Effects on the optokinetic system of midline lesions in the pretectum of monkeys

2001 ◽  
Vol 11 (2) ◽  
pp. 73-80
Author(s):  
Shoji Watanabe ◽  
Isao Kato ◽  
Kosuke Hattori ◽  
Miki Azuma ◽  
Tadashi Nakamura ◽  
...  
Keyword(s):  
Steady State ◽  
Phase Velocity ◽  
Visual Stimulation ◽  
Optic Tract ◽  
Velocity Storage ◽  
Slow Phase ◽  
Rapid Rise ◽  
Posterior Commissure ◽  
Time Constants ◽  
Slow Phase Velocity

The nucleus of the optic tract (NOT), an important visuo-motor relay between the retina and preoculomotor structures, is responsible for mediating horizontal optokinetic nystagmus (OKN) in monkeys, cats, rabbits and rats. In addition to its projection to the vestibular nuclei, the NOT has a prominent projection to the contralateral NOT via the posterior commissure. In order to evaluate the role of the commissural fibers between the NOTs in OKN, we cut the posterior commissure in three Macaca fuscata. The animals viewed the OKN stripes under three conditions: right eye viewing, left eye viewing, and both eyes viewing. OKN was recorded in response to counter-clockwise and clockwise stimulation at stimulus velocities of 30°/s, 60°/s and 90°/s. After control data were gathered, the posterior commissure was transected with an operating knife. Before the animal was sacrificed, biocytin, an anterograde tracer, was injected into the left NOT in order to confirm that all of the commissural fibers had been cut. Although the midline lesions decreased the initial rapid rise and steady state OKN slow-phase velocity in all three animals, there were no directional differences observed during monocular clockwise or counter-clockwise visual stimulation to either eye. In two of the three animals, there were no significant differences in the time-constants of optokinetic after nystagmus (OKAN) after the lesion. In the remaining animal, the time-constants decreased at stimulus velocities of 30°/s and 60°/s. In conclusion, gain reduction in the rapid rise and steady state slow-phase velocity of OKN can be explained by removal of an excitatory signal mediated by commissural fibers to inhibitory interneurons in the contralateral NOT. However, interrupting the commissural fibers had no effect on the velocity storage mechanism, because the time-constants of OKAN mostly remained largely unchanged by the lesion.

Spontaneous nystagmus and gaze-holding ability in monkeys after intravitreal picrotoxin injections

1992 ◽  
Vol 67 (5) ◽  
pp. 1124-1132 ◽  
Author(s):  
M. Ariel ◽  
R. J. Tusa
Keyword(s):  
Steady State ◽  
Eye Movements ◽  
Phase Velocity ◽  
Smooth Pursuit ◽  
Spontaneous Nystagmus ◽  
Velocity Storage ◽  
Slow Phase ◽  
Gamma Aminobutyric Acid ◽  
Full Field ◽  
Slow Phase Velocity

1. Eye movements were measured in three rhesus monkeys after monocular intravitreal injections of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist. The effects of this drug were tested when the animals were in a completely dark room, when they performed a smooth pursuit task, and when they viewed either a stationary pattern or a full-field optokinetic pattern rotating horizontally. 2. Between 15 and 20 min after the injection, a sustained conjugate spontaneous nystagmus developed in the dark, with the slow-phase movement in the temporal-to-nasal direction with respect to the injected eye. Peak slow-phase velocity ranged from 15 to 45 degrees/s. The nystagmus persisted for at least 1 h but stopped by the next day. 3. In a well-lit room, the nystagmus was completely suppressed, even during monocular viewing with the injected eye. When the lights were turned off, the slow-phase velocity of the spontaneous nystagmus slowly increased to a steady-state level within 70-120 s. 4. Horizontal smooth pursuit eye movements to a 1 degree target light moving in front of the animal +/- 20 degrees to either side of center of gaze at constant speeds were normal. Target speeds ranging from 15 to 60 degrees/s for both monocular and binocular viewing conditions were used. Binocular and monocular optokinetic nystagmus (OKN) to a full-field drum rotating at a constant velocity (5-90 degrees/s) were also normal. The initial pursuit and steady-state components of OKN were measured, as well as the velocity-storage component (optokinetic after nystagmus, OKAN).(ABSTRACT TRUNCATED AT 250 WORDS)

A review of the effects of space flight on the asymmetry of vertical optokinetic and vestibulo-ocular reflexes

2003 ◽  
Vol 13 (4-6) ◽  
pp. 255-263
Author(s):  
Gilles Clément
Keyword(s):  
Phase Velocity ◽  
Optokinetic Nystagmus ◽  
Visual Stimulation ◽  
Head Movements ◽  
Slow Phase ◽  
Eye Position ◽  
Slow Phase Velocity ◽  
Ocular Reflex ◽  
Vestibulo Ocular Reflex ◽  
Eye Velocity

Prolonged microgravity during orbital flight is a unique way to modify the otolith inputs and to determine the extent of their contribution to the vertical vestibulo-ocular reflex (VOR) and optokinetic nystagmus (OKN). This paper reviews the data collected on 10 astronauts during several space missions and focuses on the changes in the up-down asymmetry. Both the OKN elicited by vertical visual stimulation and the active VOR elicited by voluntary pitch head movements showed an asymmetry before flight, with upward slow phase velocity higher than downward slow phase velocity. Early in-flight, this asymmetry was inverted, and a symmetry of both responses was later observed. An upward shift in the vertical mean eye position in both OKN and VOR suggests that these effects may be related to otolith-dependent changes in eye position which, in themselves, affect slow phase eye velocity.

Spatial Orientation of Caloric Nystagmus in Semicircular Canal-Plugged Monkeys

2002 ◽  
Vol 88 (2) ◽  
pp. 914-928 ◽  
Author(s):  
Yasuko Arai ◽  
Sergei B. Yakushin ◽  
Bernard Cohen ◽  
Jun-Ichi Suzuki ◽  
Theodore Raphan
Keyword(s):  
Phase Velocity ◽  
Spatial Orientation ◽  
Velocity Vector ◽  
Semicircular Canals ◽  
Velocity Storage ◽  
Slow Phase ◽  
Coordinate Frame ◽  
Slow Phase Velocity ◽  
Caloric Nystagmus ◽  
Eye Velocity

We studied caloric nystagmus before and after plugging all six semicircular canals to determine whether velocity storage contributed to the spatial orientation of caloric nystagmus. Monkeys were stimulated unilaterally with cold (≈20°C) water while upright, supine, prone, right-side down, and left-side down. The decline in the slow phase velocity vector was determined over the last 37% of the nystagmus, at a time when the response was largely due to activation of velocity storage. Before plugging, yaw components varied with the convective flow of endolymph in the lateral canals in all head orientations. Plugging blocked endolymph flow, eliminating convection currents. Despite this, caloric nystagmus was readily elicited, but the horizontal component was always toward the stimulated (ipsilateral) side, regardless of head position relative to gravity. When upright, the slow phase velocity vector was close to the yaw and spatial vertical axes. Roll components became stronger in supine and prone positions, and vertical components were enhanced in side down positions. In each case, this brought the velocity vectors toward alignment with the spatial vertical. Consistent with principles governing the orientation of velocity storage, when the yaw component of the velocity vector was positive, the cross-coupled pitch or roll components brought the vector upward in space. Conversely, when yaw eye velocity vector was downward in the head coordinate frame, i.e., negative, pitch and roll were downward in space. The data could not be modeled simply by a reduction in activity in the ipsilateral vestibular nerve, which would direct the velocity vector along the roll direction. Since there is no cross coupling from roll to yaw, velocity storage alone could not rotate the vector to fit the data. We postulated, therefore, that cooling had caused contraction of the endolymph in the plugged canals. This contraction would deflect the cupula toward the plug, simulating ampullofugal flow of endolymph. Inhibition and excitation induced by such cupula deflection fit the data well in the upright position but not in lateral or prone/supine conditions. Data fits in these positions required the addition of a spatially orientated, velocity storage component. We conclude, therefore, that three factors produce cold caloric nystagmus after canal plugging: inhibition of activity in ampullary nerves, contraction of endolymph in the stimulated canals, and orientation of eye velocity to gravity through velocity storage. Although the response to convection currents dominates the normal response to caloric stimulation, velocity storage probably also contributes to the orientation of eye velocity.

Vertical Optokinetic Nystagmus and Optokinetic Afternystagmus in Humans

1991 ◽  
Vol 1 (3) ◽  
pp. 309-315
Author(s):  
A. Böhmer ◽  
R.W. Baloh
Keyword(s):  
Phase Velocity ◽  
Optokinetic Nystagmus ◽  
Body Position ◽  
Normal Subjects ◽  
Lateral Position ◽  
Velocity Storage ◽  
Slow Phase ◽  
Lateral Side ◽  
Slow Phase Velocity ◽  
Optokinetic Afternystagmus

Vertical optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN) were recorded in 6 normal subjects using the magnetic scleral search coil technique in order to reevaluate the up-down symmetry of these responses. The effects of body position relative to gravity were investigated by comparing OKN and OKAN elicited with the subjects in an erect and in a lateral side position. No consistent up-down asymmetry in vertical OKN was found but OKAN was asymmetric (up slow phase velocity > down slow phase velocity). Most subjects had an immediate reversal in OKAN slow phase velocity after downward stimuli. No significant effects of static head position (upright versus lateral position) on vertical OKN and OKAN were found. These features of human OKAN can be explained by the summation of two oppositely directed velocity storage mechanisms.

Vestibular Function and Motion Sickness Susceptibility: Videonystagmographic Evidence From Oculomotor and Caloric Tests

2020 ◽  
Vol 29 (2) ◽  
pp. 188-198
Author(s):  
Cynthia G. Fowler ◽  
Margaret Dallapiazza ◽  
Kathleen Talbot Hadsell
Keyword(s):  
Phase Velocity ◽  
Motion Sickness ◽  
Repeated Measures ◽  
Short Form ◽  
Vestibular Function ◽  
Slow Phase ◽  
Test Results ◽  
Normal Range ◽  
Slow Phase Velocity ◽  
Caloric Tests

Purpose Motion sickness (MS) is a common condition that affects millions of individuals. Although the condition is common and can be debilitating, little research has focused on the vestibular function associated with susceptibility to MS. One causal theory of MS is an asymmetry of vestibular function within or between ears. The purposes of this study, therefore, were (a) to determine if the vestibular system (oculomotor and caloric tests) in videonystagmography (VNG) is associated with susceptibility to MS and (b) to determine if these tests support the theory of an asymmetry between ears associated with MS susceptibility. Method VNG was used to measure oculomotor and caloric responses. Fifty young adults were recruited; 50 completed the oculomotor tests, and 31 completed the four caloric irrigations. MS susceptibility was evaluated with the Motion Sickness Susceptibility Questionnaire–Short Form; in this study, percent susceptibility ranged from 0% to 100% in the participants. Participants were divided into three susceptibility groups (Low, Mid, and High). Repeated-measures analyses of variance and pairwise comparisons determined significance among the groups on the VNG test results. Results Oculomotor test results revealed no significant differences among the MS susceptibility groups. Caloric stimuli elicited responses that were correlated positively with susceptibility to MS. Slow-phase velocity was slowest in the Low MS group compared to the Mid and High groups. There was no significant asymmetry between ears in any of the groups. Conclusions MS susceptibility was significantly and positively correlated with caloric slow-phase velocity. Although asymmetries between ears are purported to be associated with MS, asymmetries were not evident. Susceptibility to MS may contribute to interindividual variability of caloric responses within the normal range.

Visually evoked slow eye movements, visual-vestibular interaction, and infratentorial lesions

1983 ◽  
Vol 91 (1) ◽  
pp. 76-80 ◽  
Author(s):  
Carsten Wennmo ◽  
Nils Gunnar Henriksson ◽  
Bengt Hindfelt ◽  
Ilmari PyykkÖ ◽  
MÅNs Magnusson
Keyword(s):  
Eye Movements ◽  
Phase Velocity ◽  
Brain Stem ◽  
Smooth Pursuit ◽  
Maximum Velocity ◽  
Slow Phase ◽  
Slow Phase Velocity ◽  
Velocity Gain ◽  
Visual Vestibular Interaction ◽  
Slow Eye Movements

The maximum velocity gain of smooth pursuit and optokinetic, vestibular, and optovestibular slow phases was examined in 15 patients with pontine, 10 with medullary, 10 with cerebellar, and 5 with combined cerebello — brain stem disorders. Marked dissociations were observed between smooth pursuit and optokinetic slow phases, especially in medullary disease. A cerebellar deficit enhanced slow phase velocity gain during rotation in darkness, whereas the corresponding gain during rotation in light was normal.

Monocular Nystagmic Responses to Caloric Stimulation

1979 ◽  
Vol 88 (1) ◽  
pp. 79-85 ◽  
Author(s):  
James W. Wolfe
Keyword(s):  
Phase Velocity ◽  
Rhesus Monkeys ◽  
Cold Water ◽  
Normal Subjects ◽  
Closed Circuit ◽  
Slow Phase ◽  
Vestibular Nystagmus ◽  
Differential Activation ◽  
Slow Phase Velocity ◽  
Left And Right

Twenty-five normal subjects and 173 clinical patients received standard bithermal caloric testing. Vestibular nystagmus was evaluated for cumulative slow phase velocity from the summated horizontal eye recording and independent recording of the left and right eye. These data revealed that cold water stimulation produced more intense activation of the ipsilateral eye. Simultaneous closed-circuit video and D.C. electro-oculographic recordings from eight normal rhesus monkeys in response to cold water irrigations confirmed the fact that this stimulus leads to differential activation of the extraocular muscles. A possible explanation for this finding is discussed.

The Velocity Storage Mechanism of the Optokinetic Nystagmus Under Apparent Stimulus Movements in Squirrel Monkeys

1997 ◽  
Vol 7 (6) ◽  
pp. 441-451
Author(s):  
J. Kröller ◽  
F. Behrens ◽  
V.V. Marlinsky
Keyword(s):  
Steady State ◽  
Brain Stem ◽  
Apparent Movement ◽  
Squirrel Monkeys ◽  
Constant Light ◽  
Velocity Storage ◽  
Slow Phase ◽  
Stripe Pattern ◽  
Storage Mechanism ◽  
The Brain

Experiments in two awake untrained squirrel monkeys were performed to study the velocity storage mechanism during fast rise of OKN slow phase velocity. This was done by testing the monkey’s capability to perform OKN in response to a stationary-appearing stroboscopically illuminated stripe pattern of a horizontally rotating drum. Nystagmus was initially elicited during constant illumination lasting between 0.6 and 25 s. The periodicity of the stripe pattern was 2.37°. When after the constant light the flash illumination was switched on again, two types of behavior could occur, depending on the length of the constant light interval (CLI): 1) when the CLI was shorter than a threshold value of 6.2 seconds, the OKN ceased under the flash stimulation. Then a “post-OKN” occurred that increased with the length of the CLIs, indicating that the intermittently illuminated pattern did not provoke fixation suppression of OKN aftereffects. 2) when the CLI was above threshold, the OKN continued under the flash light: it will he called “apparent movement OKN.” The threshold CLI between the type 1 and the type 2 response did not depend on drum velocities between 21.5°/s and 71.3°/s. The average gain of the apparent movement OKN was 0.83 ± 0.04; gain and stability of slow phase eye movement velocity did not deviate systematically from the usually elicited OKN. OKAN after apparent movement OKN did not deviate from OKAN after constantly illuminated moving patterns. In response to the OKN initiation by a constantly illuminated pattern up to pattern velocities of 100°/s, the OKN steady state gain was reached within the first 2 or 3 nystagmus beats. We ascribe the increase of the post-OKN with CLI and the existence of a threshold constant light interval to activity-accumulation in the common velocity-to-position integrator (velocity storage) of the brain stem. Loading of the velocity storage takes place after the OKN gain has already reached the steady-state value. Apparent movement OKN could also be elicited in guinea pigs that lack an effective smooth pursuit system. We suggest that apparent movement OKN is produced by mechanisms located in the brain stem.

Efficacy of histaminergic drugs in experimental motion sickness

2008 ◽  
Vol 17 (5-6) ◽  
pp. 313-321
Author(s):  
E.I. Matsnev ◽  
E.E. Sigaleva
Keyword(s):  
Phase Velocity ◽  
Healthy Volunteers ◽  
Motion Sickness ◽  
Slow Phase ◽  
High Susceptibility ◽  
Double Blind ◽  
Slow Phase Velocity ◽  
Betahistine Dihydrochloride ◽  
The Mean ◽  
Oculomotor Activity

The purpose of this investigation was to evaluate the efficacy of the histaminergic drug "Betahistine dihydrochloride" in experimental motion sickness in 10 healthy volunteers (mean age 19.4 y.o.) with high susceptibility to motion sickness. Motion sickness was modeled using Coriolis (precession) accelerations (cumulative Coriolis stimulation test – CCST). Each subject took 32 mg of "Betahistine dihydrochloride" or placebo under "double – blind" conditions 1 hour before testing. The duration and slow phase velocity of the post-rotational nystagmus, the pursuit eye tracking test, and the latency, velocity and accuracy of saccades were estimated. The tolerability level of the CCST in volunteers in the betahistine series was shown to be significantly (p < 0.001) higher, as compared to placebo and baseline. The mean illusory sensations score for the experimental series was significantly lower than that in the placebo and baseline series (p < 0.01). It was found that "Betahistine" demonstrated antimotion sickness efficacy and improved oculomotor activity (increased gain during pursuit movements, faster and more accurate saccades).

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