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PubMed2005

Spontaneous activity in the inferior colliculus of CBA/J mice after manipulations that induce tinnitus.

Several physiological studies have linked experimentally induced tinnitus to increases in the spontaneous activity of auditory neurons. These results have led to the proposal of hyperactivity models of tinnitus in which elevated neural activity in the absence of auditory stimulation is perceived as phantom sound. Such models are appealing in their simplicity but remain controversial because a generalized elevation of spontaneous rates may not be observed after treatments that induce tinnitus in humans and experimental animals. Our study addressed these issues by characterizing the effects of common methods of tinnitus induction on spontaneous activity in the central nucleus of the inferior colliculus (ICC). The ICC is an interesting structure in tinnitus research because its diverse inputs include putative generator sites in the dorsal cochlear nucleus, as well as brainstem sources that appear to remain normal after tinnitus induction. Groups of CBA/J mice were subjected to one of three induction methods: bilateral or unilateral sound exposure, and acute salicylate intoxication. Relative to normal baselines, bilaterally exposed mice showed increases in the spontaneous rates of neurons with tuning near the exposure frequency. When the sample was separated into physiologically defined response classes, exposure effects were strongest among neurons with broad excitatory bandwidths. By contrast, salicylate decreased the spontaneous rates of low-frequency neurons with transient sound-evoked activity. Our results suggest that the disordered processes of hearing that give rise to tinnitus do not involve a pervasive elevation of spontaneous activity or a single mode of induction.

Animals↗

PubMedDate not supplied

Presbyacusis and calcium-binding protein immunoreactivity in the cochlear nucleus of BALB/c mice.

The BALB/c mouse is an established model for the early development of sensorineural hearing loss, and is homozygous for the Ahl allele (age-related hearing loss). The present study was designed to determine how auditory peripheral pathology influences calcium-binding protein immunoreactivity in the cochlear nucleus in aged BALB/c mice. To address this issue the loss of hair cells, spiral ganglion neurons (SGN), and neurons in the dorsal (DCN) and posteroventral (PVCN) cochlear nucleus of BALB/c mice at 1 and 24 months of age were quantified using CAST stereological methods. These values were then compared to the percent increase in immunopositive calcium-binding proteins in the cochlear nucleus. By 24 months of age there was a near complete loss of all outer hair cells (OHC). The inner hair cell (IHC) loss was near complete in the more apical and basal regions, while in the mid-regions approximately 50% were missing. The SGN in the apical and middle turns show a 20% loss (re: 1 month) and the basal turn up to 80% loss. A statistically significant decrease in the density of DCN and PVCN neurons (25%) was found at 24 months of age compared to the one month old animals. The percentage of parvalbumin and calretinin positive neurons in the DCN and the PVCN in relation to the density of Nissl stained neurons showed significant increases at 24 months compared to the 1 month old animals. We also determine the relationship between peripheral pathology and the percent increase in calcium-binding protein immunoreactivity. In the DCN, the percent increase of calretinin and parvalbumin was correlated to the loss of SGN, IHCs and OHCs. In the PVCN, parvalbumin was correlated to SGN, IHC, and OHC loss. The percent increase in calbindin immunoreactivity was not correlated to any peripheral pathology. The data here suggest a percent increase in calcium-binding protein immunoreactivity in the cochlea nucleus in the 24 month old mice may reflect an endogenous protective strategy that is designed to counteract calcium overload that is prominent during aging and degeneration. These results will be valuable for understanding the relationship among the peripheral and central auditory system in a model demonstrating a rapidly progressive presbyacusis.

Aging↗

PubMed2004

Hearing evaluation in two sisters with a T8993G point mutation of mitochondrial DNA.

We report on two sisters with a T8993G point mutation of mitochondrial DNA, and their hearing evaluation. Considering auditory function, hearing in the elder sister remains almost normal. However, in the younger sister, the auditory brainstem response (ABR) threshold has fluctuated remarkably during a 3-year follow-up. The threshold changes of ABR in the younger sister suggest that her hearing problems may well be caused by both cochlear nerves and retrocochlear lesions. Our experience is clinically important because there have been only a few reports on hearing evaluation in patients with a T8993G point mutation of mitochondrial DNA.

Audiometry, Pure-Tone↗

PubMed2001

Expression of multidrug resistance protein 1 (MRP1) in the rat cochlea with special reference to the blood-inner ear barrier.

Expression of multidrug resistance protein 1 (MRP1) was detected in the rat cochlea by RT-PCR and immunohistochemistry using anti-MRP monoclonal antibody MRPr1. Use of primers specific for rat mrp1 gene resulted in the amplification of an expected 394 bp fragment prepared from brain and cochlear tissues. Immunohistochemically, MRP was found in the choroid plexus, stria vascularis, spiral ligament, spiral prominence and cochlear nerve in the modiolus. From these results, it was suggested that MRP in the rat cochlea might function as an extrusion pump and play an important role in the blood-inner ear barrier.

ATP Binding Cassette Transporter, Subfamily B↗

PubMed2003

Computed tomography of common congenital lesions of the temporal bone.

This pictorial review describes the application of high-resolution computed tomography to the investigation and pre-operative work-up of the common lesions of congenital hearing loss, including congenital aural dysplasia, various congenital ossicular anomalies, inner ear dysmorphology, large vestibular aqueduct syndrome, and congenital absence of cochlear nerve and labyrinthitis ossificans from previous infection. The aim is to help radiologists to provide a more accurate diagnosis of underlying aetiology and assist in surgical planning.

Cochlea↗

PubMed2001

Auditory brainstem response and temporal bone pathology findings in a brain-dead infant.

The criteria for assessing adult brain death have been already established, but those for infant brain death have not been yet established in Japan. We report auditory brainstem response (ABR) and postmortem pathology of the temporal bone and brain of a brain-dead 9-month-old female. During the comatose state, her ABR showed only waves I and II bilaterally. Autopsy revealed the presence of a left cerebellar astrocytoma, herniation and anoxic encephalopathy. The pathological examination of the temporal bone revealed the destruction of the inner ear particularly on the left side. In the auditory pathway of brain-dead patients, degeneration occurs first in the cerebrum, followed by the cochlear nerve. Thus, ABR is one of the useful means to assess brain death even in infants.

Astrocytoma↗

PubMedDate not supplied

Brainstem auditory evoked response in HIV-infected patients with and without AIDS.

BACKGROUND: The purpose of this paper is to determine the type and frequency of brainstem auditory evoked potential abnormalities in HIV-infected patients with and without acquired immune deficiency syndrome (AIDS). METHODS: Brainstem auditory evoked potentials were performed in 44 HIV-infected patients; 22 of these patients were asymptomatic carriers and 22 presented clinical manifestation of AIDS at the time of the study. Twenty healthy young adults were studied as controls. When brainstem auditory evoked potentials were performed, none of the HIV-infected patients had neurologic clinical findings. RESULTS: The interwave intervals I-V showed significant differences (p <0.05) between both HIV-infected groups and the control group. There were non-significant differences between the two groups including HIV-infected patients with or without clinical features of AIDS. CONCLUSIONS: It is concluded that the HIV infection may produce subclinical pathologic changes in the cochlear nerve and brainstem, which can be detected by BAEP test.

AIDS Dementia Complex↗

PubMed1995

Significance of auditory brain stem response and gadolinium-enhanced magnetic resonance imaging for idiopathic sudden sensorineural hearing loss.

Previous studies tried to correlate prognosis and response to oral corticosteroids in patients with idiopathic sudden sensorineural hearing loss to such factors as the age of the patient, presence of vertigo, shape of the audiogram, or severity of the hearing loss. However, temporal bone histopathologic evidence shows that idiopathic sudden sensorineural hearing loss may be caused by cochleitis or cochlear nerve neuritis. Herein we report results of a retrospective study of 96 consecutive patients with idiopathic sudden sensorineural hearing loss who were evaluated with auditory brain stem responses and gadolinium-enhanced magnetic resonance imaging. Results of the auditory brain stem response and magnetic resonance imaging were correlated with hearing outcome. Follow-up was available for 65 patients: 14 with abnormal and 51 with normal auditory brain stem responses. The overall rate of hearing recovery or improvement was 65% in the normal auditory brain stem response group compared with 43% in the abnormal auditory brain stem response group (p = 0.07). Among the 38 patients treated with a tapering course of oral corticosteroids, the recovery or improvement rate was 83% for those with normal auditory brain stem responses and 56% for those with abnormal auditory brain stem responses (p < 0.05). Of the 27 patients who did not receive steroid therapy, the improvement rate was 41% in those with normal auditory brain stem responses and 20% in those with abnormal auditory brain stem responses (p = 0.09). Magnetic resonance imaging with gadolinium was obtained on all 14 patients with abnormal auditory brain stem responses but on none with normal auditory brain stem responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMedDate not supplied

Sensorineural and vascular changes in an ear with acoustic neurinoma.

The temporal bones from a 55-year-old woman with deafness and dizzy spells caused by a right-sided acoustic neurinoma were examined by the techniques of microdissection, surface preparations, and celloidin sections. Sensorineural degeneration was present in the basal end of the right cochlea but was not severe enough to explain the deafness. The compression of the cochlear nerve by the tumor was postulated to have caused deafness by injury to neurons adjacent and central to the tumor. There was profound degeneration of the vestibular nerve and sensory cells. A gelatinous material occluded the scala vestibuli, and the vestibular fluid spaces contained an amorphous proteinaceous substance. Fewer erythrocytes were seen in the vessels of the right cochlea, but there was no atrophy of capillaries to indicate long-term reduction of circulation. Vasculoneogenesis of venous vessels had occurred in the scala tympani, probably as a result of venous stasis.

Acoustic Maculae↗

PubMedDate not supplied

Otosclerosis and sensorineural hearing loss: a histopathologic study.

The precise role and mechanism whereby otosclerosis is associated with sensorineural hearing loss remains unclear. Previous histopathologic reports are inconsistent with regard to the location of the otosclerotic focus, invasion of the otic capsule, and the number of remaining peripheral sensorineural elements. From the combined temporal bone collections of the University of Chicago and the Mayo Clinic, we identified a group of 125 ears from 80 patients, all with confirmed otosclerosis. Six of these ears were associated clinically with sensorineural hearing loss without stapes fixation. The histopathology of the otosclerotic focus was reviewed in terms of its location and depth of invasion. The cochlea and spiral ganglion were reconstructed, and the state of the organ of Corti and the presence or absence of peripheral cochlear nerve fibers were noted. Correlations with ganglion cell counts were made. The present study showed that the pattern of degeneration of peripheral sensory and neural elements in the cases presented is very similar to that found in cases of age-related processes such as presbycusis.

Aged↗

PubMed1997

Effect of prostaglandin E1 on the rat inner ear microvascular thrombosis.

1. The effect of prostaglandin E1 was investigated with a two-rat model of hearing disturbance and equilibrium dysfunction associated with inner ear microvascular thrombosis. 2. The inner ear microvascular thrombosis was induced by photochemical reaction between Rose Bengal and transmural green light (540 nm). Photochemical reaction causes endothelial injury followed by platelet adhesion, aggregation, and formation of a platelet- and fibrin-rich thrombus. 3. Under anesthesia, the cochlea or the vestibule was irradiated with green light to induce hearing disturbance or equilibrium dysfunction. 4. In the hearing disturbance model, a compound cochlear nerve action potential was recorded by electrocochleography every minute after the beginning of photoirradiation in the presence of Rose Bengal. 5. In the equilibrium dysfunction model, the photoirradiation was applied for 10 min after Rose Bengal administration. The behavior of rats was observed in the swimming test, and nystagmus was observed 24 hr after the end of photoirradiation. 6. Prostaglandin E1 significantly (P < 0.05) prolonged the time required to suppress the action potential. In the swimming test, 3 of the 6 animals treated with prostaglandin E1 did not rotate about their longitudinal axes (equilibrium dysfunction) and the duration of well-balanced swimming was significantly prolonged (P < .001). Prostaglandin E1 significantly (P < 0.05) suppressed the appearance of nystagmus. 7. In conclusion, prostaglandin E1 potentially prevents hearing disturbance and equilibrium dysfunction due to inner ear microvascular disorders.

Action Potentials↗

PubMed2001

Between sound and perception: reviewing the search for a neural code.

This review investigates the roles of representation, transformation and coding as part of a hierarchical process between sound and perception. This is followed by a survey of how speech sounds and elements thereof are represented in the activity patterns along the auditory pathway. Then the evidence for a place representation of texture features of sound, comprising frequency, periodicity pitch, harmonicity in vowels, and direction and speed of frequency modulation, and for a temporal and synchrony representation of sound contours, comprising onsets, offsets, voice onset time, and low rate amplitude modulation, in auditory cortex is reviewed. Contours mark changes and transitions in sound and auditory cortex appears particularly sensitive to these dynamic aspects of sound. Texture determines which neurons, both cortical and subcortical, are activated by the sound whereas the contours modulate the activity of those neurons. Because contours are temporally represented in the majority of neurons activated by the texture aspects of sound, each of these neurons is part of an ensemble formed by the combination of contour and texture sensitivity. A multiplexed coding of complex sound is proposed whereby the contours set up widespread synchrony across those neurons in all auditory cortical areas that are activated by the texture of sound.

Animals↗

PubMed2004

Transient focal cooling at the round window and cochlear nucleus shows round window CAP originates from cochlear neurones alone.

We have measured the compound action potential (CAP) evoked by very brief high-frequency tone-bursts (20 kHz, 1/4 ms) at the round window (RW) and at the surface of the cochlear nucleus (CN) in guinea pigs before, during and after a localised chilling of either the cochlea or CN, with a non-toxic 'freeze spray'. CN chilling almost abolished the negative-going component of the CAP measured in the CN (generated by the CN and here called the cochlear nucleus response or CNR), leaving a positive-going localised response from the cochlear neurones as they leave the internal auditory meatus. Within 3 min, the CNR recovered to control values. During that time, the N(1) component of the RW CAP was slightly increased and the P(1) was larger, even though the CNR was abolished, indicating that the P(1) was not due to electrotonic spread of current from the CN. The N(2) and successive peaks at the RW were also abolished, but returned after 30 s. When the cochlea was chilled, the RW CAP was initially reduced in amplitude, presumably due to a drop in the number of cochlear neurones spiking in response to sound, but recovered within 3 min to be larger than the control waveform, with a more prominent N(1) peak which was delayed slightly, making the CAP more monophasic. At the same time, the CNR was smaller, presumably due to fewer cochlear neurones responding, but overall the CN CAP was altered little in waveshape. These experiments indicate that that RW CAP is generated almost solely by cochlear neurones. We also suggest that some of the changes in the RW CAP during the chills were due to changes in the firing of the lateral olivo-cochlear system of efferent neurons.

Acoustic Stimulation↗

PubMed2004

Determinants of the spectrum of the neural electrical activity at the round window: transmitter release and neural depolarisation.

In this paper we summarise the changes we have observed in the electrical activity at the round window (RW) of guinea pigs during transient cooling of the RW or cochlear nucleus (CN), transient hypoxia, low frequency acoustic biasing, ablation of the CN, and DC current injection into the basal cochlear turn. We have measured the compound action potential (CAP), the spectrum of the average CAP waveform (SAW) evoked by brief tone-bursts, and the spectrum of the neural noise (SNN). We discuss how the changes we have observed can be understood in terms of changes in transmitter release from inner hair cells (that controls stochastic neural firing), or changes in the membrane potential of the primary afferent neurones (that controls the neural firing waveshape and the spectral content of the SAW and SNN). We note that changes in sound intensity produce a simple increase in the stochastic release of transmitter from inner hair cells, without much change in the waveform of the neural response, but manipulations of the auditory brainstem, cooling and current injection all appear to alter neural firing rate and the neural response waveform, producing a baseline shift in the CAP and changes in 1000 Hz peak and low frequency content of the SAW and SNN. We also discuss the use of the CAP, SAW and SNN as an indication of cochlear and auditory brainstem neural activity.

Action Potentials↗

PubMed2004

Ventral cochlear nucleus coding of voice onset time in naturally spoken syllables.

These experiments examined the coding of the voice onset time (VOT) of six naturally spoken syllables, presented at a number of intensities, by ventral cochlear nucleus (VCN) neurons in rats anesthetized with urethane. VOT is one of the cues for the identification of a stop consonant, and is defined by the interval between stop release and the first glottal pulse that marks the onset of voicing associated with a vowel. The syllables presented (/bot/, /dot/, /got/, /pot/, /tot/, /kot/) each had a different VOT, ranging between 10 and 108 ms. Extracellular recordings were made from single neurons (N=202) with a wide range of best frequencies (BFs; 0.66-10 kHz) that represented the major VCN response types - primary-like (67.8% of sample), chopper (19.8%), and onset (12.4%) neurons. The different VOTs of the syllables were accurately reflected in sharp, precisely timed, and statistically significant changes in average discharge rate in all cell types, as well as the entire VCN sample. The prominence of the response to stop release and voice onset, and the level of activity prior to the VOT, were influenced by syllable intensity and the spectrum of stop release, as well as cell BF and type. Our results suggest that the responses of VCN cells with BFs above the first formant frequency are dominated by their sensitivity to the onsets of broadband events in speech, and allows them to convey accurate information about a syllable's VOT.

Acoustic Stimulation↗

PubMed2001

Tinnitus suppression by electrical promontory stimulation (EPS) in patients with sensorineural hearing loss.

OBJECTIVE: Almost 10-15% of the population suffer from chronic tinnitus. There are clinical indications that a 'pathological sound' may be induced by any level of the auditory pathways. Theraupeutical difficulties and many hypotheses about tinnitus and places from which they originate might indicate various methods of treatment. Electrostimulation tinnitus suppression was achieved by many authors from 22 (Graham, Hazell) to 87% (Portman). The aim of our study was to define the usefulness of electrostimulation in treatment of persistent noise induced cochlear lesion tinnitus (group I - 43 men) and compare the results with the non noise induced tinnitus group II (68 patients). METHODS: Otolaryngological and audiological examination of the patients was made before and after electrostimulation, and at 90 days. The stimulation system consisted of a prototype tinnitus suppressor, the active platino-iridium needle electrode and silver surface electrode located on the forehead. Transtympanal electrical stimulation was performed using positive polarity direct current. Parameters of electrical impulse were individually different and depended on tinnitus parameters and patients sensation. The current levels ranged from 20 to 600 microA and frequency ranged from 60 to 10000 Hz. Average time of EPS was 60 s. RESULTS: The control examination 90 days after stimulation in group I showed subjective improvement in 18 (41.9%) patients, 22 (51.2%) did not notice any change and tinnitus deteriorated in 3 (6.9%) of the patients. In the comparative group II improvement was occurred in 34 (50%) persons including 2 (17.6%) in whom tinnitus was abolished, in 30 (44.1%) tinnitus was unchanged and 4 (0.6%) became worse. In both groups our method did not have a destructive influence on hearing. Electrical stimulation to relieve tinnitus has been used for nearly 200 years, but it is unclear how electrical stimulation works to suppress tinnitus. CONCLUSION: In our opinion electrical stimulation by using positive DC changes the spontaneous activity of cochlear nerve fibres. According to our results it is suggested that the mechanism of beneficial effects is due to increased microcirculation in part of the auditory pathways. Poorer results in patients with noise induced tinnitus could be explained by greater damage of the cochlea outer hair cells. In our opinion EPS could be a method of treatment for persistent tinnitus in cases which fail to respond to other methods.

Adolescent↗

PubMed2001

The learning curve in post-operative hearing results in vestibular schwannoma surgery.

PURPOSE: We chronologically investigated whether the hearing preservation (HP) rate improved or not in vestibular schwannoma (VS) surgery. SUBJECTS AND METHODS: HP surgery has been attempted in 127 VS patients with pre-operative class A and B hearing from 1976 to 1999. The HP rate was chronologically compared with hearing level and tumor size. RESULTS: The preservation rate of pre-operative class A hearing which was preserved post-operatively as class A has recently been increasing especially in patients with an intracanalicular (IC) tumor. This rate was improved to 67% from 1995, although this was 33% from 1989 to 1994. However, the preservation rate of pre-operative class B in patients with an IC tumor and that of pre-operative class A hearing which was preserved as class A in patients with a larger tumor extending into the posterior fossa, have not improved over the last 10 years. CONCLUSION: These results indicate that the improvement of the HP rate is mainly due to the increased number of patients with an IC tumor with class A pre-operative hearing. In patients with a tumor of 4-20 mm in size, especially in those showing pre-operative class B hearing, there may be histologically some limitations such as gliosis in the cochlear nerve in the preservation rate of good quality (class A or B) of hearing.

Adolescent↗

PubMed1999

Lidocaine test in patients with tinnitus: rationale of accomplishment and relation to the treatment with carbamazepine.

OBJECTIVES: There is strong evidence in the literature about the effect of local anesthetics such as lidocaine in controlling tinnitus; these agents act by stabilizing hair cell membrane and cochlear nerve fibers. However, the effect of intravenous lidocaine is transient, and its oral analog (tocainide) does not have the same efficacy for long-term treatment in patients with tinnitus. Some oral anti-epileptic drugs (carbamazepine, for instance) have been used alternatively in several studies. The aim of this work is to evaluate the response to intravenous lidocaine in patients with intractable tinnitus and the effect of oral carbamazepine in long-term maintenance of tinnitus relief. PATIENTS AND METHODS: We studied prospectively 50 patients (28 females and 22 males; mean age 50.9 years) who underwent the lidocaine test, performed by a 3-min intravenous infusion of 2% lidocaine chloridrate. The patients who experienced any relief after the test started treatment with oral carbamazepine in ascending dosages (50-600 mg/day). RESULTS: The results were classified as tinnitus abolition (18%), marked relief (32%), partial relief (26%), unchanged (22%), or worsening (2%). The lidocaine test showed favorable results in 76% of patients, especially those with bilateral tinnitus (P < 0.001). Afterwards, 50% of patients treated with carbamazepine maintained the improvement of tinnitus (P = 0.0034). CONCLUSION: The authors conclude that intravenous lidocaine is effective in reducing intractable tinnitus and that there is a close association between lidocaine and oral carbamazepine effects. Therefore, carbamazepine can be used for the treatment of tinnitus when the patient achieves improvement of symptom after the lidocaine test.

Administration, Oral↗