Central Auditory Pathway Research Articles

Study of auditory pathways in type 1 diabetes mellitus through brainstem auditory evoked potentials and contralateral acoustic reflex.

To investigate the functionalities of the neural pathways through the auditory evoked potentials of the brainstem and the contralateral stapedial acoustic reflexes in normal-hearing individuals with type 1 diabetes mellitus, in order to detect possible alterations in the central auditory pathways. This is a cross-sectional study with a comparison group and a convenience sample, consisting of 32 individuals with type 1 diabetes mellitus and 20 controls without the disease. All subjects had hearing thresholds within normal limits and type A tympanometric curves. The acoustic reflex arc and brainstem auditory potentials were investigated. Statistical analyses were performed using the SPSS 17.0. The Chi-square test, Student´s t-test, and Multiple linear regression were used. The auditory thresholds of the acoustic reflex were statistically lower in the group with the disease at frequencies of 0.5 kHz and 1.0 kHz in the left ear (p=0.01 and p=0.01, respectively). The absolute latencies III and V of the auditory potentials of the brainstem in the right ear and V in the left ear were increased in subjects with type 1 diabetes mellitus (p=0.03, p=0.02 and p=0.03, respectively). The findings suggest that subjects with type 1 diabetes mellitus are more likely to present alterations in the central auditory pathways, even with auditory thresholds within normal limits.

Hearing Loss among the Elderly at a Geriatric Centre in South-west Nigeria

Background: Aging is an unavoidable process that is connected with several health issues, including presbycusis, a degenerative disease of the cochlear hair cells and central auditory pathways with a resultant reduction in hearing acuity. In developing countries like Nigeria, little attention is given to the elderly population with possible underreporting of presbycusis, hence the need for this study. Aim: The aim of this study was to investigate hearing loss, the type, and associated risk factors among the elderly attending a geriatric clinic in South-west Nigeria. Patients, Materials and Methods: It was a cross-sectional study of patients aged 60 years and above in a geriatric centre. All consented participants were given a structured questionnaire to collect important data such as demographics, history of hearing loss, family history of hearing loss, risk factors, and so on. Ear examinations, otoscopy, pure-tone audiometry, distortion-product otoacoustic emissions, and tympanometry were also performed on all patients. Results: Ninety-five participants, comprising 33 males and 62 females, were recruited, and their ages ranged from 60 to 89 years (74.5 ± 7.6 years). The mean pure-tone average was 42.2 dB ± 17.4 and 39.21 dB ± 17.4 in the right and left ears, respectively. About 80% of them have a hearing threshold above 15 dB, with 13 (13.7%) being conductive hearing loss, 48 (50.6%) sensorineural hearing loss, and 15 (15.8) mixed hearing loss. Presbycusis was diagnosed in 37 (38.9%) participants. There was a significant correlation between the pure-tone average and distortion-product otoacoustic emissions results in both ears of the participants (P = 0.0001). Tympanograms were abnormal in 21 (22%) right ears and 27 (28%) left ears. Conclusion: Hearing loss is highly prevalent among the elderly, with presbycusis being the most common type. Periodic hearing screening for the elderly is hereby recommended.

Management of Badhirya(Sensory Loss Of Hearing) with Ayurveda

Sensory neural hearing loss occurs when there is a problem in the sensory apparatus -cochlea (sensory) or in the pathways of conduction of nerve impulses to the brain. Sensory neural hearing loss can be Peripheral and Central (auditory pathway or cortex).It can be congenital or acquired. Congenital: present at birth, due to anomalies of inner ear or due to pre or perinatal factors. In present study we have discussed a case of a 12-year-old male child who came to OPD with complains of Sensory neural hearing Loss since childhood. Audiometry report showed Right ear moderate to profound mixed hearing loss Left ear -moderate to severe sensory neural hearing loss. First Ayurvedatreatment of Sensory neural hearing loss with three sittings of MarshaNasyafrom Anu Taila, 3 sittings of Karnapuranafrom Bilwadi Taila And Sarivadi Vatiwith the dose of 250mg thrice a day with luke warm water or milk for 1 month were given in a month and same procedure followed for 6 months. After that his hearing improved showing audiometric findings of Moderate hearing in both ear. After six months repeat Audiometry was done. Patient also felt better hearing in both ears. Decreased hearing due to Sensory neural hearing loss is result of Damage of hair cells, which can be managed with the help of Ayurvedatreatment Marsha Nasya, Karnapurana with Rasayanatreatment. Hearing loss to school going children is a very serious problem affecting their education, skills and socialrelationship with others.

Low Intensity Noise Exposure Enhanced Auditory Loudness and Temporal Processing by Increasing Excitability of DCN.

Sound stimulation is generally used for tinnitus and hyperacusis treatment. Recent studies found that long-term noise exposure can change synaptic and firing properties in the central auditory system, which will be detected by the acoustic startle reflex. However, the perceptual consequences of long-term low-intensity sound exposure are indistinct. This study will detect the effects of moderate-level noise exposure (83 dB SPL) on auditory loudness, and temporal processing was evaluated using CBA/CaJ mice. C-Fos staining was used to detect neural activity changes in the central auditory pathway. With two weeks of 83 dB SPL noise exposure (8 hours per day), no persistent threshold shift of the auditory brainstem response (ABR) was identified. On the other hand, noise exposure enhanced the acoustic startle response (ASR) and gap-induced prepulse inhibition significantly (gap-PPI). Low-level noise exposure, according to the findings, can alter temporal acuity. Noise exposure increased the number of c-Fos labeled neurons in the dorsal cochlear nucleus (DCN) and caudal pontine reticular nucleus (PnC) but not at a higher level in the central auditory nuclei. Our results suggested that noise stimulation can change acoustical temporal processing presumably by increasing the excitability of auditory brainstem neurons.

Electroacupuncture Promotes Neuroplasticity of Central Auditory Pathway: An Auditory Evoked Potentials Study.

Our previous studies found that electroacupuncture at the right Zhongzhu acupoint (TE3) can enhance auditory recovery in rats with noise-induced hearing loss. Here, we investigated the changes in auditory brainstem response (ABR) and long late latency (LLR) evoked potential to explain the mechanisms of electroacupuncture at TE3. The auditory evoked potentials were recorded, including ABR and LLR, at baseline and on day 3 (D3), D5, and D8 after baseline. The 2-Hz electroacupuncture at the right TE3 was applied on D3, D4, and D5 in the electroacupuncture group but not in the control group. In ABR, compared with the control group, the latency shift of waves I (0.298 ± 0.033 vs -0.045 ± 0.057 ms), III (0.718 ± 0.038 vs -0.163 ± 0.130 ms), and V (1.160 ± 0.082 vs -0.207 ± 0.138 ms) on D3 (all p < 0.01) and of wave V (0.616 ± 0.433 vs -0.352 ± 0.209 ms, p < 0.05) on D5 was greater in the electroacupuncture group than that in the control group. Moreover, the interpeak latency shift of I-III (0.420 ± 0.041 vs -0.118 ± 0.177 ms) and I-V (0.863 ± 0.088 vs -0.162 ± 0.156 ms) on D3 (both p < 0.05) and of III-V (0.342 ± 0.193 vs -0.190 ± 0.110 ms) and I-V (0.540 ± 0.352 vs -0.343 ± 0.184 ms) on D5 (both p < 0.05) was greater in the electroacupuncture group than that in the control group. In LLR, the latency shift of P0 was greater in the electroacupuncture group than in the control group on D3 (3.956 ± 2.975 vs -1.178 ± 1.358 ms, p < 0.01) and D5 (2.200 ± 1.889 vs -0.311 ± 1.078 ms, p < 0.05). These findings indicate that electroacupuncture at the right TE3 can modulate the neuroplasticity of the central auditory pathway, including the brain stem and the primary and secondary auditory cortex.

Neurotransmitter phenotype and axonal projection patterns of VIP-expressing neurons in the inferior colliculus

Neurons in the inferior colliculus (IC), the midbrain hub of the central auditory pathway, send ascending and descending projections to other auditory brain regions, as well as projections to other sensory and non-sensory brain regions. However, the axonal projection patterns of individual classes of IC neurons remain largely unknown. Vasoactive intestinal polypeptide (VIP) is a neuropeptide expressed by subsets of neurons in many brain regions. We recently identified a class of IC stellate neurons that we called VIP neurons because they are labeled by tdTomato (tdT) expression in VIP-IRES-Cre x Ai14 mice. Here, using fluorescence in situ hybridization, we found that tdT+ neurons in VIP-IRES-Cre x Ai14 mice express Vglut2, a marker of glutamatergic neurons, and VIP, suggesting that VIP neurons use both glutamatergic and VIPergic signaling to influence their postsynaptic targets. Next, using viral transfections with a Cre-dependent eGFP construct, we labeled the axonal projections of VIP neurons. As a group, VIP neurons project intrinsically, within the ipsilateral and contralateral IC, and extrinsically to all the major targets of the IC. Within the auditory system, VIP neurons sent axons and formed axonal boutons in higher centers, including the medial geniculate nucleus and the nucleus of the brachium of the IC. Less dense projections terminated in lower centers, including the nuclei of the lateral lemniscus, superior olivary complex, and dorsal cochlear nucleus. VIP neurons also project to several non-auditory brain regions, including the superior colliculus, periaqueductal gray, and cuneiform nucleus. The diversity of VIP projections compared to the homogeneity of VIP neuron intrinsic properties suggests that VIP neurons play a conserved role at the microcircuit level, likely involving neuromodulation through glutamatergic and VIPergic signaling, but support diverse functions at the systems level through their participation in different projection pathways.

Amyloid Pathology in the Central Auditory Pathway of 5XFAD Mice Appears First in Auditory Cortex.

Effective treatment of Alzheimer's disease (AD) will hinge on early detection. This has led to the search for early biomarkers that use non-invasive testing. One possible early biomarker is auditory temporal processing deficits, which reflect central auditory pathway dysfunction and precede cognitive and memory declines in AD. Gap detection is a measure of auditory temporal processing, is impaired in human AD, and is also impaired in the 5XFAD mouse model of AD. Gap detection deficits appear as early as postnatal day 60 in 5XFAD mice, months before cognitive deficits or cell death, supporting gap detection as an early biomarker. However, it remains unclear how gap detection deficits relate to the progression of amyloid pathology in the auditory system. To determine the progression of amyloid pathology throughout the central auditory system and across age in 5XFAD mice. We quantified intracellular and extracellular antibody labelling of Aβ42 in 6 regions of the central auditory system from p14 to p150. Pathology appeared first in primary auditory cortex (A1) as intracellular accumulation of Aβ42 in layer 5 pyramidal neurons by age p21. Extracellular plaques appeared later, by age p90, in A1, medial geniculate body, and inferior colliculus. Auditory brainstem structures showed minimal amyloid pathology. We also observed pathology in the caudal pontine reticular nucleus, a brainstem structure that is outside of the central auditory pathway but which is involved in the acoustic startle reflex. These results suggest that Aβ42 accumulation, but not plaques, may impair gap detection.

Brainstem auditory pathway maturation in term neonates with congenital cytomegalovirus infection: a cohort study.

Congenital cytomegalovirus infection (cCMVi) is a leading cause of sensorineural hearing loss (SNHL) and developmental delay. Brainstem auditory evoked potentials (BAEPs) recording allows assessment of central auditory pathway maturation in neonates. We aimed to characterize the effect of cCMVi on the maturation of the brainstem auditory pathway in term neonates. We retrospectively reviewed medical records of neonates born with cCMVi in 2010-2018 and characterized their auditory pathway maturation using brainstem auditory-evoked potentials (BAEPs). We compared inter-peak latency differences (IPLDs) of the main BAEP components (I-V, I-III, and III-V) in terms of cCMVi patients and healthy controls and described their changes in cCMVi patients throughout the first year of life. Of 101 cCMVi patients, 57 (56.4%) were considered symptomatic, 6 (5.9%) were small for gestational age, 6 (5.9%) had microcephaly, 4 (4%) had thrombocytopenia, 5 (6.6%) had hepatitis, 2 (2.1%) had retinitis, 47 (49.5%) had typical abnormalities on head ultrasound, 9 (8.9%)developed SNHL, and 34 (59.6%) received antiviral therapy. No significant difference was found between IPLDs of full-term cCMVi patients compared to controls throughout the entire auditory pathway (I-III, III-V, and I-V IPLDs), for both ears (p > 0.05). On serial BAEP examinations, cCMVi patients presented decreased IPLDs throughout the first year of life (p < 0.05 ofcompared 1st, 2nd, and 3rd BAEPs in both ears). Conclusions: Intrauterine cytomegalovirus infection does not affect the auditory brainstem maturation process in term neonates. Our findings support previous studies noting the normal neurodevelopmental outcome of asymptomatic cCMVi patients, suggesting antiviral treatment is not warranted in these cases. What is Known: •cCMVi is a leading cause of developmental delay and hearing loss. Treatment is recommended for patients with symptomatic diseases who are at significant risk of long-term sequelae. • It is unknown whether cCMVi affects the central nervous system maturation process. What is New: •We performed a neurophysiological evaluation of brainstem conduction by recording the BAEPs. We found that cCMVi has no significant impact on central conduction times along the auditory pathways in the brainstem at birth nor changes the neuronal maturation process during the first year of life. •Our findings suggest that cCMVi does not universally affect central nervous system maturation, supporting a highly selective approach when considering the benefits of antiviral therapy.

Neuroethology of sound localization in anurans.

Albert Feng pioneered the study of neuroethology of sound localization in anurans by combining behavioral experiments on phonotaxis with detailed investigations of neural processing of sound direction from the periphery to the central nervous system. The main advantage of these studies is that many species of female frogs readily perform phonotaxis towards loudspeakers emitting the species-specific advertisement call. Behavioral studies using synthetic calls can identify which parameters are important for phonotaxis and also quantify localization accuracy. Feng was the first to investigate binaural processing using single-unit recordings in the first two auditory nuclei in the central auditory pathway and later investigated the directional properties of auditory nerve fibers with free-field stimulation. These studies showed not only that the frog ear is inherently directional by virtue of acoustical coupling or crosstalk between the two eardrums, but also confirmed that there are extratympanic pathways that affect directionality in the low-frequency region of the frog's hearing range. Feng's recordings in the midbrain also showed that directional information is enhanced by cross-midline inhibition. An important contribution toward the end of his career involved his participation in neuroethological research with a team of scientists working with frogs that produce ultrasonic calls.

Noise-induced hearing loss vulnerability in type III intermediate filament peripherin gene knockout mice.

In the post-natal mouse cochlea, type II spiral ganglion neurons (SGNs) innervating the electromotile outer hair cells (OHCs) of the ‘cochlear amplifier' selectively express the type III intermediate filament peripherin gene (Prph). Immunolabeling showed that Prph knockout (KO) mice exhibited disruption of this (outer spiral bundle) afferent innervation, while the radial fiber (type I SGN) innervation of the inner hair cells (~95% of the SGN population) was retained. Functionality of the medial olivocochlear (MOC) efferent innervation of the OHCs was confirmed in the PrphKO, based on suppression of distortion product otoacoustic emissions (DPOAEs) via direct electrical stimulation. However, “contralateral suppression” of the MOC reflex neural circuit, evident as a rapid reduction in cubic DPOAE when noise is presented to the opposite ear in wildtype mice, was substantially disrupted in the PrphKO. Auditory brainstem response (ABR) measurements demonstrated that hearing sensitivity (thresholds and growth-functions) were indistinguishable between wildtype and PrphKO mice. Despite this comparability in sound transduction and strength of the afferent signal to the central auditory pathways, high-intensity, broadband noise exposure (108 dB SPL, 1 h) produced permanent high frequency hearing loss (24–32 kHz) in PrphKO mice but not the wildtype mice, consistent with the attenuated contralateral suppression of the PrphKO. These data support the postulate that auditory neurons expressing Prph contribute to the sensory arm of the otoprotective MOC feedback circuit.

ISL1 is necessary for auditory neuron development and contributes toward tonotopic organization.

A cardinal feature of the auditory pathway is frequency selectivity, represented in a tonotopic map from the cochlea to the cortex. The molecular determinants of the auditory frequency map are unknown. Here, we discovered that the transcription factor ISL1 regulates the molecular and cellular features of auditory neurons, including the formation of the spiral ganglion and peripheral and central processes that shape the tonotopic representation of the auditory map. We selectively knocked out Isl1 in auditory neurons using Neurod1Cre strategies. In the absence of Isl1, spiral ganglion neurons migrate into the central cochlea and beyond, and the cochlear wiring is profoundly reduced and disrupted. The central axons of Isl1 mutants lose their topographic projections and segregation at the cochlear nucleus. Transcriptome analysis of spiral ganglion neurons shows that Isl1 regulates neurogenesis, axonogenesis, migration, neurotransmission-related machinery, and synaptic communication patterns. We show that peripheral disorganization in the cochlea affects the physiological properties of hearing in the midbrain and auditory behavior. Surprisingly, auditory processing features are preserved despite the significant hearing impairment, revealing central auditory pathway resilience and plasticity in Isl1 mutant mice. Mutant mice have a reduced acoustic startle reflex, altered prepulse inhibition, and characteristics of compensatory neural hyperactivity centrally. Our findings show that ISL1 is one of the obligatory factors required to sculpt auditory structural and functional tonotopic maps. Still, upon Isl1 deletion, the ensuing central plasticity of the auditory pathway does not suffice to overcome developmentally induced peripheral dysfunction of the cochlea.

Is there an unmet medical need for improved hearing restoration?

Hearing impairment, the most prevalent sensory deficit, affects more than 466 million people worldwide (WHO). We presently lack causative treatment for the most common form, sensorineural hearing impairment; hearing aids and cochlear implants (CI) remain the only means of hearing restoration. We engaged with CI users to learn about their expectations and their willingness to collaborate with health care professionals on establishing novel therapies. We summarize upcoming CI innovations, gene therapies, and regenerative approaches and evaluate the chances for clinical translation of these novel strategies. We conclude that there remains an unmet medical need for improving hearing restoration and that we are likely to witness the clinical translation of gene therapy and major CI innovations within this decade.

Effects of Noise and Chemical Exposure on Peripheral and Central Auditory Pathways in Normal-hearing Workers.

To assess the effects of noise and chemical exposure on peripheral and central auditory pathways in normal-hearing workers exposed to chemicals or high noise levels and compare the groups with each other and with workers not exposed to either of these agents. A total of 54 normal-hearing workers were divided into three groups (chemical, noise, control) and submitted to the following assessments: conventional and extended high-frequency pure-tone audiometry; transient and distortion-product otoacoustic emissions, the inhibitory effect of the efferent auditory pathway; and Staggered Spondaic Word (SSW) and Pitch Pattern Sequence (PPS) test. There were no significant differences between the groups in extended high-frequency hearing thresholds. Significantly lower amplitudes were observed in the noise group for otoacoustic emissions. There were significantly more absences of the inhibitory effect of the efferent system in the noise group. There was no difference between the groups in the SSW test, while in PPS, the noise group performed worse than the control group. These findings suggest that noise exposure produced deleterious effects on the workers' peripheral and central auditory systems, despite their normal hearing thresholds. The chemical group did not have significantly different results from those of the control group. It is important that individuals exposed to noise or chemicals have their auditory pathways monitored with complementary assessments.

Evaluation of age-related changes in middle-ear structures by wideband tympanometry

Background Presbycusis is bilateral sensorineural hearing loss associated with the progressive degeneration of cochlear and central auditory pathways with aging. Aims/Objectives We aimed to reveal age-related changes in middle ear function by using wideband tympanometry (WBT). Materials and Methods Fifty-eight patients diagnosed with presbycusis were compared to 52 audiologically healthy participants. WBT measurement was performed on both ears via wideband click stimulus with a tympanometer device using probe tone frequencies of 226–8000 Hz. Results There were no statistically significant differences detected among the resonance frequencies or maximum absorbance ratios measured in both ears between groups (p > .05). The mean absorbance of the right and left ears at 4000 and 8000 Hz was statistically higher in the patient group than in the healthy controls (r = 0.038, 0.030; l = 0.015, 0.012). Moreover, mean compliance values were found to be significantly lower in the patient group than in the control group (r = 0.030 and l = 0.040). Conclusion The significant differences detected in compliance and absorbance values for high frequencies in presbycusis patients were remarkable. Thus, it has been shown that WBT yields an advantage compared to traditional tympanometry in the diagnosis and treatment of middle ear diseases.

Aging process and central auditory pathway: a study based on auditory brainstem evoked potential and frequency-following response.

ABSTRACTObjective To analyze age-related changes in the central auditory pathway in healthy elderly individuals.Methods A prospective, quantitative cross-sectional study. The caseload comprised 18 adults (mean age, 22.78 years) and 18 elderly individuals (mean age, 66.72 years) of both sexes, who met inclusion criteria. Subjects were submitted to basic audiological evaluation and related electrophysiologic tests: brainstem auditory evoked potential with click stimulus and frequency-following response.Results Elderly individuals had higher wave and interpeak latencies (waves I, III and V and interpeaks I-V and III-V) of brainstem auditory evoked potential. Latencies of frequency following response waves A, E, F and O were also higher in elderly individuals. Frequency following response amplitudes were better in A than in D, F and O waves in these subjects. Likewise, interpeak intervals (V-A and V-O) were larger in elderly relative to adult individuals. Lower slope values were observed in elderly individuals.Conclusion Brainstem auditory evoked potential and frequency-following response allowed appropriate assessment of age-related changes in the auditory pathway. Slower neural response to auditory stimuli suggests reduced synchrony between neural structures.

Correlation of Blast-Induced Tympanic Membrane Perforation with Peripheral Cochlear Synaptopathy.

The auditory organs, including the tympanic membrane, cochlea, and central auditory pathway, are the most fragile components of the human body when exposed to blast overpressure. Tympanic membrane perforation (TMP) is the most frequent symptom in blast-exposed patients. The impact of TMP on the inner ear and central auditory system, however, is not fully understood. We aimed to analyze the effect of blast-induced TMP on the auditory pathophysiological changes in mice after blast exposure. Mice aged seven weeks were exposed to blast overpressure to induce TMP and allowed to survive for two months. All TMP cases had spontaneously healed by week three after the blast exposure. Compared with controls, blast-exposed mice exhibited a significant elevation in hearing thresholds and an apparent disruption of stereocilia in the outer hair cells, regardless of the occurrence or absence of TMP. The reduction in synapses in the inner hair cells, which is known as the most frequent pathology in blast-exposed cochleae, was significantly more severe in mice without TMP. A decrease in the number of excitatory central synapses labeled by VGLUT-1 in the cochlear nucleus was observed, however, regardless of the absence or presence of TMP. Our findings suggest that blast-induced TMP mitigates peripheral cochlear synaptic disruption but leaves the central auditory synapses unaffected, indicating that central synaptic disruption is independent of TMP and peripheral cochlear synaptic disruption. Synaptic deterioration in the peripheral and central auditory systems can contribute to the promotion of blast-induced hearing impairment, including abnormal auditory perception.

Time Course of Activity-Dependent Changes in Auditory Nerve Synapses Reveals Multiple Underlying Cellular Mechanisms.

Abnormal levels of acoustic activity can result in hearing problems such as tinnitus and language processing disorders, but the underlying cellular and synaptic changes triggered by abnormal activity are not well understood. To address this issue, we studied the time course of activity-dependent changes that occur at auditory nerve synapses in mice of both sexes after noise exposure and conductive hearing loss. We found that EPSC amplitude and synaptic depression decreased within 2 d of noise exposure through a decrease in the probability of vesicle release (Pr). This was followed by a gradual increase in EPSC amplitude through a larger pool of releasable vesicles (N). Occlusion of the ear canal led to a rapid decrease in EPSC amplitude through a decrease in N, which was followed by an increase in EPSC amplitude and synaptic depression through an increase in Pr After returning to normal sound levels, synaptic depression recovered to control levels within 1-2 d. However, repeated exposure to noise for as little as 8 h/d caused synaptic changes after 7 d, suggesting recovery did not fully offset changes. Thus, there appear to be three activity-dependent mechanisms in auditory nerve synapses-bidirectional changes in Pr in 1-2 d, slower bidirectional changes in N through synaptic growth or retraction, and rapid downregulation of N with low activity. The dynamic changes indicate that multiple mechanisms are present to fine-tune synaptic fidelity across different acoustic conditions in a simple relay.SIGNIFICANCE STATEMENT Hearing impairments can arise from exposure to noise or conductive hearing loss. This appears to result from changes in the brain, but the mechanisms are not well understood. We study this issue by studying the synapses made by auditory nerve fibers called endbulbs of Held. These synapses undergo bidirectional changes in size and release probability of neurotransmitter in response to increased or decreased activity. Here, we made a close examination of how quickly these synaptic characteristics change, which indicates there are at least three cellular mechanisms underlying changes. Furthermore, repeated exposure to brief periods of noise can produce cumulative effects. These changes could significantly affect hearing, especially because they occur at the start of the central auditory pathway.

HP01: Usefulness of auditory brainstem evoked response in the assessment of bilirubin-induced auditory toxicity in infants with jaundice: A case-control study

To assess ABR alterations due to hyperbilirubinemia in jaundiced infants compared to a control group. Background: Bilirubin-induced neurotoxicity has predilection to specific areas of the brain including the auditory pathway structures. These latter are assessed by auditory brainstem evoked response (ABR). Methods: This was a retrospective study including two groups: jaundiced infants (G1) and age-matched (p>0.05) infants without jaundice (G2). All infants underwent ABR on each ear to screen deafness. Responses obtained at 90 dB were studied. Responses of G2 were normal. The Mann-Whitney U test was used to compare the responses between the two groups. Results: Twenty infants (40 ears) were included with a mean age of 33.5±13 months. G1 and G2 included 18 and 20 ears, respectively. Wave-I latency was significantly more prolonged in G1 (1.71±0.2 ms) compared to G2 (1.56±0.1 ms) with p=0.02. There was no difference in I-III interpeak interval (IPL). The III-V IPL was significantly increased in G1 (2.04±0.1 ms) compared to G2 (1.92±0.1 ms) with p=0.04. I-V IPL was more prolonged in G1. Discussion: Both peripheral and central auditory pathways may be altered in infants with jaundice. Bilirubin-induced toxicity may affect the inner part of the ear. The central dysfunction may occur at the brainstem level between the bulbo-protuberant junction and the inferior colliculus. This may be due to the hyperbilirubinemia-induced changes in the central synaptic transmission. Conclusion: Hyperbilirubinemia-induced auditory toxicity can occur at different levels of the auditory pathway. Therefore, there is a need for an early ABR assessment in jaundiced infants.

Disturbed Balance of Inhibitory Signaling Links Hearing Loss and Cognition.

Neuronal hyperexcitability in the central auditory pathway linked to reduced inhibitory activity is associated with numerous forms of hearing loss, including noise damage, age-dependent hearing loss, and deafness, as well as tinnitus or auditory processing deficits in autism spectrum disorder (ASD). In most cases, the reduced central inhibitory activity and the accompanying hyperexcitability are interpreted as an active compensatory response to the absence of synaptic activity, linked to increased central neural gain control (increased output activity relative to reduced input). We here suggest that hyperexcitability also could be related to an immaturity or impairment of tonic inhibitory strength that typically develops in an activity-dependent process in the ascending auditory pathway with auditory experience. In these cases, high-SR auditory nerve fibers, which are critical for the shortest latencies and lowest sound thresholds, may have either not matured (possibly in congenital deafness or autism) or are dysfunctional (possibly after sudden, stressful auditory trauma or age-dependent hearing loss linked with cognitive decline). Fast auditory processing deficits can occur despite maintained basal hearing. In that case, tonic inhibitory strength is reduced in ascending auditory nuclei, and fast inhibitory parvalbumin positive interneuron (PV-IN) dendrites are diminished in auditory and frontal brain regions. This leads to deficits in central neural gain control linked to hippocampal LTP/LTD deficiencies, cognitive deficits, and unbalanced extra-hypothalamic stress control. Under these conditions, a diminished inhibitory strength may weaken local neuronal coupling to homeostatic vascular responses required for the metabolic support of auditory adjustment processes. We emphasize the need to distinguish these two states of excitatory/inhibitory imbalance in hearing disorders: (i) Under conditions of preserved fast auditory processing and sustained tonic inhibitory strength, an excitatory/inhibitory imbalance following auditory deprivation can maintain precise hearing through a memory linked, transient disinhibition that leads to enhanced spiking fidelity (central neural gain⇑) (ii) Under conditions of critically diminished fast auditory processing and reduced tonic inhibitory strength, hyperexcitability can be part of an increased synchronization over a broader frequency range, linked to reduced spiking reliability (central neural gain⇓). This latter stage mutually reinforces diminished metabolic support for auditory adjustment processes, increasing the risks for canonical dementia syndromes.

Normative data for brainstem auditory evoked potential responses in North Indian menopausal females

Background: Ovarian hormones are known to influence central neuronal functioning. Many studies have established the brainstem auditory evoked potential (BAEP) pattern vis-à -vis the cyclical fluctuations of these hormones in young females; however, there is a paucity of research involving BAEP patterns among menopausal females. Aim: This study was conducted to provide normative values for various BAEP parameters in menopausal females from North India. Materials and Methods: A cross-sectional study was done on 100 females aged 46–70 years. BAEP recording was done using a standardized protocol. The data were analyzed using SPSS software. It consisted of mean wave latencies I, II, III, IV, and V and interpeak latencies (IPL) I-V, I-III, and III-V. Student's unpaired t-test was used for statistical analysis. Results: The average value of means of wave latencies and IPL from both the ears was obtained. The latencies of waves I, II, III, IV, and V were 1.82 ± 0.27 ms, 2.81 ± 0.27 ms, 4.09 ± 0.35 ms, 4.87 ± 0.33 ms, and 6.19 ± 0.31 ms, respectively. The mean values of IPL I-V, I-III, and III-V were 4.37 ± 0.38 ms, 2.26 ± 0.33 ms, and 2.1 ± 0.32 ms, respectively. Conclusion: The study findings compared favorably with already existing data from similar studies conducted elsewhere. The data from the present study would prove useful to the clinicians to detect subtle neurodegenerative changes at an early stage within the central auditory pathways, even in the absence of any perceptible hearing loss, in this subset of population.