Selective Inner Hair Cell Loss in Prematurity: A Temporal Bone Study of Infants from a Neonatal Intensive Care Unit

Amatuzzi, Mônica Gondim; Liberman, M. Charles; Northrop, Clarinda

doi:10.1007/s10162-011-0273-4

Cited by 40 publications

(33 citation statements)

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“…This is similar to the research conducted by Pourarian et al and Santoso, that sepsis is not a risk factor for cochlear dysfunction. [15,16] However, these results differ from previous studies conducted by Meyer et al revealed that infants with a history of sepsis have a risk of 2.57 (95% CI 1.12 to 5.91) underwent cochlear dysfunction. [8] The un significant sepsis as risk factors cochlear dysfunction may be caused by the development of early detection of sepsis and the development of antibiotics in the treatment of sepsis in infants so that better management of sepsis and further complications can be prevented.…”

Section: Discussioncontrasting

confidence: 56%

Risk Factors Association with Cochlear Dysfunction on the First Hearing Screening in the Neonatal Intensive Care Unit

2015

IJSR

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Section: Discussioncontrasting

confidence: 56%

Risk Factors Association with Cochlear Dysfunction on the First Hearing Screening in the Neonatal Intensive Care Unit

2015

IJSR

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“…Pathological insults to different cochlea locations and auditory neurons are not uniform in patients with ANSD and patients with SNHL (e.g. Amatuzzi et al, 2011; He et al, 2012; Makary et al, 2011), which might account for, at least partially, the variations in group effects on these dependent variables at different electrodes. No difference in averaged N1 latency was observed between children with ANSD and children with SNHL.…”

Section: Discussionmentioning

confidence: 99%

Temporal Response Properties of the Auditory Nerve in Implanted Children with Auditory Neuropathy Spectrum Disorder and Implanted Children with Sensorineural Hearing Loss

Abbas

Doyle

et al. 2016

Ear &Amp; Hearing

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Objective This study aimed to 1) characterize temporal response properties of the auditory nerve in implanted children with auditory neuropathy spectrum disorder (ANSD); and 2) compare results recorded in implanted children with ANSD with those measured in implanted children with sensorineural hearing loss (SNHL). Design Participants included 28 children with ANSD and 29 children with SNHL. All subjects used Cochlear Nucleus devices in their test ears. Both ears were tested in six children with ANSD and three children with SNHL. For all other subjects, only one ear was tested. The electrically-evoked compound action potential (ECAP) was measured in response to each of the 33 pulses in a pulse train (excluding the second pulse) for one apical, one middle-array, and one basal electrode. The pulse train was presented in a monopolar-coupled stimulation mode at four pulse rates: 500, 900, 1800 and 2400 pulses per second (pps). Response metrics included the averaged amplitude, latencies of response components and response width, the alternating depth and the amount of neural adaptation. These dependent variables were quantified based on the last six ECAPs or the six ECAPs occurring within a time window centered around 11–12 ms. A Generalized Linear Mixed Model (GLMM) was used to compare these dependent variables between the two subject groups. The slope of the linear fit of the normalized ECAP amplitudes (re. amplitude of the first ECAP response) over the duration of the pulse train was used to quantify the amount of ECAP increment over time for a subgroup of nine subjects. Results Pulse train evoked ECAPs were measured in all but eight subjects (five with ANSD and three with SNHL). ECAPs measured in children with ANSD had smaller amplitude, longer averaged P2 latency and greater response width than children with SNHL. However, differences in these two groups were only observed for some electrodes. No differences in averaged N1 latency or in the alternating depth were observed between children with ANSD and children with SNHL. Neural adaptation measured in these two subject groups was comparable for relatively short durations of stimulation (i.e. 11–12 ms). Children with ANSD showed greater neural adaptation than children with SNHL for a longer duration of stimulation. Amplitudes of ECAP responses rapidly declined within the first few milliseconds of stimulation, followed by a gradual decline up to 64 ms after stimulus onset in the majority of subjects. This decline exhibited an alternating pattern at some pulse rates. Further increases in pulse rate diminished this alternating pattern. In contrast, ECAPs recorded from at least one stimulating electrode in six ears with ANSD and three ears with SNHL showed a clear increase in amplitude over the time course of stimulation. The slope of linear regression functions measured in these subjects was significantly greater than zero. Conclusions Some but not all aspects of temporal response properties of the auditory nerve measured in this study differ between implanted...

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“…For example a high incidence of auditory neuropathy is found in infants born prematurely (Xoinis et al, 2007). Recently, a study of infant temporal bones revealed that 30% of preterm babies who died in the NICU had selective inner hair cell (IHC) loss, while only 3% of full-term infants presented such a phenotype (Amatuzzi et al, 2011). This high prevalence for such a rare histopathology (Schuknecht, 1993) suggested that selective IHC loss might be a common cause of auditory neuropathy.…”

Section: Introductionmentioning

confidence: 99%

Perinatal thiamine deficiency causes cochlear innervation abnormalities in mice

et al. 2016

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Neonatal thiamine deficiency can cause auditory neuropathy in humans. To probe the underlying cochlear pathology, mice were maintained on a thiamine-free or low-thiamine diet during fetal development or early postnatal life. At postnatal ages from 18 days to 22 wks, cochlear function was tested and cochlear histopathology analyzed by plastic sections and cochlear epithelial whole-mounts immunostained for neuronal and synaptic markers. Although none of the thiamine-deprivation protocols resulted in any loss of hair cells or any obvious abnormalities in the non-sensory structures of the cochlear duct, all the experimental groups showed significant anomalies in the afferent or efferent innervation. Afferent synaptic counts in the inner and outer hair cell areas were reduced, as was the efferent innervation density in both the outer and inner hair cell areas. As expected for primary neural degeneration, the thresholds for distortion product otoacoustic emissions were not affected, and as expected for subtotal hair cell de-afferentation, the suprathreshold amplitudes of auditory brainstem responses were more affected than the response thresholds. We conclude that the auditory neuropathy from thiamine deprivation could be produced by loss of inner hair cell synapses.

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Selective Inner Hair Cell Loss in Prematurity: A Temporal Bone Study of Infants from a Neonatal Intensive Care Unit

Cited by 40 publications

References 32 publications

Risk Factors Association with Cochlear Dysfunction on the First Hearing Screening in the Neonatal Intensive Care Unit

Risk Factors Association with Cochlear Dysfunction on the First Hearing Screening in the Neonatal Intensive Care Unit

Temporal Response Properties of the Auditory Nerve in Implanted Children with Auditory Neuropathy Spectrum Disorder and Implanted Children with Sensorineural Hearing Loss

Perinatal thiamine deficiency causes cochlear innervation abnormalities in mice

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