Threshold shift

threshold shift is an increase in the hearing threshold for a particular sound frequency. It means that the hearing sensitivity decreases and that it becomes harder for the listener to detect soft sounds. Threshold shifts can be temporary or permanent.

temporary threshold shift (TTS) is a temporary shift in the auditory threshold. It may occur suddenly after exposure to a high level of noise, a situation in which most people experience reduced hearing. A temporary threshold shift results in temporary hearing loss.

The opposite of a temporary threshold shift is a permanent threshold shift. A permanent threshold shift (PTS) is when the ability to hear is reduced permanently, which causes a permanent hearing loss. A professional hearing test can measure the level of the threshold shift and the results can be seen on an audiogram. PTS is sensorineural and varies across frequencies, depending on characteristics of the exposure, the transmission characteristics of the external and middle ears, and the innate sensitivity of different regions of the cochlea to damage.

Exposure to intense sound can produce TTS, acute changes in hearing sensitivity that recover over time, or PTS, a loss that does not recover to pre-exposure levels. In general, a threshold shift ≥ 10 dB at 2, 3 and 4 kHz is required for reporting purposes in human studies. The high-frequency regions of the cochlea are most sensitive to noise damage. Resonance of the ear canal also results in a frequency region of high noise sensitivity at 4–6 kHz. A primary noise target is the cochlear hair cell. While the mechanisms that underlie such hair cell damage remain unclear, there is evidence to support a role for reactive oxygen species, stress pathway signaling and apoptosis.

Another target is the synapse between the hair cell and the primary afferent neurons. Large numbers of these synapses and their neurons can be lost after noise, even though hearing thresholds may return to normal. This affects auditory processing and detection of signals in noise. The consequences of TTS and PTS include significant deficits in communication that can impact performance of military duties or obtaining/retaining civilian employment. Tinnitus and exacerbation of post-traumatic stress disorder are also potential sequelae.

Characteristics of temporary threshold shift

TTS is a change in hearing threshold that recovers to pre-exposure levels (baseline) over time. The amount of time to recover to baseline may be relatively fast (minutes to hours) or slow (days to weeks). The severity of the initial insult, as well as the time course of the recovery, are dependent on a number of factors including: the type of insult or trauma, the intensity and duration of the insult (single vs repeated, short vs long exposures), and the stimulus type (impulse/impact sound or continuous noise including wide or narrow-band noise).

Individual susceptibility is dependent on the use of hearing protective devices, the quiet time or rest between exposures, and the level of hearing loss prior to exposure. Individual susceptibility to TTS may also be influenced by age, sex, prior history of noise exposure, diabetes, genotype and other personal or environmental factors such as smoking and diet. While these factors are at play for PTS as well, unlike PTS, TTS is a change in hearing sensitivity which recovers to baseline or within test/retest criteria in minutes, hours, days or weeks with the upper limit being 30 days post exposure. TTS and PTS outcomes will vary as a function of the insult and individual factors.

Mechanisms of temporary threshold shift

Historically, TTS was largely thought to be a mechanical process that involved structures within the outer and middle ear including the ear drum, ossicular chain and middle ear muscles through the acoustic reflex. Extremely intense noise exposure is also known to mechanically damage the cochlea, disrupting the connections between the tectorial membrane and outer hair cell stereocilia, damaging the stereocilia themselves, breaching the integrity of the reticular lamina or even disrupting the basilar membrane.

However, recent work in several preclinical studies has demonstrated a significant involvement of several sensorineural inner ear structures including hair cells and their stereocilia, supporting cells within the organ of Corti, endothelial cells and fibrocytes within the stria vascularis and spiral ligament, and dendritic processes of the auditory nerve. Molecular and biochemical changes have been identified that include pro-inflammatory and pro-apoptotic processes. These changes have been shown to alter the normal function of several critical processes within the cochlea including the endolymphatic potential that drives hair cell depolarization, cellular membranes and mitochondria responsible for hair cell and supporting cell activity, and neural innervation of the inner hair cell that conduct impulses to the auditory brainstem. In addition, changes in the activity or metabolism of neurons in the cochlear nucleus, superior-olivary complex and inferior colliculus have been observed. In support of this noise-induced change in inner ear biology and pharmacology and its relevance in establishing the TTS, several preclinical studies have demonstrated a significant reduction in TTS when the animals were administered otoprotective compounds or drugs immediately prior to noise exposure.

Characteristics of permanent threshold shift

Noise damage is typically most extensive at frequencies above those of the exposure, a phenomenon well explained by nonlinearities in the cochlear mechanical response to sound. This is most apparent for TTS and for low levels of PTS. However, noises to which human ears are exposed often are broadband in frequency composition.

These signals are shaped (some frequencies amplified, others reduced by filtering) by passage through the external and middle ears. Resonance in the ear canal produces amplification of acoustic frequencies whose wavelengths are approximately 4 times the length of the canal, which for humans results in enhancement of frequencies around 4 kHz. This contributes to an enhanced “notch” of PTS at 4–6 kHz for exposure to broad-band stimuli.

Finally, as with many other forms of damage, the basal cochlea appears to be most vulnerable to noise. While the reason for this is not entirely clear, it may be related to higher levels of antioxidants in apical hair cells as well as higher rates of metabolic activity in basal hair cells. This basal sensitivity results in a tendency for TTS and PTS to be more extensive at high frequencies.

Mechanisms of permanent threshold shift

While intense sounds such as blast can damage the conductive apparatus of the outer and middle ears, producing permanent hearing loss through tympanic membrane rupture or ossicular dislocation, PTS is generally considered to be a sensorineural phenomenon restricted to the cells of the cochlea. The most recognized cause of PTS is damage to and loss of cochlear hair cells. The mechanisms by which this damage can occur are not known with certainty. However, there is extensive evidence implicating the generation of reactive oxygen species (ROS) within hair cells during and after overexposure. This leads to the activation of stress signaling pathways such as the JNK MAP kinase cascade, which can in turn lead to cell damage, apoptosis and/or necrosis. The biochemical pathways leading to hair cell damage/death are undoubtedly complex, and also appear to include competing survival pathways that attempt to rescue hair cells and restore their function. It is the balance of these competing pathways that determine the fate of the cell. The outer hair cells, responsible for the exquisite sensitivity and frequency and selectivity of the cochlea, are the most sensitive to damage.

Noise also can target hair cell synapses and neurons directly, even when the hair cells themselves remain and recover normal function. The insult is seen acutely as a glutamate-like ‘excitotoxicity’ that includes swelling and retraction of afferent terminals from beneath inner hair cells. Recent work in animal models shows that noise-induced loss of synapses and afferent terminals is rapid and permanent. Loss of spiral ganglion neurons is comparatively slow, and can be ‘primary,’ that is, occurring without noise-induced hair cell loss or ‘secondary’ to the loss of their inner hair-cell targets. Such synaptic and neural loss can exacerbate the functional consequences of noise exposure by reducing the ability of the VIIIth nerve to encode auditory signals with fidelity, with or without loss of threshold sensitivity. Thus, lack of PTS does not imply that auditory function is normal.


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