efferent fiber stimulation on auditory nerve afferent activity. In his experiment, an electrode delivered a shock to medulla of a cat, and clicks of varying intensity were presented to the cat’s cochlea. His experiments found that auditory nerve firing to weak-moderate intensity click was reduced or inhibited by electrical stimulation of floor of medulla. In order to inhibit effectively, shock stimulation must be at cross-over point of olivocochlear pathway, not merely at surrounding landmarks. Histological findings revealed that inhibition remained intact only in specimens whose olivocochlear bundles had not been severed. Peripheral ablation resulted in no change in suppression of N1. In other words, this phenomenon continued after bones and muscles of middle ear were removed. When the OCB is functioning, it “suppresses the expected inflow of auditory nerve activity to normal acoustic stimuli” (Galambos, 1956).


Galambos’ work was ground-breaking. Using electric stimulation to observe the function of the olivocochlear bundle remained popular until other researchers, such as Pickles, Comis, and Dewson began utilizing other methods, such as surgical ablation and biochemistry.


In 1968, James Dewson, previously inspired by electrophysiological work performed by himself and others, conducted a new experiment. He trained monkeys to discriminate between human speech sounds presented at 70 dB SPL in 2,400 Hz low-pass noise. After being trained to distinguish vowel sounds reliably, a group of monkeys underwent surgery to ablate their olivocochlear bundles. Dewson’s findings demonstrated the importance of the olivocochlear bundle in discriminating speech in noise. The group that underwent surgery was found to have impaired performance on the speech (in noise) discrimination task after section of OCB. However, there was no loss in ability to discriminate between signals when noise was absent or soft. The deficit appeared to be related to “perceptual signal-to-noise ratio.” High intensity noise could not worsen performance if speech stimuli was insufficiently masked. Additionally, the extent of deficit depended upon how destructed the OCB fibers were.


Five years later, Pickles and Comis (1973) launched a project that studied the effects of pharmacology on the role of the olivocochlear bundle. Having recently published their findings on how to perform this examination, the duo put it into practice in this study. They administered a local injection of different drugs (atropine and pentobarbital) to cochlear nucleus of cat and then behaviorally measured changes in detection of masked and unmasked tone pips. Their findings indicated a significant difference between the effects of the drugs across various conditions. Atropine, which blocks efferent pathways with cholinergic properties, raised masked thresholds more than absolute thresholds. This deficit was greater for wide-band masking than narrow-band. Efferent pathways to cochlear nucleus help with signal detection in noise. Pentobarbital (a general depressant) raised absolute thresholds but did not affect masked thresholds. These findings suggested that the efferent pathways are directly involved in the detection of signals in noise and are sensitive to various signal to noise ratios. This involvement was achieved by controlling the critical bandwidth.


Some years later an important and different approach to measuring OCB suppression was introduced. Folsom and Owsley in 1987 began examining the interaction of contralateral noise and the olivocochlear bundle. By examining N1 (Wave I) amplitude and latency of the auditory brainstem response (ABR) in the presence of contralateral noise, it was found that contralateral noise reduced the amplitude of N1 but no effect was found for the latency. This amplitude effect was not due to acoustic reflex activation, because an increase in latency would be expected due to reduced input level. Williams, Brookes, and Prasher (1993) would later echo these findings and interpretation. What likely was happening was that the reduction in amplitude of wave I could be occurring at the basilar membrane due to the mechanical movement of outer hair cells innervated by the OCB.


Cooper and Guinan (2006) gave support to previous findings in their study on efferent control of basilar membrane motion. Their study delineated two possible factors controlling the basilar membrane. They discussed a fast and slow form of inhibition present at the basilar membrane. The slow form of inhibition is reflective of decreased outer hair cell motility, while the fast form could show decreased electromotility. Both forms were found to be similar in terms of frequency and intensity dependence, and it was unclear whether these two inhibitory processes serve different purposes or if they are merely two paths to the same destination.


Now having discussed the OCB and suppression let us return to OAEs. With several techniques for examining the olivocochlear bundle already established, research began to focus on its relationship to otoacoustic emissions, and more specifically, the inhibition of otoacoustic emissions. Williams, Brookes, and Prasher (1993) examined contralateral acoustic stimulation on otoacoustic emissions in vestibular neurectomy patients. In this study, a patient with normal hearing and a labyrinthine disorder underwent a vestibular neurectomy. Control for the study was obtained from un-operated side. This study was of considerable significance due to the related anatomy which showed that the OCB tracts coursed along with the vestibular nerves in the internal auditory meatus. Therefore this was among the first human models for examining the effects of removing efferent auditory innervation on otoacoustic emissions.


After vestibular neurectomy, there was no inhibition of contralateral OAEs, and the patient’s un-operated side showed reduced amplitude and phase lead during contralateral stimulation. In order to ensure that the reduced measured amplitudes were not due to bilateral acoustic reflex activation, noise and stimuli were presented at a low level. The mechanism for contralateral inhibition is possibly activation of medial efferent system. The fibers attached to outer hair cells were thought to change the mechanical response of these cells, altering the production of OAEs. This study supported the hypothesis that contralateral suppression of OAEs mirrors cellular events at the organ of Corti, secondary to OCB actions.  Once the OCB is severed, contralateral inhibition was stopped.


In 1993, Kawase and Liberman opened the door  to another line of research regarding the OCB which will only be briefly mentioned here. They delineated the function of the olivocochlear bundle in relation to contralateral noise. In their study, they compared responses to tone pips in the presence and absence of contralateral noise and before and after cutting the olivocochlear bundle. While contralateral noise was useful for evaluating contralateral olivocochlear fibers, it did not reveal much about the fibers that innervate ipsilaterally. The main benefit of noise came from its repeatability. The responses were measured as compound action potentials (CAP). It was found that the CAP of cats increased when contralateral noise was presented at moderate levels. Additionally, when noise of equal levels was presented binaurally, and the OCB was cut, CAP amplitudes from masked tone pips decreased. This decrease corresponded to about 6 dB SNR.


Kawase and Liberman found that the observed antimasking could be explained by medial olivocochlear fibers suppressing responses to continuous noise. Adaptation to this background noise allowed the signal to be enhanced perceptually. Liberman and Kujawa would examine the effects of frequency and level of DPOAEs and olivocochlear effects in 2001, finding that ipsilateral olivocochlear effects were greater in high frequencies than lows.


Also in 1993, Berlin et al. began to search for clinical implications of contralateral suppression. A study examined several patients with robust OAEs who lacked contralateral suppression. These same patients did not have auditory brainstem responses. Berlin’s study examined how a lack of afferent activation could possibly lead to the type II efferent fibers not receiving the input needed to activate. While these patients may have been sensitive to pure tones, the efferent fibers did not respond sufficiently to produce an ABR.


While otoacoustic emissions are valuable for evaluating the attenuation of the OCB, Chabert’s 2002 study using cats corroborated Kawase and Liberman’s use of CAP, finding that while neural attenuation varied with frequency and the level of contralateral noise, attenuation values of up to 10 dB were noted.  Chabert also stated that most studies using OAEs report an attenuation value no greater than 2-4 dB for transient evoked OAEs. Further, to this point, Moulin, Collet, and Duclaux (1993) found contralateral broadband noise to provide an average of 0.5-2 dB of attenuation using OAEs. Granted, approaches and the nature of these studies differed but as is well known, OAE suppression effects in humans often range only form 1-3 dB.


The role of the olivocochlear bundle in contralateral inhibition has many possible explanations. As a possible attenuator of unwanted noise, its function poses a possibly large benefit if fully understood. Potential applications for management of excess noise, protective abilities, and even a seeming ability to perceptually improve signal-to-noise ratio are among the presumed benefits that this system provides. Although these functions are incredibly valuable to signal detection and speech understanding in noise, contralateral suppression has not made is way to the clinic. The values currently found in research are both too small and too variable to provide a clear benefit to clinicians.


As it stands, measuring the suppression of otoacoustic emissions is a noninvasive way to evaluate the function of the medial olivocochlear bundle. Its function is clear, but its application remains difficult to pinpoint. Some researchers, such as Stuart and Cobb (2015) have begun to quantify the reliability of these measures. Results point towards a future need for studies examining the specificity and sensitivity of tests evaluating the medial olivocochlear complex.   Perhaps in the future these tests will become part of a clinician’s repertoire, but for now, more research is needed.





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