Current insights in noise-induced hearing loss: A literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Current insights in noise-induced hearing loss: A literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

This comprehensive review by four University of British Columbia in the Journal of Otolaryngology – Head & Neck Surgery provides a nice update on the pathophysiology, investigations, prevalence of asymmetry, associated symptoms, and current strategies on the prevention and treatment of noise-induced hearing loss (NIHL); and is available in its’ entirety for free. For brevity, we’re providing only the abstract; and then, presenting our own observations; and also including additional “For Further Reading” articles, gleaned from this article’s references.

Here is the abstract:
Background:

Noise-induced hearing loss is one of the most common forms of sensorineural hearing loss, is a major health problem, is largely preventable and is probably more widespread than revealed by conventional pure tone threshold testing. Noise-induced damage to the cochlea is traditionally considered to be associated with symmetrical mild to moderate hearing loss with associated tinnitus; however, there is a significant number of patients with asymmetrical thresholds and, depending on the exposure, severe to profound hearing loss as well.

Main body:

Recent epidemiology and animal studies have provided further insight into the pathophysiology, clinical findings, social and economic impacts of noise-induced hearing loss. Furthermore, it is recently shown that acoustic trauma is associated with vestibular dysfunction, with associated dizziness that is not always measurable with current techniques. Deliberation of the prevalence, treatment and prevention of noise-induced hearing loss is important and timely. Currently, prevention and protection are the first lines of defence, although promising protective effects are emerging from multiple different pharmaceutical agents, such as steroids, antioxidants and neurotrophins.

Conclusion:

This review provides a comprehensive update on the pathophysiology, investigations, prevalence of asymmetry, associated symptoms, and current strategies on the prevention and treatment of noise-induced hearing loss.

Read the rest of the article here.

Our own observations:
  • We profoundly disagree with dismissing any asymmetrical hearing loss without medical intervention via MRI. Period. Even if you, the clinician, have a good idea the asymmetry was caused by NIHL, the presence of a vestibular schwannoma (formerly called “acoustic neuroma”) must be conclusively ruled out: “When In Doubt, Refer It Out!” What’s More, as we documented in Two Study Findings Call ABR’s Into Question For Detecting Vestibular Schwannomas, a VS can either grow slowly, causing auditory dys-synchrony due to pressure on the auditory nerve Not Detected in the ABR; or can be fast growing cochlear poisoning due to ototoxic secretions causing sensorineural hearing loss Not Detected by the speech rollover test, which is Much More Dangerous;
  • We’re pleased to see Harvard’s Sharon Kujawa’s work on “Hidden Hearing Loss” (due to glutamate excitotoxicity, triggering cochlear synaptopathy and spiral ganglion neurodegeneration) heavily cited; and we wrote about this subject 3½ years ago in Uh Oh! Here Comes Noise-Induced Cochlear Synaptopathy …And It Just May Up-End Everything We Know About Hearing Conservation;
  • Although otacoustic emission (OAE) measurement of outer hair cell integrity is a valuable clinical tool for detecting early signs of NIHL, we don’t believe this will actually detect cochlear synaptopathy and spiral ganglion neurodegeneration itself, as those are two different lesion sites, as well as inner hair cell integrity. We remind the reader that presence or absence of OAE’s is .NOT. part of the differential diagnosis for ANSD;
  • We especially like the discussion of the possible ways to attempt to quantify hidden hearing loss as, by definition, it does not show up on the audiogram. Some of the authors’ suggested methods are through speech perception testing in both quiet & noise, acoustic auditory brainstem evoked response (aABR) analysis of Wave I amplitude (pay attention, pay attention!), changes in acoustic (stapedial) reflex thresholds, and (New!) vestibular function disruptions;
  • On The Other Hand, that instead of the aABR, we think hidden hearing loss can be better detected through a careful analysis of the electrocochleogram (ECochG): As  first observed by Starr, Zeng, Michalewski, & Moser in 2008 [mirror copy] — and we expanded on 3½ years ago — the result of these lesions is a widening and lowering of the action potential (AP). At the time, we wrote,

    A good way of looking at what happens to the neural firing synchrony is to relate it to signal jitter;2 or a bit more closely, Lag-Only Cyclic phase jitter,3 which are “rapid, repeated phase perturbations that result in the intermittent shortening or lengthening of signal elements,” which in the case of cochlear synaptopathy is lengthening only, as you can see in the grey arrows, which yield a lower and longer action potential (AP) on the electrocochleogram (ECochG), and hence ABR wave I.

    Figure 2 from Perspectives on Auditory Neuropathy: Disorders of Inner Hair Cell, Auditory Nerve, and Their Synapse: A representation of the patterns of activity of afferent auditory nerve fibers with synaptic connections to an inner hair cell. The onset of a transient stimulus is indicated by the vertical line below. The occurrence of fiber activity in a normally functioning system is represented by black arrows while fiber activity in an abnormal system is represented by gray arrows. The patterns of activity in the two conditions are shown below. The abnormalities of fiber activity that are represented include (a) variable delay in the latency of discharge and (b) absence of a response in 30%of the fibers. Note the short latency and synchrony of the population’s response when the system is normal and the delayed latency, temporal dispersion, and reduced amplitude of the population’s response when the system is abnormal. We suggest that the pattern of abnormality of activity would be similar whether the disorder were at inner hair cell, the synapse including neurotransmitter release, reuptake and binding to receptor sites, or in the nerve fibers. However, the extent of latency delay and variability as well as in the proportion of fibers that are activated would vary according to the type and extent of the pathological processes.

    Figure 2 from Perspectives on Auditory Neuropathy: Disorders of Inner Hair Cell, Auditory Nerve, and Their Synapse:1 A representation of the patterns of activity of afferent auditory nerve fibers with synaptic connections to an inner hair cell. The onset of a transient stimulus is indicated by the vertical line below. The occurrence of fiber activity in a normally functioning system is represented by black arrows while fiber activity in an abnormal system is represented by gray arrows. The patterns of activity in the two conditions are shown below. The abnormalities of fiber activity that are represented include (a) variable delay in the latency of discharge and (b) absence of a response in 30%of the fibers. Note the short latency and synchrony of the population’s response when the system is normal and the delayed latency, temporal dispersion, and reduced amplitude of the population’s response when the system is abnormal. We suggest that the pattern of abnormality of activity would be similar whether the disorder were at inner hair cell, the synapse including neurotransmitter release, reuptake and binding to receptor sites, or in the nerve fibers. However, the extent of latency delay and variability as well as in the proportion of fibers that are activated would vary according to the type and extent of the pathological processes.

References:
  1. Perspectives on Auditory Neuropathy: Disorders of Inner Hair Cell, Auditory Nerve, and Their Synapse, by Arnold Starr, Fan-Gang Zeng, H J Michalewski, and Tobias Moser (2008) | Mirror copy
  2. Definition of jitter
  3. Definition of cyclic phase jitter
For Further Reading:

 

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About the author

Dan Schwartz

Electrical Engineer, via Georgia Tech

2 Comments

  1. James Oliver
    September 9, 2018 at 10:11 am

    There are so many typos in this post, it immediately lacks credibility! Can’t trust it.


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