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[Intraoperative monitoring with transtympanic electrocochleography].

Transtympanic electrocochleography (ECoG) enables auditory evoked potentials to be recorded directly from the peripheral organ, and ECoG recordings can be used as a routine during operations. Examples of cochlear and eighth nerve monitoring in middle ear, inner ear, and cerebellopontine angle surgery are given. This monitoring tool provides a continuous feedback to the surgeon of the effects of the operation on the cochlea and the auditory pathway.

Acoustic Stimulation↗

Malformations in cochlear implant patients.

OBJECTIVE: To report on cochlear implantation in children with bony inner ear malformations. PATIENTS: 30 children with bony inner ear malformations who have received cochlear implants. INTERVENTIONS: High-resolution spiral computed tomography is used to identify malformations. Magnetic resonance imaging is used to detect the presence of an acoustic nerve and determine the integrity of the auditory pathway and central nervous system structures. Both imaging techniques may be used intraoperatively, as well as facial nerve monitoring and electrical auditory brainstem response monitoring. Three-dimensional reconstructions are helpful in preoperative planning. Large vestibular aqueducts and vestibular malformations can be successfully managed. RESULTS: Postoperative results have been encouraging, although children with malformations tend to occupy the lower third of rehabilitation results of all children with implants.

Child↗

Auditory brain-stem responses evoked by electrical stimulation of the cochlear nucleus in human subjects.

When auditory nerve function is lost due to surgical removal of bilateral acoustic tumors, a sense of hearing may be restored by means of an auditory brain-stem implant (ABI), which electrically stimulates the auditory pathway at the level of the cochlear nucleus. Placement of the stimulating electrodes during surgical implantation may be aided by electrically evoked auditory brain-stem responses (EABRs) recorded intra-operatively. To establish preliminary standards for human EABRs evoked by electrical stimulation of the cochlear nucleus, short-latency evoked potentials were recorded from 6 ABI patients who were either already implanted or undergoing implantation surgery. Neural responses were distinguished from stimulus artifact and equipment artifact by their properties during stimulus polarity reversal and amplitude variation. Other properties contributed to further identification of the evoked potentials as auditory responses (EABRs). The response waveforms generally had 2 or 3 waves. The peak latencies of these waves (approximately 0.3, 1.3, and 2.2 msec) and the brain-stem localization of the region from which they could be elicited are consistent with auditory brain-stem origin.

Adult↗

Middle latency response: frequency and intensity effects.

Auditory middle latency responses (MLR) and auditory brainstem responses (ABR) were measured with epidural electrodes in unanesthetized gerbils. Response thresholds of simultaneously recorded MLRs and ABRs, and latencies and amplitudes of MLR peaks were analyzed with respect to stimulus intensity (10-80 dB SPL) and frequency (0.5, 1, 2, 4, 8 and 16 kHz). Only minor changes in the latencies of the MLR were associated with increases in stimulus intensity. Changes in latencies were more apparent for waves A and B as compared to wave C, and were significant only at low intensities. Latencies did not change significantly as a function of stimulus frequency. Amplitudes of the MLR were highly variable between animals, particularly waves B and C, and showed complex changes with intensity. In general, wave amplitudes were inversely related to stimulus frequency. The gerbil MLR resembles MLRs recorded under similar conditions in guinea pig, cat, and rat. Some qualitative similarities between gerbil and human MLRs are apparent. Results indicate that the MLR is a less sensitive measure of hearing threshold relative to the fast waves of the ABR at frequencies above 1 kHz. However, clearly defined MLRs are elicited with a wide range of stimulus frequencies. Because the surface recorded MLR reflects activation of central auditory pathways, including the cortex, it may provide an electrophysiological measure which can be utilized to study central components of normal and pathological auditory function.

Acoustic Stimulation↗

In vivo visualization of the cochlear nerve and nuclei with fluorescent axonal tracers.

In recent years multichannel neuroprostheses have been developed which directly stimulate the central auditory pathway. Substantially these have been used in cases of total hearing loss caused by neurofibromatosis type 2 where bilateral damage to the auditory nerve prevents more peripheral stimulation. The electrode carrier of the auditory brainstem implant (ABI) is designed to be placed on the cochlear nucleus complex residing at the lateral brainstem surface. Despite altered anatomy due to tumor growth or preceding surgery, correct electrode placement is essential to maximize the variety of pitch percept elicited during electrical stimulation with the ABI without producing side-effects. In order to assist intraoperative identification of the proximal auditory nerve and cochlear nuclei, the non-toxic fluorescent axonal tracers Fast Blue or Fluorogold were injected into the cochlea of rats and Java monkeys. Four to seven days after tracer application, labeling of the eighth cranial nerve, its entrance into the brainstem and the primary radiation of auditory fibers into the cochlear nucleus could be demonstrated as colored fluorescence on the living brain under appropriate ultraviolet illumination. Additional histological processing revealed groups of retrogradely labeled neuronal cell bodies in both species. Our results suggest that this method could also be used in humans in order to aid surgeons with the proper positioning of the electrode array.

Amidines↗

[Detection of central auditory compensation in unilateral deafness with functional magnetic resonance tomography].

BACKGROUND: Functional magnetic resonance imaging (fMRI) is a noninvasive method to detect focal brain activity at high spatial resolution. Acoustic stimulation induces an increase of regional cerebral blood flow in the primary auditory cortex. This entails an increased concentration of diamagnetic oxyhemoglobin in the capillaries and the venous system. The resulting decrease of the local magnetic susceptibility was detected as a signal increase in T2*-weighted images. The central auditory pathways predominantly cross to the contralateral hemisphere in normally hearing subjects. The aim of the present study was to investigate the primary auditory cortex after acoustic stimulation in unilateral deaf patients using fMRI. METHODS: Magnetic resonance images were acquired on a 1.5 T Siemens Vision scanner. For fMRI, a single shot gradient recalled, echo planar imaging (EPI) sequence with decreasing excitation order was used, allowing the aquisition of 9 slices within 1.8 s. The 9 slices covered a slab of 3.6 cm in cranio-caudal extension in the region of the temporal lobes. For statistical processing of the raw image data the SPM96 software package was used. A p-value of p < 0.01 was applied to differentiate between activated and non-activated. The resulting functional activation maps were superimposed onto the EPI scan. The number of activated pixels was used to quantitate the cortical response upon acoustic stimulation. Stimulation consisted of a 1000-Hz sine tone (100 dB SPL at the distal end of the head phone, pulsed at 6 Hz) to which the patients were asked to listen passively. A piezoelectric loudspeaker was mounted on the subject table and connected to a plastic tube system leading to a combination of bilateral ear- and headphones. Auditory paradigms require disentangling experimental excitation from the scanner noise that approximates 90 dB. Headphones suppress noise by approximately 30 dB. To decrease the acoustic background-to-stimulation ratio and to keep background noise constant during stimulation and resting, we employed short scanning (1.8 s) and long resting periods (10.2 s; TR = 12 s). This acquisition mode allows sufficient recovery during off-periods and sufficient excitation during on-periods. 14 unilateral deaf patients were examined. The mean duration of deafness was 22.5 years. RESULTS: Acoustic stimulation of the deaf ear revealed only weak cortical activation which could be explained by sound transmission via bone conduction to the other ear. A significant increase of BOLD (blood oxygen level dependent)-activation in the primary auditory cortex could be demonstrated in all patients after stimulation of the hearing ear. However, remarkable individual differences were noticed concerning the absolute number of activated pixels. The lateralization ratio was calculated by the number of activated pixels on the hearing side divided by the number of activated pixels on the deaf side. A mean lateralization ratio of 0.9 (Stdv +/- 0.6) was found. The mean lateralization ratio for patients with a right deaf ear (n = 8) and those with a left deaf ear (n = 5) was 1.1 (Stdv +/- 0.7) and 0.6 (Stdv +/- 0.3) respectively. However, the difference was not significant (Wilcoxon test: p = 0.08). CONCLUSIONS: Central-auditory compensation by bilateral cortical activation was demonstrated in unilateral deaf patients. Moreover, a tendency towards a dominance of the left primary auditory cortex was found, although the difference between both hemispheres was not significant. The lateralization ratio in unilateral deaf patients is similar to findings after binaural stimulation in normally hearing subjects.

Acoustic Stimulation↗

The Gunn rat: an experimental model for central deafness.

The Gunn rat which develops neonatal hyperbilirubinemia has been used as an experimental model to evaluate the effect of bilirubin on the auditory system. Electrocochleographic and morphological studies (including light microscopy, surface preparations and transmission electron microscopy) did not reveal any cochlear abnormality in homozygous Gunn rats. Brainstem auditory evoked potentials showed morphological and amplitude changes suggesting a functional damage in the brainstem auditory pathways. These results suggest that hearing loss, when observed in kernicterus, is primarily due to neuronal damage at the level of brainstem auditory nuclei.

Animals↗

Some pathologies of sensory and neural hearing loss.

Recently surgical implantation of devices to stimulate the auditory nerve in man makes it apparent that sensory and neural pathologies of deafness need to be differentiated from each other. In this paper 10 exemplary cases are presented. In addition, an attempt is made to compile the information now available about sensory and neural pathologies in the various diseases that cause deafness. Superficially, it would appear that most such entities are sensory in nature and thus theoretically might be amenable to auditory nerve stimulation. However, loss of supporting cells seems to be associated with cochlear nerve fibre degeneration. Many individuals may, therefore, eventually develop combined pathology. The paucity of knowledge of pathology of the auditory pathways and their radiations in deaf persons is recognized as a limiting factor in attempts to predict which patients might benefit from auditory nerve stimulation. It is not within the scope of this paper to delineate the possible deleterious effects that cochlear implants might have on the auditory nerve.

Adult↗

[Cortical responses evoked by vibrotactile sensations in deaf children].

Vibrotactile evoked responses (VER) to 250 and 500 Hz presented respectively at 50 and 70 dB HL by BC vibrator placed on right thumb, were recorded in 20 children (10 with pathological EEG) with severe sensorineural hearing loss, or deaf since birth, both to control accuracy of cortical responses to high intensity auditory stimuli and to diagnose central non auditory pathways lesions. The results have shown that: VER are present in subjects with severe sensorineural hearing loss or deaf; in children with auditory lesions VER have parameters different from auditory evoked response (AER); VER recording is not related both to the presence of auditory lesions and to neurological pathology.

Cerebral Cortex↗

Maturation of binaural interaction components in auditory brainstem responses of young guinea pigs with monaural or binaural conductive hearing loss.

Reversible conductive hearing loss created during the first 4 weeks post partum caused marked alterations in the maturation of binaural interaction components in the auditory brainstem responses of guinea pigs. In untreated control animals all three components investigated demonstrated postnatal development in terms of latency shortening that was completed during the first 3 weeks of life. Plugging of both external ear canals caused a significant delay in the maturation of the late component DN2, where latency values of the controls were reached only 2 weeks after the end of the treatment, i.e. after 6 weeks of life. Monaural deprivation likewise led to a retarded development of peak latencies during the phase of imbalanced sensory input. After the end of the one-sided conductive hearing loss the maturation process was markedly enhanced, even resulting in latency values for DN2 and DP1 that were significantly shorter than those of the controls. This phenomenon persisted until the end of the study period and was the case for both plugged and untreated ears in this group of animals. The time course of latencies in two other groups of experimental animals which were deprived in the same way as adults suggests that the effects observed are due to a sensitive period in the maturation process of the auditory pathway.

Age Factors↗

Further differences between brain-stem auditory potentials evoked by rarefaction and condensation clicks as revealed by vector analysis.

Vectorial analysis of the brain-stem auditory evoked potential (BAEP) elicited by either condensation and rarefaction stimuli was performed in 22 healthy subjects. Besides differences in latency of components III and V ('R' longer than 'C'), a significant difference was found between the directions of the vector calculated over the descending limb of wave III, with an ascending direction for 'C' responses and a contralateral direction for 'R' responses. The possible origins of these differences are discussed. It is concluded that the use of alternating or isolated single polarity clicks is not recommended, mainly when assessing integrity of central auditory pathways.

Acoustic Stimulation↗

Role of serotonin in the nicotine-induced depression of the brainstem auditory evoked response.

We have examined the role of serotonergic and/or dopaminergic mechanism in the mediation of the nicotine-induced depression of brainstem auditory evoked responses (BAER) to auditory stimuli. Nicotine produced dose- and time-dependent decreases in BAER amplitude. Administration of serotonin-depleting drugs (reserpine or p-chlorophenylalanine (PCPA), prevented this decrease. Administration of catecholamine-depleting drugs (alpha-methyl-p-tyrosine, disulfiram or Dopa), on the other hand, had no effect. These data thus suggest a role for serotonergic mechanisms in the mediation of nicotine-induced depression of the brainstem auditory pathway.

Animals↗

Unusual pattern of somatosensory and brain-stem auditory evoked potentials after cardio-respiratory arrest.

Two patients in coma after cardio-pulmonary arrest showed bilateral absence of all brain-stem auditory evoked potentials contrasting with normal brain-stem reflexes and normal somatosensory cortical evoked potentials. In both patients pre-existing dysfunction of peripheral auditory structures could be ruled out. Subsequent neuropathological analysis showed that the anoxic-ischaemic lesions were restricted to Sommer's sector and the Purkinje cells. These unusual data suggest the hypothesis that a severe hypoxic-ischaemic insult may impair cochlear function and interfere with the activation of the intact auditory pathways.

Aged↗

Effect of selective attention on the latency of human frequency-following potentials.

While effects of attention on late and middle latency components of the evoked potential have been demonstrated, similar effects on brain stem evoked potentials--in particular on the human frequency-following potential (FFP)--are controversial. The FFP is a response to tone bursts in the frequency range of human language (optimum approximately 350 Hz). It has a latency of approximately 6.3 ms and is probably generated at a site peripheral to the inferior colliculus. We present data showing that the latency of the FFP can be shortened significantly (45 microseconds) if the subject is required to attend to the evoking auditory tone burst, while the amplitude of the FFP remains unaffected. This indicates an attention-controlled influence on signal processing in the earliest parts of the auditory pathway.

Acoustic Stimulation↗

Auditory brainstem evoked response as a hearing test in infants and children: a follow up study.

In recent years the auditory brainstem evoked response (BSER) has become an established aid in assessing hearing in unco-operative subjects. We have reviewed our experience with this technique in 293 infants and children aged less than 11 years. We have found that the threshold for click BSER correlates well with the average audiometric threshold in the 2-4 kHz range. We have had encouraging preliminary experience to support the claim by other workers that 500 Hz stimuli may be used to assess low tone auditory function. In interpreting results it is important to appreciate that hearing levels may fluctuate with disorders such as otitis media and occasionally in cases of meningitis. Caution is also advised in interpreting results in cases where central nervous system pathology capable of affecting auditory pathways is known to exist.

Audiometry↗

Effect of interaction between noise and toluene on auditory function in the rat.

Rats were exposed to toluene (1000 ppm, 16 h/d, 5 d/w, 2 w), or noise (100 dB Leq, 10 h/d, 7 d/w, 4 w) or toluene followed by noise. Auditory function was tested by brainstem audiometry using a 1/3 octave filtered sine wave stimulus at the frequencies 1.6, 3.15, 6.3, 12.5 and 20.0 kHz. A high-frequency auditory impairment was observed after exposure to toluene alone and noise alone. A slight recovery was recorded 1 and 6 months after the toluene exposure. Toluene followed by noise resulted in a higher threshold at all frequencies. A slight recovery was recorded 6 months post-exposure. The threshold shift exceeded the summated loss caused by toluene alone and by noise alone, particularly at 3.15 and 6.3 kHz. The latencies varied only slightly. The results indicate that the major cause of the auditory impairment was cochlear damage and that only minor injury was caused to the auditory pathways.

Animals↗

Spontaneous otoacoustic emissions in neonates and effect of contralateral white noise stimulation.

Neonates younger than the age of 12 weeks (10 full-term, 20 preterm) had an audiological assessment consisting of brainstem audiometry, tympanometry, transiently evoked otoacoustic emissions, and spontaneous otoacoustic emissions with contralateral white noise stimulation. Results from brainstem audiometry, tympanometry, and transiently evoked otoacoustic emissions suggested normal middle ear function and normal cochlear function. All full-term neonates had multiple spontaneous otoacoustic emissions, and contralateral white noise stimulation resulted in enhancement of emissions in 80%, whereas in 20% the emissions were suppressed. In preterm neonates, spontaneous otoacoustic emissions were present in 55%. These emissions were mostly solitary and, in 64%, showed suppression with contralateral white noise stimulation. Embryological data taken into consideration suggest that the pattern of spontaneous otoacoustic emissions in preterm neonates is more likely related to immaturity of the central auditory pathway rather than the cochlea.

Acoustic Stimulation↗

[Effect of nicotine on auditory functions in the rat, studied by electrocochleography and auditory evoked potentials of the brain stem].

The rôle of nicotine (100 micrograms/kg) on brainstem auditory evoked responses (FFP) and electrocochleography (EcoG) in rats anaesthetized with pentobarbital has been studied. Each component of FFP and EcoG was analysed in terms of its latency and amplitude. Nicotine failed to produce any significant changes in the latencies of the FFP and EcoG components. Nicotine after 30 min increases significantly the amplitude I, I', II and III, of the FFP components, and decreases no significantly IV and V components. These finding suggests the presence of muscarinic and nicotinic effect of nicotine, in the mediation of the brainstem auditory pathway.

Animals↗