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Correlations of neuroanatomical measures to auditory brain stem response latencies.

Magnetic resonance imaging (MRI) was used to obtain measures presumed to scale the dimensions of the lower auditory pathway in humans for the purpose of further defining the relationship between length of the auditory pathway and auditory brain stem response (ABR) latencies. Specifically, measurements of soft tissue structures, that is, the eighth nerve and brain stem, were made for comparison with skull dimensions and ABR latencies. It was hypothesized that the brain stem dimensions covary significantly with skull dimensions and that the ABR parameters covary with both skull and brain stem dimensions. In general, only weak correlations were obtained with coefficients failing to reach statistical significance for most comparisons. These findings suggest that variance in ABR latencies cannot be attributed completely to variance in brain stem dimensions and raise suspicion that skull dimensions do not directly reflect brain stem dimensions.

Acoustic Impedance Tests↗

Mismatch negativity in the neurophysiologic/behavioral evaluation of auditory processing deficits: a case study.

The subject of this case report is an 18-year-old woman with grossly abnormal auditory brain stem response (ABR), normal peripheral hearing, and specific behavioral auditory processing deficits. Auditory middle latency responses (MLRs) and cortical potentials N1, P2, and P300 were intact. The mismatch negativity (MMN) was normal in response to certain synthesized speech stimuli and impaired to others--consistent with her behavioral discrimination of these stimuli. Behavioral tests of auditory processing were consistent with auditory brain stem dysfunction. A neuropsychological evaluation revealed normal intellectual and academic performance. The subject was in her first year of college at the time of the evaluation. This case study is important because: (1) Although there have been several reports of absent/abnormal ABR with preserved peripheral hearing and deficits in auditory processing, little is known about the specific nature of the auditory deficits experienced by these individuals. Such information may be valuable to the clinical management of patients with this constellation of findings. (2) Of interest is the information that the mismatch negativity (MMN) cortical event-related potential can bring to the evaluation of patients with auditory processing deficits. The MMN reflects central auditory processing of small acoustic differences and may provide an objective measure of auditory discrimination. (3) From a theorectical standpoint, a patient with neural deficits affecting specific components of the auditory pathway provides insight into the relationship between evoked potentials and physiological mechanisms of auditory processing. How do various components of the auditory pathway contribute to speech discrimination? How might evoked potentials reflect the processes underlying the neural coding of specific features of speech stimuli such as timing and spectral cues?

Achievement↗

Central auditory development in children with cochlear implants: clinical implications.

A common finding in developmental neurobiology is that stimulation must be delivered to a sensory system within a narrow window of time (a sensitive period) during development in order for that sensory system to develop normally. Experiments with congenitally deaf children have allowed us to establish the existence and time limits of a sensitive period for the development of central auditory pathways in humans. Using the latency of cortical auditory evoked potentials (CAEPs) as a measure we have found that central auditory pathways are maximally plastic for a period of about 3.5 years. If the stimulation is delivered within that period CAEP latencies reach age-normal values within 3-6 months after stimulation. However, if stimulation is withheld for more than 7 years, CAEP latencies decrease significantly over a period of approximately 1 month following the onset of stimulation. They then remain constant or change very slowly over months or years. The lack of development of the central auditory system in congenitally deaf children implanted after 7 years is correlated with relatively poor development of speech and language skills [Geers, this vol, pp 50-65]. Animal models suggest that the primary auditory cortex may be functionally decoupled from higher order auditory cortex due to restricted development of inter- and intracortical connections in late-implanted children [Kral and Tillein, this vol, pp 89-108]. Another aspect of plasticity that works against late-implanted children is the reorganization of higher order cortex by other sensory modalities (e.g. vision). The hypothesis of decoupling of primary auditory cortex from higher order auditory cortex in children deprived of sound for a long time may explain the speech perception and oral language learning difficulties of children who receive an implant after the end of the sensitive period.

Auditory Cortex↗

Central auditory imperception.

The development of clinically applicable techniques for the evaluation of hearing impairment caused by lesions of the central auditory pathways has increased clinical interest in the anatomy and physiology of these pathways. A conceptualization of present understanding of the anatomy and physiology of the central auditory pathways is presented. Clinical tests based on reduction of redundancy of the speech message, degradation of speech and binaural interations are presented. Specifically performance-intensity functions, filtered speech tests, competing message tests and time-compressed speech tests are presented with the emphasis on our experience with time-compressed speech tests. With proper use of these tests not only can central auditory impairments by detected, but brain stem lesions can be distinguished from cortical lesions.

Animals↗

Altered pathways for auditory discrimination and recognition memory in preterm infants.

Preterm infants are at increased risk for cognitive disorders, including impairments in recognition memory. This study evaluated the effects of extreme prematurity on the neural pathway for auditory recognition memory using event-related potentials (ERPs), a neurophysiological technique widely used in cognitive neuroscience. ERPs were recorded at term postmenstrual age in 35 preterm infants born at less than 32 weeks' gestation (22 males, 13 females; mean birthweight ([BW] 1154g, SD 374g) with normal brain ultrasounds, compared with 40 healthy, term newborns (1 to 3 days of age; 20 males, 20 females; BW 3672g, SD 420g). Because infants must be able to detect and discriminate sounds before recognizing them, two paradigms were used to assess these functions. The first evaluated the detection and discrimination of speech sounds. The second tested recognition of the mother's voice compared with a stranger's. Results showed significantly different patterns of speech sound discrimination in preterm infants compared with term infants. No evidence of maternal voice recognition was elicited from the preterm infants. No specific patterns of auditory detection or discrimination were associated with patterns of recognition memory, suggesting that the function of multiple neural pathways may have been altered in this group of preterm infants. These results provide a functional corroboration of magnetic resonance imaging studies showing effects of prematurity on early brain development, even among preterm infants with normal cranial ultrasonography.

Auditory Cortex↗

P1 latency as a biomarker for central auditory development in children with hearing impairment.

We used the latency of the P1 cortical auditory-evoked potential (CAEP) as a biomarker for the development of central auditory pathways in three children who received intervention through hearing aids and/or cochlear implants. Our goal was to examine the clinical feasibility of using the latency of the P1 CAEP as an objective tool to evaluate whether acoustic amplification for hearing-impaired children has provided sufficient stimulation for normal development of central auditory pathways. If clinicians have such a marker, then they can more confidently make a decision about whether to provide a child with a cochlear implant following an appropriate hearing-aid trial. Using the same marker, clinicians will also be able to monitor the maturation of central auditory pathways once electrical stimulation is initiated.

Auditory Pathways↗

Auditory plasticity and hyperactivity following cochlear damage.

This paper will review some of the functional changes that occur in the central auditory pathway after the cochlea is damaged by acoustic overstimulation or by carboplatin, an ototoxic drug that selectively destroys inner hair cells (IHCs) in the chinchilla. Acoustic trauma typically impairs the sensitivity and tuning of auditory nerve fibers and reduces the neural output of the cochlea. Surprisingly, our results show that restricted cochlear damage enhances neural activity in the central auditory pathway. Despite a reduction in the auditory-nerve compound action potential (CAP), the local field potential from the inferior colliculus (IC) increases at a faster than normal rate and its maximum amplitude is enhanced at frequencies below the region of hearing loss. To determine if this enhancement was due to loss of sideband inhibition, we recorded from single neurons in the IC and dorsal cochlear nucleus before and after presenting a traumatizing above the unit's characteristic frequency (CF). Following the exposure, some neurons showed substantial broadening of tuning below CF, less inhibition, and a significant increase in discharge rate, consistent with a model involving loss of sideband inhibition. The central auditory system of the chinchilla can be deprived of some of its cochlear inputs by selectively destroying IHCs with carboplatin. Selective IHC loss reduces the amplitude of the CAP without affecting the threshold and tuning of the remaining auditory nerve fibers. Although the output of the cochlea is reduced in proportion to the amount of IHC loss, the IC response shows only a modest amplitude reduction, and remarkably, the response of the auditory cortex is enhanced. These results suggest that the gain of the central auditory pathway can be up- or down regulated to compensate for the amount of neural activity from the cochlea.

Animals↗

MR imaging of 495 consecutive cases with sensorineural hearing loss.

PURPOSE: To examine patients with sensorineural hearing loss (SNHL) with MR. MATERIAL AND METHODS: 495 consecutive patients with SNHL and 120 age-matched healthy controls were examined. Spin-echo (SE) and fast spin-echo (FSE) images were used with 1.5 T equipment. RESULTS: An intracranial abnormality was found in 211 (42.6%) of the patients with 95 (19.2%) along the acoustic pathway. Eleven of the 95 patients had sensory hearing loss while 84 had neural hearing loss with the retrocochlear auditory pathway affected by lesions. In 62 of the 84 patients, the internal acoustic canal and cerebellopontine angle were involved. Twenty-two patients had intra-axial lesions. The controls had no pathologic changes along the auditory pathway. CONCLUSION: MR imaging in a patient with SNHL must cover the entire acoustic pathway from the cochlea to the superior temporal gyrus, and all the components of the auditory pathway should be scrutinized. The FSE-technique can be used to detect the lesions causing SNHL. FSE-sequences can replace SE-sequences.

Adolescent↗

Healthy-side dominance of middle- and long-latency neuromagnetic fields in idiopathic sudden sensorineural hearing loss.

Any lesion along the neural axis may induce a subsequent functional reorganization at the level above. The present study used magnetoencephalography to investigate auditory-evoked magnetic fields [a component of the middle-latency auditory evoked fields peaking at approximately 50 ms (P50m) and a component of the long-latency auditory evoked fields peaking at approximately 100 ms (N100m)] on stimulation of both healthy and affected ears in patients with acute unilateral idiopathic sudden sensorineural hearing loss (ISSNHL) of moderate degree in order to elucidate the functional plasticity of the auditory system. Sixteen right-handed, previously untreated adult patients with acute unilateral left (n = 8) or right (n = 8) ISSNHL of moderate degree were studied. Sixteen right-handed healthy volunteers with normal hearing served as control. Auditory neuromagnetic responses, measured by a whole-head 306-channel neuromagnetometer, were detected by monaural tone stimulation applied to affected and healthy ears, respectively, in different sessions. Intragroup and intergroup interhemispheric differences of peak dipole strengths and latencies of P50m and N100m, respectively, to monaural tones were evaluated. Healthy-side amplitude dominance of both P50m and N100m was found in ISSNHL, i.e. contralateral dominance was preserved on affected-ear stimulation but ipsilateral dominance was seen on healthy-ear stimulation. The phenomena could be attributed to the combined contralateral attenuation and ipsilateral enhancement of P50m and N100m activity in response to healthy-ear stimulation. Our findings confirmed that functional modulation can occur within the first few tens of milliseconds of evoked response at the auditory cortex in ISSNHL. The mechanisms of healthy-side dominance might be ascribed to a functional retune of auditory pathways, i.e. conjoined contralateral inhibition and ipsilateral excitation of the auditory pathway in response to healthy-ear stimulation. The effect could be registered in cortical responses.

Acoustic Stimulation↗

Neurotoxic effects of rubber factory environment. An auditory evoked potential study.

The effects of rubber factory environment on functional integrity of auditory pathway have been studied in forty rubber factory workers using Brainstem Auditory Evoked Potentials (BAEPs) technique to detect early subclinical impairments. Results indicate that 47 percent of the workers showed abnormalities in prolongations of either peak latencies or interpeak latencies when compared with age and sex matched control subjects not exposed to rubber factory environment. The percent distribution of abnormalities (ears affected) were in the order of extrusion and calendering (75%) > vulcanising (41.66%) > mixing (28.57%) > loading and dispatch (23.07%) > tubing (18.75%) sections of the factory. This incidence of abnormalities may be attributed to solvents being used in these units of rubber factory. These findings suggest that rubber factory environment does affect auditory pathway in the brainstem.

Adolescent↗

[The auditory evoked brain stem potential andits value for clinical diagnosis].

Auditory evoked brain stem potentials (seven waves within the first 10 milliseconds after the stimulus) obtained from the intercalated nuclei within the auditory pathway by averaging are suitable for a functional diagnosis of the brain stem. Disorders affecting the auditory pathway (direct or indirect tumour pressure or infiltrates, demyelinisation processes, traumatic brain stem injuries, ischemia) from the acoustic nerve through the cochlear nuclei, the superior olivary nuclei, the nuclei of the lateral lemnisci, the inferior collicular nuclei, to the medial geniculate bodies can be identified and used for the topical diagnosis.

Adolescent↗

Auditory evoked responses during different phases of menstrual cycle.

The electrophysiological correlates of changes in sensory function during menstrual cycle has already been studied and attributed to the hormonal influence. Effects of estrogen and progesterone on waves of auditory brainstem responses (ABR) have been reported and a hypothesis has been proposed that sex steroids have more influence on central auditory pathways. As mid-latency responses (MLRs) and slow vertex responses (SVRs) are better indicators of central auditory pathways, so MLRs and SVRs were also recorded besides ABRs in the present study. Waves of ABRs, MLRs & SVRs were recorded in 20 normal cycling females in 4 different phases of menstrual cycles from Cz-A1 and Cz-A2 position with alternating 90dB sound pressure click stimuli. Contralateral ear was masked with a white noise of -40 dBHL. With the same setting by changing the number of click stimuli, intervals of stimuli and filter bandpass the above 3 recordings were taken. The evoked responses in females having ovulatory cycles were compared within the four phases using ANOVA test. There is a trend of increase in peak latencies of ABR waves III and V and IPL I-V in estrogen-peak midcycle while decrease in latencies in progesterone-peak (interpeak latency) midluteal phase. Peak latencies of MLR waves No, Po, Na, Pa and Pb also show a same trend. SVR waves P2 and N2 are significantly delayed in mid-cycle (178.80 +/- 20.49, 276.65 +/- 18.32) while conduction is faster in midluteal phase (166.45 +/- 17.41, 261.95 +/- 21.07). Smallest latencies of all the waves are occurring during menstruation. These findings are suggesting that normal cyclical variations in the levels of estrogen and progesterone during menstrual cycle do affect the auditory pathways and effects are better seen on the central component.

Acoustic Stimulation↗

A map of visual space induced in primary auditory cortex.

Maps of sensory surfaces are a fundamental feature of sensory cortical areas of the brain. The relative roles of afferents and targets in forming neocortical maps in higher mammals can be examined in ferrets in which retinal inputs are directed into the auditory pathway. In these animals, the primary auditory cortex contains a systematic representation of the retina (and of visual space) rather than a representation of the cochlea (and of sound frequency). A representation of a two-dimensional sensory epithelium, the retina, in cortex that normally represents a one-dimensional epithelium, the cochlea, suggests that the same cortical area can support different types of maps. Topography in the visual map arises both from thalamocortical projections that are characteristic of the auditory pathway and from patterns of retinal activity that provide the input to the map.

Animals↗

Influence of unilateral deafness on auditory evoked magnetic field.

To investigate the effect of unilateral deafness on central auditory mechanisms, we examined patients with unilateral deafness of various durations. Auditory evoked magnetic fields (AEF) were recorded using a whole-head neuromagnetometer. In patients who had unilateral deafness for more than 3 weeks, the average N100m latency in the ipsilateral hemisphere did not differ from that in the contralateral hemisphere. In addition, in some patients with congenital or early onset deafness, the equivalent current dipole (ECD) moment was larger in the ipsilateral hemisphere than in the contralateral hemisphere. These findings suggest that unilateral deafness may cause reorganization of the central auditory pathway. They also suggest that central auditory pathway in adults has some plasticity, though not as much as in childhood.

Adult↗

Direct projections from cochlear nuclear complex to auditory thalamus in the rat.

It is known that the dorsal cochlear nucleus and medial geniculate body in the auditory system receive significant inputs from somatosensory and visual-motor sources, but the purpose of such inputs is not totally understood. Moreover, a direct connection of these structures has not been demonstrated, because it is generally accepted that the inferior colliculus is an obligatory relay for all ascending input. In the present study, we have used auditory neurophysiology, double labeling with anterograde tracers, and retrograde tracers to investigate the ascending projections of the cochlear nuclear complex. We demonstrate that the dorsal cochlear nucleus and the small cell cap of the ventral cochlear nucleus have a direct projection to the medial division of the medial geniculate body. These direct projections from the cochlear nucleus complex bypass the inferior colliculus and are widely distributed within the medial division of the medial geniculate, suggesting that the projection is not topographic. As a nonlemniscal auditory pathway that parallels the conventional auditory lemniscal pathway, its functions may be distinct from the perception of sound. Because this pathway links the parts of the auditory system with prominent nonauditory, multimodal inputs, it may form a neural network through which nonauditory sensory and visual-motor systems may modulate auditory information processing.

Animals↗

Auditory brainstem anomalies in albino cats. I. Evoked potential studies.

The amount of melanin pigmentation in the inner ear is positively correlated with the general pigmentation of the body and specifically with the amount of pigment in the eye. The misrouting of retinofugal projections which accompanies ocular and oculocutaneous albinism has been thought to be a defect in decussation unique to the visual system. Evidence suggests that functional abnormalities may also exist in the auditory systems of albino humans and animals. To evaluate this possibility, evoked potential techniques were used to examine the functional anatomy of decussating brainstem auditory pathways in albino and pigmented cats. Auditory brainstem responses (ABRs) were recorded from albino, pigmented, and Siamese cats using monaural stimulation. ABRs were recorded ipsilateral and contralateral to the stimulated ear. The albinos were complete tyrosinase-negative (cc), not the dominant white (W) variety associated with deafness. In pigmented cats, the amplitudes of ABRs recorded with the reference electrode ipsilateral to the stimulated ear and the ABRs recorded using the reference contralateral to the stimulated ear did not differ by more than 40% for individual components appearing between 2 and 4 ms after stimulus onset. In albino cats the components at these latencies were obliterated or greatly attenuated in the ABR recorded using the reference contralateral to the stimulated ear. These data indicate that anomalies may exist in the brainstem at the level of the acoustic striae, superior olivary nuclei and/or trapezoid body in tyrosinase-negative albino cats.

Animals↗

Comparison of the effects of lesions in nucleus basalis and field 'L' on vocal learning and performance in the budgerigar (Melopsittacus undulatus).

Lesions were placed in either nucleus basalis (Bas) or the primary thalamorecipient portion of Field 'L' (i.e. centered in Field L2a) in budgerigars at 3-5 weeks posthatching and as adults. The calls of birds sustaining Bas lesions before fledging, or as adults, were markedly abnormal in that they showed little frequency modulation and individual distinctiveness. Call durations, however, were similar for lesioned and unlesioned birds. In contrast, the calls of Field 'L' lesioned birds were similar to those of siblings and cagemates. This implies that the roles of the isthmofrontal (i.e., direct projections from the ventrolateral nucleus of the lateral lemniscus to Bas) and thalamotelencephalic (i.e., direct projections from nucleus ovoidalis thalami to Field L2a) auditory pathways in providing auditory feedback during vocal learning and performance are different and that the isthmofrontal pathway plays an essential role in these processes throughout the life of the animal.

Animals↗

Morphological changes in the cochlear nucleus of congenitally deaf white cats.

Investigations in animal models and humans have indicated that congenital deafness produces degenerative changes in the central auditory pathway. The cochlear nucleus is the first central structure that receives cochlear input, and may be considered the origin of ascending auditory pathways. In this context, we studied congenitally deaf white cats, who express early onset cochlear receptor loss, in order to assess the nature of structural changes in cells of the cochlear nucleus. It is conceivable that pathologic alterations in higher auditory structures are transneuronally distributed through this nucleus. The cochlear nuclei of nonwhite cats with normal hearing were compared to those of deaf white cats exhibiting hearing loss in excess of 70 dB SPL. The cochlear nuclei of the deaf white cats were smaller in volume by roughly 50%, with the ventral and dorsal divisions being equally affected. Cell body silhouette area was determined for spherical bushy cells of the anteroventral cochlear nucleus (AVCN), pyramidal cells of the dorsal cochlear nucleus (DCN), sensory neurons from the principal trigeminal nucleus, and motoneurons of the facial nucleus. We found no statistical difference in neuronal cell body size between nonauditory neurons of these two groups of cats, whereas auditory neurons of deaf white cats were 30.8-39.4% smaller than those of normal cats. These data imply that neuronal changes in congenitally deaf cats are specific to the auditory pathway. Although cochlear nucleus volume loss was uniform for both divisions, there was a differential effect on cell density: AVCN cell density increased by 40%, whereas DCN cell density was relatively unaffected (10% increase). Astrocyte density was also greater in the AVCN (52%) compared to that in the DCN (5%). These observations reveal a differential impact on cells in the cochlear nucleus to congenital deafness, suggesting selective processing impairment at this level. If similar patterns of degeneration occur in humans, such pathologies may underlie reduced processing of input from cochlear implants in congenitally deaf adults.

Animals↗