182 research outputs found

    Chapitre V: Etiologies non génétiques

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    This chapter reviews the numerous non-genetic risk factors and medical conditions known to be potentially associated with an Auditory Neuropathy/Auditory Dys-synchrony. Among the most frequently cited conditions, one finds prematurity and its many complications, perinatal hypoxia and neonatal hyperbilirubinaemia. The latter condition may cause a reversible Auditory Neuropathy/Auditory Dys-synchrony. When contemplating the list of the diverse other conditions ranging from cochlear nerve agenesis to paramyxovirus infections and Refsum's disease, it clearly appears that Auditory Neuropathy/Auditory Dys-synchrony is far from being a single morbid entity. This label indicates a peculiar profile of psycho-acoustic and physiological anomalies having in common a deficit in the temporal representation of auditory stimuli at the level of the cochlear nerve.SCOPUS: re.jinfo:eu-repo/semantics/publishe

    Chapitre II: Bilan fonctionnel neurophysiologique

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    This chapter reviews the respective contributions of three categories of evoked responses to the evaluation of Auditory Neuropathy/Auditory Dys-synchrony. 1. Short-latency evoked potentials and Oto-Acoustic Emissions. The definite diagnosis of Auditory Neuropathy/Auditory Dys-synchrony relies on an operational definition which requires the demonstration of profoundly altered Auditory Brainstem Responses including wave I, combined with preserved physiological response of Outer Hair Cells. When Oto-Acoustic Emissions are present the latter condition is easy to document In practice however, emissions are often absent, either because of abnormal middle ear status or because they disappear as disease progresses. This means that in many cases the presence of an isolated Cochlear Microphonic Potential is the only remaining clue to the correct diagnosis. This chapter explains and illustrates the various recording strategies that contribute to a correct detection and identification of the Cochlear Microphonic Potential. These include: a. Systematic comparison of both acoustic polarities of the stimulus. b. Stimulus delivery incorporating an acoustic delay in order to avoid confusion with electromagnetic artifacts radiated by the transducer. c. Checking the pre-synaptic nature of the recorded signal i.e. a fixed latency across intensities, the absence of adaptation to high stimulation rates and persistence in presence of masking noise. 2. Long-Latency cortical Evoked Potentials. Some data suggest that they could, when preserved, be associated with a less severe form of desynchronization and be associated with a favourable response to conventional amplification. 3. Auditory Steady Stats Evoked Potentials. They can be absent, but in most cases are obtained at intensities for which the brainstem potentials are absent, thus adding another type of paradoxical result to the overall picture. However, behavioural thresholds cannot be reliably estimated from neurophysiological ones.SCOPUS: re.jinfo:eu-repo/semantics/publishe

    Etude neurophysiologique de la déficience auditive chez l'Homme: vers une optimalisation de l'usage des potentiels de courte latence évoqués par des clics

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    Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe

    LES OTO-EMISSIONS ACOUSTIQUES ET LEURS RELATIONS AVEC LES ACOUPHENES

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    SCOPUS: NotDefined.jinfo:eu-repo/semantics/publishe

    Chapitre I: La neuropathie auditive / désynchronisation auditive: Définition et généralités

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    The term Auditory Neuropathy was coined by Starr et al. in 1996 to label a peculiar hearing disorder due to poor synchronization of neural activity in the cochlear nerve. Since selective Inner Hair Cells loss or defects of the synapse between these cells and the cochlear nerve can lead to similar signs and symptoms, the condition is now referred to as Auditory Neuropathy/ Auditory Dys-synchrony. The condition reveals itself through a series of paradoxical findings distinguishing it from the usual cochlear hearing losses. Speech comprehension scores are typically poorer than those predicted from the audiograms. Auditory Brainstem Responses (including wave I) cannot be obtained to supra-threshold clicks and Outer Hair Cell responses (Cochlear Microphonic potential and/or Oto-Acoustic Emissions) are preserved despite threshold values associated with the abolition of the Oto-Acoustic Emissions in usual cochlear hearing losses. Estimations of prevalence in the population with confirmed Hearing Loss range from 4 to 11%.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

    Négativité de discordance et mécanismes de perception de la parole

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    info:eu-repo/semantics/nonPublishe
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