PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cochlear Nerve”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 541 records · Page 30Linked to original sources
PubMed1998

Detectability of cochlear, acoustic nerve and brainstem potentials in a group of 'normal' preterm newborns recorded with insert earphone.

Thirty-four 'normal' preterm newborns were tested at 40 weeks postconceptional age. To separate electromagnetic artifacts from cochlear potentials and subsequent auditory brainstem responses, a test was given using an insert earphone at 90, 70, 50, 30 dB nHL. The detectability of receptor potentials, waves I, III, V, as a function of stimulus intensity is described: at 90 dB nHL exclusively, we could always identify these peaks because of the better morphological distinctiveness of each potential. When trying to evaluate the acoustic pathway in premature newborns, we suggest that brainstem response audiometry should be performed at 90 dB nHL with an insert earphone.

Acoustic Stimulation↗
PubMedDate not supplied

[Acoustically guided behavior in the early ontogeny of the long-eared owl: the development of hearing sensitivity].

The development of hearing sensitivity was studied in 15 nestlings and 7 adult long eared owls by cochlear recording potentials. The dynamic of frequency threshold characteristics of cochlear microphonic, action potential of cochlear nerve, and electromyogram of reflectory contraction of middle ear muscle were followed from the 1st to 40 day posthatching. The upper limit of hearing determined by cochlear microphonic, was about 3 kHz on the 1st day after hatching, 7 kHz on the 6th day, and 10 kHz on the 11th. Within 11 days after hatching the low-frequency range of higher sensitivity was revealed (with the maximum at 0.5 kHz), which was the same as that of monotonic signals effective for stimulation of the feeding reaction. The middle frequency range of higher sensitivity corresponded to the spectrum of own vocalization of the nestlings. During the period of formation of the patterned vision there was a delay in development of low- and middle-frequency sensitivity of cochlear microphonic while the high-frequency thresholds continued to decrease. After this period the guiding stimulation for eliciting feeding reaction changes from the auditory for the visual. The action potential of the cochlear nerve could be recorded from the 6th day simultaneously with the appearance of locating head movements and the reflectory contraction of the middle ear muscle.

Acoustic Stimulation↗
PubMed1989

A degenerative disorder of the central auditory system of the gerbil.

A previously unidentified disorder which affects primarily the cochlear nucleus was observed in two species of gerbils, Meriones unguiculatus and M. libycus. Unusual lesions were observed in the cochlear nucleus bilaterally in all animals examined. In light and electron microscopic specimens these lesions were characterized by the presence of microcysts and vacuolar neuronal degeneration. The microcysts resembled large holes, containing trabeculae, organelles and cellular remnants. Also observed were light and dark degeneration of neuronal perikarya and degenerated axons, dendrites, and synapses, accompanied by phagocytosis. Astrocytosis was not conspicuous. In the one cochlea examined, no microcysts were observed. In young animals the microcysts were prevalent in the cochlear nerve root region and the posteroventral cochlear nucleus. In older animals the microcysts increased in number and area. In the oldest animals, the microcysts had spread to other central auditory structures, including the superior olivary complex, the nuclei of the lateral lemniscus, and the inferior colliculus. Other regions of the brain were largely free of microcysts. The etiology and behavioral manifestations of this disorder are unknown, although it is clearly neurodegenerative and perhaps genetically determined.

Animals↗
PubMed1991

Cochlear implant histopathology.

Twenty-two temporal bones and one brain stem from 13 cochlear implant patients were examined histologically. Sixteen temporal bones had undergone one or more implant procedure. Results of analysis suggested that the ganglion cells were the responding elements to the implant and that useful auditory sensation could result from as few as 10 percent of the normal number of ganglion cells. All implanted bones exhibited varying amounts of fibrosis (some ossified) in the basal turn of the cochlea and beyond in some cases. Usually there was damage to the surviving elements of the organ of Corti and the dendrites throughout the extent of the electrode insertion. However, the ganglion cell population was not affected. Prolonged electrical stimulation (up to 14 years) did not affect ganglion cell survival in three cases, and had no effect on the cochlear nerves in two cases or on cochlear nuclei in one case.

Adult↗
PubMed1992

Gamma-D-glutamylaminomethyl sulfonic acid (GAMS) distinguishes subtypes of glutamate receptor in the chick cochlear nucleus (nuc. magnocellularis).

Because kainic acid (KA) is more potent than other excitatory amino acids (EAAs) in affecting synaptic transmission in the cochlear nucleus, previous reports have concluded that primary afferent neurotransmission to the cochlear nucleus in birds and mammals is mediated by KA-preferring non-N-methyl-D-aspartate (non-NMDA) EAA receptors. Since this conclusion is at odds with a number of studies suggesting that rapid excitatory neurotransmission in the CNS is mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring non-NMDA receptors, we re-examined the pharmacology of synaptic transmission between the cochlear nerve and nucleus magnocellularis (NM) in chickens, using bath application of drugs and recording of field potentials evoked in NM by electrical stimulation of the cochlear nerve in vitro. A series of EAA agonists produced complete, concentration-dependent and reversible suppression of postsynaptic responses: the order of potency was domoic acid (DO) greater than KA greater than AMPA much greater than quisqualic acid much greater than L-glutamic acid (Glu). Three quinoxalinedione antagonists of non-6-nitro-7-sulphamobenzo[f]quinoxaline-2,3-dione NMDA receptors also produced complete, concentration-dependent and reversible suppression of postsynaptic responses in NM without affecting the presynaptic action potential; the half-maximal inhibitory concentrations (IC50's) were 2.7 +/- 0.4 microM for 6-nitro-7-sulphamobenzo[f]quinoxaline-2,3-dione (NBQX), 5.3 +/- 0.1 microM for 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and 10.6 +/- 1.2 microM for 6,7-dinitroquinoxaline-2,3-dione (DNQX).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Evolution of vestibular schwannoma surgery: the long journey to current success.

The extraordinary improvement of patient outcome after surgical treatment for vestibular schwannomas is relatively recent and has occurred mainly over the last 30 years. The introduction of microsurgical techniques has resulted in increasing degrees of precise anatomical and functional preservation of the facial and cochlear nerves. An expanded microsurgical technique accompanied by continuous electrophysiological monitoring has resulted in marked changes in the primary goals for this surgery. Whereas in the past the primary goal of vestibular schwannoma management was to preserve the patient's life, the objective in vestibular schwannoma treatment today is to preserve neurological function. Long-term follow-up examinations show negligible recurrence rates, indicating that the aim of preservation of nerve function does not limit the completeness of tumor removal with modern neurosurgical techniques. Despite these advances in preserving the anatomical integrity of, for example, the cochlear nerve, losses of function and even deafness may occur postoperatively in some cases. Current biological and technical research in experimental and clinical settings addresses these problems. In this article, the authors report in detail the developments achieved in vestibular schwannoma surgery and the great clinicians to whom these results can be credited.

Deafness↗
PubMed2002

Correlation between auditory function and internal auditory canal pressure in patients with vestibular schwannomas.

OBJECT: Hearing loss is the most common presenting symptom in patients who harbor a vestibular schwannoma (VS). Although mechanical injury to the cochlear nerve and vascular compromise of the auditory apparatus have been proposed, the exact mechanism of this hearing loss remains unclear. To test whether pressure on the cochlear nerve from tumor growth in the internal auditory canal (IAC) is responsible for this clinical finding, the authors prospectively evaluated intracanalicular pressure (ICaP) in patients with VS and correlated this with preoperative brainstem response. METHODS: In 40 consecutive patients undergoing a retrosigmoid-transmeatal approach for tumor excision, ICaP was measured by inserting a pressure microsensor into the IAC before any tumor manipulation. Pressure recordings were correlated with tumor size and preoperative auditory evoked potential (AEP) recordings. The ICaP, which varied widely among patients (range 0-45 mm Hg), was significantly elevated in most patients (median 16 mm Hg). Although these pressure measurements directly correlated to the extension of tumor into the IAC (p = 0.001), they did not correlate to total tumor size (p = 0.2). In 20 patients in whom baseline AEP recordings were available, the ICaP directly correlated to wave V latency (p = 0.0001), suggesting that pressure from tumor growth in the IAC may be responsible for hearing loss in these patients. CONCLUSIONS: Tumor growth into the IAC results in elevation of ICaP and may play a role in hearing loss in patients with VS. The relevance of these findings to the surgical treatment of these tumors is discussed.

Adult↗
PubMed1996

Spatial selectivity in a rotationally symmetric model of the electrically stimulated cochlea.

A rotationally symmetric model of electrical stimulation of the guinea pig cochlea with active neural elements is used to study the influence of temporal stimulus parameters and electrode configurations on the spatial selectivity of electrical stimulation by cochlear implants. The width of the excitation patterns is determined with respect to the position of the stimulating electrode pairs in the cochlea. Computed O10 AB values are compared against single fibre data from the cat cochlear nerve as measured by Van den Honert and Stypulkowsky (1987). It turns out that the use of charge-balanced asymmetric rather than symmetric biphasic pulses approximately doubles the number of independent channels that can be applied in a cochlear implant with longitudinal bipolar electrodes, like a configuration with radial electrode pairs using symmetric biphasic pulse stimulation will also do. Finally, the influence on Selectivity of the physiological variation in diameter of the cochlear nerve fibres and of a possible loss of their peripheral processes is studied.

Animals↗
PubMed1997

Role of acute cochlear neuritis in sudden hearing loss in multiple sclerosis.

We report a patient with definite multiple sclerosis (MS) who developed unilateral sudden hearing loss coincident with exacerbation of central nervous system symptoms. Involvement of the peripheral cochlear nerve, suggested by auditory findings including auditory brainstem response, was confirmed by magnetic resonance imaging. The clinical, electrophysiological and neuroradiological abnormalities disappeared in response to steroid pulse therapy. These findings suggest that acute inflammatory demyelinative lesion of the peripheral cochlear nerve can occur in MS, manifesting sudden hearing loss.

Acute Disease↗
PubMed1996

Central and peripheral myelin in the rat cochlear and vestibular nerves.

In the bipolar neurons of vertebrate cochlear and vestibular nerves, the myelin envelopes without interruption the axon, the perikaryon and the dendrite. The perikaryal myelin is thin and partially loose, whereas axon and dendrite are enveloped by compacted myelin. The expression of protein 0 and myelin basic protein, constituents of peripheral and central myelin respectively, has been investigated in the rat by immunohistochemical study at the light microscopic level. Our data indicate that both in the cochlear and vestibular nerves the myelin of the perikaryon and dendrite is composed by specific peripheral myelin proteins. The axon segment between the perikaryon and the transitional zone expresses peripheral myelin proteins in the cochlear nerve, while both types of myelin proteins are present in the vestibular nerve. Between the transitional zone and the brainstem the myelin of the axon is exclusively of the central type. The peripheral-central myelin transitional zone is in close proximity to the axonal pole in the vestibular ganglion cells, while in the cochlear nerve it is near the spiral foramina, at variable distance from the axonal pole of ganglion cells.

Animals↗
PubMed1991

Auditory brainstem response (ABR) in spontaneously epileptic rats (SER) and their parent mutants.

Postnatal development of auditory brainstem response (ABR) in spontaneously epileptic rats (SER; zi/zi, tm/tm), a double mutant, their parent mutants, tremor rats (tm/tm) and zitter rats (zi/zi), and Kyo:Wistar rats (control), was studied by repeated ABR recordings from 2 to 13 weeks of age. In tremor rats and Kyo:Wistar rats at 2 weeks of age, ABR pattern was almost the same and 2 or 3 waves were identified. However, no further development in ABR was observed in tremor rats and prolongation of latency and lowering of amplitude were marked. Only wave I with prolonged latency and lowered amplitude was recognized in zitter rats, SER and SER-N (zitter phenotype without epilepsy; zi/zi, tm/+ or zi/zi, +/+). ABR pattern was almost the same from 2 to 13 weeks of age in them. Electrocochleography revealed delay of N1 latency of compound action potential in SER. Vacuolation was observed in the cochlear nuclei and the brainstem of tremor rats and SER from 3 weeks of age in histopathological examination. The organ of Corti and cochlear nerve of tremor rats and SER exhibited no remarkable histopathological findings. The deafness in SER and its parent mutants was considered to occur as a result of impairment of inner ear, cochlear nerve and brainstem as well.

Aging↗
PubMed1979

Steroid treatment in sudden idiopathic neural deafness? Experimental research.

For the recording of action potential in the auditory nerve two different methods of preparation were used in order to reach at the auditory nerve of experimental animals. The remarkable fact arose that this difference in preparation also produced a difference in signal output during the hypoxygenation experiments. In the one method a solitary P1 peak--the approaching-wave--was recorded from the cochlear nerve during the hypoxygenation, whereas in the other method this solitary P1 was never seen. An explanation for this phenomenon is formulated in this article. At the same time the analogy of the 'sudden deafness' caused by affections of the cochlear nerve is compared with Bell's palsy.

Animals↗
PubMed1993

The preservation of hearing and facial nerve function in a consecutive series of unilateral vestibular nerve schwannoma surgical patients (acoustic neuroma).

Between January 1981 and February 1992, 102 non-NF-2 patients underwent removal of a unilateral vesitbular schwannoma. There were 54 women and 48 men. Eighty-six percent of patients with normal facial function preoperatively retained normal function (House score 1 or 2) postoperatively. Of the 64 patients with a functional cochlear nerve preoperatively, five had normal hearing (PTA < 25 dB, SB > 70%), five had near normal hearing (PTA < 45 dB, SD > 70%), four patients had preserved hearing (PTA < 50 dB, SD > 50%), and three patients had preserved cochlear nerve function (PTA > 50 dB, SD < 50%) after surgery. Hearing preservation was obtained in patients whose tumors were larger than 3 cm. Radiological follow-up revealed 10 patients with recurrent tumor, all but one asymptomatic.

Adult↗
PubMed1997

Effects of early deafness on development of brain stem auditory neurons.

Early destruction of the otocyst (embryonic precursor of the inner ear) in chick embryos results in complex changes in developing central auditory pathways. In the cochlear nucleus angularis (NA) and nucleus magnocellularis (NM), 30% to 40% of the neurons die after otocyst removal, the survivors are shrunken, and some neurons in the NA migrate to an abnormal position in the brain stem. The characteristic forms of cochlear nucleus neurons develop normally in the absence of cochlear nerve input, however. In the nucleus laminaris (NL), development of normal dendritic size is dependent on a normal inner ear, but most of the highly specialized dendritic organization of this nucleus, which is important for low-frequency sound localization, can develop normally in the absence of cochlear influences. Otocyst removal induces formation of a permanent functional aberrant axonal projection to the ipsilateral NM from the contralateral NM. Although these aberrant axons form functional glutamatergic synapses, these show immature functional properties, suggesting that cochlear nerve inputs are necessary for normal maturation of glutamate receptors on auditory neurons. Treatment of chick embryo for a brief period in ovo with 6-cyano-7-nitroquinoxaline-2,3-dione, a quinoxalinedione antagonist of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate-kainate subtype of glutamate receptor, completely and permanently prevents the neuronal loss in the NM produced by otocyst removal. The work reviewed has 1) identified aspects of development in central auditory neurons that are perturbed by profound early sensorineural loss, 2) identified aspects of development that appear independent of cochlear influences, and 3) suggested a potential chemotherapeutic approach to prevention of central neuronal death after early damage to the cochlea.

Animals↗
PubMed2000

AMPA receptor binding in adult guinea pig brain stem auditory nuclei after unilateral cochlear ablation.

This study determined if an asymmetric hearing loss, due to unilateral cochlear ablation, could induce the regulation of intracellular AMPA receptors in brain stem auditory nuclei. In young adult guinea pigs, the high-affinity specific binding of [(3)H]AMPA was measured in the cochlear nucleus (CN), the superior olivary complex (SOC), and the auditory midbrain at 2-147 postlesion days. After correction for tissue shrinkage, changes in specific binding relative to that in age-matched unlesioned controls were interpreted as altered numbers and/or activity of intracellular AMPA receptors. In the CN, transient elevations and/or deficits in binding were evident in most regions, which usually recovered by 147 days. However, persistently deficient binding was evident ipsilaterally in the anterior part of the anteroventral CN (AVCNa). In the SOC, transient elevations in binding were evident at 2 days in the medial limb of the lateral superior olive (LSOmed) and the medial superior olive. Between 7 and 147 days, most SOC nuclei exhibited transient, temporally synchronized postlesion deficits in binding. However, late in the survival period, deficits persisted ipsilaterally in the LSOmed and the lateral (LSOlat) limb of the lateral superior olive. In the midbrain, transient elevations and/or deficits in binding were evident in the dorsal nucleus of the lateral lemniscus as well as in the central and dorsal nucleus of the inferior colliculus. A persistent deficit was evident in the intermediate nucleus of the lateral lemniscus. The findings implied that auditory neurons contain regulatory mechanisms that control the numbers and/or activity of intracellular AMPA receptors. Regulation was induced by cochlear nerve destruction and probably by changes in the excitation of glutamatergic neurons. Many of the regulatory changes were transient, except in the ipsilateral AVCNa and LSO, where postlesion downregulations were persistent. The downregulation in the ipsilateral AVCNa was probably induced directly by the loss of cochlear nerve endings. However, other regulatory changes may have been induced by signals carried on pathways emerging from the ipsilateral CN and on centrifugal auditory pathways.

Animals↗
PubMed1996

Enhancement of vowel coding for cochlear implants by addition of noise.

Profoundly deaf people, who gain no benefit from conventional hearing aids, can receive speech cues by direct electrical stimulation of the cochlear nerve. This is achieved by an electronic device, a cochlear implant, which is surgically inserted into the ear. Here we show physiological results from the isolated sciatic nerve of the toad Xenopus laevis, used to predict the response of the human cochlear nerve to vowels coded by a cochlear implant. These results suggest that standard analogue cochlear implants do not evoke the patterns of neural excitation that are normally associated with acoustic stimulation. Adding noise to the stimulus, however, enhanced distinguishing features of the vowel encoded by the fine time structure of neural discharges. On the basis of these results, and those concerning stochastic resonance, we advocate a cochlear implant coding strategy in which noise is deliberately added to cochlear implant signals.

Action Potentials↗
PubMed2005

Regulation of NT-3 and BDNF levels in guinea pig auditory brain stem nuclei after unilateral cochlear ablation.

Injury to areas of the central nervous system can alter neurotrophin levels, which may influence postlesion neuronal survival and plasticity. To determine if sensorineural hearing loss induces such changes, we used an enzyme-linked immunosorbent assay (ELISA) to measure neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF) levels in adult guinea pig brain stem auditory nuclei 3-60 days after a unilateral cochlear ablation (UCA). After UCA, which destroyed the cochlea and cochlear nerve on one side, NT-3 levels were usually depressed at 3 days by 22-44% but became elevated transiently at 7 days by 28-124%. BDNF levels were elevated transiently by 50% on the ablated side in the anteroventral (AVCN) and posteroventral (PVCN) cochlear nucleus at 3 days and may have signaled support for the survival of deafferented neurons. Coincident elevation at 3 and 7 days of BDNF or NT-3 and phosphorylated extracellular signal-regulated protein kinase 2 (ERK2-P) suggested a relationship to stimulated signal transduction activity. Elevated neurotrophin levels may have contributed to synaptogenesis in the AVCN and the superior olive and to changes in the synaptic biochemistry in the auditory nuclei after UCA. In contrast, deficiencies or failure to elevate neurotrophin levels within several days of the UCA correlated with upregulation of phosphorylated stress-activated protein kinase (SAPK-P), suggesting a relationship with stress-activated signal transduction and with the sparse degeneration of fibers observed in some of the auditory nuclei after UCA.

Animals↗