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  1. Lee MK, Hosseini Fouladi M, Narayana Namasivayam S
    Sci Rep, 2018 Oct 18;8(1):15355.
    PMID: 30337652 DOI: 10.1038/s41598-018-33645-y
    An irregular-shaped plate with dimensions identical to a guitar soundboard is chosen for this study. It is well known that the classical guitar soundboard is a major contributor to acoustic radiation at high frequencies when compared to the bridge and sound hole. This paper focuses on using an analytical model to compute the sound power of an unbraced irregular-shaped plate of variable thickness up to frequencies of 5 kHz. The analytical model is an equivalent thin rectangular plate of variable thickness. Sound power of an irregular-shaped plate of variable thickness and with dimensions of an unbraced Torres' soundboard is determined from computer analysis using ANSYS. The number of acoustic elements used in ANSYS for accurate simulation is six elements per wavelength. Here we show that the analytical model can be used to compute sound power of an unbraced irregular-shaped plate of variable thickness.
    Matched MeSH terms: Auditory Pathways
  2. Asha'ari ZA, Mat Zain N, Razali A
    Malays J Med Sci, 2010 Jan;17(1):49-51.
    PMID: 22135526 MyJurnal
    Phonophobia and hyperacusis are two separate but closely related symptoms that are often mistakenly used in clinical practice as the same entity. Here we present a case report to highlight the distinguishing features of both and discuss the steps of management in these conditions. It is vital for the attending doctors to recognise hyperacusis and phonophobia as different entities to manage them successfully.
    Matched MeSH terms: Auditory Pathways
  3. Anandan ES, Husain R, Seluakumaran K
    Atten Percept Psychophys, 2021 May;83(4):1737-1751.
    PMID: 33389676 DOI: 10.3758/s13414-020-02210-z
    Signals containing attended frequencies are facilitated while those with unexpected frequencies are suppressed by an auditory filtering process. The neurocognitive mechanism underlying the auditory attentional filter is, however, poorly understood. The olivocochlear bundle (OCB), a brainstem neural circuit that is part of the efferent system, has been suggested to be partly responsible for the filtering via its noise-dependent antimasking effect. The current study examined the role of the OCB in attentional filtering, particularly the validity of the antimasking hypothesis, by comparing attentional filters measured in quiet and in the presence of background noise in a group of normal-hearing listeners. Filters obtained in both conditions were comparable, suggesting that the presence of background noise is not crucial for attentional filter generation. In addition, comparison of frequency-specific changes of the cue-evoked enhancement component of filters in quiet and noise also did not reveal any major contribution of background noise to the cue effect. These findings argue against the involvement of an antimasking effect in the attentional process. Instead of the antimasking effect mediated via medial olivocochlear fibers, results from current and earlier studies can be explained by frequency-specific modulation of afferent spontaneous activity by lateral olivocochlear fibers. It is proposed that the activity of these lateral fibers could be driven by top-down cortical control via a noise-independent mechanism. SIGNIFICANCE: The neural basis for auditory attentional filter remains a fundamental but poorly understood area in auditory neuroscience. The efferent olivocochlear pathway that projects from the brainstem back to the cochlea has been suggested to mediate the attentional effect via its noise-dependent antimasking effect. The current study demonstrates that the filter generation is mostly independent of the background noise, and therefore is unlikely to be mediated by the olivocochlear brainstem reflex. It is proposed that the entire cortico-olivocochlear system might instead be used to alter the hearing sensitivity during focus attention via frequency-specific modulation of afferent spontaneous activity.
    Matched MeSH terms: Auditory Pathways
  4. Wilson CA, Berger JI, de Boer J, Sereda M, Palmer AR, Hall DA, et al.
    Hear Res, 2019 03 15;374:13-23.
    PMID: 30685571 DOI: 10.1016/j.heares.2019.01.009
    A common method for measuring changes in temporal processing sensitivity in both humans and animals makes use of GaP-induced Inhibition of the Acoustic Startle (GPIAS). It is also the basis of a common method for detecting tinnitus in rodents. However, the link to tinnitus has not been properly established because GPIAS has not yet been used to objectively demonstrate tinnitus in humans. In guinea pigs, the Preyer (ear flick) myogenic reflex is an established method for measuring the acoustic startle for the GPIAS test, while in humans, it is the eye-blink reflex. Yet, humans have a vestigial remnant of the Preyer reflex, which can be detected by measuring skin surface potentials associated with the Post-Auricular Muscle Response (PAMR). A similar electrical potential can be measured in guinea pigs and we aimed to show that the PAMR could be used to demonstrate GPIAS in both species. In guinea pigs, we compare the GPIAS measured using the pinna movement of the Preyer reflex and the electrical potential of the PAMR to demonstrate that the two are at least equivalent. In humans, we establish for the first time that the PAMR provides a reliable way of measuring GPIAS that is a pure acoustic alternative to the multimodal eye-blink reflex. Further exploratory tests showed that while eye gaze position influenced the size of the PAMR response, it did not change the degree of GPIAS. Our findings confirm that the PAMR is a sensitive method for measuring GPIAS and suggest that it may allow direct comparison of temporal processing between humans and animals and may provide a basis for an objective test of tinnitus.
    Matched MeSH terms: Auditory Pathways/physiology
  5. Zilany MS, Bruce IC, Carney LH
    J Acoust Soc Am, 2014 Jan;135(1):283-6.
    PMID: 24437768 DOI: 10.1121/1.4837815
    A phenomenological model of the auditory periphery in cats was previously developed by Zilany and colleagues [J. Acoust. Soc. Am. 126, 2390-2412 (2009)] to examine the detailed transformation of acoustic signals into the auditory-nerve representation. In this paper, a few issues arising from the responses of the previous version have been addressed. The parameters of the synapse model have been readjusted to better simulate reported physiological discharge rates at saturation for higher characteristic frequencies [Liberman, J. Acoust. Soc. Am. 63, 442-455 (1978)]. This modification also corrects the responses of higher-characteristic frequency (CF) model fibers to low-frequency tones that were erroneously much higher than the responses of low-CF model fibers in the previous version. In addition, an analytical method has been implemented to compute the mean discharge rate and variance from the model's synapse output that takes into account the effects of absolute refractoriness.
    Matched MeSH terms: Auditory Pathways/physiology
  6. Dzulkarnain AAA, Noor Ibrahim SHM, Anuar NFA, Abdullah SA, Tengku Zam Zam TZH, Rahmat S, et al.
    Int J Audiol, 2017 Oct;56(10):723-732.
    PMID: 28415891 DOI: 10.1080/14992027.2017.1313462
    OBJECTIVE: To investigate the influence of two different electrode montages (ipsilateral: reference to mastoid and vertical: reference to nape of neck) to the ABR results recorded using a level-specific (LS)-CE-Chirp® in normally hearing subjects at multiple intensities levels.

    DESIGN: Quasi-experimental and repeated measure study designs were applied in this study. Two different stopping criteria were used, (1) a fixed-signal averaging 4000 sweeps and, (2) a minimum quality indicator of Fmp = 3.1 with a minimum of 800 sweeps.

    STUDY SAMPLE: Twenty-nine normally hearing adults (18 females, 11 male) participated.

    RESULTS: Wave V amplitudes were significantly larger in the LS CE-Chirp® recorded from the vertical montage than the ipsilateral montage. Waves I and III amplitudes were significantly larger from the ipsilateral LS CE-Chirp® than from the other montages and stimulus combinations. The differences in the quality of the ABR recording between the vertical and ipsilateral montages were marginal.

    CONCLUSIONS: Overall, the result suggested that the vertical LS CE-Chirp® ABR had a high potential for a threshold-seeking application, because it produced a higher wave V amplitude. The Ipsilateral LS CE-Chirp® ABR, on the other hand, might also have a high potential for the site of lesion application, because it produced larger waves I and III amplitudes.

    Matched MeSH terms: Auditory Pathways/physiology*
  7. Mohd Khairi MD, Normastura AR, Wan Zaharah AW
    Singapore Med J, 2009 Sep;50(9):e324-5.
    PMID: 19787161
    The prevalence of auditory neuropathy is not known, although the majority of cases are felt to lie within the population of neonatal intensive care unit graduates. We report three cases of auditory neuropathy, out of 211 children with sensorineural hearing loss, seen at our audiology clinic from April 1, 1999 to December 31, 2003. Two patients did not have a risk factor for hearing impairment. Screening policies based solely on transient evoked otoacoustic emissions testing will not detect auditory neuropathy effectively, and may falsely reassure parents and professionals unaware of this condition.
    Study site: Audiology clinic, Hospital Universiti Sains Malaysia, Kelantan, Malaysia
    Matched MeSH terms: Auditory Pathways/physiopathology
  8. Dewey RS, Francis ST, Guest H, Prendergast G, Millman RE, Plack CJ, et al.
    Neuroimage, 2020 01 01;204:116239.
    PMID: 31586673 DOI: 10.1016/j.neuroimage.2019.116239
    In animal models, exposure to high noise levels can cause permanent damage to hair-cell synapses (cochlear synaptopathy) for high-threshold auditory nerve fibers without affecting sensitivity to quiet sounds. This has been confirmed in several mammalian species, but the hypothesis that lifetime noise exposure affects auditory function in humans with normal audiometric thresholds remains unconfirmed and current evidence from human electrophysiology is contradictory. Here we report the auditory brainstem response (ABR), and both transient (stimulus onset and offset) and sustained functional magnetic resonance imaging (fMRI) responses throughout the human central auditory pathway across lifetime noise exposure. Healthy young individuals aged 25-40 years were recruited into high (n = 32) and low (n = 30) lifetime noise exposure groups, stratified for age, and balanced for audiometric threshold up to 16 kHz fMRI demonstrated robust broadband noise-related activity throughout the auditory pathway (cochlear nucleus, superior olivary complex, nucleus of the lateral lemniscus, inferior colliculus, medial geniculate body and auditory cortex). fMRI responses in the auditory pathway to broadband noise onset were significantly enhanced in the high noise exposure group relative to the low exposure group, differences in sustained fMRI responses did not reach significance, and no significant group differences were found in the click-evoked ABR. Exploratory analyses found no significant relationships between the neural responses and self-reported tinnitus or reduced sound-level tolerance (symptoms associated with synaptopathy). In summary, although a small effect, these fMRI results suggest that lifetime noise exposure may be associated with central hyperactivity in young adults with normal hearing thresholds.
    Matched MeSH terms: Auditory Pathways/physiology*
  9. Islam, M.R., Muzaimi, M., Abdullah, J.M.
    Orient Neuron Nexus, 2011;2(1):2-9.
    MyJurnal
    Glutamate is the principal excitatory neurotransmitter in the central nervous system, and plays important roles in both physiological and pathological neuronal processes. Current understanding of the exact mechanisms involved in glutamate-induced neuronal excitotoxicity, in which excessive glutamate causes neuronal dysfunction and degeneration, whether acute or chronic, remain elusive. Conditions, due to acute insults such as ischaemia and traumatic brain injury, and chronic neurodegenerative disorders such as multiple sclerosis and motor neuron disease, suffer from the lack of translational neuroprotection in clinical setting to tackle glutamate excitotoxicity despite steady growth of animal studies that revealed complex cell death pathway interactions. In addition, glutamates are also released by non-neuronal cells including astrocytes and oligodendroglia. Thus, attempts to elucidate this complexity are closely related to our understanding of the glutamatergic circuitry in the brain. Neuronal cells develop a glutamatergic system at glutamatergic synapses that utilise glutamate as an intercellular signaling molecule to characterise the output, input, and termination of this signaling. As to signal input, various kinds of glutamate receptors have been identified and characterized. Na+-dependent glutamate transporters at the plasma membrane are responsible for the signal termination through sequestration of glutamate from the synaptic cleft. The signal output systems comprise vesicular storage and subsequent exocytosis of glutamate by using vesicular glutamate transporters. Similar to the mammalian brain, the regional differences of glutamatergic neurons and glutamate receptor neurons suggest many glutamatergic projections in the avian brain, as supported by recent evidence of glutamate-related genes distribution. Glutamatergic target areas are expected to show high activity of glutamate transporters that remove released glutamate from the synaptic clefts. This review summarises and compares glutamatergic circuits in the avian and mammalian brain, particularly in the olfactory pathway, the paffial organization of glutamatergic neurons and connection with the striatum, hippocampal-septal pathway, visual and auditory pathways, and granule cell-Purkinje cell pathway in the cerebellum. Comparative appreciation of these glutamatergic circuits, particularly with the localisation and/or expression of specific subtypes of glutamate transporters, would provide the morphological basis for physiological and pharmacological designs that supplement existing animal studies of the current proposed mechanisms that underlie glutamate-induced neuronal excitotoxicity.
    Matched MeSH terms: Auditory Pathways
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