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)

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.

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.

Analysis of vertebrate eye movements following intravitreal drug injections. IV. Drug-induced eye movements are unyoked in the turtle

1991 ◽  
Vol 65 (4) ◽  
pp. 1003-1009 ◽  
Author(s):  
M. Ariel
Keyword(s):  
Eye Movements ◽  
Contact Lenses ◽  
Spontaneous Nystagmus ◽  
Slow Phase ◽  
Dependent Manner ◽  
Drug Induced ◽  
Full Field ◽  
Optokinetic Responses ◽  
Vertebrate Eye ◽  
Stimulus Direction

1. Eye movements of awake turtles were measured from both eyes simultaneously using two search-coil contact lenses. Optokinetic nystagmus (OKN) was evoked by full field patterns moving horizontally at different stimulus velocities. Intravitreal injections of either bicuculline or 2-amino-4-phosphonobutyrate (APB) were then made into one eye, after which eye movements were again recorded under similar stimulus conditions. Several days later, eye movements were again recorded and recovery was observed. 2. The effects of these two synaptic drugs on the optokinetic responses of the injected eye were similar to those previously reported in turtles, rabbits, and decorticate cats. APB, which blocks the retinal ON pathways, completely blocked visually evoked responses to any stimulus direction or velocity presented to the injected eye. On the other hand, the uninjected eye was still responsive to optokinetic stimuli. This difference between the eyes is consistent with the nonconjugate nature of OKN in the turtle. 3. After bicuclline application, the injected eye displayed a spontaneous nystagmus with its slow phase in the temporal-to-nasal direction. The movements of the injected eye were independent of stimulus direction or a range of stimulus velocities. During that effect, the eye contralateral to the injection still responded to visual stimuli in a direction- and velocity-dependent manner. For example, if the uninjected eye was exposed to optokinetic stimuli moving temporal-to-nasal, both eyes would then move in their respective temporal-to-nasal directions. This nonconjugate ocular behavior is similar to that seen when each eye of a normal turtle was exposed to its temporal-to-nasal stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Alexander's Law During High-Speed, Yaw-Axis Rotation: Adaptation or Saturation?

2020 ◽  
Vol 11 ◽  
Author(s):  
Claudia Lädrach ◽  
David S. Zee ◽  
Thomas Wyss ◽  
Wilhelm Wimmer ◽  
Athanasia Korda ◽  
...  
Keyword(s):  
Eye Movements ◽  
Phase Velocity ◽  
High Speed ◽  
Semicircular Canals ◽  
Vertical Axis ◽  
Normal Subjects ◽  
Vestibular Nuclei ◽  
Slow Phase ◽  
Slow Phase Velocity ◽  
Alexander’S Law

Objective: Alexander's law (AL) states the intensity of nystagmus increases when gaze is toward the direction of the quick phase. What might be its cause? A gaze-holding neural integrator (NI) that becomes imperfect as the result of an adaptive process, or saturation in the discharge of neurons in the vestibular nuclei?Methods: We induced nystagmus in normal subjects using a rapid chair acceleration around the yaw (vertical) axis to a constant velocity of 200°/second [s] and then, 90 s later, a sudden stop to induce post-rotatory nystagmus (PRN). Subjects alternated gaze every 2 s between flashing LEDs (right/left or up/down). We calculated the change in slow-phase velocity (ΔSPV) between right and left gaze when the lateral semicircular canals (SCC) were primarily stimulated (head upright) or, with the head tilted to the side, stimulating the vertical and lateral SCC together.Results: During PRN AL occurred for horizontal eye movements with the head upright and for both horizontal and vertical components of eye movements with the head tilted. AL was apparent within just a few seconds of the chair stopping when peak SPV of PRN was reached. When slow-phase velocity of PRN faded into the range of 6–18°/s AL could no longer be demonstrated.Conclusions: Our results support the idea that AL is produced by asymmetrical responses within the vestibular nuclei impairing the NI, and not by an adaptive response that develops over time. AL was related to the predicted plane of eye rotations in the orbit based on the pattern of SCC activation.

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.

scholarly journals Comparing mastoid and posterior cervical muscles vibration effects on eye movement in normal subjects

2019 ◽  
Author(s):  
Moslem Shaabani ◽  
Najmeh Naghibi ◽  
Enayatollah Bakhshi
Keyword(s):  
Eye Movements ◽  
Phase Velocity ◽  
Eye Movement ◽  
Vestibular System ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Slow Phase ◽  
Vestibular Disorders ◽  
Rehabilitation Hospital ◽  
Slow Phase Velocity

Background and Aim: Vibration is a method for stimulating the vestibular system. This met­hod can unmask asymmetry between two vesti­bular systems (such as unilateral peripheral ves­tibular disorders). The occurrence of vibration-induced nystagmus (VIN) in healthy subjects can affect the diagnosis of patients with uni­lateral peripheral vestibular disorders. Thus, the evaluation of VIN in healthy subjects is critical to help the diagnosis of unilateral peripheral vestibular disorders. Methods: This study was carried out on 72 hea­lthy subjects (mean ± SD age: 27.12 ± 4.97 years) in the Auditory and Balance Clinic of Rofeideh Rehabilitation Hospital. Vibration sti­mulation with a frequency of 30 and 100 Hz was used on mastoid and posterior cervical mus­cles (PCMs) and simultaneously eye movements were recorded and analyzed using videonystag­mography. Results: The mastoid vibration with a frequ­ency of 30 and 100 Hz, respectively produced VIN in 16.67% and 27.78% of subjects and VIN observed in PCMs vibration with a frequency of 30 and 100 Hz in 4.17% and 9.72% of the subjects. Conclusion: The occurrence of VIN in healthy subjects was more probable with mastoid vib­ration in 100 Hz. In this study, VIN was pre­dominantly horizontal, its direction was toward the stimulated side, and its slow phase velocity was lower than 5 deg/s. These criteria could be used for differentiation between normal and abnormal subjects.

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.

Effects of occipital lobectomy upon eye movements in primate

1987 ◽  
Vol 58 (4) ◽  
pp. 883-907 ◽  
Author(s):  
D. S. Zee ◽  
R. J. Tusa ◽  
S. J. Herdman ◽  
P. H. Butler ◽  
G. Gucer
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Striate Cortex ◽  
Occipital Cortex ◽  
Image Motion ◽  
Velocity Storage ◽  
Slow Phase ◽  
Visually Guided ◽  
Temporal Area ◽  
Small Targets

1. Eye movements were recorded before and after bilateral occipital lobectomy in six rhesus monkeys trained to fixate and to follow small targets. Striate cortex was completely removed in two animals; small islands islands remained in the others. In all animals portions of extrastriate cortex were also removed but the medial superior temporal area in the superior temporal sulcus was largely spared. Optokinetic nystagmus (OKN) was markedly altered but not abolished in all animals. The immediate pursuit component of OKN was eliminated leading to a poor response to stimuli comprised of high frequencies. The velocity-storage component of OKN was present, but the maximum value of OKN that could be achieved was decreased to 6 and 16 degrees/s in the two most severely affected animals (preop, 65-116 degrees/s). The residual OKN was similar to that of afoveate animals with a diminished response to high velocities of retinal-image motion and a temporal to nasal predominance during monocular viewing. 2. In the initial postoperative period all animals appeared completely blind. Within 1-6 mo, however, they regained an ability to make visually guided saccades to, and smooth pursuit of, small targets. Saccades were nearly as accurate as preoperatively, but saccade amplitudes were more variable and saccade latencies increased. In the two animals with a complete removal of striate cortex, gains (eye velocity/target velocity) of smooth pursuit during sinusoidal tracking (60 degrees/s, 0.5 Hz) were 0.9 and 0.95. During tracking of step-ramp (Rashbass) stimuli with 60 degrees/s ramps, the average acceleration of the eyes during the first 120 ms of smooth pursuit was 189-278 degrees.s-1.s-1 (preop range, 154-418 degrees.s-1.s-1). In other respects, though, smooth pursuit was not normal. Latencies were increased two- to threefold, and tracking was more variable. 3. Paradoxically, as visually guided saccades and pursuit recovered, some other ocular motor functions deteriorated. Spontaneous and gaze-evoked nystagmus developed 3-6 mo after occipital lobectomy; the time constant of the neural eye-position integrator dropped to values as low as 2.6-4.8 s. The maximum slow-phase velocity of OKN also decreased. 4. The findings immediately after occipital lobectomy indicate that in normal primates occipital cortex is necessary for visually guided saccades and smooth pursuit as well as for the immediate component of OKN. Occipital cortex also makes the predominant contribution toward the generation of the velocity-storage component of OKN.(ABSTRACT TRUNCATED AT 400 WORDS)

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.

Quantitative Analysis of Abducens Neuron Discharge Dynamics During Saccadic and Slow Eye Movements

1999 ◽  
Vol 82 (5) ◽  
pp. 2612-2632 ◽  
Author(s):  
Pierre A. Sylvestre ◽  
Kathleen E. Cullen
Keyword(s):  
Eye Movements ◽  
Firing Rate ◽  
Eye Movement ◽  
Neuronal Activity ◽  
Smooth Pursuit ◽  
Slow Phase ◽  
Vestibular Nystagmus ◽  
Firing Rates ◽  
Rapid Eye Movements ◽  
Eye Velocity

The mechanics of the eyeball and its surrounding tissues, which together form the oculomotor plant, have been shown to be the same for smooth pursuit and saccadic eye movements. Hence it was postulated that similar signals would be carried by motoneurons during slow and rapid eye movements. In the present study, we directly addressed this proposal by determining which eye movement–based models best describe the discharge dynamics of primate abducens neurons during a variety of eye movement behaviors. We first characterized abducens neuron spike trains, as has been classically done, during fixation and sinusoidal smooth pursuit. We then systematically analyzed the discharge dynamics of abducens neurons during and following saccades, during step-ramp pursuit and during high velocity slow-phase vestibular nystagmus. We found that the commonly utilized first-order description of abducens neuron firing rates (FR = b + kE + rE˙, where FR is firing rate, E and E˙ are eye position and velocity, respectively, and b, k, and r are constants) provided an adequate model of neuronal activity during saccades, smooth pursuit, and slow phase vestibular nystagmus. However, the use of a second-order model, which included an exponentially decaying term or “slide” (FR = b + kE + rE˙ + uË − c[Formula: see text]), notably improved our ability to describe neuronal activity when the eye was moving and also enabled us to model abducens neuron discharges during the postsaccadic interval. We also found that, for a given model, a single set of parameters could not be used to describe neuronal firing rates during both slow and rapid eye movements. Specifically, the eye velocity and position coefficients ( r and k in the above models, respectively) consistently decreased as a function of the mean (and peak) eye velocity that was generated. In contrast, the bias ( b, firing rate when looking straight ahead) invariably increased with eye velocity. Although these trends are likely to reflect, in part, nonlinearities that are intrinsic to the extraocular muscles, we propose that these results can also be explained by considering the time-varying resistance to movement that is generated by the antagonist muscle. We conclude that to create realistic and meaningful models of the neural control of horizontal eye movements, it is essential to consider the activation of the antagonist, as well as agonist motoneuron pools.

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