Noise History, Audiometric Profile, and Acoustic Reflex Responsivity

  • V. Colletti
  • V. Sittoni
Part of the NATO ASI Series book series (NSSA, volume 111)


For several years there has been a debate in the literature on the effectiveness of the stapedius reflex in attenuating the acoustic input to the cochlea and its potential for reducing the amount of noise-induced hearing loss [1–10]. Several features of the acoustic reflex seemed to suggest that the attenuation provided by the stapedius contraction is irrelevant for protection of the inner ear to acoustic overstimulation: (1) the long latency and rise time of the stapedius reflex would allow single transient sounds to pass through the middle ear without being attenuated by the reflex [1]; (2) the attenuation resulting from the stapedius reflex is quantitatively too small to protect the inner ear from high sound levels and is effective outside the frequency range where noise-induced hearing loss primarily occurs [2–6]; (3) the response decays rapidly in the presence of continuous stimulation and thus the reflex is practically inactive for most of the exposure time [7–11]. Most of these conclusions had been derived from studies that had utilized simple acoustic stimuli (continuous pure tones and noise) and experimental laboratory conditions (low levels of background noise), which differ from the actual noise situation in industrial environments. Most frequently, noise encountered in industry is fluctuating with respect to both frequency and intensity. In addition, during the work period the noise may fall to levels below the stapedius reflex threshold between periods of high noise exposure. Given the profound differences between the stimuli encountered in laboratory and industrial situations, it is difficult to predict how the stapedius reflex would act in an industrial noise environment.


Hearing Loss Noise Exposure Hearing Threshold Group Band Noise Induce Hearing Loss 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • V. Colletti
    • 1
  • V. Sittoni
    • 1
  1. 1.ENT DepartmentUniversity of VeronaVeronaItaly

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