Human Central Auditory System Research Articles

The Physiological Bases of Hidden Noise-Induced Hearing Loss: Protocol for a Functional Neuroimaging Study.

BackgroundRodent studies indicate that noise exposure can cause permanent damage to synapses between inner hair cells and high-threshold auditory nerve fibers, without permanently altering threshold sensitivity. These demonstrations of what is commonly known as hidden hearing loss have been confirmed in several rodent species, but the implications for human hearing are unclear.ObjectiveOur Medical Research Council–funded program aims to address this unanswered question, by investigating functional consequences of the damage to the human peripheral and central auditory nervous system that results from cumulative lifetime noise exposure. Behavioral and neuroimaging techniques are being used in a series of parallel studies aimed at detecting hidden hearing loss in humans. The planned neuroimaging study aims to (1) identify central auditory biomarkers associated with hidden hearing loss; (2) investigate whether there are any additive contributions from tinnitus or diminished sound tolerance, which are often comorbid with hearing problems; and (3) explore the relation between subcortical functional magnetic resonance imaging (fMRI) measures and the auditory brainstem response (ABR).MethodsIndividuals aged 25 to 40 years with pure tone hearing thresholds ≤20 dB hearing level over the range 500 Hz to 8 kHz and no contraindications for MRI or signs of ear disease will be recruited into the study. Lifetime noise exposure will be estimated using an in-depth structured interview. Auditory responses throughout the central auditory system will be recorded using ABR and fMRI. Analyses will focus predominantly on correlations between lifetime noise exposure and auditory response characteristics.ResultsThis paper reports the study protocol. The funding was awarded in July 2013. Enrollment for the study described in this protocol commenced in February 2017 and was completed in December 2017. Results are expected in 2018.ConclusionsThis challenging and comprehensive study will have the potential to impact diagnostic procedures for hidden hearing loss, enabling early identification of noise-induced auditory damage via the detection of changes in central auditory processing. Consequently, this will generate the opportunity to give personalized advice regarding provision of ear defense and monitoring of further damage, thus reducing the incidence of noise-induced hearing loss.

The Adverse Effects of Heavy Metals with and without Noise Exposure on the Human Peripheral and Central Auditory System: A Literature Review.

Exposure to some chemicals in the workplace can lead to occupational chemical-induced hearing loss. Attention has mainly focused on the adverse auditory effects of solvents. However, other chemicals such as heavy metals have been also identified as ototoxic agents. The aim of this work was to review the current scientific knowledge about the adverse auditory effects of heavy metal exposure with and without co-exposure to noise in humans. PubMed and Medline were accessed to find suitable articles. A total of 49 articles met the inclusion criteria. Results from the review showed that no evidence about the ototoxic effects in humans of manganese is available. Contradictory results have been found for arsenic, lead and mercury as well as for the possible interaction between heavy metals and noise. All studies found in this review have found that exposure to cadmium and mixtures of heavy metals induce auditory dysfunction. Most of the studies investigating the adverse auditory effects of heavy metals in humans have investigated human populations exposed to lead. Some of these studies suggest peripheral and central auditory dysfunction induced by lead exposure. It is concluded that further evidence from human studies about the adverse auditory effects of heavy metal exposure is still required. Despite this issue, audiologists and other hearing health care professionals should be aware of the possible auditory effects of heavy metals.

Timing matters: the processing of pitch relations.

The human central auditory system can automatically extract abstract regularities from a variant auditory input. To this end, temporarily separated events need to be related. This study tested whether the timing between events, falling either within or outside the temporal window of integration (~350 ms), impacts the extraction of abstract feature relations. We utilized tone pairs for which tones within but not across pairs revealed a constant pitch relation (e.g., pitch of second tone of a pair higher than pitch of first tone, while absolute pitch values varied across pairs). We measured the mismatch negativity (MMN; the brain’s error signal to auditory regularity violations) to second tones that rarely violated the pitch relation (e.g., pitch of second tone lower). A Short condition in which tone duration (90 ms) and stimulus onset asynchrony between the tones of a pair were short (110 ms) was compared to two conditions, where this onset asynchrony was long (510 ms). In the Long Gap condition, the tone durations were identical to Short (90 ms), but the silent interval was prolonged by 400 ms. In Long Tone, the duration of the first tone was prolonged by 400 ms, while the silent interval was comparable to Short (20 ms). Results show a frontocentral MMN of comparable amplitude in all conditions. Thus, abstract pitch relations can be extracted even when the within-pair timing exceeds the integration period. Source analyses indicate MMN generators in the supratemporal cortex. Interestingly, they were located more anterior in Long Gap than in Short and Long Tone. Moreover, frontal generator activity was found for Long Gap and Long Tone. Thus, the way in which the system automatically registers irregular abstract pitch relations depends on the timing of the events to be linked. Pending that the current MMN data mirror established abstract rule representations coding the regular pitch relation, neural processes building these templates vary with timing.

Auditory training: Stimulus exposure, task execution, and response feedback affect the neural detection of sound.

The P1‐N1‐P2 cortical auditory evoked potential (AEP) has been used to study the effects of training‐related plasticity in the human central auditory system. One consistent finding is that enhanced P2 amplitudes coincide with improved perception. A typical interpretation of this result is that auditory training alters the physiological representation of the cue being trained. However, it is also possible that changes in P2 amplitude reflect other processes that are associated with, but not specific to, the improved representation of the trained cue itself. Here we isolated different components of auditory training by examining the effects of stimulus exposure, behavioral task execution, as well as task‐ plus‐feedback on the AEPs of 30 normal‐hearing young adults. For each group, AEP responses were passively obtained in response to two speech syllables differing in voice‐onset‐time, on three separate days. The first two sessions were on consecutive days and the third session occurred 1 week later. Results suggest that mere stimulus exposure alters the way sound is represented in the human auditory system, but the magnitude of P2 amplitude change is significantly greater when participants interact with the stimuli while executing a task. This point is especially true with the addition of feedback. [Work supported by NIH NIDCD Grant No. R01DC007705.]

Plasticity of tonotopic maps in humans: influence of hearing loss, hearing aids and cochlear implants

Conclusion: This paper reviews psychoacoustical and electrophysiological evidence for reorganization of the human central auditory system in case of auditory deprivation and rehabilitation. Objective: To investigate the plasticity of cortical tonotopic maps in cochlear-damaged subjects. Methods: Frequency discrimination scores were analysed in subjects with high frequency hearing loss to test for potential perceptual correlates of auditory deprivation- and rehabilitation-induced plasticity. In cochlear implant patients, electrically evoked auditory cortical responses were obtained using EEG to study scalp potential maps. Results: Perceptual changes in frequency discrimination were observed at the lesion-edge frequency of steeply sloping hearing loss. Although these results are not direct proof of cortical plasticity, no peripheral phenomenon has been found to explain them. The reversal of such auditory deprivation-induced plasticity, a phenomenon that may be termed rehabilitation plasticity, can be studied in hearing-impaired subjects fitted with a hearing aid. Cochlear implant subjects provide another interesting model for studying rehabilitation plasticity in that even profound to total deafness is made partially reversible by cochlear implantation. We found that the auditory cortex of deaf subjects with at least 3 months of cochlear implant experience is organized in a way similar to the tonotopy described in normal-hearing subjects.

Human evoked cortical activity to signal-to-noise ratio and absolute signal level

The purpose of this study was to determine the effect of signal level and signal-to-noise ratio (SNR) on the latency and amplitude of evoked cortical activity to further our understanding of how the human central auditory system encodes signals in noise. Cortical auditory evoked potentials (CAEPs) were recorded from 15 young normal-hearing adults in response to a 1000 Hz tone presented at two tone levels in quiet and while continuous background noise levels were varied in five equivalent SNR steps. These 12 conditions were used to determine the effects of signal level and SNR level on CAEP components P1, N1, P2, and N2. Based on prior signal-in-noise experiments conducted in animals, we hypothesized that SNR, would be a key contributor to human CAEP characteristics. As hypothesized, amplitude increased and latency decreased with increasing SNR; in addition, there was no main effect of tone level across the two signal levels tested (60 and 75 dB SPL). Morphology of the P1–N1–P2 complex was driven primarily by SNR, highlighting the importance of noise when recording CAEPs. Results are discussed in terms of the current interest in recording CAEPs in hearing aid users.

Assessment of auditory plasticity using psychoacoustic and electrophysiological measurements

Anatomical and physiological changes may occur under different circumstances, reflecting the plasticity of the human central and peripheral auditory system: deprivation of peripheral auditory input (plasticity induced by hearing deprivation), chronic exposition to sound in deaf subjects (plasticity induced by auditory rehabilitation), or auditory learning (learning-induced plasticity). In this review, we focus on auditory deprivation and rehabilitation-induced plasticity. We first describe some perceptual correlates of cortical plasticity induced by sensory deprivation, and then we present some of our original results showing the influence of hearing aids on perceptual performances of sensorineural hearing impaired listeners. These results are in line with the auditory acclimatization phenomenon (i.e. in monaurally fitted listeners, the aided ear performs better than the unaided ear for fine processing of high-intensity sounds). They also suggest that the auditory acclimatization phenomenon is lateralized...

Electrical Stimulation of the Midbrain for Hearing Restoration: Insight into the Functional Organization of the Human Central Auditory System

The cochlear implant can restore speech perception in patients with sensorineural hearing loss. However, it is ineffective for those without an implantable cochlea or a functional auditory nerve. These patients can be implanted with the auditory brainstem implant (ABI), which stimulates the surface of the cochlear nucleus. Unfortunately, the ABI has achieved limited success in its main patient group [i.e., those with neurofibromatosis type 2 (NF2)] and requires a difficult surgical procedure. These limitations have motivated us to develop a new hearing prosthesis that stimulates the midbrain with a penetrating electrode array. We recently implanted three patients with the auditory midbrain implant (AMI), and it has proven to be safe with minimal movement over time. The AMI provides loudness, pitch, temporal, and directional cues, features that have shown to be important for speech perception and more complex sound processing. Thus far, all three patients obtain enhancements in lip reading capabilities and environmental awareness and some improvements in speech perception comparable with that of NF2 ABI patients. Considering that our midbrain target is more surgically exposable than the cochlear nucleus, this argues for the use of the AMI as an alternative to the ABI. Fortunately, we were able to stimulate different midbrain regions in our patients and investigate the functional organization of the human central auditory system. These findings provide some insight into how we may need to stimulate the midbrain to improve hearing performance with the AMI.

Training-Related Changes in the Brain: Evidence from Human Auditory-Evoked Potentials

Auditory-evoked potentials are being used to examine training-related changes in the human central auditory system, and there is converging evidence that focused listening training, using various training methods and different types of stimuli alters evoked neural activity. Such training-related changes are often described in terms of PHYSIOLOGICAL PLASTICITY, a process whereby the neural representation of the acoustic cue is modified with training. In this review, the concept of plasticity is discussed from a broader perspective. Specifically addressed is how electrophysiological methods are being used to study physiological modifications that occur with training, and how this information might contribute to the rehabilitation of people who wear hearing aids and cochlear implants.

Lateralization, connectivity and plasticity in the human central auditory system

Although it is known that responses in the auditory cortex are evoked predominantly contralateral to the side of stimulation, the lateralization of responses at lower levels in the human central auditory system has hardly been studied. Furthermore, little is known on the functional interactions between the involved processing centers. In this study, functional MRI was performed using sound stimuli of varying left and right intensities. In normal hearing subjects, contralateral activation was consistently detected in the temporal lobe, thalamus and midbrain. Connectivity analyses showed that auditory information crosses to the contralateral side in the lower brainstem followed by ipsilateral signal conduction towards the auditory cortex, similar to the flow of auditory signals in other mammals. In unilaterally deaf subjects, activation was more symmetrical for the cortices but remained contralateral in the midbrain and thalamus. Input connection strengths were different only at cortical levels, and there was no evidence for plastic reorganization at subcortical levels.

Human central auditory plasticity associated with tone sequence learning.

We investigated learning-related changes in amplitude, scalp topography, and source localization of the mismatch negativity (MMN), a neurophysiological response correlated with auditory discrimination ability. Participants (n = 32) underwent two EEG recordings while they watched silent films and ignored auditory stimuli. Stimuli were a standard (probability = 85%) and two deviant (probability = 7.5% each for high [HD] and low [LD]) eight-tone sequences that differed in the frequency of one tone. Between recordings, subjects practiced discriminating the HD or LD from the standard for 6 min. The amplitude of the LD MMN increased significantly across recordings in both groups, whereas the amplitude of the HD MMN did not. The LD was easier to discriminate than was the HD. Thus, practicing either discrimination increased the MMN for the easier discrimination. Learning and changes in the LD MMN amplitude were highly correlated. Source localizations of event-related potentials (ERPs) to all stimuli revealed bilateral sources in superior temporal regions. Compared with the standard ERP, the LD ERP revealed a stronger source in the left superior temporal region in both recordings, whereas the right-sided source became stronger after learning. Consistent with prior studies of auditory plasticity in animals and humans, tone sequence learning induced rapid neurophysiological plasticity in the human central auditory system. The results also suggest that there is asymmetric hemispheric involvement in tone sequence discrimination learning and that discrimination difficulty influences the time course of learning-related neurophysiological changes.

Maturation of human central auditory system activity: the T-complex.

The purpose of this study was to evaluate and describe the maturation of a set of auditory evoked potentials (AEPs) described as the T-complex from a large group of children, adolescents, and young adults who ranged in age from 5 to 20 years of age. The AEPs evoked by brief trains of clicks presented to the left ear were measured at 30 scalp-electrode locations. Analyses focused on age-related latency and amplitude changes in the T-complex recorded at the temporal electrode sites T3 and T5 over the left hemisphere and T4 and T6 over the right hemisphere. The maturation of the T-complex components Na, Ta, and Tb was contrasted with those of the obligatory AEPs P1, N1b, and P2 measured at electrodes C3 and C4. T-complex activity was present in the grand average AEPs of all 14 age groups spanning ages 5-20 years. T-complex components recorded at electrodes T3 and T4 differed in both morphology and maturation rate from those recorded at T5 and T6. In contrast to the prolonged maturation of AEP latency measured at electrodes T5 and T6, the T-complex components measured at electrodes T3 and T4 did not show a significant overall change in peak latency as a function of age. Consistent amplitude and latency correlations were found between the obligatory AEP components P1, N1b and P2 recorded at C3 and C4 and the T-complex components measured at T5 and T6, but not T3 and T4. Distinct patterns of AEP maturation were measured at electrode sites commonly used to record the T-complex. At scalp electrodes located over more posterior temporal areas (T5 and T6), the AEPs were characterized by a prolonged pattern of maturation very similar to that measured at the central electrodes C3 and C4. These findings and others reported in this paper provide strong evidence that the AEPs recorded at electrodes T5 and T6 are not T-complex peaks. In contrast, the AEPs measured at electrodes T3 and T4 over more anterior temporal scalp areas appear largely independent of activity measured at the central electrode locations. The T-complex peaks Ta and Tb measured at these scalp locations mature early, with no overall significant age-related changes in peak latencies. The T-complex is recorded from the temporal electrodes T3 and T4 represents activity of secondary auditory cortex better than, and independent from, midline potentials. Its robust presence in 5-8 year olds supports its potential usefulness in assessing language impairment.

Differential ear effects of profound unilateral deafness on the adult human central auditory system.

This study investigates the effects of profound acquired unilateral deafness on the adult human central auditory system by analyzing long-latency auditory evoked potentials (AEPs) with dipole source modeling methods. AEPs, elicited by clicks presented to the intact ear in 19 adult subjects with profound unilateral deafness and monaurally to each ear in eight adult normal-hearing controls, were recorded with a 31-channel system. The responses in the 70-210 ms time window, encompassing the N1b/P2 and Ta/Tb components of the AEPs, were modeled by a vertically and a laterally oriented dipole source in each hemisphere. Peak latencies and amplitudes of the major components of the dipole waveforms were measured in the hemispheres ipsilateral and contralateral to the stimulated ear. The normal-hearing subjects showed significant ipsilateral-contralateral latency and amplitude differences, with contralateral source activities that were typically larger and peaked earlier than the ipsilateral activities. In addition, the ipsilateral-contralateral amplitude differences from monaural presentation were similar for left and for right ear stimulation. For unilaterally deaf subjects, the previously reported reduction in ipsilateral-contralateral amplitude differences based on scalp waveforms was also observed in the dipole source waveforms. However, analysis of the source dipole activity demonstrated that the reduced inter-hemispheric amplitude differences were ear dependent. Specifically, these changes were found only in those subjects affected by profound left ear unilateral deafness.

A sensitive period for the development of the central auditory system in children with cochlear implants: implications for age of implantation.

The aim of the present experiment was to assess the consequences of cochlear implantation at different ages on the development of the human central auditory system. Our measure of the maturity of central auditory pathways was the latency of the P1 cortical auditory evoked potential. Because P1 latencies vary as a function of chronological age, they can be used to infer the maturational status of auditory pathways in congenitally deafened children who regain hearing after being fit with a cochlear implant. We examined the development of P1 response latencies in 104 congenitally deaf children who had been fit with cochlear implants at ages ranging from 1.3 yr to 17.5 yr and three congenitally deaf adults. The independent variable was the duration of deafness before cochlear implantation. The dependent variable was the latency of the P1 cortical auditory evoked potential. A comparison of P1 latencies in implanted children with those of age-matched normal-hearing peers revealed that implanted children with the longest period of auditory deprivation before implantation-7 or more yr-had abnormal cortical response latencies to speech. Implanted children with the shortest period of auditory deprivation-approximately 3.5 yr or less-evidenced age-appropriate latency responses within 6 mo after the onset of electrical stimulation. Our data suggest that in the absence of normal stimulation there is a sensitive period of about 3.5 yr during which the human central auditory system remains maximally plastic. Plasticity remains in some, but not all children until approximately age 7. After age 7, plasticity is greatly reduced. These data may be relevant to the issue of when best to place a cochlear implant in a congenitally deaf child.

Maturation of human central auditory system activity: separating auditory evoked potentials by dipole source modeling

Objectives: Previous studies have shown that observed patterns of auditory evoked potential (AEP) maturation depend on the scalp location of the recording electrodes. Dipole source modeling incorporates the AEP information recorded at all electrode locations. This should provide a more robust description of auditory system maturation based on age-related changes in AEPs. Thus, the purpose of this study was to evaluate central auditory system maturation based dipole modeling of multi-electrode long-latency AEPs recordings. Methods: AEPs were recorded at 30 scalp-electrode locations from 118 subjects between 5 and 20 years of age. Regional dipole source analysis, using symmetrically located sources, was used to generate a spatio-temporal source model of age-related changes in AEP latency and magnitude. Results: The regional dipole source model separated the AEPs into distinct groups depending on the orientation of the component dipoles. The sagittally oriented dipole sources contained two AEP peaks, comparable in latency to Pa and Pb of the middle latency response (MLR). Although some magnitude changes were noted, latencies of Pa and Pb showed no evidence of age-related change. The tangentially oriented sources contained activity comparable to P 1, N 1b, and P 2. There were various age-related changes in the latency and magnitude of the AEPs represented in the tangential sources. The radially oriented sources contained activity comparable to the T-complex, including Ta, and Tb, that showed only small latency changes with age. In addition, a long-latency component labeled TP 200 was observed. Conclusions: It is possible to distinguish 3 maturation groups: one group reaching maturity at age 6 and comprising the MLR components Pa and Pb, P 2, and the T-complex. A second group that was relatively fast to mature (50%/year) was represented by N 2. A third group was characterized by a slower pattern of maturation with a rate of 11–17%/year and included the AEP peaks P 1, N 1b, and TP 200. The observed latency differences combined with the differences in maturation rate indicate that P 2 is not identical to TP 200. The results also demonstrated the independence of the T-complex components, represented in the radial dipoles, from the P 1, N 1b, and P 2 components, contained in the tangentially oriented dipole sources.

Superior formation of cortical memory traces for melodic patterns in musicians.

The human central auditory system has a remarkable ability to establish memory traces for invariant features in the acoustic environment despite continual acoustic variations in the sounds heard. By recording the memory-related mismatch negativity (MMN) component of the auditory electric and magnetic brain responses as well as behavioral performance, we investigated how subjects learn to discriminate changes in a melodic pattern presented at several frequency levels. In addition, we explored whether musical expertise facilitates this learning. Our data show that especially musicians who perform music primarily without a score learn easily to detect contour changes in a melodic pattern presented at variable frequency levels. After learning, their auditory cortex detects these changes even when their attention is directed away from the sounds. The present results thus show that, after perceptual learning during attentive listening has taken place, changes in a highly complex auditory pattern can be detected automatically by the human auditory cortex and, further, that this process is facilitated by musical expertise.

Plasticity in the adult human central auditory system: evidence from late-onset profound unilateral deafness

Experience-related changes in central nervous system (CNS) activity have been observed in the adult brain of many mammalian species, including humans. In humans, late-onset profound unilateral deafness creates an opportunity to study plasticity in the adult CNS consequent to monaural auditory deprivation. CNS activity was assessed by measuring long-latency auditory evoked potentials (AEPs) recorded from teens and adults with late-onset (post-childhood) profound unilateral deafness. Compared to monaurally stimulated normal-hearing subjects, the AEPs recorded from central electrode sites located over auditory cortical areas showed significant increases in inter-hemispheric waveform cross-correlation coefficients, and in inter-hemispheric AEP peak amplitude correlations. These increases provide evidence of substantial changes from the normal pattern of asymmetrical (contralateral>ipsilateral amplitude) and asynchronous (contralateral earlier than ipsilateral) central auditory system activation in the normal-hearing population to a much more symmetrical and synchronous activation in the unilaterally deaf. These cross-sectional analyses of AEP data recorded from the unilaterally deaf also suggest that the changes in cortical activity occur gradually and continue for at least 2 years after the onset of hearing loss. Analyses of peak amplitude correlations suggest that the increased inter-hemispheric symmetry may be a consequence of changes in the generators producing the N 1 (approximately 100 ms peak latency) potential. These experience-related changes in central auditory system activity following late-onset profound unilateral deafness thus provide evidence of the presence and the time course of auditory system plasticity in the adult brain.

Maturation of human central auditory system activity: evidence from multi-channel evoked potentials

Objective: The purpose of this study was to evaluate central auditory system maturation based on detailed data from multi-electrode recordings of long-latency auditory evoked potentials (AEPs). Methods: AEPs were measured at 30 scalp-electrode locations from 118 subjects between 5 and 20 years of age. Analyses focused on age-related latency and amplitude changes in the P 1, N 1b, P 2, and N 2 peaks of the AEPs generated by a brief train of clicks presented to the left ear. Results: Substantial and unexpected changes that extend well into adolescence were found for both the amplitude and latency of the AEP components. While the maturational changes in latency followed a pattern of gradual change, amplitude changes tended to be more abrupt and step-like. Age-related latency decreases were largest for the P 1 and N 1b peaks. In contrast, P 2 latency did not change significantly and the N 2 peak increased in latency as a function of age. Abrupt changes in P 1, P 1-N 1b, and N 2 peak amplitude (also RMS amplitude) were observed around age 10 at the lateral electrode locations C3 and C4, but not at the midline electrodes Cz and Fz. These changes in amplitude coincided with a sharp increase and plateau in AEP peak and RMS amplitude variability from 9 to 11 years of age. Conclusions: These analyses demonstrated that the observed pattern of AEP maturation depends on the scalp location at which the responses are recorded. The distinct maturational time courses observed for individual AEP peaks support a model of AEP generation in which activity originates from two or more at least partly independent central nervous system pathways. A striking parallel was observed between previously reported maturational changes in auditory cortex synaptic density and, in particular, the age-related changes in P 1 amplitude. The results indicate that some areas of the brain activated by sound stimulation have a maturational time course that extends into adolescence. Maturation of certain auditory processing skills such as speech recognition in noise also has a prolonged time course. This raises the possibility that the emergence of adult-like auditory processing skills may be governed by the same maturing neural processes that affect AEP latency and amplitude.

MAP2 expression in developing dendrites of human brainstem auditory neurons

Immunostaining of cytoskeletal elements has proved to be a useful technique for tracing ontogenetic development in the human central auditory system. In the present study, dendritic development in brainstem auditory nuclei (dorsal and ventral cochlear nuclei, medial and lateral superior olivary nuclei, and inferior colliculus) was studied using an antibody to a microtubule-associated protein, MAP2, a molecule which stabilizes dendritic processes by promoting assembly of microtubules. At 21–22 weeks of gestation, cells within the auditory nuclei first demonstrate cytoplasmic MAP2 immunoreactivity, but no dendritic structures have formed. Filamentous background staining at this stage may represent immunoreactivity in astrocytic processes. By the 24th fetal week, somata of auditory neurons are strongly immunostained and have developed short dendritic processes. During the perinatal period, dendrites extend up to 100–120 μm in length but are still sparsely branched and lack terminal formations. By the sixth postnatal month, neurons in all auditory nuclei have acquired dendritic arbors with a mature appearance. Thus MAP2 immunohistochemistry demonstrates that dendrogenesis in human brainstem auditory nuclei begins 16 weeks prior to term birth but does not reach the stage of mature dendritic morphology until several months into the postnatal period. This extended course of development implies a significant period of time during which neuronal activity could influence dendritic structure and function.

Effect of Adult-Onset Deafness on the Human Central Auditory System

Degenerative change in the central auditory system was assessed in seven subjects with profound bilateral adult-onset deafness. The degree of transneuronal atrophy was determined by measuring cell size at three levels of the brain stem auditory pathway (anteroventral cochlear nucleus, medial superior olivary nucleus, and inferior colliculus). Within subjects, the relative degree of cell shrinkage was similar across all levels of the central pathway. Across subjects, the best neuronal preservation was seen in a case of viral labyrinthitis with 1 year of bilateral dearness and a near-normal population of cochlear ganglion cells. Reduction in cell size was greatest in cases of bacterial labyrinthitis or Scheibe degeneration with reduced populations of ganglion cells and longer periods of deafness. At the level of the cochlear nucleus, there was no consistent difference in cell size between the side stimulated by a functioning prosthetic device and the nonstimulated side.