Frequency sensitivity and selectivity of acoustically evoked potentials after complete cochlear hair cell destruction.
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Biomedical subjects
Publications and source records attributed to Y Cazals.
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The occasional suppression of tinnitus during electrical stimulation of the ear with positive currents has been investigated in 106 patients presenting with any degree of hearing impairment (whether of known or unknown aetiology) from profound deafness to near-normal pure-tone thresholds. Seventy-four percent of these patients presented with tinnitus localized in the ipsilateral ear at the time of examination. The suppression was totally effective in 60% of patients during stimulation through a round-window electrode. The suppression, partial or complete, was obtained in only 43% of patients when stimulation was from the promontory electrode, which served first as a recording electrode for electrocochleography. The sensations (hearing induction and/or tinnitus suppression, and dizziness) during and after the stimulation were evaluated with respect to polarity, intensity and frequency of the electrical impulses. This procedure had several objectives: (1) to confirm the eventual suppression of tinnitus by positive currents; (2) to serve as a tool to differentiate between various types of tinnitus; (3) to assess the possible clinical application for the long-term relief to some patients suffering from tinnitus; (4) to evaluate the possibility of artificial auditory stimulation in profoundly deaf subjects; and (5) to bring some hope to highly disturbed patients.
Acoustically evoked neural activity has been recorded from the brainstem and auditory cortex of guinea pigs after complete destruction of the organ of Corti by the aminoglycosidic antibiotic amikacin. These responses to sound differ in important respects from the evoked potentials normally recorded from the auditory pathways. At the brainstem level they resemble the potentials reported by others after stimulation of the vestibular nerve.
Thresholds of the auditory nerve compound action potential (CAP) responses to filtered clicks from 0.5 to 40 kHz, defining a CAP frequency threshold curve, have been determined in the same guinea pigs: (1) in acute conditions, the animal still anesthetized at the end of the operation for permanent implantation of a round-window electrode, and (2) several days later in the implanted awake and unrestrained animal. The results show higher CAP thresholds for high frequencies in acute conditions as compared to chronic recordings. This difference appears above about 12.5 kHz and increases progressively to around 40 dB at 40 kHz. Similar effects, although somewhat less pronounced, were observed during anesthesia alone in already implanted guinea pigs. Thes observations could explain the discrepancies which appear between electrophysiological thresholds, acutely recorded either from single fibers or whole-nerve responses, and behavioral audiograms. Moreover, in the accurate evaluation of the cochlea, slight impairments may be masked by this phenomenon as illustrated in guinea pigs treated with low doses of ototoxic antibiotic.
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Electrophysiological and histological observations in guinea pig's cochleas after amikacin treatment (14 X 450 mg/kg) confirm the results obtained in a former experiment: clear, short-latency, click-evoked responses were recorded in cochleas with only very few hair cells remaining at the extreme apex. Detailed analysis of these responses strongly indicates a neural origin and confirms their low-frequency sensitivity. Careful histological observations confirm the extensive hair cell loss and the preservation of nerve fibers in the remnants of the organ of Corti and of the vestibular sense organs. These results suggest that the acoustical vibrations either stimulate the vestibular receptors or act directly or through some kind of mechano-electrical transduction on the remaining cochlear nerve fibers.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The possibility of stimulating the ear by way of an electrode on the round window in order to relieve tinnitus or to produce auditory sensations has been investigated experimentally in guinea pigs. The deleterious effects of DC currents applied to a normal cochlea clearly demonstrate that this means is unsuitable for use in relieving tinnitus in hearing patients. Although AC currents do not cause further damage in ears with the organ of Corti already destroyed by aminoglycosides, the effects of DC currents in such cases have still to be investigated before they can be recommended for the relief of tinnitus in totally deaf patients. Electrical stimulation of the round window combined with masking has made it possible to record responses of auditory neural elements from the eighth nerve to the auditory cortex. This technique could be promising for the basic study of the central auditory nervous system, both experimentally and clinically, and could lead to a more accurate evaluation of candidates for cochlear prostheses.
Electrical stimulation of the ear in humans was performed with an extracochlear electrode on the round window. With positive currents, suppression of tinnitus could be induced. With negative currents, auditory sensations were evoked. Since electrical stimulation with DC currents may be hazardous in the long term, it cannot yet be proposed for the suppression of tinnitus. However, electrically evoked hearing sensations with AC currents seem to be of definite interest for some totally deaf patients.
While investigating the possibilities of electrically induced hearing in cases of profound deafness, we observed that very often an appropriate stimulation of the cochlea could result in tinnitus cancellation. We present here a progress report on that phenomenon, including 15 subjects. Such a cancellation was restricted to tinnitus subjectively localized in the ear under test, we observed no effect on noises localized in the other ear, or centrally. This suppression occurred so long as the cochlea was stimulated and stopped when the stimulation ceased. This phenomenon was very reproducible and did not seem to affect simultaneous normal acoustic hearing. It is hypothesized that this phenomenon acts through an inhibition of abnormal activity of sensorineural elements of the electrically stimulated cochlea.
In guinea pigs that had been treated with very large doses of the aminoglycoside amikacin (14 x 450 mg/kg/day, i.m.) clear, short-latency responses to various click stimuli could be recorded at the round window. When the same cochleas were examined histologically, no outer or inner hair cells could be found along the entire length of the basilar membrane, save for a very few outer hair cells remaining at the apex. The response patterns resembled that of the compound action potential, and various characteristics suggest that they were of neural origin. Vestibular function, investigated by electronystagmography during rotation, appeared normal, as did most of the saccular and utricular hair cells. Transmission electron microscopy revealed a significant number of cochlear nerve fibres still innervating the remnants of Corti's organ. In other cochleas with similarly extensive destruction induced by another aminoglycoside (sisomycin, 14 x 125 mg/kg/day, 15 days as well as 3 months post-Rx), no responses could be recorded from the round window. Cochleas that were less affected, with the upper turns preserved, gave only small, long-latency responses. These preliminary observations are confirmed by further experiments now in progress. They suggest that unless a considerable number of inner hair cells remained undetected in the lower basal turn, a possibility that appears highly unlikely, there was either a direct mechanical excitation of cochlear nerve fibres, or an acoustical stimulation of vestibular sense organs.
A series of patients presenting with subsequently surgically confirmed central tumour involving the auditory pathways were investigated using both transtympanic electrocochleography (TT ECochG) and surface recordings of brainstem evoked responses (BER). While ECochG allows a detailed study of peripheral function, BER allow the investigation of neural conduction up to the level of the inferior colliculus. Valuable information can be obtained from: (1) comparison of the amplitudes of the sensory and neural components of the ECochG; (2) comparison of ECochG, BER and auditory thresholds; (3) time interval measurements between the auditory nerve response (N1 on the ECochG) and the inferior colliculus (wave P4-5 on BER); (4) contralateral comparisons. Similar measurements performed in pure cochlear pathologies, mainly in Meniere's disease, yielded very significant differences.
A series of acoustically evoked potentials can be recorded from the cochlea up to the auditory cortex in guinea pigs where the organ of Corti has been totally destroyed after extensive treatment with amikacin, but where some of the spiral ganglion neurons always remain and where the vestibular receptors are only slightly affected. The cochlear responses have been monitored in guinea pigs permanently implanted with a round window electrode and receiving such treatment. The normal auditory nerve compound action potential disappears within a few days, while the very typical response (diphasic, short latency (0.3 ms) small amplitude) appears. This response then remains remarkably constant in time as far as we could observe (up to almost one year). This response might be a component of the normal response, undiscernible under normal conditions but revealed by the selective impairment of the labyrinth by amikacin, in contrast to the global effect of every other known otodestructive agent. Some basic questions still remain: which fibres are effectively stimulated (cochlear or vestibular), what are their central projections, and what kind of sensation is conceivably associated with these responses?
Morphological changes of the eighth nerve were observed in the guinea pig between 1 month and 1 year after treatment with large doses of the antibiotic amikacin which resulted in complete cochlear hair cell destruction. The neural retrograde degeneration was found to be relatively fast, with a considerable loss (30 to 55%) of ganglion cells one month after treatment, continuously increasing (up to 85) after one year. Gross changes in the habenula perforata and in the spiral ganglion are described, together with ultrastructural alterations of organelles important for the cell metabolism and axonal transport. The rapid degeneration and the morphological findings suggest a direct influence of toxic substances on the ganglion cells.
After complete destruction of cochlear but preservation of vestibular hair cells in the guinea pig acoustically evoked responses can still be recorded from the round window up to the auditory cortex. At all levels these responses differ from those observed in normal animals but their frequency sensitivity and selectivity make them akin to responses from auditory organs. In a series of experiments a complete cochlear destruction was combined with a total or partial destruction of the vestibule. After complete cochlear and vestibular hair cell destruction no acoustic response could be recorded. But in cases of total cochlear and drastic ampullar and utricular destruction together with an almost undamaged saccular sensory epithelium the same peculiar acoustic responses could be observed. These results support the hypothesis of a functional acoustic reception by the saccule in a mammal.