Superior canal dehiscence: mechanisms of pressure sensitivity in a chinchilla model.

BACKGROUND: Patients with superior canal dehiscence syndrome may experience vertigo and nystagmus when pressure changes occur in the external auditory canal, the middle ear, or the intracranial space. The cause is a defect in the bone of the superior canal. OBJECTIVE: To study the mechanisms of pressure sensitivity of the labyrinth in superior canal dehiscence syndrome and its surgical repair in a chinchilla model. METHODS: We investigated the changes in firing rates of vestibular nerve afferents in the chinchilla in response to changes in external auditory canal pressure before and after fenestration of the superior canal, and after repair of the fenestra. RESULTS: Before superior canal fenestration, external auditory canal pressure changes caused no responses in horizontal canal or otolith afferents, and only 1 of 9 superior canal afferents responded to pressure. After fenestration, all superior canal afferents were excited by positive pressure and inhibited by negative pressure. Half of 18 otolith and most (21 of 33) horizontal canal afferents were unaffected by pressure. The superior canal afferents had higher pressure gain than the horizontal canal afferents (P =.03). Pressure responses could be abolished only by applying a rigid seal to the fenestra. CONCLUSIONS: Fenestration of the superior canal rendered all superior canal afferents sensitive to pressure, whereas less than half of the other afferents became pressure sensitive. The direction of the superior canal afferent responses agreed with the predictions of our model of endolymph flow within the superior canal. A rigid seal applied to the fenestra abolished pressure sensitivity while maintaining physiologic rotational sensitivity.

Symptoms and signs in superior canal dehiscence syndrome.

Patients with superior canal dehiscence (SCD) syndrome experience vertigo and oscillopsia in response to loud sounds and to stimuli that result in changes in middle ear or intracranial pressure. They may also experience hyperacusis to bone-conducted sounds. The evoked eye movements in this syndrome align with the plane of the dehiscent superior canal. The symptoms and signs can be understood in terms of the effect of the dehiscence in creation of a third mobile window into the inner ear. The SCD syndrome has been diagnosed in 28 patients who were examined in the neuro-otology clinics at the Johns Hopkins Medical Institutions from May 1995 through January 2001. The diagnosis is best established based upon the symptoms that are characteristic for the syndrome, the vertical-torsional eye movements evoked by sound or pressure stimuli noted on examination performed with Frenzel goggles, the lowered thresholds for responses to vestibular-evoked myogenic potentials, and CT imaging of the temporal bones.

Translational vestibulo-ocular reflex evoked by a "head heave" stimulus.

The gain and symmetry of vestibulo-ocular reflexes for high-frequency, high-acceleration movements of the head are altered following unilateral vestibular lesions. These changes have been well characterized for rotational head movements (thrusts), and provide reliable markers of dysfunction in individual semicircular canals. Alterations in the vestibulo-ocular reflex (VOR) evoked by lateral, whole-body translations have also been observed. In an approach directed at the development of a bedside test of otolith function, we have recorded (scleral search coil) the VOR evoked by brief, high-acceleration lateral translations (heaves). We delivered these stimuli manually and also developed a "head sled" device that minimizes any rotational contaminating component of the stimulus. Our geometrical analysis of the stimuli enables us to take into account the translational and rotational components of the movement, and to calculate an ideal response required for stabilization of images on the fovea at different fixation distances. We observed a tracking response (visually assisted VOR) that was close to ideal for image stabilization when these methods were used to analyze responses to slow, low-amplitude lateral translations of the head. When applied to rapid, high-acceleration (0.5 g) translations, the VOR was found to be less than compensatory in subjects with normal vestibular function. In a patient with unilateral vestibular hypofunction following intratympanic gentamicin injections, both the rotational and the translational VOR were asymmetric. Responses for translations toward the treated side had lower gain than those for translations toward the normal side. These findings provide a basis for further development of this technique as a clinical test and as a method for quantitative evaluation of otolith function.

Horizontal vestibuloocular reflex evoked by high-acceleration rotations in the squirrel monkey. IV. Responses after spectacle-induced adaptation.

The horizontal angular vestibuloocular reflex (VOR) evoked by sinusoidal rotations from 0.5 to 15 Hz and acceleration steps up to 3,000 degrees /s(2) to 150 degrees /s was studied in six squirrel monkeys following adaptation with x2.2 magnifying and x0.45 minimizing spectacles. For sinusoidal rotations with peak velocities of 20 degrees /s, there were significant changes in gain at all frequencies; however, the greatest gain changes occurred at the lower frequencies. The frequency- and velocity-dependent gain enhancement seen in normal monkeys was accentuated following adaptation to magnifying spectacles and diminished with adaptation to minimizing spectacles. A differential increase in gain for the steps of acceleration was noted after adaptation to the magnifying spectacles. The gain during the acceleration portion, G(A), of a step of acceleration (3,000 degrees /s(2) to 150 degrees /s) increased from preadaptation values of 1.05 +/- 0.08 to 1.96 +/- 0.16, while the gain during the velocity plateau, G(V), only increased from 0.93 +/- 0.04 to 1.36 +/- 0.08. Polynomial fits to the trajectory of the response during the acceleration step revealed a greater increase in the cubic than the linear term following adaptation with the magnifying lenses. Following adaptation to the minimizing lenses, the value of G(A) decreased to 0.61 +/- 0.08, and the value of G(V) decreased to 0.59 +/- 0.09 for the 3,000 degrees /s(2) steps of acceleration. Polynomial fits to the trajectory of the response during the acceleration step revealed that there was a significantly greater reduction in the cubic term than in the linear term following adaptation with the minimizing lenses. These findings indicate that there is greater modification of the nonlinear as compared with the linear component of the VOR with spectacle-induced adaptation. In addition, the latency to the onset of the adapted response varied with the dynamics of the stimulus. The findings were modeled with a bilateral model of the VOR containing linear and nonlinear pathways that describe the normal behavior and adaptive processes. Adaptation for the linear pathway is described by a transfer function that shows the dependence of adaptation on the frequency of the head movement. The adaptive process for the nonlinear pathway is a gain enhancement element that provides for the accentuated gain with rising head velocity and the increased cubic component of the responses to steps of acceleration. While this model is substantially different from earlier models of VOR adaptation, it accounts for the data in the present experiments and also predicts the findings observed in the earlier studies.

Vestibular-evoked myogenic potentials in the diagnosis of superior canal dehiscence syndrome.

Patients with superior canal dehiscence (SCD) syndrome have vertigo and oscillopsia induced by loud noises and by stimuli that result in changes in middle ear or intracranial pressure. We recorded vestibular-evoked myogenic potentials (VEMP responses) in 10 patients with SCD syndrome. The diagnosis had been confirmed in each case by evoked eye movements and by high-resolution CT scans of the temporal bones that showed a dehiscence overlying the affected superior canal. For the 8 patients without prior middle ear disease, the VEMP threshold from the dehiscent ears measured 72 +/- 8 dB NHL (normal hearing level) whereas the threshold from normal control subjects was 96 +/- 5 dB NHL (p < 0.0001). The VEMP threshold measured from the contralateral ear in patients with unilateral dehiscence was 98 +/- 4 dB NHL (p > 0.9 with respect to normal controls). Two patients with apparent conductive hearing loss from middle ear disease, and SCD, had VEMP responses from the affected ears. In the absence of dehiscence, VEMP responses would not have been expected in the setting of conductive hearing loss. These findings confirm earlier studies demonstrating that patients with SCD syndrome have lowered VEMP thresholds. Conditions other than SCD syndrome may also lead to lowered VEMP thresholds. Rather than being based upon a single test, the diagnosis of SCD syndrome is best established when the characteristic symptoms, signs, VEMP response, and CT imaging all indicate SCD.

Relationship between time- and frequency-domain analyses of angular head movements in the squirrel monkey.

We used the three-dimensional magnetic search-coil recording technique to study the range of active angular head movements made by squirrel monkeys. There were two goals in this study: (1) to determine the range of angular velocities and accelerations as well as the bandwidth and other frequency characteristics of active head movements and (2) to compare analyses of transients of velocity and acceleration that are studied by residual analysis, Fourier transform, and wavelet transform of the head velocity signal. The residual analysis showed that the shape and duration of the transients affected the bandwidth. During the time after the head had begun to accelerate, the frequency content of the head movement extended into the range of 6 to 12 Hz. When considering all three planes of rotation, approximately 75% of the transients had peak acceleration between 2,000 and 10,000 deg/s(2) and a peak velocity of 50 to 400 deg/s. A peak acceleration of >10,000 deg/s(2) was recorded in 10% of the transients. These findings indicate that active head movements in squirrel monkeys cover a higher range of frequencies, accelerations, and velocities than have typically been used in previous eye-movement and neuronal studies of the reflexes that control gaze. We further conclude that the choice of a method for analyzing transient, time-varying biological signals is dependent on the desired information. Residual analysis provides detailed resolution in the time domain, but estimation of the frequency content of the signal is dependent on the portions selected for analysis and the choice of filters. Fourier transform provides a representation of the power spectrum in the frequency domain but without any inherent temporal resolution. We show that the wavelet transform, a novel method as applied to the signal analysis goals of this study, is the most useful technique for relating time- and frequency-domain information during a continuous signal.

Central versus peripheral origin of vestibuloocular reflex recovery following semicircular canal plugging in rhesus monkeys.

We have previously shown that there is a slowly progressing, frequency-specific recovery of the gain and phase of the horizontal vestibuloocular reflex (VOR) in rhesus monkeys following plugging of the lateral semicircular canals. The adapted VOR response exhibited both dynamic and spatial characteristics that were distinctly different from responses in intact animals. To discriminate between adaptation or recovery of central versus peripheral origin, we have tested the recovered vestibuloocular responses in three rhesus monkeys in which either one or both coplanar pairs of vertical semicircular canals had been plugged previously by occluding the remaining semicircular canals in a second plugging operation. We measured the spatial tuning of the VOR in two or three different mutually orthogonal planes in response to sinusoidal oscillations (1.1 Hz, +/-5 degrees, +/-35 degrees /s) over a period of 2-3 and 12-14 mo after each operation. Apart from a significant recovery of the torsional/vertical VOR following the first operation we found that these recovered responses were preserved following the second operation, whereas the responses from the newly operated semicircular canals disappeared acutely as expected. In the follow-up period of up to 3 mo after the second operation, responses from the last operated canals showed recovery in two of three animals, whereas the previously recovered responses persisted. The results suggest that VOR recovery following plugging may depend on a regained residual sensitivity of the plugged semicircular canals to angular head acceleration.

Horizontal vestibuloocular reflex evoked by high-acceleration rotations in the squirrel monkey. III. Responses after labyrinthectomy.

The horizontal angular vestibuloocular reflex (VOR) evoked by high-frequency, high-acceleration rotations was studied in four squirrel monkeys after unilateral labyrinthectomy. Spontaneous nystagmus was measured at the beginning and end of each testing session. During the period that animals were kept in darkness (4 days), the nystagmus at each of these times measured approximately 20 degrees /s. Within 18-24 h after return to the light, the nystagmus (measured in darkness) decreased to 2.8 +/- 1.5 degrees /s (mean +/- SD) when recorded at the beginning but was 20.3 +/- 3.9 degrees /s at the end of the testing session. The latency of the VOR measured from responses to steps of acceleration (3,000 degrees /s(2) reaching a velocity of 150 degrees /s) was 8.4 +/- 0.3 ms for responses to ipsilesional rotations and 7.7 +/- 0.4 ms for contralesional rotations. During the period that animals were kept in darkness after the labyrinthectomy, the gain of the VOR measured during the steps of acceleration was 0.67 +/- 0.12 for contralesional rotations and 0.39 +/- 0.04 for ipsilesional rotations. Within 18-24 h after return to light, the VOR gain for contralesional rotations increased to 0.87 +/- 0.08, whereas there was only a slight increase for ipsilesional rotations to 0.41 +/- 0. 06. A symmetrical increase in the gain measured at the plateau of head velocity was noted after the animals were returned to light. The VOR evoked by sinusoidal rotations of 2-15 Hz, +/-20 degrees /s, showed a better recovery of gain at lower (2-4 Hz) than at higher (6-15 Hz) frequencies. At 0.5 Hz, gain decreased symmetrically when the peak amplitude was increased from 20 to 100 degrees /s. At 10 Hz, gain was decreased for ipsilesional half-cycles and increased for contralesional half-cycles when velocity was raised from 20 to 50 degrees /s. A model incorporating linear and nonlinear pathways was used to simulate the data. Selective increases in the gain for the linear pathway accounted for the recovery in VOR gain for responses at the velocity plateau of the steps of acceleration and for the sinusoidal rotations at lower peak velocities. The increase in gain for contralesional responses to steps of acceleration and sinusoidal rotations at higher frequencies and velocities was due to an increase in the contribution of the nonlinear pathway. This pathway was driven into cutoff and therefore did not affect responses for rotations toward the lesioned side.

Dehiscence or thinning of bone overlying the superior semicircular canal in a temporal bone survey.

OBJECTIVE: To determine the incidence and etiology of dehiscences of bone overlying the superior semicircular canal in a temporal bone archive. DESIGN: A microscopic study was performed of 1000 temporal bones from 596 adults in a university hospital registry. Specimens were sectioned vertically in the plane of the superior semicircular canal. Measurements of minimum bone thickness over the superior canal were made in a subset of 108 randomly chosen specimens. All bones were examined for thinning or dehiscence relative to these norms. Clinical histories, when available, were reviewed. RESULTS: Complete dehiscence of the superior canal was identified in 5 specimens (0.5%), at the middle fossa floor (n = 1) and where the superior petrosal sinus was in contact with the canal (n = 4). In 14 other specimens (1.4%), the bone at the middle fossa floor (n = 8) or superior petrosal sinus (n = 6) was no thicker than 0.1 mm, significantly less than values measured in the control specimens (P<.001). Abnormalities were typically bilateral. Specimens from infants demonstrated uniformly thin bone over the superior canal in the middle fossa at birth, with gradual thickening until 3 years of age. CONCLUSIONS: Dehiscence of bone overlying the superior canal occurred in approximately 0.5% of temporal bone specimens (0.7% of individuals). In an additional 1.4% of specimens (1.3% of individuals), the bone was markedly thin (< or =0.1 mm), such that it might appear dehiscent even on ultra-high-resolution computed tomography of the temporal bone. Sites affected were in the middle fossa floor or a deep groove for the superior petrosal sinus, often bilaterally. These abnormalities may arise from failure of postnatal bone development. Thin areas of bone over the superior canal may be predisposed to disruption by trauma.

Superior canal dehiscence syndrome.

OBJECTIVE: To present the symptoms, signs, and findings on diagnostic tests of patients with the superior canal dehiscence syndrome and to describe the surgical procedures used to treat the dehiscence in five patients. DESIGN AND SETTING: Prospective study of a series of patients identified as having this syndrome at a tertiary care referral center. PATIENTS AND RESULTS: Seventeen patients with vertigo, oscillopsia, or both evoked by intense sounds or stimuli that caused changes in middle ear and/or intracranial pressure were identified over a 4-year period. The evoked eye movements had vertical and torsional components, with the direction corresponding to the effect of the stimuli in causing excitation (Valsalva against pinched nostrils, tragal compression, sounds) or inhibition (Valsalva against a closed glottis or jugular venous compression) of the affected superior semicircular canal. Thirteen (76%) of these patients also experienced chronic dysequilibrium that was often the most debilitating symptom. Dehiscence of bone overlying the superior semicircular canal on the affected side was confirmed with computed tomographic scans in each case. Surgical procedures through the middle fossa approach to plug or resurface the superior canal were performed in five patients (canal plugging in three cases and resurfacing of the dehiscence without plugging in two). The debilitating symptoms resolved or improved after the procedures. Signs of vestibular hypofunction, without loss of hearing, were noted in one patient after plugging of the superior canal and in one other patient after resurfacing of the canal. CONCLUSIONS: The superior canal dehiscence syndrome is identified based on characteristic symptoms, signs, and computed tomographic findings. The clinical presentation and findings can be understood in terms of the effect of the dehiscence on the physiology of the labyrinth. The syndrome is a treatable cause of vestibular disturbance.

Eye movements in patients with superior canal dehiscence syndrome align with the abnormal canal.

BACKGROUND: The superior canal dehiscence (SCD) syndrome consists of sound- or pressure-induced nystagmus and vertigo caused by a defect in bone overlying the superior semicircular canal. The SCD syndrome is diagnosed based upon characteristic symptoms, signs, and findings on CT imaging of the temoral bones. However, SCD syndrome is often misdiagnosed as perilymphatic fistula (PLF), and the symptoms of sound- and pressure-induced vertigo are more commonly attributed to the vestibular utricle, rather than to the superior semicircular canal. This study explored the role of the superior canal and the utricle in the pathophysiology of SCD syndrome. METHODS: Three-dimensional scleral search coils were used to record eye movements in 11 patients with SCD syndrome. RESULTS: Ten patients developed nystagmus with upward torsional slow phases characteristic of superior canal activation when loud tones were presented to the affected ear or when the patients performed a Valsalva maneuver. Visual fixation led to a suppression of the nystagmus and the appearance of a sustained torsional deviation of the eyes. Two patients also had sound-evoked head movements in the same direction as the ocular slow phases. The response of the affected superior canal to rapid head rotations was tested in nine patients. The response was diminished in those with large (>/=5 mm) defects in the bone overlying the superior canal. CONCLUSIONS: The evoked eye movements in patients with SCD syndrome arise from the superior canal, not the utricle. The syndrome is recognized by the characteristic nystagmus evoked by tones or maneuvers that change middle ear or intracranial pressure. Examination for this nystagmus should be performed under conditions that prevent visual fixation.

Hyperventilation-induced nystagmus in patients with vestibular schwannoma.

OBJECTIVE: To analyze the nystagmus evoked by hyperventilation in patients with unilateral vestibular schwannoma and to use this information to predict the effects of hyperventilation on individual ampullary nerves. METHODS: Three-dimensional scleral search coil eye movement recording techniques were used to record the magnitude and time course of eye movements in six patients with unilateral vestibular schwannoma and hyperventilation-induced nystagmus. The presenting complaints in five of these patients were vertigo or dysequilibrium. RESULTS: The eye movement response to hyperventilation was a "recovery" nystagmus with slow-phase components corresponding to excitation of the affected vestibular nerve. Projection of the eye velocity vector into the plane of the semicircular canals revealed that fibers arising from the ampulla of the horizontal canal were most affected by hyperventilation with lesser activation of fibers to the superior canal and smaller, more variable responses from posterior canal fibers. CONCLUSIONS: The three-dimensional characteristics of the nystagmus evoked by hyperventilation in patients with vestibular schwannoma provide insight into the vestibular end organs affected by the tumor and the mechanism responsible for the nystagmus. This finding indicates that hyperventilation resulted in a transient increase in activity from these partially demyelinated axons.

High-frequency dynamics of regularly discharging canal afferents provide a linear signal for angular vestibuloocular reflexes.

Regularly discharging vestibular-nerve afferents innervating the semicircular canals were recorded extracellularly in anesthetized chinchillas undergoing high-frequency, high-velocity sinusoidal rotations. In the range from 2 to 20 Hz, with peak velocities of 151 degrees/s at 6 Hz and 52 degrees/s at 20 Hz, 67/70 (96%) maintained modulated discharge throughout the sinusoidal stimulus cycle without inhibitory cutoff or excitatory saturation. These afferents showed little harmonic distortion, no dependence of sensitivity on peak amplitude of stimulation, and no measurable half-cycle asymmetry. A transfer function fitting the data predicts no change in sensitivity (gain) of regularly discharging afferents over the frequencies tested but shows a phase lead with regard to head velocity increasing from 0 degrees at 2 Hz to 30 degrees at 20 Hz. These results indicate that regularly discharging afferents provide a plausible signal to drive the angular vestibuloocular reflex (VOR) even during high-frequency head motion but are not a likely source for nonlinearities present in the VOR.

Horizontal vestibuloocular reflex evoked by high-acceleration rotations in the squirrel monkey. I. Normal responses.

The horizontal angular vestibuloocular reflex (VOR) evoked by high-frequency, high-acceleration rotations was studied in five squirrel monkeys with intact vestibular function. The VOR evoked by steps of acceleration in darkness (3,000 degrees /s(2) reaching a velocity of 150 degrees /s) began after a latency of 7.3 +/- 1.5 ms (mean +/- SD). Gain of the reflex during the acceleration was 14.2 +/- 5.2% greater than that measured once the plateau head velocity had been reached. A polynomial regression was used to analyze the trajectory of the responses to steps of acceleration. A better representation of the data was obtained from a polynomial that included a cubic term in contrast to an exclusively linear fit. For sinusoidal rotations of 0.5-15 Hz with a peak velocity of 20 degrees /s, the VOR gain measured 0.83 +/- 0.06 and did not vary across frequencies or animals. The phase of these responses was close to compensatory except at 15 Hz where a lag of 5.0 +/- 0.9 degrees was noted. The VOR gain did not vary with head velocity at 0.5 Hz but increased with velocity for rotations at frequencies of >/=4 Hz (0. 85 +/- 0.04 at 4 Hz, 20 degrees /s; 1.01 +/- 0.05 at 100 degrees /s, P < 0.0001). No responses to these rotations were noted in two animals that had undergone bilateral labyrinthectomy indicating that inertia of the eye had a negligible effect for these stimuli. We developed a mathematical model of VOR dynamics to account for these findings. The inputs to the reflex come from linear and nonlinear pathways. The linear pathway is responsible for the constant gain across frequencies at peak head velocity of 20 degrees /s and also for the phase lag at higher frequencies being less than that expected based on the reflex delay. The frequency- and velocity-dependent nonlinearity in VOR gain is accounted for by the dynamics of the nonlinear pathway. A transfer function that increases the gain of this pathway with frequency and a term related to the third power of head velocity are used to represent the dynamics of this pathway. This model accounts for the experimental findings and provides a method for interpreting responses to these stimuli after vestibular lesions.

Horizontal vestibuloocular reflex evoked by high-acceleration rotations in the squirrel monkey. II. Responses after canal plugging.

The horizontal angular vestibuloocular reflex (VOR) evoked by high-frequency, high-acceleration rotations was studied in four squirrel monkeys after unilateral plugging of the three semicircular canals. During the period (1-4 days) that animals were kept in darkness after plugging, the gain during steps of acceleration (3, 000 degrees /s(2), peak velocity = 150 degrees /s) was 0.61 +/- 0.14 (mean +/- SD) for contralesional rotations and 0.33 +/- 0.03 for ipsilesional rotations. Within 18-24 h after animals were returned to light, the VOR gain for contralesional rotations increased to 0. 88 +/- 0.05, whereas there was only a slight increase in the gain for ipsilesional rotations to 0.37 +/- 0.07. A symmetrical increase in the gain measured at the plateau of head velocity was noted after animals were returned to light. The latency of the VOR was 8.2 +/- 0. 4 ms for ipsilesional and 7.1 +/- 0.3 ms for contralesional rotations. The VOR evoked by sinusoidal rotations of 0.5-15 Hz, +/-20 degrees /s had no significant half-cycle asymmetries. The recovery of gain for these responses after plugging was greater at lower than at higher frequencies. Responses to rotations at higher velocities for frequencies >/=4 Hz showed an increase in contralesional half-cycle gain, whereas ipsilesional half-cycle gain was unchanged. A residual response that appeared to be canal and not otolith mediated was noted after plugging of all six semicircular canals. This response increased with frequency to reach a gain of 0.23 +/- 0.03 at 15 Hz, resembling that predicted based on a reduction of the dominant time constant of the canal to 32 ms after plugging. A model incorporating linear and nonlinear pathways was used to simulate the data. The coefficients of this model were determined from data in animals with intact vestibular function. Selective increases in the gain for the linear and nonlinear pathways predicted the changes in recovery observed after canal plugging. An increase in gain of the linear pathway accounted for the recovery in VOR gain for both responses at the velocity plateau of the steps of acceleration and for the sinusoidal rotations at lower peak velocities. The increase in gain for contralesional responses to steps of acceleration and sinusoidal rotations at higher frequencies and velocities was due to an increase in the gain of the nonlinear pathway. This pathway was driven into inhibitory cutoff at low velocities and therefore made no contribution for rotations toward the ipsilesional side.

Relationship of the utriculus and sacculus to the stapes footplate: anatomic implications for sound-and/or pressure-induced otolith activation.

One hundred thirty human temporal bones that were sectioned in the vertical plane were examined to evaluate the relationship between the stapes footplate and the otolith organs. The shortest distance between the footplate and the utriculus was 0.58+/-0.10 mm in the posterior third of the oval window, 1.04+/-0.20 mm in the middle third, and 1.51+/-0.20 mm in the anterior third. The distance from the sacculus to the footplate was 1.33+/-0.20 mm in the middle third of the oval window and 1.31+/-0.18 mm in the anterior third. Membranous connections extending between the utriculus and the footplate were found in 26% of temporal bones. These membranous connections in coexistence with additional anatomic factors such as stapes hypermobility and/or dehiscence of bone within labyrinthine structures may predispose patients to sound- and/or pressure-induced otolith activation. The findings may have implications for different causes of the Tullio phenomenon.