Noise Flashcards
Murillo-Cuesta et al. (2009)
Murillo-Cuesta et al. (2009) compared albino mice to mice with melanin precursors (such as L-DOPA) and found that the albino mice experience a higher incidence of profound hearing loss and have poorer recovery of thresholds after noise exposure.
(Chen et al., 1977; Morioka et al., 1977)
Gratton et al., 1990
Two ototoxic medications that have synergistic effects with noise on hearing include gentamicin (Chen et al., 1977; Morioka et al., 1977) and cisplatin (Gratton et al., 1990).
(Kujawa & Liberman, 2009) Introduction
Noise can lead to the presence of increased reactive oxygen species and toxic free radicals; there is extensive evidence implicating the generation of reactive oxygen species (ROS) within hair cells during and after overexposure (Kujawa & Liberman, 2009).
(Pirvola et al., 2000)
Bohne, Harding, & Lee, 2007
Noise can lead to the presence of increased reactive oxygen species and toxic free radicals; there is extensive evidence implicating the generation of reactive oxygen species (ROS) within hair cells during and after overexposure (Kujawa & Liberman, 2009). This leads to the activation of stress signaling pathways such as the JNK MAP kinase cascade (Pirvola et al., 2000), which can in turn lead to cell damage, apoptosis and/or necrosis (Bohne, Harding, & Lee, 2007).
Fetoni et al. (2015)
Fetoni et al. (2015) conducted a study in rats that investigated the effects of antioxidant treatment in animals that were exposed to noise. The authors hypothesized that if noise causes cochlear oxidative imbalance, then use of antioxidant treatments may be able to reduce the effects of noise. The results suggest that antioxidant protection does prevent noise-exposed rats from acquiring hearing loss due to noise. This is important to the patient who wants to prevent hearing loss, since cochlear oxidative stress may lead to damaged outer hair cells, cochlear synaptopathy, and degeneration of the spiral ganglion neurons, which then has implications for alterations in the morphology of the auditory cortex.
Harris, Bielefeld, and Henderson (2006)
Antioxidant levels can be increased in the cochlea endogenously and/or exogenously. Endogenous increases in antioxidant levels can occur with sound conditioning. According to Harris, Bielefeld, and Henderson (2006), sound conditioning by exposure to low-level noise endogenously increases the availability of antioxidant enzymes in the cochlea; as such, increased antioxidant levels from prophylactic sound conditioning can protect the ear against oxidative stress induced by traumatic noise exposure. This study put experimental group chinchillas through a sound conditioning regimen and then introduced the animals to Paraquat (a generator of superoxide). Compared to control animals that did not undergo sound conditioning, significantly less damage (e.g. threshold shifts and inner hair cell loss) occurred for the animals who received the sound conditioning treatment.
(Campbell et al., 2007)
Exogenous increases of antioxidant levels in the cochlea can be accomplished through application either directly onto the cochlea or systemically into the body. For example, antioxidant levels can be increased with the ingestion or uptake of significant amounts of D-methionine (Campbell et al., 2007). D-methionine functions as a reactive oxygen species scavenger. By reducing reactive oxygen species, production of nitric oxide (an antioxidant) is stimulated and provides a significant protective effect on sensory cells. Second, D-methionine increases the intracellular presence of another antioxidant, mitochondrial glutathione; as a result, the usual efflux of glutathione from the cell that can occur because of cellular injury is avoided, which is significant, since the probability of hair cell survival after noise exposure is related to mitochondrial function.
(Claussen et al., 2013)
In a chinchilla model, D-met administration in advance of noise-exposure (2-3 days), without subsequent administration, significantly protected the animals from noise-induced ABR threshold shift and OHC loss (Claussen et al., 2013).
Kujawa and Liberman (2009).
The presence of clinically normal pure-tone thresholds in conjunction with patient reports of trouble hearing in noise or other difficult environments is likely a reflection of cochlear synaptopathy and related degeneration in the auditory system that is described by Kujawa and Liberman (2009). This research suggests that exposure to noise levels which cause temporary threshold shifts may leave cochlear hair cells intact, yet trigger long-term metabolic changes, such as delayed degeneration of the auditory nerve secondary to a loss of afferent nerve terminals. This concept was evaluated in a CBA/CaJ mouse model using clinical measures, as well as cochlear functional assays and confocal imaging of the inner ear. At 16 weeks old, experimental mice were exposed to an 8-16 kHz octave band of noise at 100 dB SPL for 2 hours to induce a temporary threshold shift. At 1 day, 3 days, 2 weeks, and 8 weeks post noise exposure, distortion product otoacoustic emissions (DPOAEs) and auditory brainstem response (ABR) measures were obtained. From these data, it was apparent that thresholds for DPOAEs and ABRs returned to baseline within 2 weeks. However, supra-threshold ABR data, particularly for wave I, did not demonstrate a total recovery in response to high frequencies. This permanent attenuation of responses is consistent with the loss of neurons in some regions of the cochlea. The fibers affected by this degree of noise exposure are suspected to be low spontaneous rate/high threshold fibers, which are utilized in auditory system in response to loud level inputs (rather than inputs near threshold).
(Ruggles, Bharadwaj, & Shinn-Cunningham, 2011)
Clinical audiometry measures utilized in routine testing are not sensitive to the loss of ribbon synapses and delayed degeneration of the auditory nerve fibers from noise exposure. With intact cochlear hair cells, threshold measures are not expected to worsen significantly, and thresholds of audibility often used to define “normal hearing” in the clinic do not capture important differences in basic sensory encoding that have important consequences for communicating in everyday situations (Ruggles, Bharadwaj, & Shinn-Cunningham, 2011).
(e.g. Kujawa & Lieberman, 2009; Furman, Kujawa, & Lieberman, 2013)
This body of literature (e.g. Kujawa & Lieberman, 2009; Furman, Kujawa, & Lieberman, 2013) suggests the use of non-threshold measures for a screening procedure to evaluate a patient’s performance when cochlear synaptopathy is suspected.
Gallun et al. (2012)
Gallun et al. (2012) tested blast-exposed participants on a battery of behavioral and electrophysiological assessments and found that the blast-exposed participants performed abnormally with reference to normative values established as the mean performance on each test by the control subjects plus or minus two standard deviations; these results were noted on measures of Gaps-In-Noise, Masking Level Difference, Staggered Spondaic Words, and the Quick Speech-In-Noise tests. These results suggest that, for some patients, blast exposure may lead to difficulties with hearing in complex auditory environments, even when peripheral hearing sensitivity is near normal limits.
(Kujawa & Lieberman, 2009)
suggest a screening protocol
Additionally, the use of ultra-high frequency pure-tone testing and otoacoustic emissions testing may reveal a decrease in sensitivity prior to a shift in standard audiometric assessment may reveal a decrease in sensitivity, which is consistent with animal model findings of cochlear synaptopathy and may provide additional information about the integrity of the cochlea and auditory nerve. (Kujawa & Lieberman, 2009).
What are the implications of delayed effects of noise for treatment, both from a pharmacologic perspective?
Unexpected high level noise exposure can occur in certain professions (emergency workers, miners, military personnel), for recreational exposure (concerts and power equipment), or from protective mechanisms in everyday life (air bag deployment and alarm systems). Pharmacological, it may be possible to protect against permanent ABR threshold shift and OHC loss up to a certain amount of time after noise exposure through injections of ingestion of certain antioxidants or other biochemical compounds.
What are the implications of delayed effects of noise for treatment, both from an AR perspective?
From an aural rehabilitation perspective, with delayed effects, the association between a harmful experience (unprotected exposure to loud noise levels) and its ramifications (increased difficulty understanding speech in noise) is lost. Additionally, clinicians can not predict the degree to which or timespan over which a patient’s hearing will progress after noise exposure, making interventions and counseling more difficult. But if we can prevent these delayed effects of noise from occurring, less people may require hearing aids, cochlear implants or other assistive technology to communicate effectively and there may be a reduced burden of these experiences on the quality of life of affected individuals.
