A connection between the Efferent Auditory System and Noise-Induced Tinnitus Generation. Reduced contralateral suppression of TEOAEs in patients with noise-induced tinnitus

Med Sci Monit. 2011 Jul;17(7):MT56-62. doi: 10.12659/msm.881835.

Abstract

Background: Subjective tinnitus is an auditory perception that is not caused by external stimulation, its source being anywhere in the auditory system. Furthermore, evidence exists that exposure to noise alters cochlear micromechanics, either directly or through complex feed-back mechanisms, involving the medial olivocochlear efferent system. The aim of this study was to assess the role of the efferent auditory system in noise-induced tinnitus generation.

Material/methods: Contralateral sound-activated suppression of TEOAEs was performed in a group of 28 subjects with noise-induced tinnitus (NIT) versus a group of 35 subjects with normal hearing and tinnitus, without any history of exposure to intense occupational or recreational noise (idiopathic tinnitus-IT). Thirty healthy, normally hearing volunteers were used as controls for the efferent suppression test.

Results: Suppression of the TEOAE amplitude less than 1 dB SPL was considered abnormal, giving a false positive rate of 6.7%. Eighteen out of 28 (64.3%) patients of the NIT group and 9 out of 35 (25.7%) patients of the IT group showed abnormal suppression values, which were significantly different from the controls' (p<0.0001 and p<0.045, respectively).

Conclusions: The abnormal activity of the efferent auditory system in NIT cases might indicate that either the activity of the efferent fibers innervating the outer hair cells (OHCs) is impaired or that the damaged OHCs themselves respond abnormally to the efferent stimulation.

MeSH terms

  • Acoustic Impedance Tests
  • Acoustic Stimulation
  • Adult
  • Analysis of Variance
  • Cochlea / physiopathology*
  • Efferent Pathways / physiology
  • Female
  • Hearing / physiology*
  • Humans
  • Male
  • Otoacoustic Emissions, Spontaneous / physiology*
  • Tinnitus / physiopathology*