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At least 343 records · Page 19Linked to original sources
PubMed2005

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↗
PubMed2000

Auditory agnosia and auditory spatial deficits following left hemispheric lesions: evidence for distinct processing pathways.

Auditory recognition and auditory spatial functions were studied in four patients with circumscribed left hemispheric lesions. Patient FD was severely deficient in recognition of environmental sounds but normal in auditory localisation and auditory motion perception. The lesion included the left superior, middle and inferior temporal gyri and lateral auditory areas (as identified in previous anatomical studies), but spared Heschl's gyrus, the acoustic radiation and the thalamus. Patient SD had the same profile as FD, with deficient recognition of environmental sounds but normal auditory localisation and motion perception. The lesion comprised the postero-inferior part of the frontal convexity and the anterior third of the temporal lobe; data from non-human primates indicate that the latter are interconnected with lateral auditory areas. Patient MA was deficient in recognition of environmental sounds, auditory localisation and auditory motion perception, confirming that auditory spatial functions can be disturbed by left unilateral damage; the lesion involved the supratemporal region as well as the temporal, postero-inferior frontal and antero-inferior parietal convexities. Patient CZ was severely deficient in auditory motion perception and partially deficient in auditory localisation, but normal in recognition of environmental sounds; the lesion involved large parts of the parieto-frontal convexity and the supratemporal region. We propose that auditory information is processed in the human auditory cortex along two distinct pathways, one lateral devoted to auditory recognition and one medial and posterior devoted to auditory spatial functions.

Aged↗
PubMed1994

Intra- and extra-uterine development of neonatal 3-channel Lissajous' trajectory of auditory brainstem evoked potentials.

This study compared intra- and extra-uterine maturation of the auditory pathway, using auditory brainstem evoked potentials (ABEPs), recorded with three orthogonal differential electrode configurations. From the three records of each subject, 3-channel Lissajous' trajectories (3CLTs) were derived and analyzed. 107 newborns were compared at the same gestational and post-conceptional (gestational+postnatal) age, from 29 weeks (wks) up to 43 wks. In addition, we explored the effects and neurophysiological consequences of early exposure to extra-uterine life, on the peripheral and central portions of the auditory pathway. Our findings indicate that exposure of premature infants to the extra-uterine environment is associated with advanced peripheral development, but slower central conduction compared to intra-uterine development.

Analysis of Variance↗
PubMed1992

Transient neonatal hypothyroxinemia and the auditory brainstem evoked response.

Ten premature infants with low serum thyroxine levels (less than 84 nmol/L) were compared with 10 biochemically euthyroid infants to determine whether hypothyroxinemia in such infants can lead to alterations in the auditory pathway. The auditory pathway was studied between 6 and 11 wk of life by analyzing brainstem evoked potentials elicited by a 10/s, 75 dB above normal adult hearing level click stimulus presented at the infant's ears. Peak latencies of components I, III, and V and interpeak latencies I-III, III-V, and I-V did not yield statistically significant differences between groups. The present study indicates that untreated neonatal hypothyroxinemia does not lead to abnormalities of auditory brainstem evoked response.

Evoked Potentials, Auditory, Brain Stem↗
PubMed2004

Auditory neural pathway evaluation on sensorineural hearing loss using diffusion tensor imaging.

Diffusion tensor imaging is a new in vivo tool not only for the assessment of white matter structural integrity but also for diagnosis and assessment of disease conditions which disturb tissue structural coherence. In this study, we investigated the integrity of auditory pathway in patients of sensorineural hearing loss by means of fractional anisotropy of water diffusion to see any subtle changes of auditory pathways resulting from sensorineural hearing loss. In addition, this study suggests that the diffusion anisotropy measured by diffusion tensor imaging is highly sensitive to otherwise subtle disease processes not normally seen with conventional magnetic resonance imaging or computed tomography contrast.

Adolescent↗
PubMed2001

Early identification of hearing impairment in patients with type 1 diabetes mellitus.

OBJECTIVE: The aim of this study was to evaluate the cochlear micromechanics and central auditory function in patients with type I diabetes mellitus and to identify the site of possible dysfunction. METHODS: Cochlear activity was evaluated by recording distortion product otoacoustic emissions (DPOAEs). DPOAEs were performed using an ILO 92 Otodynamics Analyser. Functional changes in the retrocochlear auditory pathway were evaluated by auditory brainstem responses (ABRs). DPOAEs and ABRs were measured in 42 normally hearing patients with type 1 diabetes mellitus aged 21 to 42 years, and 33 age- and sex-matched nondiabetic control subjects. RESULTS: Both of the groups (diabetic and control) had normal and undifferentiated results in tonal and impedance audiometry. ABR peripheral transmission time (wave I) and central transmission time (interpeak latencies I-V) were significantly delayed in the diabetic compared with normal subjects, and the mean amplitudes of various DPOAEs were significantly reduced in the diabetic patients compared with the control subjects. CONCLUSIONS: Combined use of different procedures for monitoring central and peripheral portions of the auditory pathway in diabetic patients showed alterations in cochlear micromechanics and the retrocochlear auditory pathway. Hearing impairment in diabetic patients is usually mild and subclinical, and can be detected early by accurate and objective audiometric methods.

Acoustic Impedance Tests↗
PubMed1999

A review of objective methods of evaluating auditory neural pathways.

OBJECTIVES: Review physiological methods of evaluating function of the auditory neural pathways in infants, children, and adults. Present two case studies to demonstrate the usefulness of physiological measures in assessing abnormalities of the auditory neural pathways. STUDY DESIGN: Review of applications of physiological measures of auditory neural function. METHODS: Review otoacoustic emissions, auditory evoked potentials, and efferent reflexes, and discuss their use in identifying disorders of the auditory neural pathways from the cochlea to the cortex. RESULTS: Auditory disorders occur from peripheral to central areas of the neural system. Patients with disorders of the peripheral nerve and/or the input from the cochlear inner hair cells, such as the patients presently described as having auditory neuropathy, demonstrate abnormal efferent reflexes, including middle ear muscle reflexes and efferent suppression of otoacoustic emissions, as well as grossly abnormal brainstem evoked potentials. In contrast, patients with more central disorders can be differentiated by normal results on tests of the neural periphery and abnormal findings on cortical evoked potentials and other measures of central function. CONCLUSIONS: Physiological measures are sensitive, objective, and less variable in assessing neural disorders than traditional behavioral measures such as pure-tone or speech audiometry.

Adolescent↗
PubMed2001

Delay analysis in the auditory brainstem of the rat: comparison with click latency.

Many cells in the auditory brainstem 'phase lock' to tone stimuli. From the changing phase relationship between the stimulus and the neural response in phase-locking cells, the delay between them can be estimated. This delay, however, is consistently greater than the latency measured in response to click stimuli, an important discrepancy. In this paper the different measures of delay, namely phase delay, group delay and signal-front delay are re-examined. An improved method for computing the average group delay is presented, which accounts for the cyclical nature of the phase data. Data were collected from units in successive processing sites of auditory pathway: the auditory nerve, the cochlear nucleus, the trapezoid body and the medial nucleus of the trapezoid body. Low-characteristic frequency (CF) units gave multimodal post-stimulus-time histograms in response to clicks, and showed stepwise decreases in latency with increasing intensity, with the appearance of earlier peaks in the response, rather than shifts in the timing of the peaks. The separation of peaks corresponded to the inverse of the unit's CF. High-CF units also showed a decline in click latency with intensity, but to a lesser degree than low CF units. We present an analysis which explains the difference between click latency and delay, and which in contrast to previous accounts is experimentally testable. We demonstrate that this new framework accounts for the discrepancy between the two measures of delay, and in addition accounts for the observed stepwise shifts in click latency for low-CF units.

Acoustic Stimulation↗
PubMed1993

40-Hz steady state response in awake cats after bilateral chronic lesions in auditory cortices or inferior colliculi.

To reveal the generators of 40-Hz steady state response, the following investigations in awake cat were performed: (i) analyses of 40-Hz SSR without any lesions, and study of stimulus rate; (ii) effect of chronic lesions in the bilateral auditory cortex; (iii) effect of chronic lesions in the bilateral inferior colliculus. The maximum amplitudes were obtained at stimulus rates of 40-50 Hz. In cat with lesions in the bilateral auditory cortex, the wave configurations and the phase were retained but the amplitude was reduced to 90%. In cat with lesions in the inferior colliculus, the wave configurations and the phase were retained but the amplitude was reduced to 60%. These data suggest the following conclusions: (i) cat was a suitable animal model for human's 40-Hz SSR; (ii) the auditory cortex could be one of the generators of 40-Hz SSR; (iii) the inferior colliculus could be an important generator of 40-Hz SSR; (iv) 40-Hz SSR seems to be generated through not only primary auditory pathways, but also nonspecific auditory pathways, which receive auditory information in parallel from the brainstem, thalamus, and cerebrum.

Animals↗
PubMed1996

Anatomical basis for audio-vocal integration in echolocating horseshoe bats.

Neurophysiological recordings suggest that audio-vocal neurons located in the paralemniscal tegmentum of the midbrain in horseshoe bats provide an interface between the pathways for auditory sensory processing and those for the motor control of vocalization. To verify these physiological results anatomically, the projection pattern of the audio-vocally active area in the paralemniscal tegmentum was investigated by using extracellular tracer injections of wheat germ agglutinin conjugated to horseradish peroxidase. Several nuclei of the lemniscal auditory pathway (dorsal nucleus of the lateral lemniscus, central nucleus of the inferior colliculus, lateral superior olive) as well as the nucleus of the central acoustic tract appear to project to the paralemniscal tegmentum. Other possible sources of afferent projections are a small but distinctly labeled structure within the lateral hypothalamic area, the substantia nigra pars compacta, the deep mesencephalic nucleus, the rostral portion of the inferior colliculus, the deep and intermediate layers of the superior colliculus, and several small areas in the rhombencephalic reticular formation. No direct efferent projection from the audio-vocally active area of the paralemniscal tegmentum to primarily auditory structures was found. Instead, the main targets were structures that are involved in the control of different motor patterns. These targets include the deep and intermediate layers of the superior colliculus and the dorsomedial portion of the facial nucleus, both of which most probably control pinna movements in cats, and the reticular formation medial and caudal to the facial nucleus and rostral to the nucleus ambiguus, which represents an area involved in the control of vocalization. Hence, the anatomical projection pattern suggests that the paralemniscal tegmentum in horseshoe bats serves as a link between the processing of auditory information and the control of vocalization and related motor patterns.

Animals↗
PubMed2006

Axon guidance cues in auditory development.

The innervation of the cochlear sensory epithelium is intricately organized, allowing the tonotopy established by the auditory hair cells to be maintained along the ascending auditory pathways. These auditory projections are patterned by several gene families that regulate neurite attraction and repulsion, known as axon guidance cues. In this review, the roles of various axon guidance molecules, including fibroblast growth factor, ephs, semaphorins, netrins and slits, are examined in light of their known contribution to auditory development. Additionally, morphogens are discussed in the context of their recently described influence on axonal pathfinding in other sensory systems. The elucidation of these various mechanisms may guide the development of therapies aimed at maximizing the connectivity of auditory neurons in the context of congenital or acquired sensorineural hearing loss, especially as pertains to cochlear implants. Further afield, improved understanding of the molecular processes which regulate innervation of the organ of Corti during normal development may prove useful in connecting regenerated hair cells to the central nervous system.

Auditory Pathways↗
PubMed1991

The dentate nucleus is a short-latency relay of a primary auditory transmission pathway.

Recordings of unit activity showing 4-6 ms latency responses to a click stimulus provided evidence that the dentate nucleus could function as a short-latency auditory relay. On the basis of these findings, plus fiber fillings from injections of phaseolus leucoagglutinin into the dentate, a new auditory pathway between dorsal and ventral cochlear nuclei, dentate nucleus, and rostral thalamus is proposed. The pathway could provide direct, short-latency transmissions to the motor cortex that bypass the classical auditory receptive cortex.

Acoustic Stimulation↗
PubMed1997

Cochlear dysfunction in IDDM patients with subclinical peripheral neuropathy.

OBJECTIVE: To investigate the function of the auditory pathway from the cochlea to the auditory cortex in subjects with IDDM. RESEARCH DESIGN AND METHODS: Brain stem, middle-, and long-latency auditory-evoked responses and evoked otoacoustic emissions were measured in 48 normally hearing IDDM patients and in age- and sex-matched nondiabetic subjects. Peripheral neuropathy was diagnosed by nerve conduction velocity (NCV) at the peroneal and sural nerves. Auditory brain stem responses (ABRs) reflect auditory pathway function within the brain stem; middle-latency responses (MLRs) and long-latency responses (LLRs) originate from the auditory cortex; and evoked otoacoustic emissions (EOAEs) give objective information about preneural, mechanical elements of the cochlear function. RESULTS: A subclinical peripheral neuropathy was found in 12 diabetic patients. We found higher latencies of waves I (t = 4.4, P < 0.0001), III (t = 3.7, P = 0.0004), and V (t = 2.7, P = 0.008) of ABRs in diabetic patients (I: 1.7 +/- 0.13 ms; III: 3.9 +/- 0.17 ms; V: 5.7 +/- 0.24 ms), compared with those of the control group (I: 1.6 +/- 0.13 ms; III: 3.7 +/- 0.18 ms; V: 5.6 +/- 0.17 ms). However, neither central transmission time (i.e., the wave interpeak I-V) nor MLRs and LLRs were found to be significantly different in diabetic and control subjects. Mean EOAE amplitude was found to be significantly reduced (F = 4.2, P = 0.02) in diabetic patients with a reduced NCV (7.6 +/- 3.9 dB; Scheffé test: P = 0.03), but not in those without neuropathy (9.1 +/- 4.2 dB), compared with the control group (10.8 +/- 3.1 dB). No correlations were found between duration of diabetes and EOAEs or between sural NCV and peroneal NCV and metabolic control. EOAEs were not correlated with peroneal and sural NCVs. CONCLUSIONS: Our results indicate that the early preneural dysfunction of cochlear receptors causes a prolonged activation of the peripheral portion of the auditory pathway, while signal conduction along the central auditory pathway was shown to be normal in diabetes.

Adult↗
PubMed1991

Familial spastic paraplegia: an electrophysiological study of central sensory conduction pathways.

An electrophysiological assessment has been performed studying somatosensory, visual and auditory pathways in clinically affected and unaffected members from 4 pedigrees with the autosomal form of 'pure' familial spastic paraplegia (n = 32). In some members from 2 families, testing of all 3 sensory pathways showed abnormal results, even in those clinically unaffected. In another family, some had abnormal somatosensory and visual pathways, with no involvement of the auditory pathway. In a further family, the somatosensory and brainstem auditory pathways were abnormal, with sparing of the visual pathway. These findings indicate that the neuronal degeneration in familial spastic paraplegia extends beyond the spinal cord and involves the visual and auditory pathways. The differences between families, and the asymptomatic abnormalities in clinically unaffected members, suggest diversity in the expression of the genetic defect.

Evoked Potentials, Auditory, Brain Stem↗
PubMed2005

Evidence for corticofugal modulation of peripheral auditory activity in humans.

Active cochlear micromechanisms, involved in auditory sensitivity, are modulated by the medial olivocochlear efferent system, which projects directly onto the organ of Corti. Both processes can be assessed non-invasively by means of evoked otoacoustic emissions. Animal experiments have revealed top-down control from the auditory cortex to peripheral auditory receptor, supported by anatomical descriptions of descending auditory pathways from auditory areas to the medial olivocochlear efferent system and organ of Corti. Through recording of evoked otoacoustic emissions during presurgical functional brain mapping for refractory epilepsy, we showed that corticofugal modulation of peripheral auditory activity also exists in humans. In 10 epileptic patients, electrical stimulation of the contralateral auditory cortex led to a significant decrease in evoked otoacoustic emission amplitude, whereas no change occurred under stimulation of non-auditory contralateral areas. These findings provide evidence of a cortico-olivocochlear pathway, originating in the auditory cortex and modulating contralateral active cochlear micromechanisms via the medial olivocochlear efferent system, in humans.

Action Potentials↗
PubMed2000

Auditory dysfunction in stroke.

The auditory and vestibular systems share the same end organ and cranial nerve, yet vestibular signs and symptoms are common with stroke, whereas hearing disturbances are much less frequent. Several reasons would appear to account for this striking dissimilarity. One is that the auditory pathway is less ubiquitous than the vestibular pathways. The likelihood that a stroke involves the auditory pathway is, therefore, less on this basis alone. A second difference, to our knowledge not previously reported, is that the auditory pathway is often spared by the most common strokes. This is because major parts of the auditory pathway, such as the cochlear nucleus, inferior colliculus and medial geniculate body, have multiple sources of blood supply. A third well-recognized factor is the redundancy of the central auditory system and its strong bilateral representation above the level of the cochlear nuclei. Consequently, rostral to the cochlear nuclei gross deficits in hearing, such as those measured by standard pure-tone audiometry and speech discrimination, only occur if lesions are bilateral. Furthermore, widespread bilateral lesions of the auditory system typically render the patient unable to respond or are incompatible with life. In contrast, language disorders are more frequent because language is usually unilaterally represented in the cortex. Certainly, cerebral stroke often includes the auditory system, resulting in various types of auditory disorders, but most hemispherical lesions produce subtle hearing dysfunctions that can only be detected with sophisticated psychoacoustic and electrophysiological testing. The purpose of this review is to provide an overview of the auditory system and its blood supply and to review how auditory processing can be affected by stroke. Psychoacoustic and electrophysiological test procedures for identifying lesions in the central auditory system are described. The literature of hearing disorders due to stroke is reviewed and illustrative cases are presented.

Audiometry, Pure-Tone↗
PubMed1996

Effects of (-)-baclofen, clonazepam, and diazepam on tone exposure-induced hyperexcitability of the inferior colliculus in the rat: possible therapeutic implications for pharmacological management of tinnitus and hyperacusis.

Recent investigations in the authors' laboratory have shown that acute tone exposure (4 kHz continuous tone, 104 dB sound pressure level (SPL), 30-min duration) induces increases in the amplitude of click-evoked potentials in the inferior colliculus (IC). These increases have been attributed to a decrease in GABAA-mediated inhibition on IC neurons. In the present study, we examined the effects of three compounds (diazepam, clonazepam, and (-)-baclofen) that are known to enhance GABAergic inhibition on these tone exposure-induced increases and on changes in temporal integration in the IC. (-)-Baclofen was the only one of the three compounds tested that reversed in a dose-dependent manner the effects of tone exposure on both the amplitude of the click-evoked potentials recorded from the IC and on measures of the changes in temporal integration based on these potentials. Diazepam and clonazepam exhibited remarkably different effects on the click-evoked potentials recorded from the surface of the IC. Diazepam caused a dose-dependent decrease in one of the components of the IC potentials that reflects postsynaptic activity in the IC, whereas clonazepam caused a dose-dependent decrease in a peak that reflects input to the IC from the superior olivary complex (SOC). At dosages up to 40 mg/kg, neither diazepam nor clonazepam reversed the changes in temporal integration in the IC that were induced by the tone exposure; diazepam caused a small, but statistically significant, enhancement of the effects of tone exposure on this function. The results of this study show that (-)-baclofen is a potent modulator of both the excitability of neurons in the ascending auditory pathway and the processing of auditory information by IC neurons. The finding of the present study that two benzodiazepines (clonazepam and diazepam) have remarkably different effects on evoked potentials, which reflects both input to the IC and postsynaptic events in the IC neurons, suggests heterogenicity of the GABAA receptor from one structure to another in the ascending auditory pathway. We suggest that (-)-baclofen may be clinically useful in treating disorders of the auditory system that are caused by plasticity in the ascending auditory pathway.

Acoustic Stimulation↗
PubMed1979

"Paradoxic" ear extinction in dichotic listening: possible anatomic significance.

"Paradoxic" extinction in dichotic listening tasks has been attributed to lesions in the interhemispheric auditory pathways, the anatomic courses of which are unknown. The localization of cerebral lesions related to abnormal patterns of dichotic listening was studied in computerized tomographic (CT) scans with a method of anatomic templates. Paradoxic extinction was found consistently with lesions near the lateral wall of the lateral ventricles at the level of the trigone in both left and right hemispheres. On the basis of these findings, we propose that the pathway leaves the auditory cortex traveling backward and upward to arch around the lateral ventricles and join the callosum in its posterior region.

Adolescent↗