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Cochlear Implants and Auditory Brainstem Implants
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
Rajeev Mathew, Deborah Vickers, Patrick Axon, Manohar Bance
Assessment should be performed by a multidisciplinary team including but not limited to surgeons, audiologists and rehabilitationists. It is crucial that patients have realistic expectations of their hearing outcome and adequate pre-operative counselling is necessary. Behavioural audiological assessment involves age appropriate assessment of hearing thresholds and in adults also includes word recognition tests. This can be supplemented with objective measurements including otoacoustic emissions (assessment of auditory neuropathy spectrum disorder; see Chapter 16), auditory brainstem responses (ABRs; for hearing threshold estimation; see Chapter 4) and auditory cortical responses (for assessing benefit from hearing aids; see Chapter 4). This is particularly important in young children and in patients with suspected non-organic hearing loss. Transtympanic electrocochleography is occasionally used in patients in whom there is concern about the presence/function of the cochlear nerve.
Current and Emerging Clinical Applications of the auditory Steady-State Response
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Rance et al. (2005) generalized ASSR findings into four different categories. First, correlation of ASSR and behavioral hearing threshold was high (0.96–0.98) for stimulus frequencies of 500–4000 Hz. Second, the correlation of ASSR versus pure tone thresholds was rather poor for children with diagnosis of auditory neuropathy spectrum disorder (ANSD) (0.46–0.55). Third, as already noted, ASSR usually overestimates thresholds in normal hearers. Finally, hearing threshold estimation improves with the degree of hearing loss. He also pointed out that the ASSR threshold for normal hearers was significantly higher than tone burst ABR thresholds. Therefore, ASSR cannot differentiate normal hearers with those with mild to moderate hearing loss (Rance et al., 2005).
Hearing Aids for the Pediatric Population
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Katia de Almeida, Maria Cecíli Martinelli
Children with auditory neuropathy spectrum disorder (ANSD) should have an amplification trial as soon as it can be established that: (i) hearing sensitivity is sufficiently poor; and (ii) speech at conversational levels is noteasily audible. Based on the potential for improved speech recognition and the difficulty in predicting hearing aid benefit from audiological characteristics, a trial with an appropriately fit amplification for ANSD children is recommended, prior to a candidacy evaluation for a cochlear implant. Until hearing thresholds can reliably be established, careful observation of the responsiveness of the child to sounds while wearing hearing aids is essential, with adjustments to the degree of amplification as necessary (AAA, 2013).
Auditory brainstem responses obtained with randomised stimulation level
Published in International Journal of Audiology, 2023
Marta Martinez, Joaquin T. Valderrama, Isaac M. Alvarez, Angel de la Torre, Jose L. Vargas
Tracking the ABR components as a function of the stimulus level can be of particular interest to visually determine the presence of a neurophysiological response in complex scenarios where the ABR morphology diverges from standard patterns, such as (i) in individuals with hearing loss (whose ABR components are delayed and present a smaller amplitude; Hall, 2007; Sininger, 2007); (ii) in individuals with auditory central nervous system disorders, including acoustic neuroma (where ABRs present prolonged waves I–V interpeak latencies compared to the normal-appearing ABR; Naito et al., 1999) and auditory neuropathy spectrum disorder (present cochlear microphonics but absent or severely abnormal ABRs; Hood, 2007); or (iii) when ABRs are elicited by an electrical stimulus (where ABRs are substantially distorted by the electrical artefact and the latency of their components is shorter; Hey et al., 2007).
Agreement/disagreement between caloric and video head impulse tests: does it reveal something? Report from three individuals with auditory neuropathy spectrum disorder
Published in Hearing, Balance and Communication, 2019
Sujeet Kumar Sinha, Shalini Bansal, Anuj Kumar Neupane
Auditory neuropathy spectrum disorder (ANSD) is characterized as abnormal or absent auditory brainstem responses (ABRs), with presence of otoacoustic emissions (OAEs) and/or cochlear microphonics, absence of acoustic reflexes, puretone hearing loss that could vary from normal to profound hearing loss with poor speech identification score disproportionate to the degree of hearing loss [1]. The abnormality in ANSDcould be at the level of the inner hair cells, the synapse between inner hair cells and cochlear nerve fibers, the spiral ganglions, or may be a combination of all of the above [2].The possible etiologies of ANSD include neonatal illnesses such as prematurity, low birth weight, anoxia, hyperbilirubinemia ischemic-hypoxic neuropathy, and other hereditary sensory motor neuropathies [2,3].
Evolving the concept of APD
Published in International Journal of Audiology, 2018
An example of using a spectral approach to advance the conceptualisation of an auditory disorder can be seen in auditory neuropathy spectral disorder (ANSD). While the original concept of auditory neuropathy was reconceptualised as ANSD in the 1990s, Rance and Starr (2015) have recently argued for its declassification as a spectrum disorder based on recent evidence that the disorder is underpinned by at least four separate mechanisms (sites of dysfunction). These authors argue that while ANSD may have been appropriate when objective measures of the disorder were lacking and our understanding of its underlying aetiologies was limited, recent advances in the field have made the term ANSD redundant. This offers some argument for reconceptualising APD as a spectrum disorder in two respects. First, objective measures of APD are lacking and our understanding of its underlying mechanisms remains limited. Second, our understanding of APD is likely to advance to a point that supersedes considering APD as a spectral disorder as sufficient evidence is obtained to define APD as a clinical entity or a series of clinical entities. Alternatively, the evidence may accrue such that the term APD becomes redundant. One possibility in this regard is the concept of auditory neuropathy could subsume all bottom-up AP deficits, leaving top-down processing deficits to be better characterised by their origin as deficits of cognition or language.