Auditory Brainstem Response Wave Research Articles

Alpha9alpha10 knockout mice show altered physiological and behavioral responses to signals in masking noise.

Medial olivocochlear (MOC) efferents modulate outer hair cell motility through specialized nicotinic acetylcholine receptors to support encoding of signals in noise. Transgenic mice lacking the alpha9 subunits of these receptors (α9KOs) have normal hearing in quiet and noise, but lack classic cochlear suppression effects and show abnormal temporal, spectral, and spatial processing. Mice deficient for both the alpha9 and alpha10 receptor subunits (α9α10KOs) may exhibit more severe MOC-related phenotypes. Like α9KOs, α9α10KOs have normal auditory brainstem response (ABR) thresholds and weak MOC reflexes. Here, we further characterized auditory function in α9α10KO mice. Wild-type (WT) and α9α10KO mice had similar ABR thresholds and acoustic startle response amplitudes in quiet and noise, and similar frequency and intensity difference sensitivity. α9α10KO mice had larger ABR Wave I amplitudes than WTs in quiet and noise. Other ABR metrics of hearing-in-noise function yielded conflicting findings regarding α9α10KO susceptibility to masking effects. α9α10KO mice also had larger startle amplitudes in tone backgrounds than WTs. Overall, α9α10KO mice had grossly normal auditory function in quiet and noise, although their larger ABR amplitudes and hyperreactive startles suggest some auditory processing abnormalities. These findings contribute to the growing literature showing mixed effects of MOC dysfunction on hearing.

Investigating the Effects of Level-Specific CE-Chirp on Auditory Brainstem Response Waves in Normal Hearing Infants.

Auditory brainstem response (ABR) to the level-specific (LS) CE-Chirp has been reported to provide optimum neural synchrony along cochlear partitions, theoretically improving ABR waveform resolution. Despite this promising finding, limited studies have been conducted to contrast the results between LS CE-Chirp and Click stimuli. The current study aimed to compare the results of ABR between the two stimuli (Click and LS CE-Chirp). Sixty-seven normal-hearing infants, both with and without risk factors, aged less than 7 months old, participated in this study. The ABR test was conducted at 70 dBnHL using 33.3 stimulus repetition rates with both Click and LS CE-Chirp stimuli. The signal averaging was stopped at a maximum fixed signal average of 2,500 sweeps. Data were statistically compared between the two stimuli using the Wilcoxon signed-rank test. The waves I and V ABRs elicited by LS CE-Chirp exhibited significantly larger amplitudes than the Click stimulus. However, the amplitude of wave III and absolute latencies were similar in both stimuli at a supra-threshold level. LS CE-Chirp has the advantage of larger amplitudes than the ABR from Click at the supra-threshold level (70 dBnHL) in normal-hearing infants.

Sound elicits stereotyped facial movements that provide a sensitive index of hearing abilities in mice

Sound elicits rapid movements of muscles in the face, ears, and eyes that protect the body from injury and trigger brain-wide internal state changes. Here, we performed quantitative facial videography from mice resting atop a piezoelectric force plate and observed that broadband sounds elicited rapid and stereotyped facial twitches. Facial motion energy (FME) adjacent to the whisker array was 30 dB more sensitive than the acoustic startle reflex and offered greater inter-trial and inter-animal reliability than sound-evoked pupil dilations or movement of other facial and body regions. FME tracked the low-frequency envelope of broadband sounds, providing a means to study behavioral discrimination of complex auditory stimuli, such as speech phonemes in noise. Approximately 25% of layer 5-6 units in the auditory cortex (ACtx) exhibited firing rate changes during facial movements. However, FME facilitation during ACtx photoinhibition indicated that sound-evoked facial movements were mediated by a midbrain pathway and modulated by descending corticofugal input. FME and auditory brainstem response (ABR) thresholds were closely aligned after noise-induced sensorineural hearing loss, yet FME growth slopes were disproportionately steep at spared frequencies, reflecting a central plasticity that matched commensurate changes in ABR wave 4. Sound-evoked facial movements were also hypersensitive in Ptchd1 knockout mice, highlighting the use of FME for identifying sensory hyper-reactivity phenotypes after adult-onset hyperacusis and inherited deficiencies in autism risk genes. These findings present a sensitive and integrative measure of hearing while also highlighting that even low-intensity broadband sounds can elicit a complex mixture of auditory, motor, and reafferent somatosensory neural activity.

Ambient sound stimulation tunes axonal conduction velocity by regulating radial growth of myelin on an individual, axon-by-axon basis

Adaptive myelination is the emerging concept of tuning axonal conduction velocity to the activity within specific neural circuits over time. Sound processing circuits exhibit structural and functional specifications to process signals with microsecond precision: a time scale that is amenable to adjustment in length and thickness of myelin. Increasing activity of auditory axons by introducing sound-evoked responses during postnatal development enhances myelin thickness, while sensory deprivation prevents such radial growth during development. When deprivation occurs during adulthood, myelin thickness was reduced. However, it is unclear whether sensory stimulation adjusts myelination in a global fashion (whole fiber bundles) or whether such adaptation occurs at the level of individual fibers. Using temporary monaural deprivation in mice provided an internal control for a) differentially tracing structural changes in active and deprived fibers and b) for monitoring neural activity in response to acoustic stimulation of the control and the deprived ear within the same animal. The data show that sound-evoked activity increased the number of myelin layers around individual active axons, even when located in mixed bundles of active and deprived fibers. Thicker myelination correlated with faster axonal conduction velocity and caused shorter auditory brainstem response wave VI-I delays, providing a physiologically relevant readout. The lack of global compensation emphasizes the importance of balanced sensory experience in both ears throughout the lifespan of an individual.

Evaluation of cochlear and auditory brainstem functions in COVID-19 patients; a case control study

BackgroundMany viral infections can cause hearing loss due to affection of cochlear hair cells or neurogenic pathway. Although, the damage secondary to viral infections is mainly cochlear affection; auditory brainstem can be affected as well. It was predicted that SARS-COV-2 infection can similarly affect the auditory system. This study aimed to detect affection in auditory system and if present investigate the possible site of lesion (up to the level of the brain stem) in relation to COVID-19 infection.MethodsThis is a case control study, where the study group constituted of thirty adults, diagnosed with COVID-19 at least 2 weeks prior to testing and up to 6 months, without previous auditory complaints pre-COVID-19 or other risk factors that could affect the auditory pathway. Fifteen adult participants that were age and gender matched to the study group with no previous history of covid-19 infection constituted the control group. Audiological evaluations done to all participants were pure-tone and speech audiometry, tympanometry, transient-evoked otoacoustic emission with and without contralateral suppression and auditory brainstem response measurements.ResultsThe study group showed significantly worse pure tone thresholds at high frequencies 4 and 8 kHz (p < 0.01), significantly worse transient-evoked otoacoustic emission signal to noise ratio at 2800 Hz and 4000 Hz (p < 0.05) and significantly lower total suppression index (p<0.05). On the other hand, there was no significant difference between both groups in auditory brainstem response wave latencies (p > 0.05).ConclusionCOVID-19 had subtle effect on cochlear basal turn, and it is shown that the auditory efferent system may also be affected, while the auditory nerve and afferent brainstem pathways seems to be spared. Moreover, the absence of the symptoms of auditory dysfunction postcovid-19 does not guarantee normal auditory functions.

A Time-Saving Alternative to "Peak-Picking" Algorithms: A Gaussian Mixture Model Feature Extraction Technique for the Neurodiagnostic Auditory Brainstem Response.

The accurate and efficient analysis of neurodiagnostic auditory brainstem responses (ABR) plays a critical role in assessing auditory pathway function in human and animal research and in clinical diagnosis. Traditional analysis of the neurodiagnostic ABR analysis involves visual inspection of the waveform and manually marking peaks and troughs. Visual inspection is a tedious and time-consuming task, especially in research where there may be hundreds or thousands of waveforms to analyze. "Peak-picking" algorithms have made this task faster; however, they are prone to the same errors as visual inspection. A Gaussian mixture model-based feature extraction technique (GMM-FET) is a descriptive model of ABR morphology and an alternative to peak-picking algorithms. The GMM-FET is capable of modeling multiple waves and accounting for wave interactions, compared with other template-matching approaches that fit single waves. The present study is a secondary analysis applying the GMM-FET to 321 ABRs from adult humans from 2 datasets using different stimuli and recording parameters. Goodness-of-fit of the GMM-FET to waves I and V and surrounding waves, that is, the summating potential and waves IV and VI, was assessed, and latency and amplitude estimations by the GMM-FET were compared with estimations from visual inspection. The GMM-FET had a similar success rate to visual inspection in extracting peak latency and amplitude, and there was low RMS error and high intraclass correlation between the model and response waveform. Mean peak latency differences between the GMM-FET and visual inspection were small, suggesting the two methods chose the same peak in the majority of waveforms. The GMM-FET estimated wave I amplitudes within 0.12 µV of visual inspection, but estimated larger wave V amplitudes than visual inspection. The results suggest the GMM-FET is an appropriate method for extracting peak latencies and amplitudes for neurodiagnostic analysis of ABR waves I and V.

Auditory Neural Responses and Communicative Functioning in Children With Microcephaly Related to Congenital Zika Syndrome.

Children with microcephaly exhibit neurodevelopmental delays and compromised communicative functioning, yielding challenges for clinical assessment and informed intervention. This study characterized auditory neural function and communication abilities in children with microcephaly due to congenital Zika syndrome (CZS). Click-evoked auditory brainstem responses (ABR) at fast and slow stimulation rates and natural speech-evoked cortical auditory evoked potentials (CAEP) were recorded in 25 Brazilian children with microcephaly related to CZS (M age: 5.93 ± 0.62 years) and a comparison group of 25 healthy children (M age: 5.59 ± 0.80 years) matched on age, sex, ethnicity, and socioeconomic status. Communication abilities in daily life were evaluated using caregiver reports on Vineland Adaptive Behavior Scales-3. Caregivers of children with microcephaly reported significantly lower than typical adaptive functioning in the communication and socialization domains. ABR wave I latency did not differ significantly between the groups, suggesting comparable peripheral auditory function. ABR wave V absolute latency and waves I-V interwave latency were significantly shorter in the microcephaly group for both ears and rates. CAEP analyses identified reduced N2 amplitudes in children with microcephaly as well as limited evidence of speech sound differentiation, evidenced mainly by the N2 response latency. Conversely, in the comparison group, speech sound differences were observed for both the P1 and N2 latencies. Exploratory analyses in the microcephaly group indicated that more adaptive communication was associated with greater speech sound differences in the P1 and N2 amplitudes. The trimester of virus exposure did not have an effect on the ABRs or CAEPs. Microcephaly related to CZS is associated with alterations in subcortical and cortical auditory neural function. Reduced ABR latencies differ from previous reports, possibly due to the older age of this cohort and careful assessment of peripheral auditory function. Cortical speech sound detection and differentiation are present but reduced in children with microcephaly. Associations between communication performance in daily life and CAEPs highlight the value of auditory evoked potentials in assessing clinical populations with significant neurodevelopmental disabilities.

Hearing ability of prairie voles (Microtus ochrogaster).

The hearing abilities of mammals are impacted by factors such as social cues, habitat, and physical characteristics. Despite being used commonly to study social behaviors, hearing of the monogamous prairie vole (Microtus ochrogaster) has never been characterized. In this study, anatomical features are measured and auditory brainstem responses (ABRs) are used to measure auditory capabilities of prairie voles, characterizing monaural and binaural hearing and hearing range. Sexually naive male and female voles were measured to characterize differences due to sex. It was found that prairie voles show a hearing range with greatest sensitivity between 8 and 32 kHz, binaural hearing across interaural time difference ranges appropriate for their head sizes. No differences are shown between the sexes in binaural hearing or hearing range (except at 1 kHz), however, female voles have increased amplitude of peripheral ABR waves I and II and longer latency of waves III and IV compared to males. The results confirm that prairie voles have a broad hearing range, binaural hearing consistent with rodents of similar size, and differences in amplitudes and thresholds of monaural physiological measures between the sexes. These data further highlight the necessity to understand sex-specific differences in neural processing that may underly variability in responses between sexes.

Estrogen as a guardian of auditory health: Tsp1–CD47 axis regulation and noise-induced hearing loss

Objectives This study aimed to analyze the role of estrogen in noise-induced hearing loss (NIHL) and uncover underlying mechanisms. Methods An ovariectomized Sprague-Dawley rat model (OVX) was constructed to investigate the hearing threshold and auditory latency before and after noise exposure using the auditory brainstem response (ABR) test. The morphological changes were assessed using immunofluorescence, scanning electron microscopy and transmission electron microscopy. Proteomics and bioinformatics were used to analyze the mechanism. The findings were further verified through western blot and Luminex liquid suspension chip technology. Results After noise exposure, OVX rats exhibited substantially elevated hearing thresholds. A conspicuous delay in ABR wave I latency was observed, alongside increased loss of outer hair cells, severe collapse of stereocilia and pronounced deformation of the epidermal plate. Accordingly, OVX rats with estrogen supplementation exhibited tolerance to NIHL. Additionally, a remarkable upregulation of the thrombospondin 1 (Tsp1)–CD47 axis in OVX rats was discovered and verified. Conclusions OVX rats were more susceptible to NIHL, and the protective effect of estrogen was achieved through regulation of the Tsp1–CD47 axis. This study presents a novel mechanism through which estrogen regulates NIHL and offers a potential intervention strategy for the clinical treatment of NIHL.

Gentamicin administration leads to synaptic dysfunction in inner hair cells

Ototoxicity is a major side effect of aminoglycosides, which can cause irreversible hearing loss. Previous studies on aminoglycoside-induced ototoxicity have primarily focused on the loss of sensory hair cells. Recent investigations have revealed that aminoglycosides can also lead to the loss of ribbon synapses in inner hair cells (IHCs). However, the functional implications of ribbon synapse loss and the underlying mechanisms remain unclear. In this study, we intraperitoneally injected C57BL/6 J mice with 300 mg/kg gentamicin once daily for 3, 10, and 20 days. Then, we performed immunofluorescence staining, patch-clamp recording, proteomics analysis and western blotting to characterize the changes in ribbon synapses in IHCs and the associated mechanisms. After gentamicin treatment, the auditory brainstem response (ABR) threshold was elevated, and the ABR wave I amplitude was decreased. We also observed loss of ribbon synapses in IHCs. Interestingly, ribbon synapse loss occurred on both the modiolar and pillar sides of IHCs. Whole-cell patch-clamp recordings in IHCs revealed a reduction in the calcium current amplitude, along with a shifted half-activation voltage and altered calcium voltage dependency. Moreover, exocytosis of IHCs was reduced, consistent with the reduction in the ABR wave I amplitude. Through proteomic analysis, western blotting, and immunofluorescence staining, we found that gentamicin treatment resulted in downregulation of myosin VI, a protein crucial for synaptic vesicle recycling and replenishment in IHCs. Furthermore, we evaluated the kinetics of endocytosis and found a significant reduction in IHC exocytosis, possibly reflecting the impact of myosin VI downregulation on synaptic vesicle recycling. In summary, our findings demonstrate that gentamicin treatment leads to synaptic dysfunction in IHCs, highlighting the important role of myosin VI downregulation in gentamicin-induced synaptic damage.

Comprehensive behavioral and physiologic assessment of peripheral and central auditory function in individuals with mild traumatic brain injury

Auditory complaints are frequently reported by individuals with mild traumatic brain injury (mTBI) yet remain difficult to detect in the absence of clinically significant hearing loss. This highlights a growing need to identify sensitive indices of auditory-related mTBI pathophysiology beyond pure-tone thresholds for improved hearing healthcare diagnosis and treatment. Given the heterogeneity of mTBI etiology and the diverse peripheral and central processes required for normal auditory function, the present study sought to determine the audiologic assessments sensitive to mTBI pathophysiology at the group level using a well-rounded test battery of both peripheral and central auditory system function. This test battery included pure-tone detection thresholds, word understanding in quiet, sentence understanding in noise, distortion product otoacoustic emissions (DPOAEs), middle-ear muscle reflexes (MEMRs), and auditory evoked potentials (AEPs), including auditory brainstem responses (ABRs), middle latency responses (MLRs), and late latency responses (LLRs). Each participant also received magnetic resonance imaging (MRI). Compared to the control group, we found that individuals with mTBI had reduced DPOAE amplitudes that revealed a compound effect of age, elevated MEMR thresholds for an ipsilateral broadband noise elicitor, longer ABR Wave I latencies for click and 4 kHz tone burst elicitors, longer ABR Wave III latencies for 4 kHz tone bursts, larger MLR Na and Nb amplitudes, smaller MLR Pb amplitudes, longer MLR Pa latencies, and smaller LLR N1 amplitudes for older individuals with mTBI. Further, mTBI individuals with combined hearing difficulty and noise sensitivity had a greater number of deficits on thalamic and cortical AEP measures compared to those with only one/no self-reported auditory symptoms. This finding was corroborated with MRI, which revealed significant structural differences in the auditory cortical areas of mTBI participants who reported combined hearing difficulty and noise sensitivity, including an enlargement of left transverse temporal gyrus (TTG) and bilateral planum polare (PP). These findings highlight the need for continued investigations toward identifying individualized audiologic assessments and treatments that are sensitive to mTBI pathophysiology.

Electrophysiological Changes Associated with the Progression of Noise-Induced Hearing Loss.

The aim of this study is to evaluate the clinical characteristics and electrophysiological changes in patients with different degrees of noise-induced hearing loss compared with those of normal controls to elucidate the progression of auditory neural damage attributed to noise exposure. A retrospective cohort study was conducted through a review of the medical records for the patients who presented to a tertiary referral center. Sixty-nine participants were included in the study: 29 had noise-induced hearing loss, and 40 were healthy controls. All the participants underwent electrophysiological tests and pure-tone audiometry. Nine patients showed mild hearing loss (mild hearing loss group), while the others showed worse than moderate hearing loss on puretone audiometry (severe hearing loss group). Significantly reduced wave I and V amplitudes of auditory brainstem response were present in both mild and severe hearing loss groups compared to the control group (P -lt; .001 and P=.002, respectively), without significant differences between the mild and severe hearing loss groups. In the multivariate analysis, auditory brainstem response wave V amplitude was negatively associated with auditory brainstem response wave I-V inter-peak latency delay (B=-0.48, P=.02). The results of the present study confirm the similarity in the electrophysiological characteristics between the mild and severe hearing loss groups. Thus, widespread disruption in the auditory neural conduction could have been established in the early period when the patient developed mild hearing loss following noise exposure.

Wave In in auditory brainstem response suggests a high possibility of a high jugular bulb.

Wave In, which refers to the negativity between waves I and II in auditory brainstem response (ABR), is an electrophysiological phenomenon observed in previous studies. The term "high jugular bulb" (HJB) describes a jugular bulb that is located in a high position in the posterior aspect of the internal acoustic canal. The present study aimed to explore the correlation between wave In and the possibility of a HJB. This retrospective study included a cohort of pediatric patients diagnosed with profound hearing loss who were enrolled in a government-sponsored cochlear implantation program at an academic medical center between January 2019 and December 2022. The analysis involved examining the results obtained from the ABR test and high-resolution computed tomography (HRCT) of the temporal bone in the patients. The position of the jugular bulb was classified according to the Manjila and Semaan classification. A total of 221 pediatric patients were included in the study. Twenty-four patients, with a median age of 3 years and a range of 1-7 years, showed significant bilateral (n = 21) or unilateral (n = 3) wave In (mean latency: right ear, 2.16 ms ± 0.22 ms; left ear, 2.20 ms ± 0.22 ms). The remaining 197 patients showed an absence of ABR. The HRCT images revealed that 18 of the 24 patients (75%) had HJB, but only 41 of the 197 patients who lacked ABR (20.8%) showed signs of HJB. The ratio difference was considered statistically significant based on the chi-squared test (χ2 = 32.10, p < 0.01). More than 50% of the HJBs were categorized as type 4 jugular bulbs, which are located above the inferior margin of the internal auditory canal. ABR wave In in pediatric patients with profound hearing loss suggests a high possibility of HJB. The physiological mechanism underlying this correlation needs further investigation.

Investigating the optimal stimulus to evoke the binaural interaction component of the auditory brainstem response

Objective assessment of spatial and binaural hearing deficits remains a major clinical challenge. The binaural interaction component (BIC) of the auditory brainstem response (ABR) holds promise as a non-invasive biomarker for diagnosing such deficits. However, while comparative studies have reported robust BIC in animal models, BIC in humans can sometimes be unreliably evoked even in subjects with normal hearing. Here we explore the hypothesis that the standard methodology for collecting monaural ABRs may not be ideal for electrophysiological assessment of binaural hearing. This study aims to improve ABR BIC measurements by determining more optimal stimuli to evoke it. Building on previous methodology demonstrated to enhance peak amplitude of monaural ABRs, we constructed a series of level-dependent chirp stimuli based on empirically derived latencies of monaural-evoked ABR waves I, IV and the binaural-evoked BIC DN1, the most prominent BIC peak, in a cohort of ten chinchillas. We hypothesized that chirps designed based on BIC DN1 latency would specifically enhance across-frequency temporal synchrony in the afferent inputs leading to the binaural circuits that produce the BIC and would thus produce a larger DN1 than either traditional clicks or chirps designed to optimize monaural ABRs. Compared to clicks, we found that level-specific chirp stimuli evoked significantly greater BIC DN1 amplitudes, and that this effect persisted across all stimulation levels tested. However, we found no significant differences between BICs resulting from chirps created using binaural-evoked BIC DN1 latencies and those using monaural-evoked ABR waves I or IV. These data indicate that existing level-specific, monaural-based chirp stimuli may improve BIC detectability and reduce variability in human BIC measurements.

Preserved Auditory Steady State Response and Envelope-Following Response in Severe Brainstem Dysfunction Highlight the Need for Cross-Checking.

Commercially available auditory steady state response (ASSR) systems are widely used to obtain hearing thresholds in the pediatric population objectively. Children are often examined during natural or induced sleep so that the recorded ASSRs are of subcortical origin, the inferior colliculus being often designated as the main ASSR contributor in these conditions. This report presents data from a battery of auditory neurophysiological objective tests obtained in 3 cases of severe brainstem dysfunction in sleeping children. In addition to ASSRs, envelope-following response (EFR) recordings designed to distinguish peripheral (cochlear nerve) from central (brainstem) were recorded to document the effect of brainstem dysfunction on the two types of phase-locked responses. Results obtained in the 3 children with severe brainstem dysfunctions were compared with those of age-matched controls. The cases were identified as posterior fossa tumor, undiagnosed (UD), and Pelizaeus-Merzbacher-Like Disease. The standard audiological objective tests comprised tympanograms, distortion product otoacoustic emissions, click-evoked auditory brainstem responses (ABRs), and ASSRs. EFRs were recorded using horizontal (EFR-H) and vertical (EFR-V) channels and a stimulus phase rotation technique allowing isolation of the EFR waveforms in the time domain to obtain direct latency measurements. The brainstem dysfunctions of the 3 children were revealed as abnormal (weak, absent, or delayed) ABRs central waves with a normal wave I. In addition, they all presented a summating and cochlear microphonic potential in their ABRs, coupled with a normal wave I, which implies normal cochlear and cochlear nerve function. EFR-H and EFR-V waveforms were identified in the two cases in whom they were recorded. The EFR-Hs onset latencies, response durations, and phase-locking values did not differ from their respective age-matched control values, indicating normal cochlear nerve EFRs. In contrast, the EFR-V phase-locking value and onset latency varied from their control values. Both patients had abnormal but identifiable and significantly phase-locked brainstem EFRs, even in a case with severely distorted ABR central waves. ASSR objective audiograms were recorded in two cases. They showed normal or slightly elevated (explained by a slight transmission loss) thresholds that do not yield any clue about their brainstem dysfunction, revealing the method's lack of sensitivity to severe brainstem dysfunction. The present study, performed on 3 sleeping children with severe brainstem dysfunction but normal cochlear responses (cochlear microphonic potential, summating potential, and ABR wave I), revealed the differential sensitivity of three auditory electrophysiological techniques. Estimated thresholds obtained by standard ASSR recordings (cases UD and Pelizaeus-Merzbacher-Like Disease) provided no clue to the brainstem dysfunction clearly revealed by the click-evoked ABR. EFR recordings (cases posterior fossa tumor and UD) showed preserved central responses with abnormal latencies and low phase-locking values, whereas the peripheral EFR attributed to the cochlear nerve was normal. The one case (UD) for which the three techniques could be performed confirms this sensitivity gradient, emphasizing the need for applying the Cross-Check Principle by avoiding resorting to ASSR recording alone. The entirely normal EFR-H recordings observed in two cases further strengthen the hypothesis of its cochlear nerve origin in sleeping children.

Histological Correlates of Auditory Nerve Injury from Kainic Acid in the Budgerigar (Melopsittacus undulatus).

Loss of auditory nerve afferent synapses with cochlear hair cells, called cochlear synaptopathy, is a common pathology in humans caused by aging and noise overexposure. The perceptual consequences of synaptopathy in isolation from other cochlear pathologies are still unclear. Animal models provide an effective approach to resolve uncertainty regarding the physiological and perceptual consequences of auditory nerve loss, because neural lesions can be induced and readily quantified. The budgerigar, a parakeet species, has recently emerged as an animal model for synaptopathy studies based on its capacity for vocal learning and ability to behaviorally discriminate simple and complex sounds with acuity similar to humans. Kainic acid infusions in the budgerigar produce a profound reduction of compound auditory nerve responses, including wave I of the auditory brainstem response, without impacting physiological hair cell measures. These results suggest selective auditory nerve damage. However, histological correlates of neural injury from kainic acid are still lacking. We quantified the histological effects caused by intracochlear infusion of kainic acid (1mM; 2.5 µL), and evaluated correlations between the histological and physiological assessments of auditory nerve status. Kainic acid infusion in budgerigars produced pronounced loss of neural auditory nervesoma (60% on average) in the cochlearganglion, and of peripheral axons, at time points 2 or more months following injury. The hair cell epithelium was unaffected by kainic acid. Neural loss was significantly correlated with reduction of compound auditory nerve responses and auditory brainstem response wave I. Compound auditory nerve responses and wave I provide a useful index of cochlear synaptopathy in this animal model.

Auditory brainstem response to different chirp (based on cochlear partition) stimulation rates

All through the last decades, hearing thresholds have been estimated by audiologists by different means, such as pure-tone assessments, auditory steady state response, auditory brainstem response, etc. Objective EEG-based measurements have been applied, such as the auditory brainstem response (ABR), which measures neural synchrony along the brainstem auditory pathway. Through ABR waves’ amplitude and latency due to a stimulus level, hearing thresholds can be estimated. Considered a short-latencyauditory evoked potential (1–20 ms), very short transient stimulus (0.1–10 ms) is needed to evoke ABR. Chirp is a stimulus that has demonstrated to evoke better response, compared with clicks (aprox twice responses amplitude). Chirp is a transient auditory stimulus designed that considers delay in basilar membrane tonotopic gradient inside the cochlea. Chirp auditory response has been suggested to represent higher amplitudes, lower latency and lower time to identify thresholds. Characterization of ABR morphology due to chirp stimulus is something that has still been studied since multiple chirp designs have been proposed to identify changes in response due to chirp parameters differences. In the present work a description of Chirp design and detailed ABR extraction is presented, looking for a comparison between 4 Chirp stimulation rates as described in literature.

Evaluation of an Investigational Hearing Screening Device (HeLe) to Demonstrate Acoustic Brainstem Response among Normal-hearing Adults

Objective. This pilot human trial demonstrates the ability of the investigational newborn hearing screening device to provide acoustic stimulation to produce evoked potentials, as well as its ability to capture and acquire auditory evoked potentials, especially the auditory brainstem response (ABR) wave V. This pilot study also demonstrates the ease of recognizing and identifying ABR waves in the graphical presentation of the evoked potentials over time.Methods. Fourteen normal-hearing adults or a total of twenty-eight (28) normal-hearing adult ears underwent auditory brainstem response testing using the investigational hearing screening device. A commercially available auditory brainstem response detection device was used to confirm that the acquired ABR waves of the investigational device are normal. The ABR waves displayed by the investigation device were also reviewed by the clinical audiologists to determine their recognizability and identifiability.Results. The pilot trial demonstrates the ability of the investigational newborn hearing screening device in providing acoustic stimulation to produce evoked potentials, and in acquiring and capturing ABR waves, specifically the wave V, among normal-hearing adult ears. The clinical audiologists recognized and identified the ABR wave V among the evoked potentials at 40dB, 60dB, and 80dB acoustic stimulation. About eighty-nine percent (89.2%) of all ears tested had identifiable and recognizable wave V upon acoustic stimulation at 40dB.Conclusion. The investigational hearing screening device: (1) can provide acoustic stimulation to produce evoked potentials, (2) can accurately capture and acquire these evoked potentials, (3) can present these evoked potentials in a voltage per time graphical display which an audiologist and trained HCP can easily read and interpret (diagnostic ABR), and (4) can present wave V auditory brainstem potentials that can be easily identified by an audiologist and trained HCP (screening ABR).Keywords: , 

Effect of Different Blood Groups on Auditory Brainstem Response Findings

Background and Aim: The human blood group system can have an effect on the health and auditory system. The present study aimed to determine the differences in the Auditory Brainstem Response (ABR) recordings among persons with different blood groups (AB, A, B, O).&#x0D; Methods: Sixty adults aged between 18 and 25 years with normal hearing sensitivity took part in the study. Further, they were grouped into four groups based on their blood groups (A, B, AB, O). Each group consisted of 15 participants. Auditory brainstem responses were recorded for all the participants at different rates (11.1/s and 90.1/s).&#x0D; Results: The results of the study showed that the amplitude of ABR waves was significantly reduced for individuals with blood group O at lower repetition rate. The amplitude and latency of wave V was reduced at higher repetition rate among individuals with blood group O. There was no significant difference for all the other parameters  across the groups.&#x0D; Conclusion: The result of the study suggests the possibility of lesser auditory nerve functioning and increased risk of cochlear synaptopathy in persons with the O blood group.&#x0D; Keywords: Auditory brainstem response; outer hair cell; auditory nerve; cochlear synaptopathy

Mefloquine-Induced Inner Ear Damage and Preventive Effects of Electrical Stimulation: An Electrophysiological Study

Introduction: Mefloquine is an antimalarial medicine used to prevent and treat malaria. This medicine has some side effects, including ototoxicity. This study, which was designed in two phases, aimed to investigate the side effects of mefloquine and evaluate the preventive effects of electrical stimulation on these side effects. Methods: In the first phase, two doses of mefloquine (50 and 200 μ<sc>M</sc>) were injected into male rats, and after 7 days, they were evaluated by an auditory brainstem response (ABR) test. In the second phase, electrical stimulation was applied for 10 days, and then a toxic dose of mefloquine was injected. Similar to the first phase of the study, the animals were evaluated by an ABR test after 7 days. Results: In the first phase, the results showed that a high dose of mefloquine increased the ABR threshold and wave I latency; however, these changes were not observed in the second phase. Conclusion: Application of electrical stimulation could prevent the ototoxic effects of mefloquine. According to the findings of the present study, electrical stimulation can be used as a preconditioner to prevent the ototoxic effects of mefloquine.