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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have described asymmetrical vertical eye movements when normal human subjects were rotated about a vertical inter-aural axis (with head rolled 90 degrees). We measured vertical eye movements induced by visual, vestibular and visual-vestibular stimuli with a magnetic scleral search coil technique while 10 normal subjects sat upright in a chair designed to rotate about the horizontal inter-aural axis at frequencies and amplitudes of natural head movements. Asymmetries in the gain of upward and downward pursuit and fixation-suppression of the VOR were found in individual subjects. However, there was no significant difference (p greater than 0.05) between the mean gain of up and down slow eye movements induced by vestibular, visual or visual-vestibular stimulation in the group of normal subjects. Systematic up-down asymmetries in vertical eye movements previously observed with testing about the vertical inter-aural axis were probably due to bias introduced by otolith stimulation and/or electro-oculographic eyelid artifact.
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PMID:Vertical visual-vestibular interaction in normal human subjects. 380 79

Vertical optokinetic nystagmus (OKN) i.e., OKN in the sagittal plane, was asymmetrical in the monkey when it was induced with animals lying on their sides in a 90 degrees roll position. In typical monkeys the slow phase velocity of downward OKN (slow phases up) increased proportionally with stimulus velocity at close to unity gain to about 60 degrees/s and saturated at about 100 degrees/s. Upward OKN (slow phases down) increased with close to unity gain only to about 40 degrees/s and saturated at about 60 degrees/s. The slow phase velocity of upward OKN was usually irregular and its frequency was lower than that of downward or horizontal OKN. Upward and downward optokinetic after-nystagmus (OKAN) were also asymmetrical. Upward OKAN was weak or absent and when present it usually saturated at 10 degrees/s. Downward OKAN was stronger, increasing with a gain of about 0.7 with regard to stimulus velocity to a saturation velocity of about 50-60 degrees/s. This was usually about 10-30 degrees/s less than the saturation velocity of horizontal OKAN. The weak or absent upward OKAN indicates that stored activity related to slow phase eye velocity contributes little to the production of upward OKN. In agreement with this, there was little or no slow rise in slow phase velocity to a steady state level during upward OKN. Instead eye velocity rose to its peak velocity at the onset of stimulation. The lack of stored velocity information is probably largely responsible for the differences in regularity, gain and frequency between upward and downward OKN. Vertical vestibular nystagmus was induced by rotating monkeys in darkness with steps of velocity about a vertical axis, while they were lying on their sides in a 90 degree roll position. The velocities of the initial upward and downward slow phases were approximately equal. Gains of the vertical VOR ranged from about 0.5 to 0.98 for stimuli up to 150 degrees/s. Despite equivalent initial gains for upward and downward nystagmus, the vertical VOR was asymmetrical in that downward nystagmus had a higher frequency and generally lasted longer than upward nystagmus. Time constants of downward nystagmus (slow phases up) were about 15 s on average and were similar to those of horizontal nystagmus. Mean time constants of upward nystagmus (slow phases down) were about 8 s. This is only slightly longer than the average time constant of afferent activity in the semicircular canal nerves induced by steps of velocity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vertical optokinetic nystagmus and vestibular nystagmus in the monkey: up-down asymmetry and effects of gravity. 660 54

A new technique was developed to test the VOR in humans. A tightly but comfortably fitting helmet was provided with an electronically controlled torque motor that rotated a mass around a vertical axis. Acceleration of the motor caused reactive torque of the helmet in the opposite direction which was transmitted to the (freely movable) head. Sinusoidal head oscillations in the frequency range 2-20 Hz (peak-to-peak amplitudes about 10 degrees and 0.1 degrees respectively) were easily achieved, as well as step displacements of the head with accelerations on the order of 1000 degrees/s2. Limitation of the maximum torque and lack of any rigid attachment of the head to a fixed structure made the technique safe and comfortable. Eye and head rotations were recorded, independently of head translations, with eye and head search coils in a homogeneous a.c. magnetic field. In normal subjects, gain was near unity at 2 Hz: above 8 Hz, gain increased progressively toward 1.1-1.3 at 20 Hz. Phase lag increased from a few degrees at 2 Hz to about 45 degrees at 20 Hz. Above 2 Hz, these results were unaffected by visual conditions; lower gains and increased phase lags were found in subjects with bilateral or unilateral vestibular loss. For step displacements, gain (measured in the first 100 ms) was near unity for normals, near zero after bilateral vestibular loss and strongly asymmetrical after unilateral vestibular loss. Thus, the technique seems highly effective in testing vestibular function with minimal contamination by other systems.
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PMID:Evaluation of the human vestibulo-ocular reflex at high frequencies with a helmet, driven by reactive torque. 874 66

To investigate the effect of asymmetrical vestibular input on the perceived straight-ahead direction, we compared 7 subjects (age 59 +/- 8 yrs, mean +/- SD) who had chronic (>10 mos) unilateral vestibular deafferentation with 10 age matched controls (age 61+/-6 younger controls (age 28 +/- 7 yrs). Despite the age difference, the two control groups performed similarly and were therefore pooled. Eye and head movements were recorded using search coils as subjects underwent 30 s trials of sinusoidal, whole body oscillation (0.4-2 Hz, peak velocities 0-120 degrees /s) in darkness while attempting to maintain gaze on a remembered target 5 m distant. As a control, most stimulus oscillations were randomly superimposed on an imperceptible, constant velocity of +/-0.5 degrees /s that produced a whole-body offset of 15 degrees by the end of the trial. Following oscillation, subjects remained motionless in darkness and were asked to orient both gaze and a manipulandum to the remembered target location. In control subjects, mean final gaze and manipulandum positions were within 15 degrees of the target for all testing conditions. There was no dependence of final gaze and manipulandum positions on the frequency or velocity of the preceding whole-body oscillations (p > 0.05). In four of seven unilaterally deafferented subjects there was an ipsilesional bias of final eye position of > or =10 degrees. These subjects moved both eye and manipulandum to the ipsilesional side, with the error increasing at higher stimulus velocities. For the 120 degrees /s peak head velocity, mean ipsilesional gaze bias ranged from 10-37 degrees and mean manipulandum bias ranged from 26-108 degrees. Although the errors depended on velocity p < 0.01), errors were independent of frequency (p > 0.1). In the remaining three subjects with vestibular deafferentation, final gaze and manipulandum positions [were not statistically different from controls.] Early gain (eye velocity / head velocity) of the VOR averaged 0.82 +/- 0.01 for the first 10 s of all trials and was similar in all groups (p > 0.1). Gain during the final 10 s gain averaged 0.78 +/- 0.01 for control subjects, but was significantly lower at 0.70 +/- 0.01 for unilaterally deafferented subjects, whose eye positions reached the limit of the ocular motor range. We conclude that many humans with chronic unilateral vestibular deafferentation have a large ipsilesional dynamic bias of eye position and the perceived straight ahead direction reflecting persistent asymmetry of vestibular processing.
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PMID:Asymmetry of ocular motor and perceptual vestibular processing in humans with unilateral vestibular deafferentation. 1145 7