External auditory canal translocation for cochlear implantation.
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Mover-Lev and colleagues reported a carbon dioxide-oxygen time-constant ratio of 3.9 for transmucosal gas exchange in guinea pigs under conditions of a large positive oxygen pressure gradient and a negative carbon dioxide gradient. That ratio is much less than the value of 19 reported previously for monkeys and used in predictive models of middle ear pressure regulation. In this report, the mathematics that underlie models of transmucosal gas exchange are developed and the conditions that allow accurate estimation of time constants are defined. The results demonstrate that the experimental and analytic methods used by Mover-Lev et al do not control for certain confounding effects or concurrently measure all required system parameters. Under the most realistic conditions, their ratio of 3.9 represents a significant underestimation of a true value on the order of 10. Also, their expectation of nonvarying, transmucosal time constant ratios for pairings that include reactive gases is simplistic and true only for identical experimental contexts.
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The round window membrane of the guinea pig was perforated with a sharp instrument, and electrocochleography, vestibular function and histological changes of cochlea were studied in 1, 2, 4, 7, 14 and 28 days. It was found that the compound action potential (AP) threshold and the latency increased at 95 dB (spl) sound stimulus, and vestibular function decreased slightly, but histologic appearance of Corti's organ was normal in the early stage. Latency and threshold of AP and vestibular function gradually recovered to normal 2 weeks later. If no obvious histological change took place in inner ear, hearing loss would not appear. There was no significant difference of SP changes between the experimental and control ears.
Changes in ambient pressure can elicit the vertigo and bodily disequilibrium known clinically as alternobaric vertigo. Our previous studies showed that changes in middle ear pressure altered the activity of the primary vestibular neuron, and the finding suggests that the pressure-induced vestibular response causes alternobaric vertigo. To investigate the roles played by the round window (RW) and the oval window (OW) in the vestibular response induced by pressure, we measured the change in perilymphatic pressure and the firing rates of primary vestibular neurons after the application of positive or negative pressure to the middle ear. We found an increase in the pressure-induced vestibular response in the group with a closed OW, and a decrease in the group with a closed RW. Measurements showed that the amplitude of the change in perilymphatic pressure in the group with a closed OW did not differ from that in the control group, whereas the amplitude of the perilymphatic pressure change in the group with a closed RW was significantly reduced. A discrepancy between the number of neurons responding and the amplitude of the perilymphatic pressure change in the closed OW group suggests that the vestibular response induced by the change in middle ear pressure was not related solely to the magnitude of the pressure change in the inner ear, but also involved the oval and round windows.
Under pressure in the tympanic cavity causes increased impedance of the middle ear. Gellé was the first to describe increased bone conduction levels following alteration of ear canal pressure in healthy ears. Up to now, no investigation which quantitatively describes the elevation of the hearing threshold induced by various levels of under pressure in the middle ear has been published. In a pressure chamber, we induced relative under pressure in the middle ears of 15 adults with normal hearing. We measured hearing thresholds and calculated medium values at four separate levels of under pressure. At an under pressure of 3.3 kPa, air conduction was reduced by a few dB at 500 and 1000 Hz. Alterations of bone conduction were first seen at 6.6 kPa accompanied by increased deterioration of air conduction. Both effects became more obvious at 10 kPa; and at a maximum under pressure of 13.3 kPa, a deterioration of air conduction by more than 25 dB was seen at 250, 500, and 1000 Hz. Bone conduction deteriorated by more than 10 dB at 500 and 1000 Hz. There was no uniformity in the development of bone conduction threshold in the condition of under pressure: Several ears expressed only slight changes, but in some ears we saw an increase of bone conduction at the same rate as air conduction. Minor alterations were observed in frequencies above 1000 Hz. These results may be only partially explained by middle ear effects like the reduction of the ostio-tympanic component of bone conduction caused by increased stiffness of the ossicles. We believe that disturbances of inner ear mechanics play a role in the deterioration of bone conduction levels, too.(ABSTRACT TRUNCATED AT 250 WORDS)
HYPOTHESIS: Despite its invasiveness, the temporary implantation of a microcatheter into the middle ear cavity is an appropriately safe method for providing continuous drug delivery to the inner ear. BACKGROUND: For the application of drugs to the inner ear, different delivery strategies are available ranging from intratympanic injections to temporarily implanted microcatheters. It has recently been demonstrated that the choice of the drug delivery system influences the pharmacokinetics in the inner ear. If a continuous drug application over several weeks is required, a secure placement of the delivery device (i.e., the microcatheter) is necessary to guarantee efficient drug delivery and to avoid unwanted side effects. STUDY DESIGN: Retrospective chart review. MATERIALS AND METHODS: During 2000 to 2005, 25 patients with acute unilateral severe-to-profound hearing loss or anacusis and failure of systemic high-dose glucocorticoid and rheological therapy were offered an intratympanic delivery of glucocorticoids via a temporarily implanted catheter and an external pump for up to 4 weeks as a salvage treatment option. The standardized surgical implantation and fixation technique developed for the microcatheter were characterized by six elements: 1) a medial and a lateral tunnel connected by a groove in the posterior wall of the bony ear canal, 2) stabilization of the catheter with bone wax and soft tissue plugs in the tunnels, 3) an ear canal packing, 4) a series of fixating sutures along the catheter, 5) an adhesive dressing, and 6) additional tapes at the connecting line between pump and catheter. At the end of the implantation period, the catheter was removed by a second surgical procedure allowing for evaluation of the catheter position and the condition of the middle ear space. RESULTS: Adverse events included catheter dislocation, catheter obstruction, formation of mild granulation tissue in the middle ear cavity, tympanic membrane defects, and ear canal skin defects. With introduction of an improved implantation and fixation technique, the number of catheter dislocations could be significantly reduced. No complications were observed on long-term follow-up. CONCLUSION: If the pharmacokinetics or pharmacodynamics of a specific local inner ear therapy approach requires a continuous intratympanic drug application (e.g., to restore hearing in patients with severe or profound hearing loss), the temporary implantation of a microcatheter by a standardized surgical technique is a feasible and appropriately safe method for providing continuous drug delivery to the inner ear.
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We report on two patients with sudden hearing loss occurring immediately after registration of an acoustically elicited acoustic reflex with pure tones of 500, 1000, 2000, and 4000 cps and 125 dB HL. Aetiology and patho-physiology of this form of acute acoustic trauma are discussed. An obvious destruction of middle ear structures or the membrane of the round and oval window can be excluded. Assuming pre-existing disposition, e.g. distortion of microcirculation in the cochlea, the acoustic stimulus is merely the trigger for the imminent sudden hearing loss. Therefore, we suggest to limit the stimulus power to 105 dB HL. In every case one should keep in mind the possible danger of this examination and perform a benefit-risk calculation in every patient.
The purpose of this study was to evaluate the average discharge rate of all fibres in the whole auditory nerve (R(wn)) when a broad-band noise with steady-state effects is applied to the ear. We assessed the R(wn) parameter by detecting the state of refractoriness of the nerve during noise stimulation using an electric stimulus (ES) as a probe. The technique, applied in awake pre-implanted guinea pigs (Charlet de Sauvage et al., 1994), made it possible to obtain electro-acoustic responses (EARs), from which an estimate of the R(wn) parameter could be deduced. Negative current pulses of 100 micros duration, each followed by an identical pulse of positive polarity for charge balance, were applied between round window and indifferent vertex electrodes at intervals of 160 ms. The 120 ms wide-band noise masker started 92 ms before every other negative ES. The signal on the stimulating electrodes was averaged over a 5.12 ms window in synchrony with the negative pulse. EARs were obtained by alternately subtracting recordings during noise from those during silence. The R(wn) parameter was determined by comparing experimental and computed EAR patterns. For this purpose, a model of unit response incorporating changes in amplitude and conduction velocity during the relative refractory period was designed. The recovery function of the firing probability in response to ES was evaluated. Fibres were classified in different categories according to their background discharge rates. The probability of response of single fibres to ES in each category was calculated on the basis of their interval histograms during silence and noise. Individual spikes were combined accordingly to obtain the computed EAR waveform. R(wn) was determined by adjusting the EAR amplitude of the model in relation to that of the experimental EAR. R(wn) generally increases in a linear fashion with respect to noise intensity expressed in dB, thus following the increase in loudness perception estimated by Weber's law. At the highest noise levels, R(wn) tends to saturate. The estimated saturation rate was found to be about 380 spikes/s.
The spatial anatomy of microfissures in the round and oval window areas was investigated in 24 randomly selected normal human temporal bones by our computer-aided three-dimensional reconstruction and measurement method. Microfissures that communicated with the middle ear surface in the round window area were seen in 21 cases (87%) and were located on the posteromediosuperior aspect of the round window niche; whereas microfissures in the oval window area, seen in seven cases (29%), were located at various sites, but mostly in the area below the oval window. Of the 21 microfissures seen in the round window niche, only four were found to be visible through the aperture of the round window niche when viewed from the lateral direction. The mean lengths of the microfissures seen on the middle ear surface in the round and oval window areas were 0.95 +/- 0.66 mm and 0.74 +/- 0.44 mm, respectively. The microfissures in the round window area were significantly longer in individuals 20 years of age and older, than in those less than 20 years (Wilcoxon test, t = 21.5, p less than 0.01); this tendency for microfissures to be longer in older subjects was also found for microfissures in the oval window area. The possible clinical and pathologic significance of these results is discussed.
The term "caloric irregularity" was coined to refer to a gross irregularity in the amplitude and/or frequency of a caloric-induced nystagmus, having a variable slow-phase velocity and prolonged duration. Twelve of 46 guinea pigs with experimentally induced perilymphatic fistula had irregular responses to the ice-water caloric test 1 week after creation of a fistula. The long-term vestibular consequences in animals with caloric irregularities were either resolution and return to normal function (i.e. caloric return) or continuing deterioration to canal paresis. Morphological examination of ears with caloric irregularity revealed that there had been partial collapse of the membranous labyrinth and the creation of a floating labyrinth.
Single unit activity of second-order vestibular neurons was recorded in alert guinea pigs. Here, we compared the spike discharge regularity (measured by calculating the coefficient of variation (CV)) of neurons from control animals with those from animals labyrinthectomized 1 week before. The mean CV (+/-SD) were the same in both groups (0.72+/-0.43 vs. 0.70+/-0.39). Furthermore, in both groups, the CV was related to the resting rate (RR) according to the same law (CV = 4/square root of RR). Because the discharge of a neuron is more regular when it is due to a pacemaker activity than when it is due to the synaptic drive, we conclude that restoration in the firing rate after labyrinthectomy is due to increase in the synaptic drive rather than to increase in the (intrinsic) pacemaker activity.
The results of a poll revealed that 96 singular neurectomies have been performed by ten surgeons in this country. Eighty-eight of these (91.7%) resulted in complete relief of benign paroxysmal positional vertigo (BPPV). In seven patients (7.3%) there was a sensorineural hearing loss as a result of this procedure. The average hospital stay for patients having this procedure ranged from 2-6 days, and the return to work time ranged from 1 to 3 weeks. These results indicate that singular neurectomy is an effective selective vestibular ablation procedure for BPPV and that the risks and disability are comparable to other routine middle ear procedures. The causes for failure of this procedure to relieve positional vertigo are a) misdiagnosis of BPPV and b) failure to recognize the singular nerve in the middle ear. Knowledge of the pathophysiology of the disorder and of the anatomical variation in the location of the singular canal will reduce these causes of failure.
Twenty-eight chinchillas received continuous or intermittent infrasound (1, 10, 20 Hz) at 150, 160, or 170 dB SPL; there were 7 controls. Serial sections of the temporal bones were examined using light microscopy. Pathologies noted were tympanic membrane perforation, stapes subluxation, bleeding from the middle ear mucosa and tensor tympani, strial pathology, Reissner's membrane rupture, endolymphatic hydrops, saccular wall rupture, hair cell damage, and blood in the cochlear scalae. Continuous infrasound was more damaging than intermittent. Only continuous infrasound produced saccular pathology and perforations of the tympanic membrane. Of the other pathologies observed, continuous infrasound exposures produced 67% of the hair cell damage, 73% of the bleeding in the cochlear scalae, 83% of the strial pathology, and 78% of the cases of cochlear hydrops. 170-dB infrasound exposures produced the highest percentage of ears with pathologies of the three exposure intensities. As frequency increased the percentage of ears with pathologies decreased.
The activity of central vestibular neurons (Vn) of the horizontal canal system was recorded in chronically hemilabyrinthectomized cats and compared with that of labyrinth intact animals. In both groups the cerebellar vermis was removed in order to assess the efficacy of the vestibular brainstem commissure alone by means of polarizing currents applied to the labyrinths. Experiments were carried out under Ketamine anaesthesia. In control animals the mean resting rates of type I and type II Vn measured 22.4 +/- 14.0 and 27.5 +/- 14.6 imp/s respectively, and the type I responses occurred ca. 3 X more frequently than type II. In the lesioned animals a drastic reduction of the number of type I responses was found on the deafferented side, while that on the intact side remained normal. The resting rates of type I Vn on the two sides did not differ significantly from each other but were significantly lower than those of control animals. In contrast, type II responses were present on the deafferented side, but almost completely missing on the intact side. Applying polarizing stimuli in control animals, it was found that both labyrinths have similar weight in driving Vn. In lesioned animals, no major changes in the efficacy of the commissural path were found when polarizing stimuli were applied to the intact side. It is concluded that vestibular nerve section causes a severe loss of type I responses in the vestibular nuclei on the side of the lesion which apparently is not compensated by an adaptive change in the commissural path and, therefore, may be mainly responsible for the VOR asymmetry observed concomitantly.
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