Medial Olivocochlear Neural Efferent Pathway in Tinnitus

Evaluation of Medial Olivocochlear Neural Efferent Pathway in Tinnitus Perception in Normal-hearing Individuals https://www.tinnitusjournal.com/articles/evaluation-of-medial-olivocochlear-neural-efferent-pathway-in-tinnitus-perception-in-normalhearing-individuals-19938.html

See first the first picture at https://carism.se/2024-2/24-impossible/pictures-oliviocochlea-and-cochlea/ as well as Pons!

“Abstract
Objective: The objective of this study is to investigate a possible role of the Medial Olivocochlear (MOC) efferent neural pathway and neural connections responsible for tinnitus generation in silence/sensory deprivation. 

Design: By placing normal hearing participants in a sound booth for 10 minutes, silence/sensory deprivation was created. This offered assessment of MOC neural pathway in normal hearing participants in silence. Hyperactivity of MOC neural pathway was assessed by its more suppressive effect on Transient Otoacoustic Emissions (TEOAEs) in silence. The required auditory measurements were recorded in the sound booth using recommended diagnostic protocols to ensure the effect of ‘only silence’ on auditory structures. TEOAE were recorded from the right ear and suppression was measured by placing noise in the left ear. Fifty-eight normal hearing male individuals between age 18-35 years were recruited as participants in this study. 

Results: Approximately, forty-one percent of the participants perceived some type of tinnitus during/after 10 minutes of silence. No statistically significant difference was found in the total TEOAE amplitude and TEOAE suppression amplitude before and after ten minutes of silence. Post silence total TEOAE suppression between tinnitus perceiving and non-perceiving tinnitus participants were not statistically significantly different. 

Conclusion: These results suggest that the medial olivocochlear efferent pathway or lower brain stem area does not appear to play a role in the emergence of temporary tinnitus in silence however indicate the involvement of higher central auditory nervous system structures in perception of the tinnitus which support the well-accepted notion that tinnitus is the central auditory processing phenomenon” 

 

Evidence of cochlear neural degeneration in normal-hearing subjects with tinnitus https://www.nature.com/articles/s41598-023-46741-5
“Tinnitus, reduced sound-level tolerance, and difficulties hearing in noisy environments are the most common complaints associated with sensorineural hearing loss in adult populations. This study aims to clarify if cochlear neural degeneration estimated in a large pool of participants with normal audiograms is associated with self-report of tinnitus using a test battery probing the different stages of the auditory processing from hair cell responses to the auditory reflexes of the brainstem. Self-report of chronic tinnitus was significantly associated with (1) reduced cochlear nerve responses, (2) weaker middle-ear muscle reflexes, (3) stronger medial olivocochlear efferent reflexes and (4) hyperactivity in the central auditory pathways. These results support the model of tinnitus generation whereby decreased neural activity from a damaged cochlea can elicit hyperactivity from decreased inhibition in the central nervous system.”

More is to come


Svenska

”Tinnitus, minskad ljudnivåtolerans och svårigheter att höra i bullriga miljöer är de vanligaste besvären i samband med sensorineural hörselnedsättning i vuxna populationer. Denna studie syftar till att klargöra om cochleär neural degeneration uppskattad i en stor pool av deltagare med normala audiogram är förknippad med självrapportering av tinnitus med hjälp av ett testbatteri som undersöker de olika stadierna av den auditiva bearbetningen från hårcellssvar till hjärnstammens hörselreflexer. Självrapportering av kronisk tinnitus var signifikant associerad med (1) minskade cochleanervsvar, (2) svagare muskelreflexer i mellanörat, (3) starkare mediala olivokokleära efferenta reflexer och (4) hyperaktivitet i de centrala hörselbanorna. Dessa resultat stöder modellen för tinnitusgenerering där minskad neural aktivitet från en skadad cochlea kan framkalla hyperaktivitet från minskad hämning i det centrala nervsystemet.”

Kommer mera  ….