[Deafness syndrome caused by efferent retrocochlear inhibition]

Acta Otorrinolaringol Esp. 1993 Jul-Aug;44(4):253-6.
[Article in Spanish]

Abstract

Under the name of RIED syndrome (retrocochlear inhibition efferent deafness syndrome). I would like to introduce the clinical subject of sudden neurosensorial deafness, or rapidly progressive deafness, which is accompanied by tinnitus, and occasionally by dizziness; all this is related to stressful situations, undergone by tense and perfectionist people who are unable to relax. The possible mechanism of this active efferent inhibition can work whether in one or both ears, from the cortex, going through the medial geniculate body to the low colliculus, and from here to the olivary cochlear set, whose efferent neurons terminate in the external ciliate cells. The possible way in which this efferent retrocochlear inhibition might work, could be in altering the usual operation of the external ciliate cells, which would stop their amplifying and modulating function, causing deafness and tinnitus; this possibly happens because of the immediate alteration of the signal that originates in the internal ciliate cells and that reaches the cortex through the afferent canal; due to the personality of the people that suffer from retrocochlear inhibition efferent deafness syndrome, it is assumed that there could be some disorder in the neurotransmitters; this is very similar to what happens with endogenous depression, and this malfunctioning would take place in the medial geniculate nuclei and inferior colliculus, disturbing the efferent control that this has over the cochlea.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Cochlea / physiopathology*
  • Deafness / etiology*
  • Deafness / physiopathology
  • Diagnosis, Differential
  • Female
  • Geniculate Bodies / physiopathology*
  • Humans
  • Male
  • Neurotransmitter Agents / physiology
  • Stress, Psychological / physiopathology*
  • Syndrome
  • Tinnitus / etiology
  • Tinnitus / physiopathology

Substances

  • Neurotransmitter Agents