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Sensorineural Hearing Loss
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Linnea Cheung, David M. Baguley, Andrew McCombe
Initially, excessive noise exposure causes a temporary threshold shift (TTS), resulting in a temporary HL. The high-frequency regions of the cochlea are most sensitive (between 3 and 6 kHz). Recovery of the TTS occurs over hours, days, or weeks following exposure. Expected recovery time is dependent on the loudness and duration of the noise presented. However, a permanent threshold shift (PTS) can occur at the initial insult, or it may evolve where there is continuous or repeated excessive noise exposure at levels that would only have otherwise caused a TTS. It is thought that this may be caused by metabolic factors such as excessive neurotransmitter release, changes in cochlear blood flow, and oxidative stress within the hair cells. Structural factors like depolymerisation of actin filaments in the stereocilia, swelling of the stria vascularis, and damage to afferent nerve endings and supporting cells are also thought to play a part. Synaptic connections between inner hair cells and spiral ganglion cells may also be susceptible to noise damage. Importantly, in animal studies, these synapses can be the first site of damage, even without an HL (‘hidden hearing loss’, or synaptopathy). Additionally, genetic susceptibility, smoking and cardiovascular disease, and diabetes have been implicated as risk factors.
Effect of Noise Exposure on Human Auditory Function: Hidden Versus Not-So-Hidden Hearing Loss
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Early experiments in which noise-induced synaptopathy was first described used noise exposures that produced a relatively large TTS even at 24-h after the noise exposure. In studies in which TTS was 40–50 dB at the most affected frequencies, the day after the noise exposure, a significant decrease in the number of synaptic connections between the IHCs and the afferent neurons was shown, with data obtained both from mice (Fernandez et al., 2015; Kujawa and Liberman, 2009; Wang and Ren, 2012) and from guinea pigs (Furman et al., 2013; Lin et al., 2011). In general, the exposure paradigms have used 100 dB SPL octave-band noise for 2 h in mouse models, and 106 dB SPL octave-band noise for 2 h in guinea pig models. There is one report of synaptopathy in a mouse model subsequent to 1-week long exposure to 84-dB SPL (Maison et al., 2013). However, the interpretation of those data has been questioned based on both the small number of control animals in which synapse counts were completed, and the differences between the control animals in that study and larger numbers of control animals from the same mouse strain that were used in other studies from the same laboratory [see Le Prell and Brungart (2016), and Spankovich et al. (2014)].
Acute Acoustic Trauma and Blast-Related Hearing Loss
Published in Mansoor Khan, David Nott, Fundamentals of Frontline Surgery, 2021
Jameel Muzaffar, Christopher Coulson, Jonathan D. E. Lee, Linda E. Orr
Some consider a TTS of up to 50 dB may recover completely, though this opinion is far from universal and controversy exists as to the length of time at which a change should be classified as a PTS. Most TTS recovery is expected within 16–24 hours, but animal studies have shown improvement up to three weeks post-exposure. More recent animal studies (mice, rats, chinchillas, and non-human primates) have shown that even in animals, following noise exposure where complete recovery of hearing thresholds has been noted, histological examination of the cochlear demonstrates the loss of up to 90% of the synapses between the inner hair cell and the spiral ganglion neurone (the first part of the auditory nerve). This suggests that the idea that a TTS is harmless may not be true and, if this is correct, current health and safety guidelines regarding safe levels and durations of exposure are based on a misconception. Second, whilst outer hair cells are responsible for amplification within the cochlea, it is the inner hair cell/spiral ganglion area that is responsible for the encoding of complex signals, such as speech in background noise. Poor-quality encoding due to injury at this synapse could explain the tinnitus and hyperacusis often associated with blast injury – as a result of increased central gain – as a compensatory mechanism for impaired encoding. Human studies looking for ‘Hidden Hearing Loss’ – Cochlear Synaptopathy, as it is more accurately termed – have not yet provided any firm evidence and studies, including that of Armed Forces personnel are ongoing. It may be that humans are more resistant to this phenomenon than animals, but it is more likely that either current test measures are not sensitive enough to detect synaptopathy without histological analysis of the temporal bone or that the civilian populations studied so far have not had sufficient noise exposure to induce it. Improved understanding of the site of lesion within the auditory pathway is an essential stepping stone to the validation of novel therapeutics that are currently in animal and early phase human trials for the regeneration of inner ear structures, or for pharmacological protection of structures prior to noise exposure.
Listening effort in individuals with noise-induced hearing loss
Published in Hearing, Balance and Communication, 2022
Hemanth Narayan Shetty, Suma Raju, Yashwanth Kumar, Sanjana S. Singh
Furthermore, the correlation analysis revealed a significant strong positive relation between recall and repeat scores. This indicated that the recall score was reduced with a decrease in recognition score. It was seen in both groups, but it was more pronounced in the NIHL group. It can thus be inferred that any condition making the primary task difficult results in less spare mental capacity to perform the secondary task. The performance of the primary task (repeat score) tells us the effort the listeners have to put in on the secondary task (recall). Thus, the alternative hypothesis is accepted where a person exposed to noise expends more effort in listening to understand speech because of the competencies of the cognitive capacities (metal and spare capacity) are affected by the exposure to noise over a prolonged period. To conclude, synaptopathy can coexist with some degree of measurable hearing loss and the individuals can exhibit deficits in suprathreshold testing. Thus, at an early stage, individuals with noise exposure often complain of difficulty understanding speech. A test to assess listening effort can be included in the test battery to assess ease of communication among individuals who are exposed to noise.
Speech perception in noise, gap detection and amplitude modulation detection in suspected hidden hearing loss
Published in Hearing, Balance and Communication, 2021
Srikar Vijayasarathy, Meghana Mohan, Pratibha Nagalakshmi, Animesh Barman
Perceptual effects of possible synaptopathy, however, have remained ambiguous due to differing findings reported in the literature. Some studies in humans suggest that synaptopathy can lead to speech perception in noise deficits [23–25]. Affected phoneme discrimination [26] and deviant hemispheric lateralization [27] have also been reported in noise-exposed subjects. Poorer signal detection in noise has been observed in the frequency ranges associated with a permanent reduction in wave I amplitude in mice exposed to neuropathic noise [28]. However, many other studies have not reported a correlation between noise exposure and speech perception in noise [9,29–32]. Valderrama et al. [8] reported a positive correlation between wave I amplitude and speech in noise perception, but not with noise exposure itself. Grose et al. [33] also reported a tendency for a reduced wave I amplitude in those with frequent attendance of music venues but did not report any perceptual consequences. Similarly, while some studies suggest poorer temporal processing, phase-locking ability, and delayed latencies of onset responses in those exposed to noise [12,24,34,35], many others do not support this conclusion [29,30,33].
ABR findings in musicians with normal audiogram and otoacoustic emissions: evidence of cochlear synaptopathy?
Published in Hearing, Balance and Communication, 2020
Dimitrios Kikidis, Aikaterini Vardonikolaki, Zoe Zachou, Andriana Razou, Pavlos Pantos, Athanasios Bibas
Findings from studies attempting to investigate the existence of synaptopathy in humans are inconclusive [15]. Possible factors include different measurement settings, possible reduced synaptic vulnerability in humans compared to animals, insufficient noise exposure (either in terms of intensity or time of exposure) to induce either detectable or clinically evident synaptopathy, existence of synaptopathy in normal population (and thus difficulty in detecting small differences) and confounding effect of co-existing OHC functional pathology [15]. The main hypothesis of this study is that the possible existence of synaptopathy might be reflected in different electrophysiological responses when different stimuli presentation rates are used. The rational is that apparently ABR normal responses in cases of CS may become abnormal at high stimulation rates. One of the main findings in our study is that there was a significantly greater reduction in wave I amplitude as well as in wave Ι/V amplitude ratio as the stimulus presentation rate increased from 11/s to 33/s in musicians compared to the CG, which supports this hypothesis.