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PubMed2004

Noise trauma alters D-[3H]aspartate release and AMPA binding in chinchilla cochlear nucleus.

Exposure of adults to loud noise can overstimulate the auditory system, damage the cochlea, and destroy cochlear nerve axons and their synaptic endings in the brain. Cochlear nerve loss probably results from the death of cochlear inner hair cells (IHC). Additional degeneration in the cochlear nucleus (CN) is hypothesized to stem from overstimulation of the system, which may produce excitotoxicity. This study tested these predictions by exposing one ear of anesthetized adult chinchillas to a loud noise, which damaged the ipsilateral cochlea and induced degeneration in the glutamatergic cochlear nerve. During the first postexposure week, before cochlear nerve axons degenerated, glutamatergic synaptic release in the ipsilateral CN was elevated and uptake was depressed, consistent with hyperactivity of glutamatergic transmission and perhaps with the operation of an excitotoxic mechanism. By 14 days, when cochlear nerve fibers degenerated, glutamatergic synaptic release and uptake in the CN became deficient. By 90 days, a resurgence of transmitter release and an elevation of AMPA receptor binding suggested transmission upregulation through plasticity that resembled changes after mechanical cochlear damage. These changes may contribute to tinnitus and other pathologic symptoms that precede and accompany hearing loss. In contrast, the other ear, protected with a silicone plug during the noise exposure, exhibited virtually no damage in the cochlea or the cochlear nerve. Altered glutamatergic release and AMPA receptor binding activity in the CN suggested upregulatory plasticity driven by signals emanating from the CN on the noise-exposed side.

Animals↗

PubMed1996

[Hearing preservation and tinnitus following removal of acoustic neurinomas].

Thirty-five cases of unilateral acoustic neurinomas were analyzed with special reference to the postoperative eighth cranial nerve function. An additional three cases of bilateral acoustic neurinomas associated with neurofibromatosis were also analyzed. Out of a total of 40 neurinomas in all, 38 cases were retrospectively reviewed. The thirty-five cases of unilateral acoustic neurinomas were summarized as follows. The patients' age ranged from 23 to 69 years old. The tumor size varied as follows; 7 cases were confined to the internal acoustic meatus, 4 cases were 20 mm or less in their maximum diameter, 13 cases were 30 mm or less, and 11 cases were more than 30 mm. The consistency of the tumor was classified as being solid in 27 cases, and being cystic in 8 cases. Hearing had been maintained in 27 cases on admission, serviceable in 17 cases, unserviceable in 10 cases and deaf in 8 cases. Operations were performed via the retromastoid suboccipital approach in all cases. The facial nerve was anatomically preserved in all cases. On the other hand, the cochlear nerve was anatomically preserved in 14 out of 35 cases (40%). The preservation ratio of the cochlear nerve showed a negative correlation to the tumor size. In 17 cases with preoperative serviceable hearing, preservation of the cochlear nerve was attempted, which resulted in a 65% anatomical preservation. However, hearing was preserved in 4 cases (36%). Serviceable hearing was preserved in only 2 cases. Tinnitus developed in 20 cases preoperatively, and then occurred postoperatively in 11 cases. Tinnitus was prominently aggravated in 2 cases in which the cochlear nerves were preserved, which resulted in unserviceable hearing. There was a statistically significant correlation between cochlear nerve preservation and the postoperative presence of tinnitus (Fisher's exact probability test: P = 0.0106 < 0.05). Tinnitus was aggravated just after the operation. However, it gradually improved and vanished as the hearing showed a recovery to a slight degree in one case. Three cases of bilateral acoustic neurinomas in neurofibromatosis were also summarized. One case received the operation only on the unilateral side. The remaining two cases were operated bilaterally. To preserve serviceable hearing on at least one side, partial removal of the tumor was performed under the monitoring of auditory brain stem response and/or cochlear microphonic potential. Serviceable hearing on at least one side was maintained in all three cases. In conclusion, hearing preservation can be expected after removal of the acoustic neurinomas under the following situations; hearing acuity of less than 50-60dB in preoperative pure tone audiogram, tumor size of less than 20 mm in maximum diameter, cases with preservation of cochlear nerve and of the internal auditory artery during the operation, and no injury to the labyrinth during the operation. In some cases, tinnitus becomes aggravated in the case with cochlear nerve preservation associated with unserviceable hearing. Furthermore, the degree of tinnitus shows a decrease as postoperative hearing improves in some cases.

Adult↗

PubMed1993

Aminoglycoside antibiotics inhibit maxi-K+ channel in single isolated cochlear efferent nerve terminals.

Patch clamp recordings were obtained from isolated cochlear efferent nerve terminals. The effect of aminoglycoside antibiotics on single maxi-K+ channels was determined. At positive voltages (cytosol with respect to extracellular side), neomycin, streptomycin, and kanamycin significantly reduced the single channel current amplitude of the maxi-K+ channel from the cytosolic side. The IC50 for neomycin was 9.10(-4) M from the cytosolic side and >> 10(-3) M from the extracellular side. Streptomycin and kanamycin were less potent. No significant difference in inhibition of the single channel current amplitude by 2.5.10(-4) M cytosolic neomycin was observed between 7.10(-4) M and 10(-6) M free cytosolic Ca2+. Neomycin had no significant effect on the open probability of the maxi-K+ channel either from the cytosolic or from the extracellular side. These findings demonstrate that the maxi-K+ channel in cochlear efferent nerve terminals can be a site of action for aminoglycoside antibiotics.

Animals↗

PubMedDate not supplied

Normal canals at the fundus of the internal auditory canal: CT evaluation.

PURPOSE: Knowledge of the normal anatomy of the four bony canals located at the fundus of the internal auditory canal (IAC) is necessary during evaluation of temporal bone trauma, congenital anomalies affecting the individual nerves, and some neuro-otologic surgeries. The purpose of this work was therefore to characterize the normal appearance of the four bony canals and to measure their dimensions. METHOD: A retrospective study was performed using CT studies of the temporal bones in 50 patients to identify and characterize the bony canals for the labyrinthine segment of the facial nerve (BCFN), superior vestibular nerve (BCSVN), cochlear nerve (BCNC), and the inferior vestibular nerve (singular canal; SC) located at the fundus of the IAC. All the patients underwent high resolution temporal bone CT for evaluation of uncomplicated inflammatory (n = 49) and neoplastic (n = 1) diseases involving the temporal bone. CT studies were done using 1-mm-thick contiguous sections in axial and coronal planes. Measurements of the canals were performed by one radiologist. No patient had a prior history of trauma, vertigo, and sensorineural hearing loss or facial nerve paralysis. RESULTS: The BCFN, BCSVN, and BCNC were identified in all studies, whereas the SC was seen in 93% of studies. The BCFN, BCSVN, and BCNC arise from the fundus of the IAC, whereas the SC arises medial to the fundus. Mean +/- SD measurements (in mm) of the length and width were as follows: BCFN = 2.92+/-0.48 and 0.91+/-0.28; BCSVN = 2.36+/-0.53 and 0.89+/-0.28; BCNC = 0.93+/-0.21 and 2.13+/-0.44; and SC = 3.22+/-0.73 and 0.50+/-0.14. CONCLUSION: These small canals are routinely visualized on thin section (1 mm) CT of the temporal bone and should not be confused with fractures. This study provides baseline measurements that may be used to evaluate congenital anomalies of these canals. These data may also be helpful in the presurgical evaluation of patients undergoing singular neurectomies for benign positional vertigo.

Adolescent↗

PubMed1992

[Effect of intravenous injection of aspirin on the cochlea].

It is not yet well understood how aspirin acts on the auditory system. This study was aimed at elucidating the effects of aspirin on the cochlear hair cells and cochlear nerve of guinea pigs by recording (1) spontaneous activity of cochlear nerve fibers, (2) compound action potentials (CAPs) evoked by electrical pulses applied to the cochlea through the round window membrane, (3) acoustically evoked action potentials (APs) through the round window membrane and (4) acoustic emissions (sound pressure near the tympanic membrane) evoked by electrical pulses applied to the cochlea. The following results were obtained. (1) After guinea pigs were given aspirin (200 mg/kg) intravenously, a transient reduction in spontaneous activity of cochlear nerve fibers and elevation over the subsequent 10-20 minutes were observed in three of four fibers recorded for more than 30 minutes. The mean spontaneous discharge rate in 102 fibers after aspirin administration (200 mg/kg) was not significantly higher than the control values from 30 to 120 minutes after aspirin administration, while the rate in 112 fibers after aspirin administration (400 mg/kg) was significantly higher. (2) After injecting of 100 mg/kg, 200 mg/kg and 400 mg/kg of aspirin, the amplitude of electrically evoked CAPs decreased significantly, while their latency increased significantly only after injection of 400 mg/kg of aspirin. (3) Changes in the amplitude of acoustically evoked APs and electrically evoked CAPs were compared before and after intravenous injections of 400 mg/kg of aspirin. The AP suppression ratio at low sound intensity was significantly greater than that of CAPs at low and high current levels. (4) After injection of 400 mg/kg of aspirin, the waves of electrically evoked acoustic emissions and their peaks in the frequency analysis disappeared either reversibly or irreversibly. The observed changes in spontaneous activity of cochlear nerve fibers in response to aspirin administration to guinea pigs may represent a tinnitus-like phenomenon. The detection of electrically evoked CAPs suggests that aspirin acts on the cochlear nerve and causes a decrease in its excitability, and the discovery of acoustically evoked APs and electrically evoked acoustic emissions is interpreted as indicating that aspirin acts not only on the cochlear nerve but also on cochlear hair cells.

Acoustic Stimulation↗

PubMed2002

Regeneration of auditory nerve following complete sectioning and intrathecal application of the IN-1 antibody.

The cochlear nerve of adult Lewis rats was following microsurgical exposure in the cerebellopontine angle (CPA). The lesions completely interrupted the auditory nerve axons at the lesion site producing ipsilateral deafness in all animals. The rats were then treated with a recombinant Fab fragment of the antibody IN-1 against nerve growth inhibitory proteins for one to two weeks. An age-matched control group of rats was treated with unspecific mouse IgG antibody. Because the cochlear nerve lesions resulted in significant neuronal apoptosis of spiral ganglion cells, neurotrophin-3 (NT-3) was applied to the lesion site immediately post-injury in some rats. Electrophysiological studies were carried out by recording the brainstem auditory evoked potentials (BAEP) before and immediately after the lesion, and at regular intervals up to 2 months after injury. Cochlear nerve fibres were anterogradely traced by horseradish peroxidase (HRP) or biotinylated dextran amine (BDA) injected into the spiral ganglion. The results achieved in this study were consistent with the following conclusions: 1) transection of the adult rat cochlear nerve at the CPA results in functional deafness, disappearance of BAEP, apoptosis of parent axotomized neurons of the spiral ganglion, and interruption of labelled axons close to the lesion site; 2) NT-3 is able to partially rescue axotomized neurons of the spiral ganglion; 3) injured cochlear nerve fibres show a limited spontaneous sprouting and regrowth response which does not lead to BAEP recovery; 4) intrathecal treatment with IN-1 directed against myelin-associated neurite growth inhibitory proteins promotes significant elongation of the injured fibres; and 5) the regenerating fibres seem to navigate to correct targets, and be able to establish synaptic connections for functional recovery as depicted by BAEP examinations.

Animals↗

PubMed2002

The effect of vestibular nerve section upon tinnitus.

This paper reviews the published evidence regarding the effect of vestibular nerve section upon tinnitus. This is of relevance not only for those performing and undergoing this procedure, but also for those considering the hypothesis that auditory efferent system dysfunction may be influential in tinnitus perception. The auditory medial efferent fibres within the internal auditory canal run within the inferior vestibular nerve, only joining the cochlear nerve at the anastomosis of Oort, a bundle of 1300 fibres running from the saccular branch of the inferior vestibular nerve to the cochlear nerve. Vestibular nerve section procedures therefore section this efferent olivocochlear pathway, and ablate efferent influence upon that cochlear. If auditory efferent dysfunction is involved in tinnitus perception, this ablation might influence the tinnitus status of that patient. A literature search identified 18 papers mentioning tinnitus status after vestibular nerve section, describing the experiences of a total of 1318 patients. The proportion of patients in whom tinnitus was said to be exacerbated postoperatively ranged from 0% to 60%, with a mean of 16.4% (standard deviation 14.0). The proportion of patients in whom tinnitus was unchanged was 17% to 72% (mean 38.5%, standard deviation 15.6), and in whom tinnitus was said to be improved was 6% to 61% (mean 37.2%, standard deviation 15.2). In the majority of patients undergoing this procedure, ablation of auditory efferent input (and thus total efferent dysfunction) to the cochlea was not associated with an exacerbation of tinnitus. The finding of this review is that efferent dysfunction after vestibular nerve section does not consistently worsen tinnitus.

Humans↗

PubMed1993

Maxi-K+ channel in single isolated cochlear efferent nerve terminals.

Patch clamp recordings were obtained from isolated cochlear efferent nerve terminals. Channel activity was found in 85% of membrane patches, was present in on-terminal and excised patches and was characterized to originate from a maxi-K+ channel. An average of 2.0 +/- 0.1 (N = 33) maxi-K+ channels were found per active patch. In symmetrical solutions, the current-voltage relationship was linear and the single-channel conductance was 221 +/- 5 pS (N = 22). The open probability of the maxi-K+ channel increased with depolarization of the membrane potential and with an increasing free Ca2+ concentration on the cytosolic side. The open probability was insensitive to changes in the free Ca2+ concentration on the extracellular side. TEA (20 mM) and charybdotoxin (10(-7) M) decreased the open probability to nearly zero from the extracellular side but had no effect from the cytosolic side. The high incidence with which this channel was found suggests that the maxi-K+ channel is physiologically relevant which might include protection against overstimulation of the efferent synapse.

Animals↗

PubMed1985

Similarity of dynamic range adjustment in auditory nerve and cochlear nuclei.

Rate versus level functions were recorded for responses to best-frequency (BF) tones of 116 cochlear nucleus units and 53 auditory-nerve fibers in the presence of interrupted tone backgrounds and continuous noise backgrounds of various intensities. The backgrounds shifted the dynamic ranges of rate-level functions to higher test intensities, so in the presence of backgrounds, rate saturation occurred at higher intensities than in quiet. The shift in saturation intensity evoked by each background was measured by comparing the rate-level function recorded with the background to one recorded without. The relation between change in saturation intensity and background intensity could be approximated by the formula (formula: see text) delta Isat is the shift in saturation intensity, I is the background intensity, theta is the threshold for evoking shift, and A is the ratio of shift to background intensity re theta. In the appendix, it is shown that A is a measure of a unit's ability to avoid saturation by the background stimulus. The optimal value of A is unity, at which point a unit's operating range is infinite. The value of A depended on BF for interrupted tone backgrounds, but not for continuous noise backgrounds. For BF less than 10 kHz, the mean value of A for tone backgrounds was 0.33 in the auditory nerve, 0.37 in the ventral cochlear nuclei (VCN), and 0.47 in the dorsal cochlear nucleus (DCN). The difference between auditory nerve and VCN was not statistically significant. For BF greater than 10 kHz, the mean A was 0.16 in auditory nerve and 0.30 in VCN. The mean value of A for noise backgrounds was 0.79 in auditory nerve, 0.86 in VCN, 0.86 in DCN units of response types II and III, and 1.04 in DCN type IV units. Only the differences between DCN type IV and the non-DCN unit groups were statistically significant. The qualitative changes produced in rate-level functions by tone and noise backgrounds were similar in auditory nerve and cochlear nuclei except for DCN type IV units. The shifts in rate functions produced by interrupted tone backgrounds did not prevent saturation of the rate response at background intensities above the dynamic range of the unit as recorded in quiet. However, the rate response to test tones was preserved in the presence of all noise background levels used (up to a 30-dB spectrum level). The shift in rate function produced by the noise was almost sufficient to allow the unit to encode test intensity relative to noise background intensity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1976

Synaptic events and discharge patterns of cochlear nucleus cells. II. Frequency-modulated tones.

Responses of 99 cochlear nucleus cells and 24 cochlear nerve fibers were studied with FM signals; 14 cochlear nerve fibers and 57 cochlear nucleus cells were studied at four rates of modulation and several signal intensities. Classification of FM response patterns as symmetrical, asymmetrical, or unidirectional was based on the calculation of a symmetry factor (S), which compared the number of discharges evoked by the ascending and by the descending phases of the FM sweep. Certain FM response patterns could not adequately be described by the symmetry factor along and variables of modulation rate and signal intensity had significant influence. A correspondence was found between the four response classes evoked by a steady-frequency tone burst (primarylike, buildup, onset, and pause) and the FM response pattern. Cochlear nerve fibers showed symmetrical response patterns to FM stimulation. Primarylike units were similar to eighth nerve fibers and generally showed symmetrical FM responses. Occasional eighth nerve fibers and primarylike cells developed asymmetry at the fastest rate of modulation (50 sps). Buildup units showed a variety of response patterns to FM signals. Onset units generally showed asymmetrical response patterns with the greater response occurring to the ascending than to the descending phase of the FM sweep. Pause units showed a characteristic inhibition of activity at 5 sps (rate-dependent inhibition). Of the 57 cochlear nuclear cells studied in response to FM signals, 16 were symmetrical, another 16 were symmetrical except at the fastest modulation rate, 12 were asymmetrical, 3 were unidirectional, and 10 showed complex responses to certain signal rates or intensities. It is clear the the cat cochlear with its complex cytoarchitecture is involved in the recoding of acoustic information. Some units in cochlear nucleus demonstrate differential responses to the direction and to the rate of frequency movement. Other cochlear nucleus cells respond as eighth nerve fibers and may serve as simple "relays" in transmitting information from the cochlea to higher auditory centers.

Acoustic Stimulation↗

PubMed1997

Neuronal and transneuronal degeneration of auditory axons in the brainstem after cochlear lesions in the chinchilla: cochleotopic and non-cochleotopic patterns.

Terminal axonal degeneration in the brain following cochlear lesions was studied with the Nauta-Rasmussen method. Losses of hair cells and myelinated cochlear fibers were assessed. The cochleotopic map projected, from apex to base, on the ventral-to-dorsal axes of the cochlear nuclei. The cochleotopic correspondence was better for loss of cochlear nerve fibers and inner hair cells, than for outer hair cells. Cochlear fibers were traced to all parts of the cochlear nucleus, including the small-cell shell, also to cell-group Y and the flocculus. Terminal axonal degeneration in nuclei of the superior olivary complex, lateral lemniscus, and inferior colliculus was interpreted as transynaptic, since degenerated axons could not be traced to these locations from the cochlear nerve or trapezoid body. Moreover, biotinylated dextran amine injection in the basal turn of scala media of a normal cochlea labeled cochlear nerve fibers projecting to the high-frequency regions of the cochlear nuclei and to the flocculus, but not to more central auditory nuclei. This is the first detailed account of transynaptic degeneration in the ascending auditory pathway resulting from cochlear damage in an adult mammal. These findings are consistent with a dystrophic process depending on hair-cell loss and/or direct damage to cochlear nerve fibers.

Animals↗

PubMed1983

Selective labeling of spiral ganglion and granule cells with D-aspartate in the auditory system of cat and guinea pig.

The present study sought to locate putative glutamatergic or aspartatergic pathways in the auditory system of cats and guinea pigs. We injected 0.06 to 3 mM D-[3H] aspartate (D-Asp) in the cochlear nucleus before preparation for light microscopic autoradiography. At short survival times (15 and 40 min) there was heavy labeling of astrocytic somata. Labeling patterns typical of cochlear nerve endings decorated neurons in the cochlear nucleus, e.g., cell bodies and dendritic trunks of octopus cells. Labeling patterns consistent with retrograde axonal transport by the parallel fibers of granule cells appeared in the molecular layer of the dorsal cochlear nucleus and in the external granular layer. Retrograde labeling of the cochlear nerve root fibers also occurred. Consistent with these results are companion biochemical findings on the rapidly dissected cochlear nuclei of guinea pigs. The dorsal, anteroventral, and posteroventral cochlear nuclei, each, evinced uptake of D-Asp. Subsequently, electrical stimulation of each nucleus released a portion of the accumulated amino acid. Most of this release probably came from synaptic endings. Another group of experiments compared autoradiographic localization of 0.06 to 3 mM D-Asp to that of horseradish peroxidase (HRP) 6 hr to 2 d after injections in the cochlear nucleus. Astroglial cell bodies were no longer labeled by D-Asp, but spiral ganglion cell bodies in the cochlea and granule cell bodies in the cochlear nucleus were. Perikarya of the periolivary and ventral cochlear nuclei projecting to the dorsal cochlear nucleus were labeled by HRP and not by D-Asp. Thus, comparisons with the HRP findings indicate that D-Asp labeling resulted from a selective retrograde transport. There was no evidence for a selective anterograde axonal transport. The present observations support the hypothesis that cochlear nerve fibers and granule cells may use L-glutamate and/or L-aspartate as a transmitter in the cochlear nucleus.

Animals↗

PubMed2004

[Anatomohistologic study of von Oort's vestibulocochlear anastomosis].

OBJECTIVES: The vestibulocochlear anastomosis was first described in 1918 by von Oort. It is situated deeply at the bottom of the internal acoustic meatus, and spreads from the saccular nerve before its terminal ramifications, to the cochlear nerve before its penetration into the cochlea. Nerve fibers of the cochlear efferent system are thought to pass through it. The aim of our study was to investigate the anatomy of the vestibulocochlear anastomosis and characterize its histological features. METHOD: [corrected] Ten human temporal bones were dissected. Serial sections were obtained for histological evaluation. RESULTS: The vestibulocochlear anastomosis was found in seven of the specimens, perfectly visualized in six. Average diameter was 0.5 mm with lengths varying from 0.5 to 1 mm. Serial histological sections demonstrated the nervous nature of the anastomosis and its relations with the saccular and cochlear nerves. The epinevrium of the saccular nerve was continuous with the supposed anastomosis in five of the specimens, demonstrating the distinct nature of the anastomosis from the saccular and cochlear nerves. We did not find any evidence linking these fibers to the cochlear efferent system. DISCUSSION: The vestibulocochlear anastomosis was found in seven of our ten dissections. The anastomosis is probably an anatomic reality composed of nerve fibers. The efferent function of these fibers remains to be demonstrated.

Anastomosis, Surgical↗

PubMed1989

Analysis of the human auditory nerve.

In human temporal bones of patients with normal hearing or sensory neural deafness, the cochlear neurons were quantitatively and qualitatively evaluated at the level of the osseous spiral lamina, the spiral ganglion and the cochlear nerve. We found from 32,000 to 31,000 myelinated nerve fibres in the cochlear nerve of normal hearing individuals and any lower number in cases of sensory neural deafness. There was in general a good correspondence between the counted numbers of the myelinated nerve fibres in the osseous spiral lamina, the spiral ganglion cells and the myelinated nerve fibres in the cochlear nerve in the inner acoustic meatus. The diameter of the peripheral axons of the type I neurons are about half the diameter of the central axons. The average diameter of the central axons is 2.5 millimicrons with a narrow distribution in children, but an increasingly larger range of fiber calibers with increasing age (0.5 to 7 microns in the 40 to 50 year age group adults).

Adult↗

PubMed2002

Magnetic resonance imaging versus computed tomography in pre-operative evaluation of cochlear implant candidates with congenital hearing loss.

Recent reports indicate that the cochlear nerve may be absent in some cases of congenital sensorineural hearing loss. The aim of this prospective study was to determine the incidence of cochlear nerve anomaly in cochlear implant candidates with congenital hearing loss using magnetic resonance imaging (MRI). Twenty-seven patients with congenital profound bilateral sensorineural hearing loss who were being evaluated for the cochlear implant procedure were studied. These patients had high-resolution computerized tomography (CT), through the petrous bone in axial sections. MRI examinations consisted of T1 and turbo spin echo (TSE) T2-weighted 3 mm axial images, and additional 3D Fourier Transform T2-weighted TSE sequences obtained on three different planes (axial, perpendicular and parallel to the internal auditory canal (IAC) i.e. oblique sagittal and coronal, respectively) for the purpose of cochlear nerve demonstration. Results showed that all of the 14 patients with normal CT of the temporal bone, had four distinct nerves in the distal part of the IAC on TSE-MRI. Thirteen patients demonstrated various bony malformations of the cochleovestibular system on CT. MRI revealed the absence of the cochleovestibular nerve in four patients where the IAC was very narrow or completely absent on CT. One patient with severe Mondini malformation who had an enlarged IAC demonstrated an isolated absent cochlear nerve.

Adolescent↗

PubMed2007

Ultrastructural changes of the cochlea after oral and maxillofacial firearm wounds.

BACKGROUND: There have been reports that maxillofacial firearm wounds could induce hearing loss. The effects on the ultrastructure of the cochlea and cochlear nerves after oral and maxillofacial firearm wounds are still unclear. This experiment investigates the ultrastructural changes of the cochlea and cochlear nerve after oral and maxillofacial firearm wounds. METHODS: Twenty dogs were wounded by steel spheres or detonators to establish animal models of oral and maxillofacial firearms wound. At different times after trauma, the wounds were examined and the specimens of the cochlea and cochlear nerve were taken to study the ultrastructural changes. RESULTS: The ultrastructural changes of the cochlea and cochlear nerve at 1 hour after trauma were cilia disorganization, edema of the nerve, and mitochondrial denaturalization. At 6 hours, there was extensive degeneration in the cochlea and cochlear nerve, cilia falling off of hair cells, and dissolution of the nerve sheath structure. CONCLUSIONS: The ultrastructure of the cochlea and cochlear nerve after injury is severe, but in the early period the injury is reversible.

Animals↗

PubMed1990

[Acoustic neuroma: a histopathological study].

In view of recent controversy concerning the preservation of hearing in acoustic neuroma surgery, a histologic study of the nerve-tumour interface was undertaken in order to investigate cochlear nerve involvement. Twelve intact acoustic neuromas were studied by means of Masson's trichrome stain, the Luxol fast blue technique, Verhoeff's stain and an immunohistochemical technique using monoclonal antibodies to human neurofilaments. In nine out of twelve specimens, macroscopically visible adherences were present between the cochlear nerve and the tumour. The microscopical correlate was found to be the absence of a clear cleavage plane between the cochlear nerve and the tumour on the one hand, and the presence of cochlear nerve fibers, surrounded by tumoural cells, past the assumed nerve-tumour interface on the other hand.

Cochlear Nerve↗

PubMed1992

Auditory processing of complex sounds: an overview.

The past 30 years has seen a remarkable development in our understanding of how the auditory system--particularly the peripheral system--processes complex sounds. Perhaps the most significant has been our understanding of the mechanisms underlying auditory frequency selectivity and their importance for normal and impaired auditory processing. Physiologically vulnerable cochlear filtering can account for many aspects of our normal and impaired psychophysical frequency selectivity with important consequences for the perception of complex sounds. For normal hearing, remarkable mechanisms in the organ of Corti, involving enhancement of mechanical tuning (in mammals probably by feedback of electro-mechanically generated energy from the hair cells), produce exquisite tuning, reflected in the tuning properties of cochlear nerve fibres. Recent comparisons of physiological (cochlear nerve) and psychophysical frequency selectivity in the same species indicate that the ear's overall frequency selectivity can be accounted for by this cochlear filtering, at least in bandwidth terms. Because this cochlear filtering is physiologically vulnerable, it deteriorates in deleterious conditions of the cochlea--hypoxia, disease, drugs, noise overexposure, mechanical disturbance--and is reflected in impaired psychophysical frequency selectivity. This is a fundamental feature of sensorineural hearing loss of cochlear origin, and is of diagnostic value. This cochlear filtering, particularly as reflected in the temporal patterns of cochlear fibres to complex sounds, is remarkably robust over a wide range of stimulus levels. Furthermore, cochlear filtering properties are a prime determinant of the 'place' and 'time' coding of frequency at the cochlear nerve level, both of which appear to be involved in pitch perception. The problem of how the place and time coding of complex sounds is effected over the ear's remarkably wide dynamic range is briefly addressed. In the auditory brainstem, particularly the dorsal cochlear nucleus, are inhibitory mechanisms responsible for enhancing the spectral and temporal contrasts in complex sounds. These mechanisms are now being dissected neuropharmacologically. At the cortical level, mechanisms are evident that are capable of abstracting biologically relevant features of complex sounds. Fundamental studies of how the auditory system encodes and processes complex sounds are vital to promising recent applications in the diagnosis and rehabilitation of the hearing impaired.

Animals↗