Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “auditory”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources

Preservation of the auditory nerve function after translabyrinthine removal of vestibular schwannoma.

OBJECTIVE: To evaluate the function of the postoperative auditory nerve preserved after translabyrinthine (TL) vestibular schwannoma (VS) removal. METHODS: Fifteen patients, who underwent unilateral VS resection via a TL approach, were preserved auditory nerve anatomically. The size and location of VS were measured on MRI preoperatively. After surgery, the electrical stimulation test (EST) or electrically evoked auditory brainstem response (EABR) was performed. RESULTS: Four cases (27%) out of fifteen patients were retained the functional integrity of the auditory nerve after surgery. The maximum tumor size in the group with a positive response to EST or EABR was significantly smaller than that in the group with a negative response to EST. It seems to be difficult to preserve auditory nerve function in cases where a tumor extends to the fundus of internal auditory canal. CONCLUSION: These results suggest that size of tumor and/or extension of tumor to the fundus might be important factors in preserving the auditory nerve function even if using a TL approach.

Adult↗

Pyramidal cell size reduction in schizophrenia: evidence for involvement of auditory feedforward circuits.

BACKGROUND: Subjects with schizophrenia have decreased gray matter volume of auditory cortex in structural imaging studies and exhibit deficits in auditory sensory processing that might reflect impairments of feedforward and/or feedback circuits within the auditory cortex. Recently, we reported that one component of these circuits, pyramidal cells in deep layer 3 of the auditory association cortex (area 42), has reduced mean somal volume in subjects with schizophrenia. To discriminate between involvement of feedforward and feedback circuit components, we examined pyramidal cell somal volume in layer 3 of primary auditory cortex (feedforward) and layer 5 of auditory association cortex (feedback). METHODS: We estimated somal volumes of pyramidal neurons in deep layer 3 of area 41 and layer 5 of area 42 in subjects with schizophrenia (area 41, n = 16; area 42, n = 18), each of whom was matched to one normal comparison subject for gender, age, and postmortem interval. RESULTS: In deep layer 3 of area 41, mean pyramidal cell somal volume was significantly reduced, by 10.4%. No significant reduction was present in layer 5 of area 42. CONCLUSIONS: Pyramidal cell somal volume is reduced in layer 3 of area 41 and area 42, but not in layer 5 of area 42, of subjects with schizophrenia. This pattern of abnormalities is consistent with impairments of auditory feedforward projection neurons.

Adult↗

Reduced auditory processing capacity during vocalization in children with Selective Mutism.

BACKGROUND: Because abnormal Auditory Efferent Activity (AEA) is associated with auditory distortions during vocalization, we tested whether auditory processing is impaired during vocalization in children with Selective Mutism (SM). METHODS: Participants were children with SM and abnormal AEA, children with SM and normal AEA, and normally speaking controls, who had to detect aurally presented target words embedded within word lists under two conditions: silence (single task), and while vocalizing (dual task). To ascertain specificity of auditory-vocal deficit, effects of concurrent vocalizing were also examined during a visual task. RESULTS: Children with SM and abnormal AEA showed impaired auditory processing during vocalization relative to children with SM and normal AEA, and relative to control children. This impairment is specific to the auditory modality and does not reflect difficulties in dual task per se. CONCLUSIONS: The data extends previous findings suggesting that deficient auditory processing is involved in speech selectivity in SM.

Auditory Perception↗

The pattern of auditory brainstem response wave V maturation in cochlear-implanted children.

OBJECTIVE: Maturation of acoustically evoked brainstem responses (ABR) in hearing children is not complete at birth but rather continues over the first two years of life. In particular, it has been established that the decrease in ABR wave V latency can be modeled as the sum of two decaying exponential functions with respective time-constants of 4 and 50 weeks [Eggermont, J.J., Salamy, A., 1988a. Maturational time-course for the ABR in preterm and full term infants. Hear Res 33, 35-47; Eggermont, J.J., Salamy, A., 1988b. Development of ABR parameters in a preterm and a term born population. Ear Hear 9, 283-9]. Here, we investigated the maturation of electrically evoked auditory brainstem responses (EABR) in 55 deaf children who recovered hearing after cochlear implantation, and proposed a predictive model of EABR maturation depending on the onset of deafness. The pattern of EABR maturation over the first 2 years of cochlear implant use was compared with the normal pattern of ABR maturation in hearing children. METHODS: Changes in EABR wave V latency over the 2 years following cochlear implant connection were analyzed in two groups of children. The first group (n=41) consisted of children with early-onset of deafness (mostly congenital), and the second (n=14) of children who had become profoundly deaf after 1 year of age. The modeling of changes in EABR wave V latency with time was based on the mean values from each of the two groups, allowing comparison of the rates of EABR maturation between groups. Differences between EABRs elicited at the basal and apical ends of the implant electrode array were also tested. RESULTS: There was no influence of age at implantation on the rate of wave V latency change. The main factor for EABR changes was the time in sound. Indeed, significant maturation was observed over the first 2 years of implant use only in the group with early-onset deafness. In this group maturation of wave V progressed as in the ABR model of [Eggermont, J.J., Salamy, A., 1988a. Maturational time-course for the ABR in preterm and full term infants. Hear Res 33, 35-47; Eggermont, J.J., Salamy, A., 1988b. Development of ABR parameters in a preterm and a term born population. Ear Hear 9, 283-9] of normal hearing children: a sum of two decaying exponential functions, one showing an early rapid decrease in latency and the other a slower decrease. Remarkably, the time-constants fell well within the ranges described by Eggermont and Salamy (i.e., 3.9 and 68 weeks), consistent with the time-course of the neurophysiological mechanisms presumably involved in auditory pathway maturation during the first 2 years of life: i.e., myelination and increased synaptic efficacy. In contrast, relatively little change in wave V was evident in children with late-onset deafness. In agreement with the notion that EABR maturation follows an apex-to-base gradient as described for ABR, we observed that wave V latencies were longer for the basal than the apical end of the implant electrode array and remained so throughout the study period, whatever the time of onset of deafness. CONCLUSIONS: The findings in the early-onset of deafness group support the theory that auditory pathways remain "frozen" during the period of sensory deprivation until cochlear implant rehabilitation restores the normal chronology of maturational processes. In children with late-onset deafness, however, some maturational processes may occur before the onset of deafness, and thus less additional maturation is required during the first two years of implant use resulting in no significant EABR latency changes being observed in this period. The results suggest that the rehabilitation-induced plasticity of the auditory pathways is, in case of late auditory deprivation, unlikely to result in neurophysiological outcomes similar to those observed in children with early auditory deprivation. SIGNIFICANCE: Changes in EABR wave V latency over the first 2 years of cochlear implant use were found to be well fitted by the sum of two decaying exponential functions in children with early-onset deafness. This is in line with the maturation of ABR wave V latency in normal-hearing children over the first two years of life. Further studies are needed to assess whether the differences observed in terms of auditory pathways maturation are associated with consistent differences in terms of language development.

Adolescent↗

CNTFRalpha and CNTF expressions in the auditory brainstem: light and electron microscopy study.

CNTF receptor alpha (CNTFRalpha) is involved in the development, the maintenance and the regeneration of a variety of brain structures. However, its in vivo distribution has not been determined in the auditory system. CNTFRalpha expression was studied in developing and adult rat brainstem auditory nuclei using immunohistochemistry. At birth, the CNTFRalpha immunolabeling was clearly present in somata of the external nucleus of the inferior colliculus but was diffuse throughout brainstem auditory nuclei. The labeling was present in most brainstem auditory nuclei by post-natal day (PND) 6. The intensity of the staining subsequently increased to its highest level at PND21 and decreased to an adult-like appearance by the fourth post-natal week. In adult, CNTFRalpha labeling occurred in most neurons of the cochlear nucleus (CN), the lateral superior olive (LSO), the medial superior olive (MSO), and the medial nucleus of the trapezoid body (MNTB). CNTFRalpha labeling first appeared in the central nucleus of the inferior colliculus (IC) by the end of the fourth week. There was a general increase in the expression of CNTFRalpha that begins prior to the onset of hearing and reaches its highest level after this important developmental stage. Ultrastructural analysis in the adult ventral CN revealed the presence of CNTFR in post-synaptic sites. The presence of CNTF has been investigated in the adult using both Western blot and immunohistochemistry. Western blot showed the presence of CNTF in both peripheral and central auditory structures. The CNTF label was generally localized to the somatic compartment, in axons and as puncta surrounding neuronal cell bodies and dendrites. Differential CNTF labeling was observed between the different auditory nuclei. CNTF staining is present in neurons of the CN, the MNTB and the LSO, while it is restricted to axons and puncta surrounding neuronal somata in the IC. The clear presence of CNTFRalpha at post-synaptic terminals and that of its ligand the CNTF in axons and puncta surrounding neuronal cell bodies suggest an anterograde mode of action for CNTF in the central auditory system.

Animals↗

Eph proteins and the assembly of auditory circuits.

Many kinds of information are carried in the acoustic signal that reaches auditory receptor cells in the cochlea. The analysis of this information is possible in large part because of the neuronal architecture of the auditory system. The mechanisms that establish the precise circuitry that underlies auditory processing have not yet been identified. The Eph receptor tyrosine kinases and their ligands are proteins that regulate axon guidance and have been shown to contribute to the establishment of topographic projections in several areas of the nervous system. Several studies have begun to investigate whether these proteins are involved in the formation of auditory system connections. Studies of gene expression show that Eph proteins are extensively expressed in structures of the inner ear as well as in neurons in the peripheral and central components of the auditory system. Functional studies have demonstrated that Eph signaling influences the assembly of auditory pathways. These studies suggest that Eph protein signaling has a significant role in the formation of auditory circuitry.

Animals↗

Auditory processing deficits in rats with neonatal hypoxic-ischemic injury.

Hypoxia-ischemia (HI) refers to reduced blood oxygenation and/or a diminished amount of blood perfusing the brain, and is associated with premature birth/very low birth weight (VLBW). HI represents a common cause of injury to the perinatal brain. Indeed, a significant number of premature/VLBW infants go on to demonstrate cognitive/behavioral deficits, with particularly high incidence of disruptions in language development. Auditory processing deficits, in turn, have been suggested to play a causal role in the development of language impairments. Specifically, the inability to identify fast elements in speech is purported to exert cascading detrimental effects on phonological discrimination, processing, and identification. Based on this convergent evidence, the current studies address auditory processing evaluation in a rodent model of HI injury induced on postnatal days 1, 7, or 10 (which in turn is well accepted as modeling HI-related injury to the perinatal human). Induced injuries were followed by a battery of auditory testing, and a spatial maze assessment, performed both during juvenile and adult periods. Results indicate that rats suffering from these early HI insults performed significantly worse than shams on tasks requiring rapid auditory processing, and on a test of spatial learning (Morris water maze (MWM)), although these effects were not seen on simpler versions of auditory tasks or on a water escape assessment (thus ruling out hearing/motor impairments). Correlations were found between performance on rapid auditory and spatial behavioral tasks and neuroanatomical measures for HI animals such as: the volume of the hippocampus, cerebral cortex, ventricles, and/or the area of the corpus callosum. Cumulative findings suggest that perinatal HI injury in the rat may lead to neurodevelopmental damage associated, in turn, with auditory processing and/or learning and memory impairments. As such, the current model may have critical implications for the study of neurophysiological underpinnings of cognitive deficits in premature/VLBW infants.

Aging↗

Noise-induced cell death in the mouse medial geniculate body and primary auditory cortex.

Noise-induced effects within the inner ear have been well investigated for several years. However, this peripheral damage cannot fully explain the audiological symptoms in noise-induced hearing loss (NIHL), e.g. tinnitus, recruitment, reduced speech intelligibility, hyperacusis. There are few reports on central noise effects. Noise can induce an apoptosis of neuronal tissue within the lower auditory pathway. Higher auditory structures (e.g. medial geniculate body, auditory cortex) are characterized by metabolic changes after noise exposure. However, little is known about the microstructural changes of the higher auditory pathway after noise exposure. The present paper was therefore aimed at investigating the cell density in the medial geniculate body (MGB) and the primary auditory cortex (AI) after noise exposure. Normal hearing mice were exposed to noise (10 kHz center frequency at 115 dB SPL for 3 h) at the age of 21 days under anesthesia (Ketamin/Rompun, 10:1). After 1 week, auditory brainstem response recordings (ABR) were performed in noise exposed and normal hearing animals. After fixation, the brain was microdissected and stained (Kluever-Barrera). The cell density in the MGB subdivisions and the AI were determined by counting the cells within a grid. Noise-exposed animals showed a significant ABR threshold shift over the whole frequency range. Cell density was significantly reduced in all subdivisions of the MGB and in layers IV-VI of AI. The present findings demonstrate a significant noise-induced change of the neuronal cytoarchitecture in central key areas of auditory processing. These changes could contribute to the complex psychoacoustic symptoms after NIHL.

Acoustic Stimulation↗

Spatiotemporal properties of the BOLD response in the songbirds' auditory circuit during a variety of listening tasks.

Auditory fMRI in humans has recently received increasing attention from cognitive neuroscientists as a tool to understand mental processing of learned acoustic sequences and analyzing speech recognition and development of musical skills. The present study introduces this tool in a well-documented animal model for vocal learning, the songbird, and provides fundamental insight in the main technical issues associated with auditory fMRI in these songbirds. Stimulation protocols with various listening tasks lead to appropriate activation of successive relays in the songbirds' auditory pathway. The elicited BOLD response is also region and stimulus specific, and its temporal aspects provide accurate measures of the changes in brain physiology induced by the acoustic stimuli. Extensive repetition of an identical stimulus does not lead to habituation of the response in the primary or secondary telencephalic auditory regions of anesthetized subjects. The BOLD signal intensity changes during a stimulation and subsequent rest period have a very specific time course which shows a remarkable resemblance to auditory evoked BOLD responses commonly observed in human subjects. This observation indicates that auditory fMRI in the songbird may establish a link between auditory related neuro-imaging studies done in humans and the large body of neuro-ethological research on song learning and neuro-plasticity performed in songbirds.

Acoustic Stimulation↗

Cross-modal processing in auditory and visual working memory.

This study aimed to further explore processing of auditory and visual stimuli in working memory. Smith and Jonides (1997) [Smith, E.E., Jonides, J., 1997. Working memory: A view from neuroimaging. Cogn. Psychol. 33, 5-42] described a modified working memory model in which visual input is automatically transformed into a phonological code. To study this process, auditory and the corresponding visual stimuli were presented in a variant of the 2-back task which involved changes from the auditory to the visual modality and vice versa. Brain activation patterns underlying visual and auditory processing as well as transformation mechanisms were analyzed. Results yielded a significant activation in the left primary auditory cortex associated with transformation of visual into auditory information which reflects the matching and recoding of a stored item and its modality. This finding yields empirical evidence for a transformation of visual input into a phonological code, with the auditory cortex as the neural correlate of the recoding process in working memory.

Adult↗

The neural networks underlying endogenous auditory covert orienting and reorienting.

Auditory information communicated through vocalizations, music, or sounds in the environment is commonly used to orient and direct attention to different locations in extrapersonal space. The neural networks subserving attention to auditory space remain poorly understood in comparison to our knowledge about attention in the visual system. The present study investigated whether a parietal-prefrontal right-hemisphere network controls endogenous orienting and reorienting of attention to the location of sounds just as it does for visual-spatial information. Seventeen healthy adults underwent event-related functional magnetic resonance imaging (FMRI) while performing an endogenous auditory orienting task, in which peripheral cues correctly (valid) or incorrectly (invalid) specified the location of a forthcoming sound. The results showed that a right precuneus and bilateral temporal-frontal network mediated the reorienting of auditory attention at both short and long stimulus onset asynchronies (SOAs). In contrast, the more automatic stage of auditory reorienting at the shorter SOA was associated with activation in a bilateral inferior parietal-frontal oculomotor network. These findings suggest that the reorienting of auditory attention is generally supported by a similar inferior parietal-frontal network as visual attention, but in both hemispheres. However, peripheral auditory cues also appear to elicit an automatic orienting response to the spatial location of a sound followed by a period of reduced processing of information that occurs in the same location later in time.

Adult↗

Auditory hair cell explant co-cultures promote the differentiation of stem cells into bipolar neurons.

Auditory neurons, the target neurons of the cochlear implant, degenerate following a sensorineural hearing loss. The goal of this research is to direct the differentiation of embryonic stem cells (SCs) into bipolar auditory neurons that can be used to replace degenerating neurons in the deafened mammalian cochlea. Successful replacement of auditory neurons is likely to result in improved clinical outcomes for cochlear implant recipients. We examined two post-natal auditory co-culture models with and without neurotrophic support, for their potential to direct the differentiation of mouse embryonic SCs into characteristic, bipolar, auditory neurons. The differentiation of SCs into neuron-like cells was facilitated by co-culture with auditory neurons or hair cell explants, isolated from post-natal day five rats. The most successful combination was the co-culture of hair cell explants with whole embryoid bodies, which resulted in significantly greater numbers of neurofilament-positive, neuron-like cells. While further characterization of these differentiated cells will be essential before transplantation studies commence, these data illustrate the effectiveness of post-natal hair cell explant co-culture, at providing valuable molecular cues for directed differentiation of SCs towards an auditory neuron lineage.

Animals↗

Intensity coding of auditory stimuli: an fMRI study.

The effect of stimulus intensity (sound pressure level, SPL) of auditory stimuli on the BOLD response in the auditory cortex was investigated in 14 young and healthy subjects, with no hearing abnormalities, using echo-planar, functional magnetic resonance imaging (fMRI) during a verbal and a non-verbal auditory discrimination task. The stimuli were presented block-wise at three different intensities: 95, 85 and 75 dB (SPL). All subjects showed fMRI signal increases in superior temporal gyrus (STG) covering primary and secondary auditory cortex. Most importantly, the spatial extent of the fMRI response in STG increased with increasing stimulus intensity. It is hypothesized that spreading of excitation is associated with the encoding of increasing stimulus intensity levels. In addition, we found bifrontal activation supposedly evoked by the auditory-articulary loop of working memory. The results presented here should assist in the design of optimal activation strategies for studying the auditory cortex with fMRI paradigms and may help in understanding intensity coding of auditory stimuli.

Adult↗

Cortical localisation of the visual and auditory word form areas: a reconsideration of the evidence.

In this paper we examine the evidence for human brain areas dedicated to visual or auditory word form processing by comparing cortical activation for auditory word repetition, reading, picture naming, and environmental sound naming. Both reading and auditory word repetition activated left lateralised regions in the frontal operculum (Broca's area), posterior superior temporal gyrus (Wernicke's area), posterior inferior temporal cortex, and a region in the mid superior temporal sulcus relative to baseline conditions that controlled for sensory input and motor output processing. In addition, auditory word repetition increased activation in a lateral region of the left mid superior temporal gyrus but critically, this area is not specific to auditory word processing, it is also activated in response to environmental sounds. There were no reading specific activations, even in the areas previously claimed as visual word form areas: activations were either common to reading and auditory word repetition or common to reading and picture naming. We conclude that there is no current evidence for cortical sites dedicated to visual or auditory word form processing.

Adult↗

Cortical auditory disorder caused by bilateral strategic cerebral bleedings. Analysis of two cases.

The authors present the anatomical and clinical features of cortical auditory dysfunction in two patients, in whom hypertensive bleedings destroyed the cortical auditory centres in both hemispheres. The second haemorrhage occurred four years after the first bleeding in both cases. The bleedings isolated the cortical hearing centres due to the destruction of the right and left temporal white matter. During the clinical course the symptomatology has changed in both patients: pure word deafness has transformed to cortical deafness and generalised auditory agnosia. Normal pattern of brain stem auditory evoked potentials suggested intact auditory pathways. Authors conclude that transformation of clinical forms of cortical auditory disorder can be explained by the tissue reaction to the subcortical bleeding in the cortical auditory centres.

Auditory Cortex↗

Auditory cortical plasticity: a comparison with other sensory systems.

The auditory cortex has a crucial role in higher cognitive functions, including the perception of speech, music and auditory space. Cortical plasticity, as in other sensory systems, is used in the fine tuning of the auditory system for these higher functions. Auditory cortical plasticity can also be demonstrated after lesions of the cochlea and it appears to participate in generating tinnitus. Early musical training leads to an expansion in the representation of complex harmonic sounds in the auditory cortex. Similarly, the early phonetic environment has a strong influence on speech development and, presumably, on the cortical organization of speech. In auditory spatial perception, the spectral cues generated by the head and outer ears vary between individuals and have to be calibrated by learning, which most probably takes place at the cortical level. The neural mechanisms of plasticity are likely to be the same across all cortical regions. It should be useful, therefore, to relate some of the findings and hypotheses about auditory cortical plasticity to previous studies of other sensory systems.

Animals↗

Abnormal auditory neural networks in patients with right hemispheric infarction, chronic dizziness, and moyamoya disease: a magnetoencephalogram study.

The purpose of this study was to determine whether the auditory cortex is sensitive to cortical insults and to determine the specificity of the insults in three clinical situations with different cortical involvement. Auditory-evoked magnetic fields of ten normal subjects, 8 patients with right hemispheric infarction, 11 with chronic dizziness, and 2 with moyamoya disease were measured. To analyze the abnormality of auditory neural networks, the magnitude ratio and the angle difference (Deltatheta) between response vectors, which were determined from maximum current arrows corresponding to the N100m peak for contralateral and ipsilateral stimuli were used. A normal range of the parameters was defined so that abnormal values could be determined. Of the three parameters, Deltatheta was the most sensitive: 4 patients with right hemispheric infarction, 4 with chronic dizziness, and 1 with moyamoya disease had abnormal Deltatheta. The electrical activity in the patients with such abnormal Deltathetas had a circular current pattern. These findings suggest that right infarction lesions sometime affect the left auditory neural network, dizziness is caused by abnormal neural networks between the vestibular cortical area and the auditory cortex or by an imbalance between left and right auditory-cortex activities, and moyamoya-disease patients have almost normal auditory-electrical activity.

Acoustic Stimulation↗

The multichannel auditory brain stem implant: performance in twenty patients.

The auditory brain stem implant has been used effectively to provide hearing sensations to individuals deafened by bilateral auditory nerve tumors (neurofibromatosis type 2). During tumor removal, the auditory brain stem implant is implanted into the lateral recess of the fourth ventricle by a translabyrinthine approach and is intended to stimulate auditory neurons of the cochlear nucleus complex. A new eight-electrode multichannel auditory brain stem implant was developed and evaluated in 20 patients who had at least 3 months' experience with the device. Mild nonauditory sensations (primarily tingling in the head or torso) were encountered in some instances but could be managed by changing the stimulus characteristics or excluding electrodes. Testing of perceptual performance indicated significant benefit from the device for communication purposes, including sound-only sentence recognition scores in three patients ranging from 49% to 58% and ability to converse on the telephone. These results indicate that significant auditory benefit can be derived from direct multichannel electrical stimulation of the auditory portion of the human brain stem.

Acoustics↗