The vestibular evoked response to linear, alternating, acceleration pulses without acoustic masking as a parameter of vestibular function

In this study, short latency vestibular evoked potentials (VsEPs) were recorded in five guinea pigs in response to alternating linear acceleration pulses with and without acoustic masking. A steel bolt was implanted in the skull and coupled to a shaker. Linear acceleration pulses (n = 400) in upward, downward or alternating directions were given, with a peak acceleration of 4g after 0.5 msec. Tests were repeated with acoustic masking, after modiolus destruction and after application of KCl in the vestibule. Stimuli of the vestibular nerve were recorded with a platinum electrode in the bony facial nerve canal in the bulla. Unilateral linear acceleration showed a shallow plateau at 0.5 msec, which disappeared with alternating acceleration impulses and after modiolus destruction. Therefore all further tests were done with alternating impulses. After a latency time of 0.8 msec a multiwave response was seen, with a first positive peak P1 at 1.16 ms. These were followed by other positive and negative peaks (N1, P2, N2, P3, N3). With the elimination of cochlear influences by using acoustic masking, P1 remained stable, while subsequent peaks were altered or eliminated. After modiolus destruction, the P1 peak remained, although with a smaller amplitude due to vestibular damage. After application of a saturated KCl solution in the vestibule all responses, including P1, disappeared, thus confirming the vestibular origin of these responses. We conclude that the onset latency of the VsEP and the peak latency and level of the first positive peak P1 in response to alternating linear acceleration pulses without acoustic masking, measured in the facial canal, are good and stable parameters of vestibular function in guinea pigs.     

The firing properties of second-order vestibular neurons in correlation with the far-field recorded vestibular-evoked response

Action potentials of the second-order vestibular neurons of ten cats were recorded, both in rest and responding to sinusoidal and intense impulse acceleration stimuli. The data were compared with the far-field recorded vestibular-evoked response induced by the same impulse stimuli. It was found that the irregular (kinetic) neurons, which had a phase lead relative to head velocity, were capable of responding to these impulses with a latency as short as 3.5 msec after the start of head acceleration. It is assumed, therefore, that these neurons are the generators of the second wave of the vestibular-evoked response, having a similar latency. A high correlation was found between the latency of the first peak in the poststimulus time histogram in response to acceleration impulses and the phase of the response to sinusoidal rotations. The regular (tonic) vestibular neurons did not respond to acceleration impulses and probably did not contribute to the vestibular-evoked response.     

Origins of the short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses

OBJECTIVE: To verify the vestibular origin of the short latency (t < 12.5 msec) vestibular evoked potentials (VsEPs) in response to linear acceleration impulses (L-VsEPs) and to differentiate between the contributions of the otolith organs and the semi-circular canals (SCCs) to their initiation. DESIGN AND METHODS: L-VsEPs (stimulus intensity, 3 g; rise time, 1.0 to 1.5 msec) were recorded in fat sand rats (Psammomys obesus) before and after unilateral labyrinthectomy, plugging of the SCCs in the remaining ear, and bilateral labyrinthectomy. Auditory nerve brainstem evoked responses (ABRs) and VsEPs to angular acceleration impulses (A-VsEPs) were also recorded. Wave amplitudes and latencies were statistically analyzed (MANOVA, repeated t-tests). RESULTS: In the intact animal, the linear VsEPs consisted of 5 to 6 waves, several mV in amplitude, with short latencies. The latency of the first wave was 2.0 msec. These waves were abolished after bilateral labyrinthectomy. Before and after plugging of the SCCs, linear acceleration VsEP wave latencies did not change, although amplitudes were slightly reduced. Similar results were obtained with respect to ABRs recorded from the same ear. Angular acceleration VsEPs were abolished after SCC plugging. CONCLUSIONS: These and other results confirm that the linear VsEPs are compound action potentials of the vestibular pathway, the first wave is the response of the vestibular nerve, and they are initiated mainly in the otolith organs.     

The effect of changes in perilymphatic K+ on the vestibular evoked potential in the guinea pig

To investigate the effect on the functioning of the vestibular system of a rupture of Reissner’s membrane, artificial endolymph was injected in scala media of ten guinea pigs and vestibular evoked potentials (VsEPs), evoked by vertical acceleration pulses, were measured. Directly after injection of a sufficient volume to cause rupture, all ears showed a complete disappearance of VsEP, followed by partial recovery. To investigate the effect of perilymphatic potassium concentration on the vestibular sensory and neural structures, different concentrations of KCl were injected directly into the vestibule. The KCl injections resulted in a dose-dependent decrease of VsEP, followed by a dose-dependent slow recovery. This animal model clearly shows a disturbing effect of a higher than normal K⁺ concentration in perilymph on the vestibular and neural structures in the inner ear. Potassium intoxication is the most probable explanation for the observed effects. It is one of the explanations for Menière attacks.     

An intrasubject comparison of electric and acoustic middle latency responses

The middle components of the auditory evoked response (middle latency response, MLR) were evoked by acoustic clicks from the normal-hearing ear and by charge-balanced biphasic current pulses from the severe-to-profoundly hearing-impaired ears of patients undergoing labyrinthectomy for the management of intractable vertigo. A vertex-positive peak with a latency ranging from 27 msec to 38 msec (Pa) was characteristic of both the electric and the acoustic MLR. In subjects, the electric Pa always preceded the acoustic Pa in latency. In addition, the electric Pa had a sharper appearance than did the acoustic Pa. The electric MLRs were elicited by a range of stimulus intensities and persisted after the completion of labyrinthectomy.     

Intraoperative electrically evoked vestibular potentials in humans.

Electrically evoked short latency vestibular potentials were recorded in 9 patients during vestibular neurectomy. Patients were operated on because of intractable Meniere's disease. The VIIIth cranial nerve was exposed through a limited retrosigmoidal approach; the vestibular nerve was contacted in the cerebello-pontine angle with a bipolar platinum-iridium electrode and stimulated with biphasic current pulses (100 microseconds/phase, 0.75-1 mA p-p, 20/s). The responses were recorded over 12.8 ms between a forehead and an ipsilateral ear lobe electrode. Each recording consisted of 2 x 1,000 averaged responses. A systematically reproducible vertex-negative potential occurring at a latency of approximately 2 ms and having an amplitude of approximately 0.5 microV was recorded in all patients. This vertex-negative potential disappeared after selective vestibular neurectomy proximal to the stimulation site. Simultaneous continuous acoustic masking did not affect the response and no facial nerve response was observed on the facial nerve monitoring. These features strongly suggest that the characteristic vertex-negative potential constitutes a specifically evoked response of the vestibular system. Electrophysiological monitoring of the sectioning of the vestibular nerve during operation is one possible clinical application of intraoperative recording of electrically evoked vestibular potentials.     

Active head turning and correlated cerebral potentials. Experimental and clinical aspects

Fast voluntary horizontal head movements (n = 400, maximum acceleration 8,500 deg/sec2) were recorded together with surface EEG over pre- and post-central regions in 30 healthy volunteers while they were gazing at a head-fixed target in darkness. Artifacts of mechanical, myogenic and oculomotor origin could be precluded. Selective averaging of the fastest movements revealed a biphasic cortical potential. Median latency of its onset was 123.5 msec, of its first peak 189 msec, of the second peak 373 msec, with amplitudes ranging around 5.7 microV. Similar recordings in patients with uni- or bilateral vestibular nerve lesions demonstrated that strong stimulation of the joint vestibular and somatosensory (neck afferent) input facilitated characteristically related EEG activity: side differences of vestibular input could be measured on this level of the CNS, i.e. measured on the cortical level as additional information to the commonly used vestibulo-oculomotor response; patients with early, bilateral loss of vestibular functions showed a specific long-term adaptation of their related EEC activity. We conclude that clinical studies of this kind might aid in diagnosis of vertigo and related phenomena.     

Effect of white noise "masking" on vestibular evoked potentials recorded using different stimulus modalities.

Short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses (L-VsEPs) are initiated in the otolith organs (saccule and utricle). Some of the saccule afferents have been reported to respond not only to linear acceleration, but also to high intensity acoustic stimuli. If so, the L-VsEP recorded from the saccule (elicited with the stimulus orientated relative to the head so as to optimally activate the saccule, i.e. stimulus in the vertical plane, Z-VsEP) should be reduced during high intensity broad band noise (BBN) "masking". Conversely, the utricular afferents have been reported to be less auditory-sensitive. Therefore, an L-VsEP which is mainly utricular in origin (stimulus in the horizontal plane, X-VsEP) should be less affected by this noise "masking". This was investigated in rats by recording X-VsEPs and Z-VsEPs and angular VsEPs (A-VsEPs), originating in the lateral semi-circular canals, before, during and after exposure to short duration, high intensity (113 dB SPL) BBN. This intensity completely masked auditory nerve evoked responses. The Z-VsEP did appear to be slightly more affected by the noise "masking" than the X-VsEP, implying the presence of more auditory-sensitive elements in the saccule. The A-VsEP was also affected by the BBN. The overall effect was relatively small (on average, 10-25% depression of the first wave of the different VsEPs). The responses showed recovery 5 min later.     

Temporal bone abnormalities associated with hearing loss in Waardenburg syndrome

OBJECTIVES/HYPOTHESIS: The objectives were to correlate audiometric thresholds with radiological findings and to determine the prevalence of inner ear radiological abnormalities in patients with hearing loss and Waardenburg syndrome. STUDY DESIGN: The study was a retrospective review of patients with Waardenburg syndrome identified in a pediatric hearing-impaired population and human genetics clinic. METHODS: Nine children with Waardenburg syndrome were identified. Eighty-nine children without sensorineural hearing loss served as control subjects. Clinical data, audiometric thresholds, and radiographic temporal bone measurements in these children were analyzed. RESULTS: Seven children were identified with hearing loss and Waardenburg syndrome. Four children had Waardenburg syndrome type 1, and three children had Waardenburg syndrome type 2. The overall prevalence of hearing loss in the total study population with Waardenburg syndrome was 78%. The mean pure-tone average was 99 dB. All of the children had sensorineural hearing loss. The hearing outcome was stable in 86% of the children. Twelve temporal bones were available for radiological analysis by computed tomography. Enlargement of the vestibular aqueduct was found in 50% of the CT scans. There was a significant difference in measurements of vestibular aqueduct width at the midpoint between the patients with Waardenburg syndrome and the control group (P <.05). There were also significant differences in the measurements of the vestibule (P =.0484), internal auditory canal (P =.0092), and modiolus (P =.0045) between the children with Waardenburg syndrome and the control group. CONCLUSION: A profound sensorineural hearing loss was characteristic of the study population with Waardenburg syndrome. Overall, 100% of patients with hearing loss and Waardenburg syndrome had temporal bone anomalies on at least one measurement of their inner ear, and 50% had an enlargement of the vestibular aqueduct at the midpoint. As shown by computed tomography, enlargement of the vestibular aqueduct and the upper vestibule, narrowing of the internal auditory canal porus, and hypoplasia of the modiolus are features of Waardenburg syndrome.     

实验性瘘管刺激前庭诱发电位面神经管电极记录

目的研究在颅顶电极引导瘘管刺激前庭诱发电位基础上,进行面神经管电极引导方法的实验观察。方法取６只健康纯白豚鼠,同时安放颅顶电极和右面神经管电极,进行瘘管刺激前庭诱发电位测试记录。前庭刺激方法为上半规管开窗,藉特殊设计的瘘管刺激探针机械刺激壶腹嵴,诱发前庭电位。结果发现面神经管电极前庭诱发电位主要由一个振幅很大的Ｐ波构成,该波与颅顶电极法的Ｐ１波潜伏期相同。结论二者潜伏期及波宽呈正相关,提示二波源于同一神经结构,考虑到面神经管电极ＥＣｏｃｈＧ以显示听神经动作电位为主,推测Ｐ波和Ｐ１波很可能代表了前庭神经的动作电位。     

Gentamicin Applied to the Oval Window Suppresses Vestibular Function in Guinea Pigs

Intratympanic gentamicin therapy is widely used clinically to treat the debilitating symptoms of Ménière’s disease. Cochleotoxicity is an undesirable potential side effect of the treatment and the risk of hearing loss increases proportionately with gentamicin concentration in the cochlea. It has recently been shown that gentamicin is readily absorbed through the oval window in guinea pigs. The present study uses quantitative functional measures of vestibular and cochlea function to investigate the efficacy of treating the vestibule by applying a small volume of gentamicin onto the stapes footplate in guinea pigs. Vestibular and cochlea function were assessed by recording short latency vestibular evoked potentials in response to linear head acceleration and changes in hearing threshold, respectively, 1 and 2 weeks following treatment. Histopathology was analyzed in the crista ampullaris of the posterior semi-circular canal and utricular macula in the vestibule, and in the basal and second turns of the cochlea. In animals receiving gentamicin on the stapes footplate, vestibular responses were significantly suppressed by 72.7 % 2 weeks after treatment with no significant loss of hearing. This suggests that the vestibule can be treated directly by applying gentamicin onto the stapes footplate.     

鼻内镜下低温等离子射频消融治疗鼻前庭囊肿

目的：观察鼻内镜下低温等离子射频消融治疗鼻前庭囊肿的疗效。方法28例鼻前庭囊肿患者,于鼻内镜下经鼻前庭径路采用低温等离子射频消融治疗。如囊肿范围不超出鼻前庭,则开放囊腔保留囊肿底壁;如囊肿范围超出鼻前庭,则彻底去除囊壁上皮以消除囊腔。结果全部患者术后随访6～12个月,囊肿均无复发,无明显鼻前庭瘢痕及前鼻孔狭窄等后遗症。结论鼻内镜下低温等离子射频消融治疗鼻前庭囊肿具有创伤小、操作简单、疗效好、适应症广等优点,具有临床推广应用价值。     

The effect of head orientation on the vestibular evoked potentials to linear acceleration impulses in rats

OBJECTIVE: To investigate the influence of linear acceleration impulses delivered when the head is held in different static head orientations, on the first wave of the short latency vestibular evoked potential (VsEP). The first wave is the compound action potential of the primary vestibular neurons synchronously activated. BACKGROUND: It has been shown previously that the VsEP elicited in response to linear acceleration is initiated mainly in the otolith organs. These organs are responsive to both dynamic and static linear forces, including gravity. METHODS: VsEPs to linear acceleration stimuli (4g) were recorded when the rats head was oriented so that a) the plane of the utricular macula was aligned with the plane of the stimulus, b) in supine position and c) with the head pitched up and down in various angles with respect to gravity (stimulus-head spatial relation remained constant) as compared to a reference position. RESULTS: With the stimulus aligned with the plane of the utricular macula, the amplitude of the first wave of the L-VsEPs was significantly larger than in the reference position. In the supine position, the amplitude of the first wave was significantly larger and the latency was significantly shorter. The amplitude of the first VsEP wave tended to be larger in the "head up" orientations as compared to the "head down" orientations (not statistically significant). CONCLUSIONS: These results demonstrate the influence of head position and gravity on the VsEPs to linear acceleration impulses, which is in accordance with their otolithic origin.     

Short latency vestibular responses to pulsed linear acceleration

Far-field vestibular responses to pulsed linear cranial acceleration have not been reported in detail for any species. In this study, precisely defined pulsed linear accelerations were used to elicit vestibular neural responses recorded from the surfaces of the skulls of 23 White Leghorn chicks. Traditional signal averaging techniques were used to resolve responses. At moderate intensities, responses consisted of a series of four to seven dominant peaks occurring within a period of 8 ms, having amplitudes between 0.3 and 20 microV peak-to-peak. The mean response threshold was 0.120 +/- 0.045 g. Latencies and amplitudes varied systematically as a function of stimulus intensity. Hypothermia prolonged response latencies. Response peaks did not invert on stimulus inversion, were present in response to cranial but not trunk acceleration, were not attenuated by broad-band auditory masking or by ambient light conditions, and disappeared with complete bilateral destruction of the labyrinth. The results rule out major contributions from auditory, somatosensory, and visual modalities and support the hypothesis that the responses reflect bilateral neural activity in the vestibular system. The findings suggest that direct noninvasive assessment of peripheral vestibular function can be achieved using pulsed linear acceleration stimuli.     

Functional impairment of the vestibular end organ resulting from impulse noise exposure

OBJECTIVES/HYPOTHESIS: To assess the effect of exposure t o impulse noise, known to cause damage tothe cochlea, on the vestibular part of the inner ear using short latency vestibular evoked potentials (VsEPs), which is a direct and objective test for evaluating the function of the vestibular end organs. STUDY DESIGN: Prospective animal study. METHODS: Sand rats (Psammomys obesus) underwent baseline measurements of VsEPs in response to linear and angular acceleration stimuli and measurement of the auditory nerve and brainstem evoked response (ABR). The animals were then exposed to 10 gunshots generating impulse noise at an intensity of approximately 160 dB sound pressure level (SPL). Repeat measurements of the evoked potentials were conducted 2 to 4 hours, 1 week, and 6 weeks after the exposure. The amplitude and latency of the first wave of VsEPs in response to linear and angular acceleration stimuli, reflecting the function of the otolith organs and semicircular canals respectively, were compared between baseline and post-exposure measurements, as were ABR thresholds. RESULTS: The amplitude of the first wave of the VsEPs in response to linear acceleration was significantly (P <.001) reduced and the latency significantly (P <.005) prolonged 2 to 4 hours after the exposure in comparison to baselinemeasurements. The latency prolongation persisted in follow-up measurements, whereas the amplitude showed partial recovery. The first wave of VsEPs in response to angular acceleration was unchanged long-term. ABR thresholds were elevated in the long-term by 60 dB. CONCLUSION: It seems that impulse noise not only damages the cochlea, but also causes clear functional impairment to the vestibular end organs, mainly the otolith organs.     

The clinical utility of search coil horizontal vestibulo-ocular reflex testing

CONCLUSION: Testing of the horizontal vestibulo-ocular reflex (VOR) with head rotations (including head impulses) using the magnetic scleral search coil technique (SCT HHI) provides valuable additional diagnostic information in patients with persistent dizziness, oscillopsia or imbalance. It identifies high and low frequency/acceleration vestibular abnormalities that are frequently missed using other methods. OBJECTIVES: To evaluate the diagnostic utility of SCT measurement of the horizontal VOR in the multidisciplinary neurotology clinic of a tertiary referral centre. PATIENTS AND METHODS: The records of 127 consecutive patients referred for persistent dizziness, oscillopsia, imbalance, or with clinical findings suggestive of high frequency/acceleration vestibular dysfunction were reviewed. All had been tested with clinical head impulses, bithermal calorics and vestibular-evoked myogenic potentials. VOR gain (peak eye velocity/peak head velocity) had been measured both in response to sinusoidal oscillations in a rotating chair (0.1-11 Hz) and to manually delivered horizontal head rotations (peak head velocities 50-500 degrees/s) using SCT. RESULTS: Agreement between the different test modalities of horizontal semicircular canal function was moderate. Relative to SCT HHI, clinical HHI showed the highest sensitivity and the lowest specificity (both 70%). SCT HHI appeared to have the greatest diagnostic yield, when compared with calorics and SCT ROT (23% of all abnormalities shown were detected only by SCT HHI) and also allowed detection of significant asymmetries in patients with bilateral vestibular dysfunction.     

Temporal bone imaging in GJB2 deafness

OBJECTIVE: To describe temporal bone findings on computed tomography (CT) imaging in GJB2-related hearing loss (HL). We asked whether evaluation of the temporal bone is required in individuals with biallelic GJB2 mutations. STUDY DESIGN: Randomized, blinded, controlled, prospective measurement. METHODS: Blood from 264 pediatric cochlear implant users was analyzed for mutations in the GJB2 gene. Thirty-six aspects of the temporal bone on CT imaging were evaluated in 53 individuals (106 ears) with biallelic disease causing GJB2 mutations. A subset of patients was age matched and compared with normally hearing individuals. Subjects with biallelic GJB2 mutations were tested for mutations in the SLC26A4 gene to rule out Pendred syndrome as a confounding cause of large vestibular aqueduct syndrome. RESULTS: Approximately 53% of ears of subjects (72% of subjects) with biallelic GJB2 mutations had at least one temporal bone anomaly. The most common findings were 1) dilated endolymphatic fossa (28%); 2) hypoplastic modiolus (25%); 3) large vestibular aqueduct (8%); 4) hypoplastic horizontal semicircular canal (8%); 5) hypoplastic cochlea (4%). Compared with normally hearing individuals, the GJB2 group had hypoplasia of the cochlear nerve canal, lateral semicircular canal vestibule, internal auditory canal (t tests, P < .001), and were 11 times more likely to have a hypoplastic modiolus. Dilated endolymphatic fossae were 1.4 times more common in the GJB2 group, and large vestibular aqueducts were 3 times more common in the GJB2 group, as compared with normally hearing controls. CONCLUSIONS: Temporal bone anomalies are common in GJB2-related HL, and imaging of the temporal bone should be included in routine evaluation of these individuals.     

Acoustic responses of vestibular afferents in a model of superior canal dehiscence.

HYPOTHESIS: Afferents innervating the superior semicircular canal are rendered especially sensitive to acoustic stimulation when there is a dehiscence of the superior canal. Other vestibular end organs are also more sensitive to acoustic stimulation. BACKGROUND: Dehiscence of the superior semicircular canal is associated with vertigo and nystagmus caused by loud sounds (Tullio phenomenon) or changes in middle ear or intracranial pressures. The mechanisms by which acoustic stimuli act on the vestibular end organs are unclear. The nystagmus caused by acoustic stimuli generally aligns with the affected superior canal. METHODS: Responses to acoustic stimuli in the superior vestibular nerves of anesthetized chinchillas were recorded before and after fenestration of the superior canal. RESULTS: Two acoustic response patterns were seen: rapid phase locking and slow tonic changes in firing rate. Phasic responses principally occurred in irregular afferents and tonic responses in regular afferents. Afferents from all of the vestibular end organs encountered could respond to acoustic stimuli, even before fenestration. However, fenestration lowered the thresholds for acoustic stimulation in superior canal afferents with phasic responses and increased the magnitude of tonic responses. CONCLUSIONS: Superior canal dehiscence may render the irregular afferents innervating the superior canal particularly sensitive to loud sounds. Rapid phase-locking responses may explain the short latency of nystagmus seen in patients with superior canal dehiscence syndrome. The mechanisms by which acoustic stimuli activate the vestibular end organs may differ from the damped endolymph motion associated with head acceleration.     

Use of electrical vestibular stimulation to alter genioglossal muscle activity in awake cats

Prior work has shown that the vestibular system contributes to regulating activity of upper airway muscles including the tongue protruder muscle genioglossus. The goal of the present experiments was to determine whether electrical vestibular stimulation could potentially be used to alter genioglossal activity in awake animals. Six adult cats were instrumented for recording of EMG activity from genioglossus, abdominal musculature, and triceps. In addition, a silver ball electrode was implanted on the round window for stimulation of vestibular afferents. Subsequently, stimulation and recordings were conducted while animals were awake. In all cases, stimulation using single shocks or trains of pulses > 100 microA in intensity produced responses in all muscles, including genioglossus. The latency of the genioglossal response was approximately 12 msec, and delivering continuous current trains to the labyrinth chronically elevated the muscle's activity. Although a number of muscles were affected by the stimulus, animals experienced no obvious distress or balance disturbances. Vestibular stimulation remained effective in producing genioglossal responses until experiments were discontinued 1-2 months following onset. These data suggest that electrical vestibular stimulation could potentially be used therapeutically to alter upper airway muscle activity.