- Increased spontaneous firing rates in auditory midbrain following noise exposure are specifically abolished by a Kv3 channel modulator. [Journal Article]
- HRHear Res 2018 Apr 30
- Noise exposure has been shown to produce long-lasting increases in spontaneous activity in central auditory structures in animal models, and similar pathologies are thought to contribute to clinical ...
Noise exposure has been shown to produce long-lasting increases in spontaneous activity in central auditory structures in animal models, and similar pathologies are thought to contribute to clinical phenomena such as hyperacusis or tinnitus in humans. Here we demonstrate that multi-unit spontaneous neuronal activity in the inferior colliculus (IC) of mice is significantly elevated four weeks following noise exposure at recording sites with frequency tuning within or near the noise exposure band, and this selective central auditory pathology can be normalised through administration of a novel compound that modulates activity of Kv3 voltage-gated ion channels. The compound had no statistically significant effect on IC spontaneous activity without noise exposure, nor on thresholds or frequency tuning of tone-evoked responses either with or without noise exposure. Administration of the compound produced some reduction in the magnitude of evoked responses to a broadband noise, but unlike effects on spontaneous rates, these effects on evoked responses were not specific to recording sites with frequency tuning within the noise exposure band. Thus, the results suggest that modulators of Kv3 channels can selectively counteract increases in spontaneous activity in the auditory midbrain associated with noise exposure.
- Blast-induced hearing loss. [Letter]
- JZJ Zhejiang Univ Sci B 2017 Oct 18
- The incidence of blast injury has increased recently. As the ear is the organ most sensitive to blast overpressure, the most frequent injuries seen after blast exposure are those affecting the ear. B...
The incidence of blast injury has increased recently. As the ear is the organ most sensitive to blast overpressure, the most frequent injuries seen after blast exposure are those affecting the ear. Blast overpressure affecting the ear results in sensorineural hearing loss, which is untreatable and often associated with a decline in the quality of life. Here, we review recent cases of blast-induced hearing dysfunction. The tympanic membrane is particularly sensitive to blast pressure waves, since such waves exert forces mainly at air-tissue interfaces within the body. However, treatment of tympanic membrane perforation caused by blast exposure is more difficult than that caused by other etiologies. Sensorineural hearing dysfunction after blast exposure is caused mainly by stereociliary bundle disruption on the outer hair cells. Also, a reduction in the numbers of synaptic ribbons in the inner hair cells and spiral ganglion cells is associated with hidden hearing loss, which is strongly associated with tinnitus or hyperacusis.
- Psychometric Properties and Factor Structure of a New Scale to Measure Hyperacusis: Introducing the Inventory of Hyperacusis Symptoms. [Journal Article]
- EHEar Hear 2018 May 08
- CONCLUSIONS: These initial results demonstrated sound statistical properties of the IHS and usefulness as a hyperacusis measurement tool in research and clinical practice. Factor structure and scale dimensions allow for differentiation between subtypes of loudness, annoyance, fear, and pain based on responses to clusters of specific items within the dimensional factor structure of the scale, and may thus prove useful in clinical practice and research.
- Uncomfortable loudness levels among children and adolescents seeking help for tinnitus and/or hyperacusis. [Journal Article]
- IJInt J Audiol 2018 Apr 24; :1-6
- CONCLUSIONS: Among children and adolescents seen at an audiology outpatient clinic for tinnitus and hyperacusis, hyperacusis diagnosed on the basis of ULLs is very prevalent and it is often characterised by lower ULLs at 8 than at 0.25 kHz.
- Evaluation of selective attention in patients with misophonia. [Journal Article]
- BJBraz J Otorhinolaryngol 2018 Mar 21
- CONCLUSIONS: The misophonia participants presented a lower percentage of correct responses in the dichotic sentence identification test with chewing sound; suggesting that individuals with misophonia may have selective attention impairment when they are exposed to sounds that trigger this condition.
- Long-Term Effects of Middle Ear Tendon Resection on Middle Ear Myoclonic Tinnitus, Hearing, and Hyperacusis. [Journal Article]
- ANAudiol Neurootol 2018 Apr 12; 22(6):343-349
- CONCLUSIONS: METR seems to be an effective and safe treatment option for intractable MEMT, considering its high control rate of tinnitus and no long-term harmful effects on hearing and hyperacusis.
- Blast Exposure Disrupts the Tonotopic Frequency Map in the Primary Auditory Cortex. [Journal Article]
- NNeuroscience 2018 May 21; 379:428-434
- Blast exposure can cause various auditory disorders including tinnitus, hyperacusis, and other central auditory processing disorders. While this is suggestive of pathologies in the central auditory s...
Blast exposure can cause various auditory disorders including tinnitus, hyperacusis, and other central auditory processing disorders. While this is suggestive of pathologies in the central auditory system, the impact of blast exposure on central auditory processing remains poorly understood. Here we examined the effects of blast shockwaves on acoustic response properties and the tonotopic frequency map in the auditory cortex. We found that multiunits recorded from the auditory cortex exhibited higher acoustic thresholds and broader frequency tuning in blast-exposed animals. Furthermore, the frequency map in the primary auditory cortex was distorted. These changes may contribute to central auditory processing disorders.
- Acoustic Trauma Changes the Parvalbumin-Positive Neurons in Rat Auditory Cortex. [Journal Article]
- NPNeural Plast 2018; 2018:9828070
- Acoustic trauma is being reported to damage the auditory periphery and central system, and the compromised cortical inhibition is involved in auditory disorders, such as hyperacusis and tinnitus. Par...
Acoustic trauma is being reported to damage the auditory periphery and central system, and the compromised cortical inhibition is involved in auditory disorders, such as hyperacusis and tinnitus. Parvalbumin-containing neurons (PV neurons), a subset of GABAergic neurons, greatly shape and synchronize neural network activities. However, the change of PV neurons following acoustic trauma remains to be elucidated. The present study investigated how auditory cortical PV neurons change following unilateral 1 hour noise exposure (left ear, one octave band noise centered at 16 kHz, 116 dB SPL). Noise exposure elevated the auditory brainstem response threshold of the exposed ear when examined 7 days later. More detectable PV neurons were observed in both sides of the auditory cortex of noise-exposed rats when compared to control. The detectable PV neurons of the left auditory cortex (ipsilateral to the exposed ear) to noise exposure outnumbered those of the right auditory cortex (contralateral to the exposed ear). Quantification of Western blotted bands revealed higher expression level of PV protein in the left cortex. These findings of more active PV neurons in noise-exposed rats suggested that a compensatory mechanism might be initiated to maintain a stable state of the brain.
- Aggressiveness, violence, homicidality, homicide, and Lyme disease. [Journal Article]
- NDNeuropsychiatr Dis Treat 2018; 14:693-713
- CONCLUSIONS: LD and the immune, biochemical, neurotransmitter, and the neural circuit reactions to it can cause impairments associated with violence. Many LD patients have no aggressiveness tendencies or only mild degrees of low frustration tolerance and irritability and pose no danger; however, a lesser number experience explosive anger, a lesser number experience homicidal thoughts and impulses, and much lesser number commit homicides. Since such large numbers are affected by LD, this small percent can be highly significant. Much of the violence associated with LD can be avoided with better prevention, diagnosis, and treatment of LD.
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- Prolonged Exposure of CBA/Ca Mice to Moderately Loud Noise Can Cause Cochlear Synaptopathy but Not Tinnitus or Hyperacusis as Assessed With the Acoustic Startle Reflex. [Journal Article]
- THTrends Hear 2018 Jan-Dec; 22:2331216518758109
- Hearing loss changes the auditory brain, sometimes maladaptively. When deprived of cochlear input, central auditory neurons become more active spontaneously and begin to respond more strongly and syn...
Hearing loss changes the auditory brain, sometimes maladaptively. When deprived of cochlear input, central auditory neurons become more active spontaneously and begin to respond more strongly and synchronously to better preserved sound frequencies. This spontaneous and sound-evoked central hyperactivity has been postulated to trigger tinnitus and hyperacusis, respectively. Localized hyperactivity has also been observed after long-term exposure to noise levels that do not damage the cochlea. Adult animals exposed to bands of nondamaging noise exhibited suppressed spontaneous and sound-evoked activity in the area of primary auditory cortex (A1) stimulated by the exposure band but had increased spontaneous and evoked activity in neighboring A1 areas. We hypothesized that the cortically suppressed frequencies should for some time after exposure be perceived as less loud than before (hypoacusis), whereas the hyperactivity outside of the exposure band might lead to frequency-specific hyperacusis or tinnitus. To investigate this, adult CBA/Ca mice were exposed for >2 months to 8 to 16 kHz noise at 70 or 75 dB sound pressure level and tested for hypo-/hyperacusis and tinnitus using tone and gap prepulse inhibition of the acoustic startle reflex. Auditory brainstem responses and distortion product otoacoustic emissions showed evidence of cochlear synaptopathy after exposure at 75 but not 70 dB, putting a lower bound on damaging noise levels for CBA/Ca mice. Contrary to hypothesis, neither exposure significantly shifted startle results from baseline. These negative findings nevertheless have implications for startle test methodology and for the putative role of central hyperactivity in hyperacusis and tinnitus.