Auditory fatigue is defined as a temporary loss of hearing after exposure to sound. This results in a temporary shift of the auditory threshold known as a temporary threshold shift. The damage can evolve in a permanent threshold shift if sufficient recovery time is not allowed for before continued sound exposure.
When the hearing loss is rooted from a traumatic occurrence, it may be classified as noise-induced hearing loss.
According to the Occupational Health and Safety Administration, 5-10 million Americans are at risk for NIHL because they are exposed to sounds louder than 85 dBA on a sustained basis in the workplace.
More males than females are reported to have NIHL.
No clear-cut differences exist between young and older individuals in their susceptibility to NIHL.
When hearing loss is limited to the high frequencies, individuals are unlikely to have difficulty in quiet conversational situations. The first difficulty the patient usually notices is trouble understanding speech when a high level of ambient background noise is present. As NIHL progresses, individuals may have difficulty understanding high-pitched voices (eg, women's, children's) even in quiet conversational situations. Conversation on the telephone is generally unimpaired because telephones do not use frequencies above 3000 Hz.
Affected anatomy: Organ of Corti.
Excessive vibrations of the inner ear which may cause structural damages.
Metabolic activity is required in order to maintain the electrochemical gradients used in mechano-electrical and electro-mechanical transduction during noise exposure and sound recognition. The metabolic activity is associated with active displacements which are components of the sound-induced vibration involving prestin, a motor protein that causes OHC motility. Excessive vibrations require increased metabolic energy.
Extra vibrations can cause the formation of free radicals known as ROS.
Recent studies have investigated additional mechanisms of NIHL involving delayed or disabled electrochemical transmission of nerve impulses from the hair cell to and along the auditory nerve. In cases of extreme acute acoustic trauma, a portion of the postsynaptic dendrite can rupture from overstimulation, temporarily stopping all transmission of auditory input to the auditory nerve (excitotoxicity).
Generation of ROS and RNS often followed by caspase-mediated cell death by apoptosis. Activation of the c-Jun N-terminal kinase/mitogen-activated protein kinase (JNK) signaling pathway.
Production of the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor α (induced by ROS).
ROS have been detected in cochlear tissue immediately after noise exposure and seen to persist for 7–10 days. This can induce the continued cochlear injury.
Noise-induced ischemia and subsequent re-perfusion further potentiate the generation of ROS.
This Overloads cochlear antioxidant enzyme system, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase causing depletion of glutathione.
Plasma membrane fluidity of outer HCs is a consequence of excess peroxidation induced by an altered metabolic state.
Loss of mitochondrial integrity can lead to increased ROS production and release of ROS into the cytoplasm.
Excessive noise also leads to an increase in free Ca2+ in cochlear HCs (L-type Ca2+ channels), this leads to further release of Ca2+ from intracellular stores such as the ER and mitochondria. Elevated Ca2+ levels in the cochlea may link to ROS production as well as triggering apoptotic and necrotic cell death pathways independent of ROS formation.
In animals exposed to intense noise, MAPK phosphorylation in the cochlea is altered. MAPKs mediate plasma membrane bound receptor signals to activate transcription factors in the nucleus, facilitating gene expression, coordinately regulating cell proliferation, differentiation, motility, and survival .
Following the activation of MAPK and ROS stress pathways, cochlear HCs can undergo apoptosis following intense noise exposure.
Balance of Damage and Survival Signaling Determines Cochlear Damage.
Inflammatory damage can be opposed by anti-inflammatory cytokines such as IL-10 and anti-inflammatory cellular phenotypes such as alternatively activated macrophages. Similarly, there are intracellular pro-survival pathways that oppose the death and damage signaling of stress pathways such as ROS, the JNK and p38 cascades.
Antioxidants react with ROS, reducing them to eliminate or reduce toxicity. Cochlear HCs contain the antioxidant glutathione, which is the substrate by which glutathione transferases detoxify ROS.
Polymorphisms in glutathione transferase genes, which catalyze the response of glutathione with ROS, have been linked to ototoxicity and noise sensitivity in humans
There are at least two potential strategies for therapeutic intervention to reduce cochlear damage. One is to inhibit processes or pathways that lead to the damage of cochlear cells. The other is to enhance processes that enhance cochlear cell survival. Both of these strategies have been attempted, with varying degrees of success.
Evidences: high doses of vitamins A, C, and E, and magnesium, taken one hour before noise exposure and continued as a once-daily treatment for five days, was very effective at preventing permanent noise-induced hearing loss in animals.
Clinical trials using antioxidants after a traumatic noise event to reduce reactive oxygen species have displayed promising results.
Sources & further readings
Mechanisms of sensorineural cell damage, death and survival in the cochlea (2015)
Hearing and loud music exposure in a group of adolescents at the ages of 14-15 and retested at 17-18 (2014)
Age-related hearing impairment and the triad of acquired hearing loss (2015)
Glutathione S-transferase M1, T1, and P1 polymorphisms as susceptibility factors for noise-induced temporary threshold shift (2009)
Differential Impact of Temporary and Permanent Noise-Induced Hearing Loss on Neuronal Cell Density in the Mouse Central Auditory Pathway (2010)