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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A thorough study of vestibular function cannot be limited to the evaluation of VOR alone; it must also include the study of VSR which serves to control erect stance under both static and dynamic conditions. In unilateral peripheral vestibular lesions (UVL) computerized stabilometry makes it possible to perform a more accurate evaluation of the VSR complex through the quantification of "postural sway". Furthermore, the diagnostic potential of stabilometry can be further fine-tuned by introducing a sensitization test, in particular the head retroflexion (OCR) and head shaking (OC-HST) tests. In the present study 61 patients with UVL of various etiology (viral, toxic, vascular, idiopathic) were studied. Besides electrooculography, stabilometry was performed under base conditions (eyes open and closed) and with sensitizing tests (OCR, OC-HST). L and S were used as statokinesigram parameters while frequency and oscillation amplitude on the sagittal and transverse planes were used as stabilogram parameters. Of the 61 UVL patients, 47.5% showed VOR compensation while static postural alterations were found in 31.1%; this raised to 50.8% when the sensitization test was introduced. Apparently the compensation phenomena became manifest more quickly for VOR than for VSR. The introduction of the sensitization test, however, markedly reduced this variance. The two sensitization, maneuvers used provided quantitatively equivalent results although in the absence of reciprocal agreement. Agreement was not even recorded between stabilometric HST and the head shaking test. This confirms the presence of two different routes for VOR and VSR. Nonetheless, the introduction of the sensitization test made it possible to identify those "false negative" VSR cases which were really pathological, thus making it possible to properly identify the patients' condition and arrange for adequate treatment.
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PMID:[Posturography in unilateral peripheral vestibular deficiency]. 210 87

Computer aided active head shaking test has several advantages because it can be used clinical at frequencies higher than 2 Hz. In this study, VOR gain and phase were examined over age. For this experiment, we designed an original measurement system composed of EOG, an angular velocity sensor and a microcomputer. VOR gain was expressed by transfer function. Forty normal subjects ranging from 10 to 75 were examined for high frequency VOR responses to active head shaking. VOR gain at frequencies higher than 2 Hz attained the same value as that seen in children below the age of 10 years. The VOR gain was nearly 1 within 2 Hz, decreasing with frequencies above 4 Hz. The effect of aging was shown at frequencies of more than 4 Hz, and appeared in patients above 50 years of age. No obvious phase lag was observed within 5 Hz.
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PMID:Development of high frequency vestibulo-ocular responses to active head shaking. 761 Aug 83

We have examined to what extent the vertical semicircular canals contribute to the nonlinearity of the horizontal VOR imposed by the driving of primary vestibular afferents into inhibitory cutoff at high velocities of head rotation (Ewald's second law). The gain (eye velocity/head velocity) of the horizontal component of the VOR with the head pitched down 30 degrees and pitched up 30 degrees was examined during constant-velocity rotations in normal subjects and patients following unilateral vestibular nerve section. In normal subjects, VOR gain decreases as chair velocity increases from 60-300 degrees/s when the head is pitched up, but VOR gain remains constant when the head is pitched down. This finding implies that the mechanism by which the gain of the horizontal VOR gain remains constant at all velocities of rotation depends upon the pattern of labyrinthine stimulation. Following unilateral nerve section, we found that the directional preponderance (DP) in horizontal VOR depends upon whether the head is pitched up 30 (mean asymmetry = 5%) or pitched down 30 degrees (mean asymmetry = 20%). This is what is expected based on the degree to which the lateral and vertical semicircular canals sense horizontal head acceleration with the head in different degrees of pitch. Hence, following unilateral vestibular lesions, the DP of horizontal VOR gain is most easily elicited at high velocities of head rotation and with the head pitched down 30 degrees. Evidence for DP at the bedside using the "head-shaking nystagmus" technique may be optimally elicited with the head pitched down 30 degrees.
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PMID:The contribution of the vertical semicircular canals to high-velocity horizontal vestibulo-ocular reflex (VOR) in normal subjects and patients with unilateral vestibular nerve section. 883 34

The functional status of the velocity storage mechanism was studied in patients at long-term follow-up (2 to 4 years) after unilateral vestibular neurectomy. The time constant of the vestibulo-ocular reflex (VORtc), the effect of head tilt on postrotatory nystagmus, optokinetic after-nystagmus (OKAN), and nystagmus after rapid head shaking were studied in 10 patients. In agreement with previous findings, VORtc was found to be short and most patients manifested OKAN, suggesting that unilateral peripheral vestibular loss is associated with a complete loss of storage within the the VOR but only a partial loss of velocity storage for visual input. However, at postrotatory head tilt the VOR time constant was further shortened, supposedly due to discharge of functioning velocity storage. Moreover, most patients manifested nystagmus after head shaking. These findings on tilt suppression and head-shaking nystagmus suggest that velocity storage within the VOR may function even in patients with complete unilateral vestibular lesions.
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PMID:Tilt suppression, OKAN, and head-shaking nystagmus at long-term follow-up after unilateral vestibular neurectomy. 883 20

"Torso Rotation" (TR) produces an acute, reversible change in human vestibular function. Experiments were performed to determine if repeated exposure to this technique would result in long-term adaptive modifications. In one experiment, VOR gain was evaluated. Measurements were obtained before and 3 times after 30 minutes of TR, on 7 consecutive days. VOR gain dropped each day after TR, returning to normal within about 20 min. In a separate experiment with different subjects, eyes-open gaze stability was measured during voluntary head shaking between 3.0 and 0.3 Hz. The same test schedule was used. Analysis of gaze stability (limited to frequencies between 1.0 and 2.0 Hz) was complicated by an unexpected finding. Despite careful instructions, head displacement increased each day after TR, also returning to normal within about 20 min. Surprisingly, subjects were unaware of this change. Combining the 2 experiments, VOR gain and head amplitude were averaged across all 7 days, separately for the 4 daily tests. Head amplitude was plotted against VOR gain for these 4 averages. Amplitude was greater when VOR gain was reduced, with a remarkably high correlation (R2 = 0.996). These findings confirm that vestibular feedback plays an important role in the control of voluntary head movement. Furthermore, the data suggest that instability of the visual scene reported by subjects shaking their heads after TR resulted not only from a lower VOR gain, but also from the inadvertent use of higher head velocities.
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PMID:"Torso rotation" experiments; 3: Effects of acute changes in vestibular function on the control of voluntary head movements. 888 95

Directional abnormalities of vestibular and optokinetic responses in patients with cerebellar degeneration are reported. Three-axis magnetic search-coil recordings of the eye and head were performed in eight cerebellar patients. Among these patients, examples of directional cross-coupling were found during (1) high-frequency, high-acceleration head thrusts; (2) constant-velocity chair rotations with the head fixed; (3) constant-velocity optokinetic stimulation; and (4) following repetitive head shaking. Cross-coupling during horizontal head thrusts consisted of an inappropriate upward eye-velocity component. In some patients, sustained constant-velocity yaw-axis chair rotations produced a mixed horizontal-torsional nystagmus and/or an increase in the baseline vertical slow-phase velocity. Following horizontal head shaking, some patients showed an increase in the slow-phase velocity of their downbeat nystagmus. These various forms of cross-coupling did not necessarily occur to the same degree in a given patient; this suggests that different mechanisms may be responsible. It is suggested that cross-coupling during head thrusts may reflect a loss of calibration of brainstem connections involved in the direct vestibular pathways, perhaps due to dysfunction of the flocculus. Cross-coupling during constant-velocity rotations and following head shaking may result from a misorientation of the angular eye-velocity vector in the velocity-storage system. Finally, responses to horizontal optokinetic stimulation included an inappropriate torsional component in some patients. This suggests that the underlying organization of horizontal optokinetic tracking is in labyrinthine coordinates. The findings are also consistent with prior animal-lesion studies that have shown a role for the vestibulocerebellum in the control of the direction of the VOR.
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PMID:Directional abnormalities of vestibular and optokinetic responses in cerebellar disease. 1037 73

Acute, reversible changes in human vestibular function can be produced by exposure to "Torso Rotation" (TR), a method involving the overuse of certain types of simple, self-generated movements. A single session results in multiple, short-lasting aftereffects, including perceptual illusions, VOR gain reduction, gaze and postural instability, and motion sickness. With repeated exposure, motion sickness susceptibility disappears and gaze stability improves. VOR gain continues to be reduced, however. Therefore, another gaze stabilizing system must come into play. Are visual and/or neck inputs involved in this functional compensation? Six subjects participated in this 7-day experiment. Eye and head movements were measured during 2 tests: 1) voluntary "head only" shaking between 0.3 and 3.0 Hz (lights off) and 2) voluntary "head and torso" shaking, moving the upper body en bloc (neck immobilized). Measurements were obtained before and repeatedly after TR. Velocity gain (eye velocity/head velocity) was determined for each of these tests. Each day, mean velocity gain during "head only" shaking in the dark (averaged over 1.0 to 2.0 Hz) dropped significantly after TR (P < 0.01), with no long-term improvement (P > 0.9). Similar results, although more noisy, were obtained for "head and torso" shaking. As a control, EOG calibration data confirmed that gaze stability in the light did improve over the 7 days of testing. This experiment demonstrates that the reduction in gaze instability following repeated exposure to TR results from an increased use of vision. It excludes the VOR, the COR, and predictive mechanisms (including efference copy) as contributors. In addition, in the 20 minutes following TR completion, gaze stability recovered less than during previous VOR testing in the dark. These results are compatible with the motion that exposure to TR leads to a change in sensorimotor strategy involving a de-emphasis of vestibular inputs.
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PMID:"Torso Rotation" experiments. 4: the role of vision and the cervico-ocular reflex in compensation for a deficient VOR. 1037 80

Patients with bilateral vestibular failure (BVF) suffer from postural and gait unsteadiness with an increased risk of falls. The aim of this study was to elucidate the differential role of otolith, semicircular canal (SSC), visual, proprioceptive, and cognitive influences on the postural stability of BVF patients. Center-of-pressure displacements were recorded by posturography under six conditions: target visibility; tonic head positions in the pitch plane; horizontal head shaking; sensory deprivation; dual task; and tandem stance. Between-group analysis revealed larger postural sway in BVF patients on eye closure; but with the eyes open, BVF did not differ from healthy controls (HCs). Head tilts and horizontal head shaking increased sway but did not differ between groups. In the dual task condition, BVF patients maintained posture indistinguishable from controls. On foam and tandem stance, postural sway was larger in BVF, even with the eyes open. The best predictor for the severity of bilateral vestibulopathy was standing on foam with eyes closed. Postural control of our BVF was indistinguishable from HCs once visual and proprioceptive feedback is provided. This distinguishes them from patients with vestibulo-cerebellar disorders or functional dizziness. It confirms previous reports and explains that postural unsteadiness of BVF patients can be missed easily if not examined by conditions of visual and/or proprioceptive deprivation. In fact, the best predictor for vestibular hypofunction (VOR gain) was examining patients standing on foam with the eyes closed. Postural sway in that condition increased with the severity of vestibular impairment but not with disease duration. In the absence of visual control, impaired otolith input destabilizes BVF with head retroflexion. Stimulating deficient SSC does not distinguish patients from controls possibly reflecting a shift of intersensory weighing toward proprioceptive-guided postural control. Accordingly, proprioceptive deprivation heavily destabilizes BVF, even when visual control is provided.
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PMID:Postural Control in Bilateral Vestibular Failure: Its Relation to Visual, Proprioceptive, Vestibular, and Cognitive Input. 2891 78

Background: Strong static magnetic fields such as those in an MRI machine can induce sensations of self-motion and nystagmus. The proposed mechanism is a Lorentz force resulting from the interaction between strong static magnetic fields and ionic currents in the inner ear endolymph that causes displacement of the semicircular canal cupulae. Nystagmus persists throughout an individual's exposure to the magnetic field, though its slow-phase velocity partially declines due to adaptation. After leaving the magnetic field an after effect occurs in which the nystagmus and sensations of rotation reverse direction, reflecting the adaptation that occurred while inside the MRI. However, the effects of visual fixation and of head shaking on this early type of vestibular adaptation are unknown. Methods: Three-dimensional infrared video-oculography was performed in six individuals just before, during (5, 20, or 60 min) and after (4, 15, or 20 min) lying supine inside a 7T MRI scanner. Trials began by entering the magnetic field in darkness followed 60 s later, either by light with visual fixation and head still, or by continuous yaw head rotations (2 Hz) in either darkness or light with visual fixation. Subjects were always placed in darkness 10 or 30 s before exiting the bore. In control conditions subjects remained in the dark with the head still for the entire duration. Results: In darkness with head still all subjects developed horizontal nystagmus inside the magnetic field, with slow-phase velocity partially decreasing over time. An after effect followed on exiting the magnet, with nystagmus in the opposite direction. Nystagmus was suppressed during visual fixation; however, after resuming darkness just before exiting the magnet, nystagmus returned with velocity close to the control condition and with a comparable after effect. Similar after effects occurred with continuous yaw head rotations while in the scanner whether in darkness or light. Conclusions: Visual fixation and sustained head shaking either in the dark or with fixation inside a strong static magnetic field have minimal impact on the short-term mechanisms that attempt to null unwanted spontaneous nystagmus when the head is still, so called VOR set-point adaptation. This contrasts with the critical influence of vision and slippage of images on the retina on the dynamic (gain and direction) components of VOR adaptation.
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PMID:Visual Fixation and Continuous Head Rotations Have Minimal Effect on Set-Point Adaptation to Magnetic Vestibular Stimulation. 3072 56