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Biomedical subjects

Lloyd B Minor

Publications and source records attributed to Lloyd B Minor.

At least 37 records · Page 2Linked to original sources
PubMed2004

Vergence-mediated modulation of the human horizontal vestibulo-ocular reflex is eliminated by a partial peripheral gentamicin lesion.

The angular vestibulo-ocular reflex normally has an increased response during vergence on a near target. Surgical unilateral vestibular deafferentation reduces the horizontal vestibulo-ocular reflex (VOR) in response to far target viewing and eliminates this vergence effect. Intratympanic gentamicin treatment reduces VOR gain during far viewing, but the reduction is less severe than that after unilateral vestibular deafferentation. We sought to determine how gentamicin would affect vergence-mediated modulation of the VOR. The VOR in response to passive head impulses in the horizontal plane while viewing a far (124 cm) or near (15 cm) target was evaluated in 11 subjects following intratympanic gentamicin treatment. Three of these subjects had also been tested immediately prior to receiving gentamicin. The impulses were low amplitude (approximately 20 degrees ), high velocity (approximately 150 degrees /s), high acceleration (approximately 3,000 degrees /s2) horizontal head rotations administered manually by the investigator. Binocular eye and head velocity were recorded using the scleral search coil technique. The VOR gain was defined as eye velocity divided by inverted head velocity. Prior to intratympanic gentamicin, the VOR gain during rotations to either side was symmetric and showed the same vergence-mediated increase. Following gentamicin, head impulses towards the untreated side yielded VOR gains of 0.91+/-0.12 while viewing a far target and 1.27+/-0.22 while viewing a near target, an increase of 33%. Head impulses towards the treated side produced a hypometric VOR with no increase between far and near viewing. The average latency of the VOR was 7.6+/-2.5 ms towards the untreated side for either near or far viewing and 20.7+/-13.1 ms towards the treated side for either near or far viewing. Our findings show that a peripheral lesion caused by gentamicin does not ablate the VOR but does eliminate a component of the vestibular signal that is necessary for vergence-mediated modulation of the VOR. Gentamicin has preferential toxicity for the hair cells in the central zone of the crista, where irregular afferents predominate. Our findings are consistent with the hypothesis that irregular afferents provide the necessary signal for vergence-mediated modulation of the VOR.

Adult↗
PubMed2004

Ménière's disease.

PURPOSE OF REVIEW: Ménière's disease is characterized by spontaneous attacks of vertigo, fluctuating sensorineural hearing loss, aural fullness, and tinnitus. The pathologic process involves distortion of the membranous labyrinth with the formation of endolymphatic hydrops. This review describes the pathogenesis and etiology as well as the diagnosis and treatment of Ménière's disease. RECENT FINDINGS: Initial management of Ménière's disease can involve a low-salt diet and a diuretic. Treatment with intratympanic injection of gentamicin can be beneficial when vertigo persists despite optimal medical management. Recent studies have shown that gentamicin reduces vestibular function in the treated ear, although complete ablation of this vestibular function is not typically required in order to achieve control of vertigo. SUMMARY: Vertigo is often the most debilitating symptom associated with Ménière's disease. Many treatment options exist for the management of vertigo. Intratympanic injection of gentamicin (low dose) can be used in patients for whom vertigo has not been controlled by medical measures. Ongoing research is providing a greater understanding of the effects of gentamicin on vestibular function and of the mechanisms through which gentamicin leads to control of vertigo.

Combined Modality Therapy↗
PubMed2004

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.

Acoustic Stimulation↗
PubMed2004

Vestibulo-ocular physiology underlying vestibular hypofunction.

The vestibular system detects motion of the head and maintains stability of images on the fovea of the retina as well as postural control during head motion. Signals representing angular and translational motion of the head as well as the tilt of the head relative to gravity are transduced by the vestibular end organs in the inner ear. This sensory information is then used to control reflexes responsible for maintaining the stability of images on the fovea (the central area of the retina where visual acuity is best) during head movements. Information from the vestibular receptors also is important for posture and gait. When vestibular function is normal, these reflexes operate with exquisite accuracy and, in the case of eye movements, at very short latencies. Knowledge of vestibular anatomy and physiology is important for physical therapists to effectively diagnose and manage people with vestibular dysfunction. The purposes of this article are to review the anatomy and physiology of the vestibular system and to describe the neurophysiological mechanisms responsible for the vestibulo-ocular abnormalities in patients with vestibular hypofunction.

Adult↗
PubMed2003

Phase-plane analysis of gaze stabilization to high acceleration head thrusts: a continuum across normal subjects and patients with loss of vestibular function.

We investigated the vestibulo-ocular reflex (VOR) during high-acceleration, yaw-axis, head rotations in 12 normals and 15 patients with vestibular loss [7 unilateral vestibular deficient (UVD) and 8 bilateral vestibular deficient (BVD)]. We analyzed gaze stabilization within a 200-ms window after head rotation began, using phase planes, which allowed simultaneous analysis of gaze velocity and gaze position. These "gaze planes" revealed critical dynamic information not easily gleaned from traditional gain measurements. We found linear relationships between peak gaze-velocity and peak gaze-position error when normalized to peak head speed and position, respectively. Values fell on a continuum, increasing from normals, to normals tested with very high acceleration (VHA = 10,000-20,000 degrees/s2), to UVD patients during rotations toward the intact side, to UVD patients during rotations toward the lesioned side, to BVD patients. We classified compensatory gaze corrections as gaze-position corrections (GPCs) or gaze-velocity error corrections (GVCs). We defined patients as better-compensated when the value of their end gaze position was low relative to peak gaze position. In the gaze plane this criterion corresponded to relatively stereotyped patterns over many rotations, and appearance of high velocity (100-400 degrees/s) GPCs in the gaze plane ending quadrant (150-200 ms after head movement onset). In less-compensated patients, and normals at VHA, more GVCs were generated, and GPCs were generated only after gaze-velocity error was minimized. These findings suggest that challenges to compensatory vestibular function can be from vestibular deficiency or novel stimuli not previously experienced. Similar patterns of challenge and compensation were observed in both patients with vestibular loss and normal subjects.

Acceleration↗
PubMed2003

Vergence-mediated changes in the axis of eye rotation during the human vestibulo-ocular reflex can occur independent of eye position.

The aim of this study was to determine whether vergence-mediated changes in the axis of eye rotation in the human vestibulo-ocular reflex (VOR) would obey Listing's Law (normally associated with saccadic eye movements) independent of the initial eye position. We devised a paradigm for disassociating the saccadic velocity axis from eye position by presenting near and far targets that were centered with respect to one eye. We measured binocular 3-dimensional eye movements using search coils in ten normal subjects and 3-dimensional linear head acceleration using Optotrak in seven normal subjects. The stimuli consisted of passive, unpredictable, pitch head rotations with peak acceleration of approximately 2000 degrees /s(2 )and amplitude of approximately 20 degrees. During the pitch head rotation, each subject fixated straight ahead with one eye, whereas the other eye was adducted 4 degrees during far viewing (94 cm) and 25 degrees during near viewing (15 cm). Our data showed expected compensatory pitch rotations in both eyes, and a vergence-mediated horizontal rotation only in the adducting eye. In addition, during near viewing we observed torsional eye rotations not only in the adducting eye but also in the eye looking straight ahead. In the straight-ahead eye, the change in torsional eye velocity between near and far viewing, which began approximately 40 ms after the start of head rotation, was 10+/-6 degrees /s (mean +/- SD). This change in torsional eye velocity resulted in a 2.4+/-1.5 degrees axis tilt toward Listing's plane in that eye. In the adducting eye, the change in torsional eye velocity between near and far viewing was 16+/-6 degrees /s (mean +/- SD) and resulted in a 4.1+/-1.4 degrees axis tilt. The torsional eye velocities were conjugate and both eyes partially obeyed Listing's Law. The axis of eye rotation tilted in the direction of the line of sight by approximately one-third of the angle between the line of sight and a line orthogonal to Listing's plane. This tilt was higher than predicted by the one-quarter rule. The translational acceleration component of the pitch head rotation measured 0.5 g and may have contributed to the increased torsional component observed during near viewing. Our data show that vergence-mediated eye movements obey a VOR/Listing's Law compromise strategy independent of the initial eye position.

Adult↗
PubMed2003

Dehiscence of bone overlying the superior semicircular canal as a cause of an air-bone gap on audiometry: a case study.

Dehiscence of bone overlying the superior semicircular canal can result in a syndrome of vertigo and oscillopsia induced by loud noises or by maneuvers that change middle ear or intracranial pressure. Patients with this disorder can also experience a heightened sensitivity to bone-conducted sounds in the presence of normal middle ear function. High-resolution CT scans of the temporal bones demonstrate the dehiscence. The authors describe a patient with bilateral superior canal dehiscence who had bilateral low-frequency conductive hearing loss, normal middle ear function, intact acoustic reflexes, and intact vestibular-evoked myogenic potentials. These findings would not be expected on the basis of a middle ear cause of the conductive hearing loss. A high-resolution CT scan of the temporal bones in this patient revealed bilateral superior canal dehiscence. Normal acoustic immittance findings in the presence of conductive hearing loss should alert clinicians to the possibility of inner ear cause of an air-bone gap due to superior canal dehiscence.

Audiometry↗
PubMed2003

High-resolution CT findings suggest a developmental abnormality underlying superior canal dehiscence syndrome.

OBJECTIVE: Patients with superior canal dehiscence (SCD) syndrome experience vertigo and oscillopsia with loud sounds and/or stimuli that result in changes in middle ear or intracranial pressure. Findings on temporal bone CT were analyzed to determine if a developmental abnormality is associated with the syndrome. MATERIAL AND METHODS: Temporal bone CT scans [0.5 mm collimation and projections into the superior semicircular canal (SC) plane] were used to compare the bone overlying the SC in patients with SCD syndrome (20 unilateral, 7 bilateral) and in 88 patients without SCD syndrome who had undergone temporal bone CT for evaluation of other otologic disorders (controls). RESULTS: The thickness of bone overlying the SC in the controls measured 0.67 +/- 0.38 mm (mean +/- SD). For individual control subjects. the thickness of bone on one side was correlated with that on the other side (r = 0.43; p < 0.0001). The thickness of bone overlying the SC on the intact side in patients with unilateral dehiscence measured 0.31 +/- 0.23 mm, and was thinner than that noted in the controls (p < 0.0001). CONCLUSION: These findings support the notion that there is a developmental abnormality underlying SCD syndrome. When dehiscence is found on one side, the contralateral side is likely to be thin.

Case-Control Studies↗
PubMed2003

Long-term hearing outcome in patients receiving intratympanic gentamicin for Ménière's disease.

OBJECTIVE: To determine the long-term hearing outcome in patients with intractable vertigo caused by unilateral Ménière's disease who were treated with intratympanic injection of gentamicin. STUDY DESIGN: The study was a longitudinal analysis of hearing and control of vertigo in patients with unilateral Ménière's disease who received intratympanic gentamicin. METHODS: Pure-tone thresholds and speech discrimination scores on audiometry were analyzed, along with the control of vertigo. Criteria described in 1995 by the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) were used. Patients treated with intratympanic gentamicin had "definite" Ménière's disease and had intractable vertigo despite optimal medical therapy, no symptoms suggestive of Ménière's disease in the contralateral ear, and serviceable hearing in the contralateral ear. The study analyzed the outcomes of 34 patients for whom follow-up data were available for periods greater than 24 months after intratympanic gentamicin. RESULTS: Complete control of vertigo (AAOHNS Class A) was obtained in 90% of the patients. Profound sensorineural hearing loss occurred as a result of gentamicin injection in 1 of the 34 patients (3%). When data from all patients were grouped together, hearing was improved in 5 (15%), unchanged in 23 (68%), and worse in 6 (17%) patients. This distribution of hearing outcome is similar to that in patients whose symptoms of Ménière's disease were managed with medical measures. Recurrent vertigo developed in 10 patients (29%) at an interval of 4 to 15 months after initially complete control. Treatment with additional intratympanic injection(s) of gentamicin did not result in a change in hearing. CONCLUSION: The risk of hearing loss in patients treated with infrequent intratympanic injection(s) of gentamicin is low.

Adult↗
PubMed2003

Labyrinthine fistulae: pathobiology and management.

PURPOSE OF REVIEW: This article reviews literature on three manifestations of these pathologic mechanisms: leakage of perilymph from the inner ear into the middle ear, disruption of the bone of the labyrinth caused by cholesteatoma or other manifestations of chronic otitis media, and superior semicircular canal dehiscence syndrome. RECENT FINDINGS: Labyrinthine fistulae are caused by abnormal communications between the inner ear and surrounding structures. Under normal circumstances, the fluid-filled spaces of the membranous labyrinth are encased in the dense bone of the otic capsule with only two places of increased compliance: the oval window and the round window. Disruption of the labyrinthine bone can lead to areas of increased compliance, with symptoms and signs that can be understood based upon abnormal pressure transmission in the system. Communication between the endolymphatic and perilymphatic spaces of the labyrinth or passage of perilymph from the labyrinth into the middle ear or mastoid can lead to hearing loss and/or vestibular disturbances. SUMMARY: Findings on clinical examination as well as CT imaging of the temporal bone can be useful in making the diagnosis. Management is based upon the specific pathological factors and the impact of the symptoms and signs on the patient.

Cholesteatoma, Middle Ear↗
PubMed2003

Dehiscence of bone overlying the superior canal as a cause of apparent conductive hearing loss.

OBJECTIVE: To identify patients with superior semicircular canal dehiscence and apparent conductive hearing loss and to define the cause of the air-bone gap. STUDY DESIGN: Prospective study of patients with superior canal dehiscence. SETTING Tertiary referral center. PATIENTS: Vestibular and/or auditory findings indicative of canal dehiscence and demonstration of superior canal dehiscence on computed tomography of the temporal bone. INTERVENTION: Vestibular-evoked myogenic potentials, three-dimensional eye movement recordings, and surgical resurfacing of the superior canal. OUTCOME MEASURE: Association of superior canal dehiscence with an air-bone gap on audiometry. RESULTS: Four patients with dehiscence of bone overlying the superior canal were found to have air-bone gaps in the affected ears that were greatest at lower frequencies and averaged 24 +/- 7 dB over the frequency range of 250 to 4,000 Hz. Three of these patients had undergone stapedectomy before the identification of superior canal dehiscence. The air-bone gap was unchanged postoperatively. Each patient had an intact vestibular-evoked myogenic potential (VEMP) response from the affected ear, a finding that would not have been expected based on a middle ear cause of conductive hearing loss. One patient underwent resurfacing of the superior canal through a middle fossa approach. Postoperatively, his vestibular symptoms were relieved, and his air conduction thresholds were improved by 20 dB. CONCLUSIONS: Superior canal dehiscence can result in apparent conductive hearing loss. The third mobile window created by the dehiscent superior canal results in dissipation of acoustic energy and is a cause of inner ear conductive hearing loss.

Adult↗
PubMed2003

Cochlear implantation in patients with bilateral Ménière's syndrome.

OBJECTIVE: To evaluate the indications and clinical outcomes (audiologic and vestibular) in patients with Ménière's syndrome who have undergone cochlear implantation. STUDY DESIGN: This is a retrospective review of patients at a large tertiary academic medical center. PATIENTS: Nine patients were included in the study with AAO-HNS criteria for diagnosis of Ménière's syndrome as well as bilateral severe to profound sensorineural hearing loss as an indication for undergoing cochlear implantation. Audiologic criteria for implantation were considered in the context of speech recognition performance with well-fit, powerful hearing aids noting large fluctuations in performance levels in some patients. In all cases, the poorer hearing ear was implanted. Seven subjects had bilateral disease and had progressed to profound sensorineural hearing loss. The average age of the patients was 61 years. Six patients had undergone previous surgery to control vertigo, including endolymphatic shunt surgery and vestibular nerve section. No patient had received previous treatment with intra-tympanic gentamicin. Symptoms of Ménière's syndrome had been present in all patients for at least 10 years before implantation. INTERVENTION: Cochlear Implantation. MAIN OUTCOME MEASURES: Pre- and Postoperative audiometric scores (monosyllable words/phonemes, Central Institute for the Deaf (CID) sentences, Hearing in Noise Test (HINT) in quite/noise (+10 db)), pre- and postoperative vestibular symptoms (number of vestibular attacks, aural fullness, tinnitus). RESULTS: Follow-up after implantation ranged from 1 to 5 years. Average 6 month postimplantation scores were: monosyllable words/phonemes = 52%/65%, CID sentences = 82%, HINT in quiet/noise = 70%/50%. Average 1-year postimplant scores were: monosyllable words/phonemes = 60%/76%, CID sentences = 97%, HINT in quiet/noise = 89%/78%. Postoperative speech recognition scores were, on average, substantially greater than preoperative scores. While there were few complications associated with implantation, some patients experienced alterations in their implant performance in association with fluctuations in vestibular symptoms. CONCLUSIONS: Patients with advanced binaural involvement with Ménière's Disease may present a challenge to conventional criteria for cochlear implant candidacy because of fluctuating symptoms. We observed significant benefit over baseline in a consecutive series of patients with Ménière's syndrome who progressed to bilateral, severe-to-profound sensorineural hearing loss and underwent cochlear implantation. Further, previous vestibular surgery, including labyrinthectomy, does not contraindicate cochlear implantation.

Adult↗
PubMed2003

CT evaluation of bone dehiscence of the superior semicircular canal as a cause of sound- and/or pressure-induced vertigo.

PURPOSE: To describe the computed tomographic (CT) findings at different collimation widths associated with superior semicircular canal (SSC) dehiscence syndrome and to determine the frequency of these findings in a control population. MATERIALS AND METHODS: Temporal bone CT scans with 1.0-mm and/or 0.5-mm collimation were obtained in 50 patients with sound- and/or pressure-induced vestibular symptoms. The control population consisted of 50 patients undergoing CT at 1.0-mm collimation and 57 patients undergoing CT at 0.5-mm collimation for other reasons. RESULTS: SSC dehiscence was documented on CT scans in all 36 patients with the clinical syndrome, with bilateral findings in six patients. Six other patients without specific clinical signs appeared to have dehiscence on 1.0-mm-collimated scans. Intact bone overlaying the SSC was subsequently identified with 0.5-mm-collimated CT in each case. On the 1.0-mm-collimated scans in 50 control patients, an area judged as possible or definite dehiscence was identified in 18 of 100 ears. The bone overlaying the SSC was intact in each of the 114 control ears evaluated with 0.5-mm-collimated CT. CT findings from the patients with vestibular symptoms combined with those in the control population indicated that the positive predictive value of an apparent dehiscence in the diagnosis of SSC dehiscence syndrome improved from 50% with 1.0-mm-collimated CT with transverse and coronal images to 93% with 0.5-mm-collimated CT with reformation in the plane of the SSC. CONCLUSION: The positive predictive value of CT in identification of SSC dehiscence syndrome improves with 0.5-mm-collimated helical CT and reformation in the SSC plane.

Adolescent↗
PubMed2002

Semicircular canal afferents similarly encode active and passive head-on-body rotations: implications for the role of vestibular efference.

The vestibular receptors in the labyrinth receive innervation from centrifugally projecting efferent fibers. The influence of these efferents on information processing by vestibular afferents in primates has not been determined. One commonly held notion is that efferent activation during large-amplitude, active head movements would result in an increase in the resting discharge rate and in a reduction of the rotational sensitivity of afferents. Such an effect would increase the dynamic range of afferents involved in the encoding of head movements. To test this hypothesis, we recorded from afferents innervating the semicircular canals in alert macaques during passive head-on-body rotations and during active head movements that included gaze shifts and gaze pursuit. Extracellular, single-unit recordings were obtained from 24 afferent fibers innervating the horizontal, superior, and posterior canals. Based on the normalized coefficient of variation of the interspike interval for these units, our sample contained six regularly discharging, six intermediate, and 12 irregularly discharging afferents. Responses were analyzed using a least squares regression to determine the bias discharge rate of each unit and sensitivity to head velocity and acceleration. We found no difference in bias discharge rate or rotational sensitivity of the afferent responses for the different stimulus conditions tested. Our results indicate that semicircular canal afferents encode information about head rotation similarly for self generated and passively applied head-on-body movements.

Action Potentials↗
PubMed2002

Changes in the three-dimensional angular vestibulo-ocular reflex following intratympanic gentamicin for Ménière's disease.

The 3-dimensional angular vestibulo-ocular reflexes (AVOR) elicited by rapid rotary head thrusts were studied in 17 subjects with unilateral Ménière's disease before and 2-10 weeks after treatment with intratympanic gentamicin and in 13 subjects after surgical unilateral vestibular destruction (SUVD). Each head thrust was in the horizontal plane or in either diagonal plane of the vertical semicircular canals, so that each head thrust effectively stimulated only one pair of canals. The AVOR gains (eye velocity/head velocity during the 30 ms before peak head velocity) for the head thrusts exciting each individual canal were averaged and taken as a measure of the function of that canal. Prior to intratympanic gentamicin, gains for head thrusts that excited canals on the affected side were 0.91 +/- 0.20 (horizontal canal, HC), 0.78 +/- 0.20 (anterior canal, AC), and 0.83 +/- 0.10 (posterior canal, PC). The asymmetries between these gain values and those for head thrusts that excited the contralateral canals were <2%. In contrast, caloric asymmetries averaged 40% +/- 32%. Intratympanic gentamicin resulted in decreased gains attributable to each canal on the treated side: 0.40 +/- 0.12 (HC), 0.35 +/- 0.14 (AC), 0.31 +/- 0.14 (PC) (p <0.01). However, the gains attributable to contralateral canals dropped only slightly, resulting in marked asymmetries between gains for excitation of ipsilateral canals versus their contralateral mates: HC: 34% +/- 12%, AC: 24% +/- 25%, and PC: 42% +/- 13%. There was no difference in the AVOR gain for excitation of the ipsilateral HC after gentamicin in patients who received a single intratympanic injection (0.39 +/- 0.11, n = 12) in comparison to those who received 2-3 injections (0.42 +/- 0.15, n = 5, p = 0.7). Gain decreases attributed to the gentamicin-treated HC and AC were not as severe as those observed after SUVD. This finding suggests that intratympanic gentamicin causes a partial vestibular lesion that may involve preservation of spontaneous discharge and/or rotational sensitivity of afferents.

Adult↗
PubMed2002

Comparison of head thrust test with head autorotation test reveals that the vestibulo-ocular reflex is enhanced during voluntary head movements.

OBJECTIVES: To compare 2 clinical tests of vestibular function, the head autorotation test (HART) and the head thrust test (HTT), and to determine why they give disparate results in patients with known unilateral vestibular deficiency (UVD) due to labyrinthectomy. METHODS: We used scleral coils to measure the horizontal (yaw) vestibulo-ocular reflex (VOR) in 5 healthy human subjects and in 11 patients who underwent labyrinthectomy. We used 2 paradigms. Using HART, subjects visually fixated a target during self-generated, swept-frequency, sinusoidal, horizontal head rotations. Using HTT, patients fixated the target during horizontal head thrusts delivered randomly in direction and time. RESULTS: In subjects without UVD, eye movements were almost perfectly compensatory for both paradigms. In subjects with UVD, VOR gain for ipsilesional head thrusts was low for both paradigms, but significantly (P<.001) higher (less abnormal) for HART (0.60 +/- 0.13) than for HTT (0.14 +/- 0.13). Contralesional gain was reduced for both, to 0.64 +/- 0.20 for HART and to 0.57 +/- 0.17 for HTT. Because ipsilesional and contralesional gains were not statistically different for HART (P =.69), comparison of VOR gains for half-cycle responses to the HART stimulus could not reliably identify the side of the known lesion. In contrast, HTT consistently identified the side of the lesion for all subjects with UVD. To investigate whether preprogramming contributes to the boost in VOR as measured by HART, we compared the gain and response delay of eye movements during actively self-generated and passively received head thrusts. For subjects without UVD, response delays were shorter for active (6 +/- 1 milliseconds) than for passive (12 +/- 1 milliseconds) HTT. For ipsilesional rotations of subjects with UVD, active HTT yielded a significantly higher gain (0.44 +/- 0.20) (P<.001) and a shorter delay (15 +/- 6 milliseconds) (P<.001) than did passive HTT (0.14 +/- 0.13 and 37 +/- 15 milliseconds, respectively). Contralesional test results revealed a similar performance boost for active head movements. Data are given as mean +/- SD. CONCLUSION: When comparison of half-cycle gains is used to identify the lesion side, self-generated predictable head movement paradigms, such as HART and active HTT, are less accurate than passive HTT in the characterization of UVD, in part because preprogramming can augment the VOR during voluntary head movements.

Adult↗
PubMed2002

Prominent expression of Narp in central vestibular pathways: selective effect of labyrinth ablation.

Recent in vitro studies demonstrated that Narp, a secreted immediate early gene (IEG) product, induces AMPA receptor clustering. Accordingly, Narp has been implicated in mediating activity-dependent changes in synaptic efficacy. To help define the role of Narp in vivo, we conducted immunohistochemical studies of Narp in rat brain. Unexpectedly, we found robust Narp expression in several discrete areas linked to the vestibular system: the anterodorsal nucleus (ADN) of the thalamus, which relays head orientation information to the cortex, the lateral vestibulospinal (Deiters') nucleus and Purkinje cells in the flocculonodular lobe of the cerebellum. Although strong Narp expression in Deiters' nucleus and the cerebellum was present consistently, Narp expression in the ADN displayed a high degree of variability among animals. To check if this variability in ADN Narp expression reflects its dependence on fluctuating levels of vestibular input, we monitored Narp immunostaining following bilateral labyrinth ablation. This procedure significantly suppressed Narp immunostaining in the ADN, indicating that it is stimulated by naturally occurring vestibular input. In contrast, labyrinth ablation did not affect Narp staining in Deiters' nucleus or the flocculonodular lobe of the cerebellum, presumably because these areas are driven by inputs from multiple systems. As previous studies implicate Narp in synaptic plasticity, these findings suggest that this IEG may mediate ongoing adjustments in synaptic strength or connectivity in several pathways linked to the vestibular system.

Animals↗