Subjective tinnitus and contralateral suppression of otoacoustic emissions
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- Created on Thursday, 27 October 2016 15:23
- Last Updated on Thursday, 27 October 2016 22:42
- Written by Maria RIga MD, PhD et al
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About the corresponding author: Dr. Maria Riga, is currently an Assistant Professor of Otorhinolaryngology at Democritus University of Thrace, in Alexandroupolis, Greece. She was born in Thessaloniki, Greece. She graduated from the Medical School of the Aristotle University of Thessaloniki. She was specialized in Otorhinolaryngology at “P&A Aglaia Kyriakou” Children's Hospital of Athens and University Otorhinolaryngology Department of the University Hospital of Patras, Greece. Her thesis with the title «The contribution of otoacoustic emissions in the study of the ototoxicity of chemotherapeutic agents in children» was assigned as 1st by the University ENT clinic, National University of Athens, Greece. She has authored 50 publications, indexed in pubmed, and 7 book chapters in Greek and English.
ABSTRACT :
The pathophysiology of subjective tinnitus is a multifactorial and unexplored subject. The medial olivocochlear bundle (MOCB) has been assumed to have a controversial role in the pathophysiology of tinnitus, with a limited number of studies debating over its association with tinnitus in normal hearing adults, by presenting positive or negative results. The main theory underneath this assumption supports that reduction of the neural efferent control of the cochlear amplifier exerted by the MOCB may result in an increase in its gain, which may subsequently trigger enhancement of the spontaneous activity in the auditory nerve or other structures along the auditory pathway. One of the main reasons for these controversies and also one of the main reasons why this observation has limited clinical use, is that almost all the data in the literature originate from case-control studies, which by using (i) different acquisition methods and (ii) different suppression testing parameters, compare the suppression amplitudes in their study populations with those of a control group. Furthermore, the meaning of a “defective MOCB reflex function” has not been quantified yet. How do we define “normal MOCB function”? Is any suppression amplitude, no matter how low, indicative of normal MOCB function?