Vestibular Nerve Lesions Research Articles

Contralateral suppression of distortion-product otoacoustic emissions: A potential diagnostic tool to evaluate the vestibular nerve

The amplitude of distortion-product otoacoustic emission (DPOAE) is suppressed in one ear when the contralateral ear is subjected to sound stimulation. Contralateral suppression of DPOAE is the phenomenon resulted by the efferent cochlear innervation on the outer hair cells via medial olivocochlear bundle (MOCB) and inferior vestibular nerve. We assumed that DPOAE would not be suppressed by contralateral sound stimulation in patients with vestibular nerve lesion as long as the specific pathway conveying that efferent innervation is affected.To test this hypothesis, we compared the amount of DPOAE contralateral suppression in patients with vestibular neuritis and healthy controls. Twenty healthy volunteers without hearing loss and vestibulopathy, and 13 patients with vestibular neuritis were recruited. DP audiogram was measured without contralateral sound stimulation and then with contralateral sound stimulation (70dB HL of 2kHz narrow band noise, NBN). The suppression value of DPOAE was evaluated according to the f2 frequency and was defined as the amount of DPOAE suppression: An−Ao, where An represents the DPOAE amplitude in the presence of contralateral NBN, and Ao represents the DPOAE amplitude in the absence of NBN. Cervical vestibular evoked myogenic potential (cVEMP) was performed in some patients with vestibular neuritis. The suppression values of DPOAE were compared between groups and were analyzed according to the results of cVEMP. The amount of suppression of DPOAE during contralateral sound stimulation was significantly reduced in the patient group compared to control at the f2 frequencies of 1257, 1587, and 2002Hz (P=0.045, P<0.001, P=0.009, respectively). However, the results of contralateral suppression of DPOAE were not consistent with the results of cVEMP in this study.Efferent cochlear innervation was affected in vestibular neuritis. Evaluation of contralateral suppression of DPOAE can be a potential diagnostic tool to evaluate the functional integrity of the vestibular nerve. Further studies are necessary to clarify this mechanism.

The n10 component of the ocular vestibular-evoked myogenic potential (oVEMP) is distinct from the R1 component of the blink reflex

Bone-conducted vibration (BCV) in the midline at the hairline (Fz), results in short latency potentials recorded by surface electrodes beneath the eyes - the ocular vestibular-evoked myogenic potential (oVEMP). The early negative component of the oVEMP, n10, is due to vestibular stimulation, however it is similar to the early R1 component of the blink reflex. Here we seek to dissociate n10 from R1. Surface potentials were recorded from the infraorbital electromyogram of 10 healthy subjects, 6 patients with bilateral vestibular loss, 2 with unilateral vestibular loss, 4 with facial palsy and 3 with facial and vestibular nerve lesions on the same side. BCV was delivered at Fz, the inion, the glabella or the supraorbital ridge using a tendon hammer or a bone-conduction vibrator. Onset latencies of the n10 evoked by taps at Fz or inion were significantly shorter than the R1 components of blink responses to supraorbital and glabellar stimuli. Upward gaze increased the amplitude of n10 but not R1. The n10 was absent bilaterally in patients with bilateral vestibular loss and beneath the contralesional eye in patients with unilateral vestibular loss, but in both these groups of patients R1 was preserved. In severe facial palsy the R1 component was absent or delayed and attenuated ipsilesionally, but n10 was preserved bilaterally. In subjects with unilateral facial and vestibular nerve lesions (Herpes Zoster of the facial and vestibulocochlear nerves) the dissociation was complete - the ipsilesional R1 was absent or attenuated whereas the ipsilesional n10 was preserved. n10 is distinguished from R1 by its earlier onset, laterality, modulation by gaze position and dissociation in patient groups. The n10 component evoked by BCV at Fz is not the R1 component of the blink reflex.

前庭神経炎，突発性難聴における自覚的視性垂直位所見

The measurement of subjective visual vertical (SVV) is clinically used as a method to assess the degree of dysfunction in the otolith, primary vestibular nerves, and central graviceptive pathways. We measured the SVV in patients with vestibular neuritis (VN) and unilateral sudden deafness (uSD). The purpose of this study was to demonstrate the characteristics of SVV in patients with VN and uSD, and determine the relation between the SVV and other neuro-otological examinations, including vestibular evoked myogenic potentials (VEMP) and the caloric test.The SVV was measured in 25 patients suffering from VN (9 women, 16 men aged from 27 to 76 years) and 30 patients suffering from uSD (16 men and 14 women aged from 21 to 76). The SVV was tilted>2o in VN (64.0%) and in uSD (23.3%). Among the abnormal SVV patients (SVV>2o), the tilt was directed toward the affected ear in all VN patients and in 75% of uSD patients.Concerning the caloric test and VEMP in VN patients, there were no significant relationships between the percentages of abnormal SVV and the degree of canal paresis and VEMP. In uSD patients, abnormal VEMP patients tended to show an abnormal SVV. Our results suggest that the shift of the SVV was strongly affected not only by superior vestibular nerve lesions, but also by inferior vestibular lesions.

Successful treatment of hyperventilation-induced nystagmus in vestibular schwannoma with oxcarbacepine

JO N 2842 tion was performed and the lesion was monitored clinically and radiologically. To treat paroxysmal symptoms, oxcarbacepine (2 x 150 mg) was prescribed and well-tolerated. The nystagmus could no longer be provoked by hyperventilation. After a pause in medication, the hyperventilation-induced nystagmus reoccurred. Nystagmus is very infrequently induced by hyperventilation. However, patients with demyelinating lesions of the vestibular nerve (due to compression by a tumor or a small blood vessel) or in central structures (multiple sclerosis) may show hyperventilation-induced nystagmus (HIN) [4]. In acoustic neuroma, the presumed mechanism of HIN is improved axonal conduction in the partially demyelinated vestibular nerve by hyperventilation. Carbon dioxide levels have been shown to decrease after a 30-second period of hyperventilation. CSF pH rises in association with this reduction in PCO2, which leads to a reduction in extracellular ionized Ca2+. Hyperventilation hence results in a transient increase in activity from partially demyelinated axons as a result of the lowering of extracellular Ca2+ [5]. Hyperventilation can cause nystagmus beating towards the side of a vestibular nerve lesion (i.e., excitatory nystagmus) and is the only test that unmasks unilateral vestibular disease without testing the dynamic properties of the vestibulo-ocular Guido Ahle Wenke Visser Annika Juergens Uwe Schlegel

Activity‐Related Postlesional Vestibular Reorganization

The synaptic convergence patterns of semicircular canal and macular afferent nerve inputs onto second-order vestibular neurons reorganize in adult frogs after a change in the activity of vestibular nerve afferent fibers. Axotomized afferent nerve fibers become silent after a vestibular nerve lesion, and second-order vestibular target neurons become disfacilitated. These changes initiate an activity-related process that was studied in detail in vitro two months after a section of the ramus anterior (RA) of N. VIII. The postlesional reaction results in an expansion of signals, preferentially from intact, remaining afferent nerve fibers, but also from excitatory commissural and spinal ascending fibers. This process of expansion takes weeks, is graded in its extent, and reversible in case of a nerve regeneration, but is not competitive, i.e., the synaptic contacts from axotomized afferent nerve fibers are maintained without a change in their efficacy. Postlesional synaptic reorganization in the brainstem is restricted to the operated side, underlies the improved responsiveness of disfacilitated second-order vestibular neurons, but also their altered spatial response tuning. The functional consequences of this reorganization were studied in vivo two months after RA nerve section by recording abducens nerve responses during linear or angular accelerations. The vector orientations of best responses of the abducens nerve of chronic RA frogs evoked by linear or angular acceleration differed from the vector orientations of controls. In chronic RA frogs, linear acceleration evoked contralesional abducens nerve responses that originated from the utricle on the intact side and from the lagena, a vertical macular organ in frogs. Such an inadequate lagenar response component was absent in controls and in the ipsi-lesional abducens nerve of chronic RA frogs. Similar differences were detected in the direction of abducens nerve responses of chronic RA frogs during angular acceleration. Thus, compensatory vestibulo-ocular reflexes of chronic RA frogs became more symmetric in gain, but less precise in direction.

Postlesional vestibular reorganization improves the gain but impairs the spatial tuning of the maculo-ocular reflex in frogs.

The ramus anterior (RA) of N.VIII was sectioned unilaterally. Two months later we analyzed in vivo responses of the ipsi- and of the contralesional abducens nerve during horizontal and vertical linear acceleration in darkness. The contralesional abducens nerve had become responsive again to linear acceleration either because of a synaptic reorganization in the vestibular nuclei on the operated side and/or because of a reinnervation of the utricular macula by regenerating afferent nerve fibers. Significant differences in the onset latencies and in the acceleration sensitivities allowed a separation of RA frogs in a group without and in a group with functional utricular reinnervation. Most important, the vector orientation for maximal abducens nerve responses was clearly altered: postlesional synaptic reorganization resulted in the emergence of abducens nerve responses to vertical linear acceleration, a response component that was barely detectable in RA frogs with utricular reinnervation and that was absent in controls. The ipsilesional abducens nerve, however, exhibited unaltered responses in either group of RA frogs. The altered spatial tuning properties of contralesional abducens nerve responses are a direct consequence of the postlesional expansion of signals from intact afferent nerve and excitatory commissural fibers onto disfacilitated 2nd-order vestibular neurons on the operated side. These results corroborate the notion that postlesional vestibular reorganization activates a basic neural reaction pattern with more beneficial results at the cellular than at the network level. However, given that the underlying mechanism is activity-related, rehabilitative training after vestibular nerve lesion can be expected to shape the ongoing reorganization.

Spatial performance of unilateral vestibular defective patients in nonvisual versus visual navigation

The purpose of this study was to investigate the effects of unilateral vestibular neurotomy on humans ability to perform navigation tasks. These tasks provided self-motion feedback by way of either locomotor activity only (nonvisual navigation or "locomotor task") or visual motion cues only (visually simulated navigation or "visual task"). After exploration of an environment in which 4 locations were marked by different objects, subjects attempted to navigate to those locations either by reproducing the same paths as those followed during exploration, by reversing routes, or by making spatial inferences (shortcuts). Vestibular defective patients were tested one day before surgical treatment and during the recovery time course following unilateral vestibular nerve lesion (1 week, 1 month, and 3 month later). Their performance was assessed by measuring turn error and distance error in both navigation tasks and was compared to that of control subjects tested 4 times at similar time intervals. Turn error in the reproduction of previously explored routes in the locomotor task was lower in patients before surgery than in controls, suggesting the existence of compensatory processes. In the acute stage (1 week) after unilateral vestibular lesion, turn error was greater in patients than in controls for the highest level of mental representation (spatial inferences or reversing routes); impairment at making accurate rotations had disappeared by 1 month after vestibular lesion in both navigation tasks. These results point to the role of vestibular cues, in interaction with other sensory modalities, in the elaboration of an accurate internal representation of the environment. In addition, they suggest that unilateral suppression of vestibular information would induce transitory spatial memory disorganization at a high level of information processing.

Effects of vestibular nerve lesions on orientation turning in the leopard frog, Rana pipiens.

Previous articleNext article No AccessBEHAVIOR AND NEUROBIOLOGYEffects of Vestibular Nerve Lesions on Orientation Turning in the Leopard Frog, Rana pipiensJ. R. King and H. StrakaJ. R. King Search for more articles by this author and H. Straka Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by The Biological Bulletin Volume 195, Number 2October 1998 Published in association with the Marine Biological Laboratory Article DOIhttps://doi.org/10.2307/1542833 Views: 8Total views on this site Copyright © 1998 by Marine Biological LaboratoryPDF download Crossref reports no articles citing this article.

Sensation of Vertigo in Relation to Severity of Inner Ear or Vestibular Nerve Damage

The sensation of vertigo or dizziness shows individual differences in patients with inner ear or vestibular nerve damage. This study was designed to correlate the sensation of vertigo or dizziness with the severity of inner ear or vestibular nerve lesions.1. Unilateral inner ear lesionsThree months after the initial medical examination, patients no longer complained of vertigo or dizziness, and in 86%, the inner ear had recovered normal function. When the caloric response on the side of the lesion had recovered over 50% of normal function, 90% of the patients no longer complained of vertigo or dizziness.2. Unilateral vestibular nerve lesionsThree months after the initial medical examination, 90% of the patients no longer complained of vertigo or dizziness. When the caloric response on the side of the lesion had recovered over 30% of normal function, none of the patients complained of vertigo or dizziness.

障害部位別にみたＧａｌｖａｎｉｃ ｂｏｄｙ ｓｗａｙ 内耳障害・前庭神経障害・前庭神経節障害症例を中心として

障害部位別にみたＧａｌｖａｎｉｃ ｂｏｄｙ ｓｗａｙ 内耳障害・前庭神経障害・前庭神経節障害症例を中心として

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.

Evidence for glutamate as a neurotransmitter in the cat vestibular nerve: radioautographic and biochemical studies.

Evidence that glutamate acts as a neurotransmitter in vestibular nerve fibers was sought (1) by electron microscope radioautographic identification of the uptake sites of [3H]-glutamic acid after incubation of slices of cat vestibular nuclei, and (2) by measuring changes in sodium-dependent high affinity glutamate uptake in nerve endings containing homogenates from normal and deafferented vestibular nuclei 8 to 11 days after unilateral vestibular nerve lesion. Electron microscopic radioautography revealed that glutamate had been taken up by numerous nerve endings projecting over the whole vestibular nuclear complex. The biochemical approach indicated that after section of the vestibular nerve, a significant decrease in high affinity glutamate uptake occurred in the vestibular nuclei, which lost their exclusively ipsilateral projection. This decrease varied from one area of the deafferented vestibular nuclei to another, reaching -58% in the lateral area of the central part corresponding to the ventral lateral vestibular nucleus and the rostral part of the descending vestibular nucleus. It is concluded that glutamate (or aspartate) is used by the vestibular nerve fibers as a neurotransmitter in the vestibular nuclei.

Short- and long-term modifications of vestibulo-ocular response dynamics following unilateral vestibular nerve lesions in the cat.

The dynamics of the horizontal vestibuloocular reflex (VOR) were determined in the dark prior to and at various time periods after unilateral removal of the vestibular nerve. One chronic group, consisting of cats that were operated at the age of 6 weeks or as adults, was studied 10.5 to 22 months later; an adult-operated group was measured 1-244 days postoperatively (p.o.). Between measurements cats were kept in a normal environment. In control animals the VOR gain was close to unity only up to certain stimulus velocities which varied amongst cats; thereafter a sharp drop in gain occurred probably due to saturation of central and peripheral neuronal responses. Therefore, VOR gains in lesioned animals were compared to the control responses yielding high gain. It is only at these small stimulus amplitudes that the two labyrinths maximally interact and, therefore, one would expect the largest changes. The gain was computed after correction for the ocular imbalance induced by the lesion. Immediately after the lesion a drop in gain to stimulations in both directions was noted; the reduction was larger for the VOR evoked on rotation to the lesioned side. Contrary to control animals, no partial response saturation occurred in lesioned animals but, following rotation to the lesioned side, complete saturation was noted with larger stimuli. Ocular balance was greatly improved within the first 3-4 days p.o. as indicated by the strong reduction of nystagmus. The time course of p.o. adaptive gain changes could be divided into three stages: in the initial stage (1-5 days p.o.) no improvement was visible; between p.o. days 5-10 one group of cats showed an abrupt increase in gain while it remained low in others. Response symmetry showed no consistent change in either group; the 3rd stage starting p.o. day 10 and extending throughout the observation period (22 months) is characterized by slowly developing changes reducing significantly response asymmetry. The incremental gain was higher in the young than in the adult-operated chronic cats. Compared to controls the phase plot of the VOR of lesioned animals shows a parallel shift of ca. 10 degrees towards larger lead over the frequency range tested (0.05-1.0 Hz) independent of direction of rotation or p.o. stages. All lesioned animals showed a clear failure to hold eye position in the dark even in the chronic stage; a drift with an exponentially decreasing velocity of ca. 2-4 degrees/s was typical.(ABSTRACT TRUNCATED AT 400 WORDS)

Pathologic correlates of electronystagmographic tracings

Electronystagmographic tracings were correlated with the histopathologic findings in the peripheral vestibular system of 66 temporal bones of 34 patients who complained of dizziness. Although some findings (e.g., spontaneous nystagmus, unilaterally reduced caloric response, and directional preponderance) seemed to have doubtful value in localizing vestibular system disease, other findings indicated a peripheral site of the vestibular lesions. Bilaterally reduced or bilaterally absent caloric responses were consistently associated with pathologic changes in the peripheral vestibular system. Similarly, a unilaterally absent caloric response consistently indicated peripheral disease. On the other hand, positional nystagmus and bilaterally equal caloric responses seemed to indicate the absence of a peripheral site of disease in the vestibular system. Although there is no reliable way to differentiate end organ from vestibular nerve lesions, the latter were more commonly associated with positional nystagmus and absence of a caloric response. The direction of nystagmus beating correlated with the side of the diseased peripheral site in two of four patients with spontaneous nystagmus, in five of seven with positional nystagmus, and in all with unilateral reductions in or absence of caloric responses. Electronystagmographic findings in the present study seemed to reflect diffuse rather than localized pathologic changes in the peripheral vestibular system.