Homocysteine, B vitamins, and cardiovascular disease.
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Atherosclerosis↗
Biomedical subjects
John P Carey
Publications and source records attributed to John P Carey.
Axis of eye rotation changes with head-pitch orientation during head impulses about earth-vertical.
The goal of this study was to assess how the axis of head rotation, Listing's law, and eye position influence the axis of eye rotation during brief, rapid head rotations. We specifically asked how the axis of eye rotation during the initial angular vestibuloocular reflex (VOR) changed when the pitch orientation of the head relative to Earth-vertical was varied, but the initial position of the eye in the orbit and the orientation of Listing's plane with respect to the head were fixed. We measured three-dimensional eye and head rotation axes in eight normal humans using the search coil technique during head-and-trunk (whole-body) and head-on-trunk (head-only) "impulses" about an Earth-vertical axis. The head was initially oriented at one of five pitch angles (30 degrees nose down, 15 degrees nose down, 0 degrees, 15 degrees nose up, 30 degrees nose up). The fixation target was always aligned with the nasooccipital axis. Whole-body impulses were passive, unpredictable, manual, rotations with peak-amplitude of approximately 20 degrees , peak-velocity of approximately 80 degrees /s, and peak-acceleration of approximately 1000 degrees /s2. Head-only impulses were also passive, unpredictable, manual, rotations with peak-amplitude of approximately 20 degrees , peak-velocity of approximately 150 degrees /s, and peak-acceleration of approximately 3000 degrees /s2. During whole-body impulses, the axis of eye rotation tilted in the same direction, and by an amount proportional (0.51 +/- 0.09), to the starting pitch head orientation (P < 0.05). This proportionality constant decreased slightly to 0.39 +/- 0.08 (P < 0.05) during head-only impulses. Using the head-only impulse data, with the head pitched up, we showed that only 50% of the tilt in the axis of eye rotation could be predicted from vectorial summation of the gains (eye velocity/head velocity) obtained for rotations about the pure yaw and roll head axes. Thus, even when the orientation of Listing's plane and eye position in the orbit are fixed, the axis of eye rotation during the VOR reflects a compromise between the requirements of Listing's law and a perfectly compensatory VOR.
Adult↗
The effect of binocular eye position and head rotation plane on the human torsional vestibuloocular reflex.
We examined how the gain of the torsional vestibulo-ocular reflex (VOR) (defined as the instantaneous eye velocity divided by inverted head velocity) in normal humans is affected by eye position, target distance, and the plane of head rotation. In six normal subjects we measured three-dimensional (3D) eye and head rotation axes using scleral search coils, and 6D head position using a magnetic angular and linear position measurement device, during low-amplitude (approximately 20 degrees ), high-velocity (approximately 200 degrees/s), high-acceleration (approximately 4000 degrees /s2) rapid head rotations or 'impulses.' Head impulses were imposed manually and delivered in five planes: yaw (horizontal canal plane), pitch, roll, left anterior-right posterior canal plane (LARP), and right anterior-left posterior canal plane (RALP). Subjects were instructed to fix on one of six targets at eye level. Targets were either straight-ahead, 20 degrees left or 20 degrees right from midline, at distance 15 or 124 cm from the subject. Two subjects also looked at more eccentric targets, 30 degrees left or 30 degrees right from midline. We found that the vertical and horizontal VOR gains increased with the proximity of the target to the subject. Previous studies suggest that the torsional VOR gain should decrease with target proximity. We found, however, that the torsional VOR gain did not change for all planes of head rotation and for both target distances. We also found a dynamic misalignment of the vertical positions of the eyes during the torsional VOR, which was greatest during near viewing with symmetric convergence. This dynamic vertical skew during the torsional VOR arises, in part, because when the eyes are converged, the optical axes are not parallel to the naso-occipital axes around which the eyes are rotating. In five of six subjects, the average skew ranged 0.9 degrees -2.9 degrees and was reduced to <0.4 degrees by a 'torsional' quick-phase (around the naso-occipital axis) occurring <110 ms after the onset of the impulse. We propose that the torsional quick-phase mechanism during the torsional VOR could serve at least three functions: (1) resetting the retinal meridians closer to their usual orientation in the head, (2) correcting for the 'skew' deviation created by misalignment between the axes around which the eyes are rotating and the line of sight, and (3) taking the eyes back toward Listing's plane.
Adult↗
Auditory function in patients with surgically treated superior semicircular canal dehiscence.
OBJECTIVE: To characterize preoperative and postoperative audiologic findings in patients with superior semicircular canal dehiscence syndrome. STUDY DESIGN: Retrospective case review. SETTING: Tertiary referral center. PATIENTS: Patients with documented superior semicircular canal dehiscence syndrome (according to history, vestibular testing, and high-resolution computed tomography imaging) who underwent surgical repair of their dehiscence. INTERVENTION: Middle fossa craniotomy for superior semicircular canal plugging and/or resurfacing. MAIN OUTCOME MEASURES: Audiologic testing both before and after surgery with pure-tone threshold measurements of air and bone conduction. RESULTS: Twenty-nine subjects underwent surgical repair of superior semicircular canal dehiscence. Overall, there were no statistically significant differences by paired t test in hearing before or after surgery, in either air-conduction or bone-conduction thresholds, for 19 patients that had no previous surgical history. At least partial closure of air-bone gap was achieved in five patients. One patient with previous stapes surgery had significantly worse hearing both before and after canal repair compared with those without previous surgery. Two patients who had undergone previous middle fossa surgery with incomplete resolution of symptoms developed sensorineural hearing loss after revision surgery. Previous middle-ear exploration and tympanostomy tube placement did not seem to affect audiologic outcomes. Surgical hearing results did not differ according to method of canal repair (plugging versus resurfacing). CONCLUSION: Primary middle fossa repair of superior semicircular canal dehiscence is not associated with sensorineural hearing loss and, in some cases, can lead to normalization of conductive hearing loss. Revision middle fossa repair or previous stapes surgery may be associated with postoperative sensorineural hearing loss.
Adult↗
Orientation of human semicircular canals measured by three-dimensional multiplanar CT reconstruction.
Analysis of vestibulo-ocular reflex experiments requires knowledge of the absolute orientations (with respect to skull landmarks) of semicircular canals (SCC). Data relating SCC orientations to accessible skull landmarks in humans are sparse, apart from a classic study of 10 skulls, which concluded that the horizontal and anterior SCC are not mutually orthogonal (111 +/- 7.6 degrees). Multiple studies of isolated labyrinths have shown the inter-SCC angles are close to 90 degrees. We hypothesized that a larger sample would yield mean absolute SCC orientations closer to the mutual orthogonality demonstrated for isolated labyrinths. We measured canal orientations with respect to accessible skull landmarks using 3-D multiplanar reconstructions of computerized tomography scans of the temporal bones of 22 human subjects. Images were acquired with 0.5-mm thickness and reconstructed with in-plane resolution of 234 microm. There was no significant difference between the left and a mirror image of the right (p > 0.57 on multiway ANOVA of orientation vector coefficients), so data were pooled for the 44 labyrinths. The angle between the anterior and posterior SCC was 94.0 +/- 4.0 degrees (mean +/- SD). The angle between the anterior and horizontal SCC was 90.6 +/- 6.2 degrees. The angle between the horizontal and posterior SCC was 90.4 +/- 4.9 degrees. The direction angles between a vector normal to the left horizontal SCC and the positive Reid's stereotaxic X (+nasal), Y (+left), and Z (+superior) axes were 108.7 +/- 7.5 degrees, 92.2 +/- 5.7 degrees, and 19.9 +/- 7.0 degrees, respectively. The angles between a vector normal to the left anterior SCC and the positive Reid's stereotaxic X, Y, and Z axes were 125.9 +/- 5.2 degrees, 38.4 +/- 5.1 degrees, and 100.1 +/- 6.2 degrees, respectively. The angles between a vector normal to the left posterior SCC and the positive Reid's stereotaxic X, Y, and Z axes were 133.6 +/- 5.3 degrees, 131.5 +/- 5.1 degrees, and 105.6 +/- 6.6 degrees, respectively. The mean anterior SCC-contralateral posterior SCC angle was 15.3 +/- 7.2 degrees. The absolute orientations of human SCC are more nearly orthogonal than previously reported.
Adult↗
Search-coil head-thrust and caloric tests in Ménière's disease.
CONCLUSIONS: Our findings suggest that canal function is substantially preserved in subjects with active vertigo attacks as a result of Ménière's disease (MD). In these subjects, the head-thrust test (HTT) may not be as sensitive to canal dysfunction as traditional caloric testing. MD may differentially affect the low-frequency sensitivity of the canals. OBJECTIVE: Caloric tests have traditionally been used to characterize semicircular canal function in vestibular disorders, including MD. The quantitative HTT provides an objective measurement of semicircular canal function in the frequency and velocity ranges of normal head movements. The aim of this study was to compare the findings of caloric and HTTs in subjects with unilateral MD. MATERIAL AND METHODS: The study population consisted of 38 candidates for gentamicin treatment due to a high frequency of vertiginous attacks (25 males, 13 females; mean age 52.9 years; range 30-70 years). The duration of symptoms was 1-30 years (mean 5.3 years). Horizontal canal function was characterized with bithermal aqueous caloric tests and recordings of the angular vestibulo-ocular reflexes (aVORs) using the scleral search-coil technique during HTTs. The main outcomes were unilateral weakness (UW) on caloric testing and aVOR gain asymmetry (GA) during HTTs. A caloric response asymmetry of >20% was considered to be indicative of pathologic UW. A difference in GA during HTTs of >5.8% was considered significant. RESULTS: Twenty subjects (52.6%) showed abnormal results on one or both tests. Pathologic UW was present in 16 subjects (42.1%). During HTTs, 11 subjects (28.9%) showed pathologic GA. Seven subjects (18.4%) showed abnormal results on both tests. A significant correlation was found between UW and GA. However, pathologic GA during HTTs in subjects with unilateral MD was less frequent and the values smaller than those published for vestibular neuritis patients. Two subjects with unilateral MD had 100% UW, but none had >30% asymmetry on HTTs.
Adult↗
The vestibulo-ocular reflex response to head impulses rarely decreases after cochlear implantation.
OBJECTIVE: Measure vestibular function using the head impulse test and assess the change in function due to unilateral cochlear implantation. BACKGROUND: Cochlear implantation entails risks to vestibular function in the implanted ear. However, the nature and extent of this risk is not known. The head impulse test uses physiologically relevant stimuli that allow detection of subtle changes in vestibular function of individual semicircular canals. SUBJECTS: Sixteen adults (age, 28-65 years) were recruited for prospective study from the Listening Center at Johns Hopkins. Eleven of these subjects were tested 4 to 6 weeks after cochlear implantation. METHODS: Three-dimensional eye movement recordings were made using the scleral search coil technique. Stimuli were rapid, passive, transient, head-on-body rotations (acceleration approximately 3000 degrees /s) in the direction excitatory for each of the six semicircular canals. RESULTS: Of the 16 subjects measured preoperatively, 6 (36%) had low (< 0.74) VOR gains in one or both of the horizontal canals and 8 (50%) had low (< 0.64) vestibulo-ocular reflex (VOR) gains in one or more of the vertical canals. These preoperative gain deficits were bilateral in six subjects. The VOR gain did not significantly change after implantation in 10 out of the 11 subjects tested postoperatively. The remaining subject suffered a partial loss of function in the implanted ear and was the only subject who experienced transient vertigo and oscillopsia after implantation. CONCLUSIONS: Preoperative vestibular deficits were common among this group of candidates for cochlear implantation; however, significant loss of vestibular function due to cochlear implantation was uncommon.
Acceleration↗
Angular vestibulo-ocular reflex gains correlate with vertigo control after intratympanic gentamicin treatment for Meniere's disease.
OBJECTIVES: The objective of our study was to determine whether angular vestibulo-ocular reflex (aVOR) gains correlated with vertigo control after intratympanic gentamicin treatment for Meniere's disease. METHODS: We conducted a prospective study of 18 subjects with unilateral Meniere's disease treated with intratympanic gentamicin injection and followed all subjects for 1 year. We measured the gain of the aVOR elicited by rapid rotary head thrusts in each of the canal planes for each subject before and after treatment with intratympanic gentamicin by using magnetic search coils to record eye movements. RESULTS: During the follow-up period, 11 subjects ("single-treatment group"; 61%) had control of their vertigo with a single gentamicin injection. The remaining 7 subjects ("multiple-treatment group"; 39%) experienced recurrent vertigo that required a second injection of gentamicin at a mean of 6 months after the first treatment. The 11 subjects in the single-treatment group had significantly greater reduction of labyrinthine function after the first treatment, as measured by change in ipsilateral horizontal canal gain, than did the 7 subjects with vertigo recurrence. Changes in caloric asymmetry did not correlate with vertigo control. CONCLUSIONS: Our results suggest that successful treatment of Meniere's disease is closely related to attenuation of semicircular canal function as measured by horizontal canal aVOR gains.
Adult↗
Superior canal dehiscence is not due to cephalic displacement of the labyrinth.
Superior semicircular canal dehiscence syndrome may have a congenital basis. CT scans of 44 control and 21 dehiscent superior canals were examined to determine if dehiscent canals were more cephalically placed or vertically oriented than control canals. Results showed that neither was the case. Instead, the defect may be in the process of ossification above the superior canal.
Ear, Inner↗
Responses of irregularly discharging chinchilla semicircular canal vestibular-nerve afferents during high-frequency head rotations.
Mammalian vestibular-nerve afferents innervating the semicircular canals have been divided into groups according to their discharge regularity, gain at 2-Hz rotational stimulation, and morphology. Low-gain irregular afferents terminate in calyx endings in the central crista, high-gain irregular afferents synapse more peripherally in dimorphic (bouton and calyx) endings, and regular afferents terminate in the peripheral zone as bouton-only and dimorphic endings. The response dynamics of these three groups have been described only up to 4 Hz in previous studies. Reported here are responses of chinchilla semicircular canal vestibular-nerve afferents to rotational stimuli at frequencies up to 16 Hz. The sensitivity of all afferents increased with increasing frequency with the sensitivity of low-gain irregular afferents increasing the most and matching the high-gain irregular afferents at 16 Hz. All afferents increased their phase lead with respect to stimulus velocity at higher frequencies with the highest leads in low-gain irregular afferents and the lowest in regular afferents. No attenuation of sensitivity or shift in phase consistent with the presence of a high-frequency pole over the range tested was noted. Responses were best fit with a torsion-pendulum model combined with a lead operator (tau(HF1)s + 1)(tau(HF2)s + 1). The discharge regularity of individual afferents was correlated to the value of each afferent's lead operator time constants. These findings suggest that low-gain irregular afferents are well suited for encoding the onset of rapid head movements, a property that would be advantageous for initiation of reflexes with short latency such as the vestibulo-ocular reflex.
Animals↗
Effects of intratympanic gentamicin on vestibular afferents and hair cells in the chinchilla.
Gentamicin is toxic to vestibular hair cells, but its effects on vestibular afferents have not been defined. We treated anesthetized chinchillas with one injection of gentamicin (26.7 mg/ml) into the middle ear and made extracellular recordings from afferents after 5-25 (early) or 90-115 days (late). The relative proportions of regular, intermediate, and irregular afferents did not change after treatment. The spontaneous firing rate of regular afferents was lower (P < 0.001) on the treated side (early: 44.3 +/- 16.3; late: 33.9 +/- 13.2 spikes x s(-1)) than on the untreated side (54.9 +/- 16.8 spikes x s(-1)). Spontaneous rates of irregular and intermediate afferents did not change. The majority of treated afferents did not measurably respond to tilt or rotation (82% in the early group, 76% in the late group). Those that did respond had abnormally low sensitivities (P < 0.001). Treated canal units that responded to rotation had mean sensitivities only 5-7% of the values for untreated canal afferents. Treated otolith afferents had mean sensitivities 23-28% of the values for untreated otolith units. Sensitivity to externally applied galvanic currents was unaffected for all afferents. Intratympanic gentamicin treatment reduced the histological density of all hair cells by 57% (P = 0.04). The density of hair cells with calyx endings was reduced by 99% (P = 0.03), although some remaining hair cells had other features suggestive of type I morphology. Type II hair cell density was not significantly reduced. These findings suggest that a single intratympanic gentamicin injection causes partial damage and loss of vestibular hair cells, particularly type I hair cells or their calyceal afferent endings, does not damage the afferent spike initiation zones, and preserves enough hair cell synaptic activity to drive the spontaneous activity of vestibular afferents.
Afferent Pathways↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗