Fetal Central Auditory System Metabolic Response to Cochlear Implant Stimulation

2002 ◽  
Vol 127 (3) ◽  
pp. 131-137 ◽  
Author(s):  
Patrick J. Antonelli ◽  
Kenneth J. Gerhardt ◽  
Robert M. Abrams ◽  
Xinyan Huang

OBJECTIVES: The purpose of this study was to examine the effects of profound auditory deprivation and its treatment by cochlear implantation and stimulation on the metabolic activity of the central auditory system in fetal sheep. METHODS: Six ovine fetuses at 85% to 90% gestation were bilaterally deafened by kanamycin perfusion and unilaterally implanted with cochlear electrode arrays. Half of the implanted animals were stimulated with an extrauterine sound processor, and half were not. Four animals served as hearing controls. One week postoperatively, central nervous system metabolic activity was evaluated in ambient laboratory noise by quantitative autoradiography using 14C-deoxyglucose. RESULTS: Kanamycin perfusion deafened all treated animals as verified by auditory brainstem response and scanning electron microscopy. Glucose utilization in the inferior colliculus was markedly lower in deafened and unstimulated animals relative to hearing controls. Glucose utilization in implanted-stimulated animals was similar to normal controls. CONCLUSIONS: Changes in central auditory system metabolic activity associated with congenital deafness may be minimized by prompt auditory habilitation.

2020 ◽  
Vol 29 (2) ◽  
pp. 152-164 ◽  
Author(s):  
Naomi F. Bramhall ◽  
Christopher E. Niemczak ◽  
Sean D. Kampel ◽  
Curtis J. Billings ◽  
Garnett P. McMillan

Purpose Complaints of auditory perceptual deficits, such as tinnitus and difficulty understanding speech in background noise, among individuals with clinically normal audiograms present a perplexing problem for audiologists. One potential explanation for these “hidden” auditory deficits is loss of the synaptic connections between the inner hair cells and their afferent auditory nerve fiber targets, a condition that has been termed cochlear synaptopathy . In animal models, cochlear synaptopathy can occur due to aging or exposure to noise or ototoxic drugs and is associated with reduced auditory brainstem response (ABR) wave I amplitudes. Decreased ABR wave I amplitudes have been demonstrated among young military Veterans and non-Veterans with a history of firearm use, suggesting that humans may also experience noise-induced synaptopathy. However, the downstream consequences of synaptopathy are unclear. Method To investigate how noise-induced reductions in wave I amplitude impact the central auditory system, the ABR, the middle latency response (MLR), and the late latency response (LLR) were measured in 65 young Veterans and non-Veterans with normal audiograms. Results In response to a click stimulus, the MLR was weaker for Veterans compared to non-Veterans, but the LLR was not reduced. In addition, low ABR wave I amplitudes were associated with a reduced MLR, but with an increased LLR. Notably, Veterans reporting tinnitus showed the largest mean LLRs. Conclusions These findings indicate that decreased peripheral auditory input leads to compensatory gain in the central auditory system, even among individuals with normal audiograms, and may impact auditory perception. This pattern of reduced MLR, but not LLR, was observed among Veterans even after statistical adjustment for sex and distortion product otoacoustic emission differences, suggesting that synaptic loss plays a role in the observed central gain. Supplemental Material https://doi.org/10.23641/asha.11977854


2021 ◽  
Vol 15 ◽  
Author(s):  
Feifan Chen ◽  
Fei Zhao ◽  
Nadeem Mahafza ◽  
Wei Lu

Noise-induced cochlear synaptopathy (CS) is defined as a permanent loss of synapses in the auditory nerve pathway following noise exposure. Several studies using auditory brainstem response (ABR) have indicated the presence of CS and increased central gain in tinnitus patients with normal hearing thresholds (TNHT), but the results were inconsistent. This meta-analysis aimed to review the evidence of CS and its pathological changes in the central auditory system in TNHT. Published studies using ABR to study TNHT were reviewed. PubMed, EMBASE, and Scopus databases were selected to search for relevant literature. Studies (489) were retrieved, and 11 were included for meta-analysis. The results supported significantly reduced wave I amplitude in TNHT, whereas the alternations in wave V amplitude were inconsistent among the studies. Consistently increased V/I ratio indicated noise-induced central gain enhancement. The results indicated the evidence of noise-induced cochlear synaptopathy in tinnitus patients with normal hearing. However, inconsistent changes in wave V amplitude may be explained by that the failure of central gain that triggers the pathological neural changes in the central auditory system and/or that increased central gain may be necessary to generate tinnitus but not to maintain tinnitus.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Zheng-De Du ◽  
Wei Wei ◽  
Shukui Yu ◽  
Qing-Ling Song ◽  
Ke Liu ◽  
...  

Clinical data has confirmed that auditory impairment may be a secondary symptom of type 2 diabetes mellitus (T2DM). However, mechanisms underlying pathologic changes that occur in the auditory system, especially in the central auditory system (CAS), remain poorly understood. In this study, Zucker diabetic fatty (ZDF) rats were used as a T2DM rat model to observe ultrastructural alterations in the auditory cortex and investigate possible mechanisms underlying CAS damage in T2DM. The auditory brainstem response (ABR) of ZDF rats was found to be markedly elevated in low (8 kHz) and high (32 kHz) frequencies. Protein expression of NADPH oxidase 2 (NOX2) and its matching subunits P22phox, P47phox, and P67phox was increased in the auditory cortex of ZDF rats. Expression of 8-hydroxy-2-deoxyguanosine (8-OHdG), a marker of DNA oxidative damage, was also increased in the neuronal mitochondria of the auditory cortex of ZDF rats. Additionally, decreases in the mitochondrial total antioxidant capabilities (T-AOC), adenosine triphosphate (ATP) production, and mitochondrial membrane potential (MMP) were detected in the auditory cortex of ZDF rats, suggesting mitochondrial dysfunction. Transmission electron microscopy results indicated that ultrastructural damage had occurred to neurovascular units and mitochondria in the auditory cortex of ZDF rats. Furthermore, cytochrome c (Cyt c) translocation from mitochondria to cytoplasm and caspase 3-dependent apoptosis were also detected in the auditory cortex of ZDF rats. Consequently, the study demonstrated that T2DM may cause morphological damage to the CAS and that NOX2-associated mitochondrial oxidative damage and apoptosis may be partly responsible for this insult.


1994 ◽  
Vol 159 (11) ◽  
pp. 676-680 ◽  
Author(s):  
Linda L. Pierson ◽  
Kenneth J. Gerhardt ◽  
Robert M. Abrams ◽  
Scott K. Griffiths ◽  
Aemil J.M. Peters

1992 ◽  
Vol 1 (2) ◽  
pp. 63-67 ◽  
Author(s):  
A. Joyce King ◽  
Yvonne S. Sininger

A vertical recording montage (C z to the seventh cervical vertebra or C 7 ) has been shown to yield significantly lower auditory brainstem response (ABR) threshold when compared with a horizontal or anterior-posterior montage (Sininger & Don, 1989). The present study further examines the relationship between electrode placement and the amplitude of the ABR to low-level stimuli. Four electrode arrays were compared—the commonly-used clinical configuration of forehead to ipsilateral mastoid, the vertical array from the previous study (C z to C 7 ), and two additional montages employing linked mastoids as reference to either the vertex or forehead electrode. ABRs were recorded simultaneously in four channels in response to 8000 click stimuli at 10, 20, and 30 dB SL from 9 male and 9 female adult subjects with normal hearing. The effect of electrode channel was significant at <.0001, with the vertical channel revealing the largest wave V amplitudes at all stimulus levels. Female subjects, as expected, produced larger ABR amplitudes than male subjects in all recording conditions, but electrode-channel effects were independent of gender.


Author(s):  
M.J. Taylor ◽  
J.B. McMenamin ◽  
E. Andermann ◽  
G.V. Watters

ABSTRACT:Auditory brainstem responses (ABRs) and cortical auditory evoked responses (AERs) were studied in a series of 16 Friedreich’s ataxia patients who varied in age, degree of clinical involvement and duration of the disorder. The ABRs were markedly abnormal in all but the youngest patient, and the abnormalities reflected the severity and duration of the disease. The latencies of the AERs were significantly longer in the Friedreich’s ataxia patients compared to normal controls, suggesting cortical as well as peripheral involvement of the auditory system. These data are discussed in terms of the neuropathology of the disorder and the similarities with the other sensory systems in Friedreich’s ataxia patients.


2002 ◽  
Vol 13 (08) ◽  
pp. 416-427 ◽  
Author(s):  
Marcia J. Hay-McCutcheon ◽  
Carolyn J. Brown ◽  
Kelly Schmidt Clay ◽  
Keely Seyle

In this study, differences between electrically evoked whole-nerve action potential (EAP) and electrically evoked auditory brainstem response (EABR) measurements within Nucleus CI24R cochlear implant recipients were evaluated. Precurved modiolus-hugging internal electrode arrays, such as the CI24R, are designed to provide more direct stimulation of neural elements of the modiolus. If the electrode array is closer to the modiolus, electrically evoked and behavioral levels might be lower than were previously recorded for the straight electrode array, the CI24M. EAP and EABR growth functions and behavioral levels were obtained for 10 postlingually deafened adults. Results revealed no significant differences between EAP and EABR threshold levels, and these levels were not significantly lower than those obtained using the CI24M.


2002 ◽  
Vol 45 (6) ◽  
pp. 1249-1261 ◽  
Author(s):  
Flint A. Boettcher

Age-related hearing loss (ARHL or presbyacusis) is an increasingly common form of sensorineural hearing loss (SNHL) as a result of changing demographics, and the auditory brainstem response (ABR) is a common experimental and clinical tool in audiology and neurology. Some of the changes that occur in the aging auditory system may significantly influence the interpretation of the ABR in comparison to the ABRs of younger adults. The approach of this review will be to integrate physiological and histopathological data from human and animal studies to provide a better understanding of the array of age-related changes in the ABR and to determine how age-related changes in the auditory system may influence how the ABR should be interpreted in presbyacusis. Data will be described in terms of thresholds, latencies, and amplitudes, as well as more complex auditory functions such as masking and temporal processing. Included in the review of data will be an attempt to differentiate between age-related effects that may strictly be due to threshold elevation from those that may be due to the aging process.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
J. Tillein ◽  
S. Heid ◽  
E. Lang ◽  
R. Hartmann ◽  
A. Kral

To compare the development of the auditory system in hearing and completely acoustically deprived animals, naive congenitally deaf white cats (CDCs) and hearing controls (HCs) were investigated at different developmental stages from birth till adulthood. The CDCs had no hearing experience before the acute experiment. In both groups of animals, responses to cochlear implant stimulation were acutely assessed. Electrically evoked auditory brainstem responses (E-ABRs) were recorded with monopolar stimulation at different current levels. CDCs demonstrated extensive development of E-ABRs, from first signs of responses at postnatal (p.n.) day 3 through appearance of all waves of brainstem response at day 8 p.n. to mature responses around day 90 p.n.. Wave I of E-ABRs could not be distinguished from the artifact in majority of CDCs, whereas in HCs, it was clearly separated from the stimulus artifact. Waves II, III, and IV demonstrated higher thresholds in CDCs, whereas this difference was not found for wave V. Amplitudes of wave III were significantly higher in HCs, whereas wave V amplitudes were significantly higher in CDCs. No differences in latencies were observed between the animal groups. These data demonstrate significant postnatal subcortical development in absence of hearing, and also divergent effects of deafness on early waves II–IV and wave V of the E-ABR.


2020 ◽  
Vol 185 (Supplement_1) ◽  
pp. 248-255
Author(s):  
Kyle D Smith ◽  
Tao Chen ◽  
Rong Z Gan

Abstract Introduction The peripheral auditory system and various structures within the central auditory system are vulnerable to blast injuries, and even blast overpressure is at relatively mild traumatic brain injury (TBI) level. However, the extent of hearing loss in relation to blast number and time course of post-blast is not well understood. This study reports the progressive hearing damage measured in chinchillas after multiple blast exposures at mild TBI levels (103–138 kPa or 15–20 psi). Materials and Methods Sixteen animals (two controls) were exposed to two blasts and three blasts, respectively, in two groups with both ears plugged with foam earplugs to prevent the eardrum from rupturing. Auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) were measured in pre- and post-blasts. Immunohistochemical study of chinchilla brains were performed at the end of experiment. Results Results show that the ABR threshold and DPOAE level shifts in 2-blast animals were recovered after 7 days. In 3-blast animals, the ABR and DPOAE shifts remained at 26 and 23 dB, respectively after 14 days. Variation of auditory cortex damage between 2-blast and 3-blast was also observed in immunofluorescence images. Conclusions This study demonstrates that the number of blasts causing mild TBI critically affects hearing damage.


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