Static Ocular Counterroll Is Implemented Through the 3-D Neural Integrator

2003 ◽  
Vol 90 (4) ◽  
pp. 2777-2784 ◽  
Author(s):  
J. Douglas Crawford ◽  
Douglas B. Tweed ◽  
Tutis Vilis
Keyword(s):  
Equilibrium Position ◽  
Neural Mechanism ◽  
Neural Integrator ◽  
Interstitial Nucleus Of Cajal ◽  
Ocular Reflex ◽  
Ocular Counterroll ◽  
Vestibulo Ocular Reflex ◽  
Input Model ◽  
Head Roll ◽  
Static Head

Static head roll about the naso-occipital axis is known to produce an opposite ocular counterroll with a gain of approximately 10%, but the purpose and neural mechanism of this response remain obscure. In theory counterroll could be maintained either by direct tonic vestibular inputs to motoneurons, or by a neurally integrated pulse, as observed in the saccade generator and vestibulo-ocular reflex. When simulated together with ocular drift related to torsional integrator failure, the direct tonic input model predicted that the pattern of drift would shift torsionally as in ordinary counterroll, but the integrated pulse model predicted that the equilibrium position of torsional drift would be unaffected by head roll. This was tested experimentally by measuring ocular counterroll in 2 monkeys after injection of muscimol into the mesencephalic interstitial nucleus of Cajal. Whereas 90° head roll produced a mean ocular counterroll of 8.5° (±0.7° SE) in control experiments, the torsional equilibrium position observed during integrator failure failed to counterroll, showing a torsional shift of only 0.3° (±0.6° SE). This result contradicted the direct tonic input model, but was consistent with models that implement counterroll by a neurally integrated pulse.

Adaptation of the Vestibulo-Ocular Reflex with the Head in Different Orientations and Positions Relative to the Axis of Body Rotation

1993 ◽  
Vol 3 (2) ◽  
pp. 181-195
Author(s):  
Caroline Tiliket ◽  
Mark Shelhamer ◽  
H. Stevie Tan ◽  
David S. Zee
Keyword(s):  
Training Session ◽  
Head Orientation ◽  
Neural Integrator ◽  
Body Rotation ◽  
Ocular Reflex ◽  
Vestibular Adaptation ◽  
Before And After ◽  
Vestibulo Ocular Reflex ◽  
Vor Adaptation ◽  
Static Head

We investigated the influence of static head orientation and position, relative to the axis of body rotation, upon vestibular adaptation. With the head centered, displaced anterior to the axis of body rotation, or tilted 40∘ to 45∘ in roll or pitch, the gain of the vestibulo-ocular reflex (VOR) was trained (to go either up or down) for one hour using artificial manipulation of the visual surround to produce a visual-vestibular mismatch. Before and after each training session, the VOR was measured in darkness with the head in the training as well as in several non-training positions. We found that transfer of VOR adaptation to non-training positions was almost complete when comparing head eccentric versus head-centered rotations. For tilts, however, transfer of VOR learning was far less complete suggesting that static otolith signals provide a strong contextual cue that gates the expression of an adaptive VOR response. Finally, following training to increase than VOR, gain was greater for centripetally than centrifugally directed slow phases. Centripetally directed postsaccadic drift also developed. These fundings imply that the gain increase paradigm also leads to abnormal function of the velocity-to-position neural integrator, which holds eccentric positions of gaze.

Alexander's Law Revisited

2008 ◽  
Vol 100 (1) ◽  
pp. 154-159 ◽  
Author(s):  
Benjamin Jeffcoat ◽  
Alexander Shelukhin ◽  
Alex Fong ◽  
William Mustain ◽  
Wu Zhou
Keyword(s):  
Cold Water ◽  
Warm Water ◽  
Slow Phase ◽  
Neural Integrator ◽  
The Gaze ◽  
Slow Phase Velocity ◽  
Ocular Reflex ◽  
Vestibulo Ocular Reflex ◽  
Alexander’S Law ◽  
Peripheral Inhibition

Alexander's Law states that the slow-phase velocity of the nystagmus caused by unilateral vestibular lesion increases with gaze in the beat direction. Two studies have shown that this gaze effect is generalized to the nystagmus caused by unilateral cold water irrigation. This indicates that the gaze effect is not the result of central changes associated with a peripheral lesion but rather because of unilateral vestibular peripheral inhibition. In this study, we show that there is a similar gaze effect on the nystagmus produced by unilateral warm water ear irrigation. Furthermore, we examined the two hypotheses of Alexander's Law proposed in the two studies. One hypothesis is based on the gaze-dependent modulation of the vestibulo-ocular reflex (VOR) response to unbalanced canal input. The other hypothesis, however, is based on the leaky neural integrator caused by unilateral vestibular peripheral inhibition. These two hypotheses predict the same gaze effect on the nystagmus produced by cold water irrigation, but opposite gaze effects on the nystagmus produced by warm water irrigation. Our results support the first hypothesis and suggest that the second hypothesis needs to be modified.

Effects of Ketamine on Ocular Movements of the Cat

1991 ◽  
Vol 1 (4) ◽  
pp. 325-338
Author(s):  
P. Mettens ◽  
E. Godaux ◽  
G. Cheron
Keyword(s):  
Time Course ◽  
Velocity Storage ◽  
Dependent Manner ◽  
Neural Integrator ◽  
Storage Mechanism ◽  
Ocular Reflex ◽  
Ocular Movements ◽  
Vestibulo Ocular Reflex ◽  
The Given ◽  
Low Dosage

We studied the effects of ketamine, an antagonist of the N-methyl-D-aspartate receptors, on (1) the spontaneous saccades, (2) the vestibulo-ocular reflex (VOR), and (3) the optokinetic nystagmus (OKN) in 8 cats. Ketamine was given intramuscularly at four dosages (1, 2, 8, and 16 mg/kg). Eye movements were measured using the magnetic field-search coil technique. Ketamine did not prevent the occurrence of saccades, but each of them was followed by a centripetal postsaccadic drift. The time-constant of the drift induced by ketamine was 1.0 s when the given dosage was 1 mg/kg and 0.35 s when the given dosage was 16 mg/kg. Post-saccadic drift caused by a low dosage of ketamine may reflect only a mismatch between the pulse and the step commands that create saccades. The highest used dosages of ketamine aggravated the post-saccadic drift probably by disturbing the oculomotor neural integrator. To elicit the horizontal VOR, the head was submitted either to sinusoidal rotations (± 20∘; 0.05 to 1 Hz) or to a rotation at a constant velocity (100∘/s during 40 s). In darkness, the VOR step gain was reduced by ketamine in a dosage-dependent manner. VOR phase lead at 0.10 Hz oscillation in darkness increased from 4.0∘ ± 2.4∘ to 51.6∘ ± 7.5∘ after administration of ketamine at 16 mg/kg. This suggests that ketamine, at least at higher dosages, induces a failure of the neural integrator. Chemical blockade of the vestibular commissure by ketamine may also be responsible for the reduction of the VOR gain. Horizontal OKN was tested using a step stimulus (30∘/s during 40 s). When ketamine was given at 1 mg/kg, the average steady-state gain of the OKN diminished from 0.6 ± 0.2 to 0.3 ± 0.1. After administration of ketamine at 2 mg/kg, the OKN was abolished. The sensitivity of OKN to ketamine is explained at least partly by the fact that ketamine acts against the visual pathways in the retina, in the geniculate nucleus, and in the visual cortex. The time course of the optokinetic afternystagmus (OKAN) and that of the decrease of the perrotatory and postrotatory VOR were not reduced by ketamine administered at 1 or 2 mg/kg. This shows that ketamine does not affect the velocity-storage mechanism at these dosages.

Ocular Counterroll Modulates the Preferred Direction of Saccade-Related Pontine Burst Neurons in the Monkey

2001 ◽  
Vol 86 (2) ◽  
pp. 935-949 ◽  
Author(s):  
Hansjörg Scherberger ◽  
Jan-Harry Cabungcal ◽  
Klaus Hepp ◽  
Yasuo Suzuki ◽  
Dominik Straumann ◽  
...  
Keyword(s):  
Eye Movements ◽  
Reference Frame ◽  
Vertical Plane ◽  
Motor Command ◽  
Velocity Signal ◽  
Burst Neurons ◽  
Preferred Direction ◽  
Ocular Counterroll ◽  
Head Roll ◽  
Static Head

Saccade-related burst neurons in the paramedian pontine reticular formation (PPRF) of the head-restrained monkey provide a phasic velocity signal to extraocular motoneurons for the generation of rapid eye movements. In the superior colliculus (SC), which directly projects to the PPRF, the motor command for conjugate saccades with the head restrained in a roll position is represented in a reference frame in between oculocentric and space-fixed coordinates with a clear bias toward gravity. Here we studied the preferred direction of premotor burst neurons in the PPRF during static head roll to characterize their frame of reference with respect to head and eye position. In 59 neurons (short-lead, burst-tonic, and long-lead burst neurons), we found that the preferred direction of eye displacement of these neurons changed, relative to head-fixed landmarks, in the horizontal-vertical plane during static head roll. For the short-lead burst neurons and the burst-tonic group, the change was about one-fourth of the amount of ocular counterroll (OCR) and significantly different from a head-centered representation. In the long-lead burst neurons, the rotation of the preferred direction showed a larger trend of about one-half of OCR. During microelectrical stimulation of the PPRF (9 sites in 2 monkeys), the elicited eye movements rotated with about one-half the amount of OCR. In a simple pulley model of the oculomotor plant, the noncraniocentric reference frame of the PPRF output neurons could be reproduced for recently measured pulley positions, if the pulleys were assumed to rotate as a function of OCR with a gain of 0.5. We conclude that the saccadic displacement signal is transformed from a representation in the SC with a clear bias to gravity to a representation in the PPRF that is closely craniocentric, but rotates with OCR, consistent with current concepts of the oculomotor plant.

Acquired nystagmus

2020 ◽  
Vol 81 (11) ◽  
pp. 1-8
Author(s):  
Jesse Panthagani ◽  
Jasvir Virdee ◽  
Trystan MacDonald ◽  
Alice Bruynseels ◽  
Ruchika Batra
Keyword(s):  
Visual Target ◽  
Neural Integrator ◽  
The Gaze ◽  
Ocular Reflex ◽  
Surrounding Environment ◽  
Gaze Holding ◽  
Illusory Movement ◽  
Vestibulo Ocular Reflex ◽  
Acquired Nystagmus ◽  
Underlying Pathology

Nystagmus is the repetitive to and fro movement of the eyes, which may be physiological or pathological. The movements can be horizontal, vertical, torsional or a combination of these movements. It starts by a slow movement of the eye away from the visual target. The second movement brings the eye back to the visual target. If this second movement is quick, the nystagmus is called jerk nystagmus. If the second movement is slow, the nystagmus is said to be pendular. Maintaining steady gaze is dependent upon visual fixation, the vestibulo-ocular reflex and the gaze-holding neural integrator system. Pathological nystagmus typically presents with the symptom of oscillopsia, which is the illusory movement of the surrounding environment. Nystagmus that develops outside of early infancy is termed acquired nystagmus. There may be serious underlying pathology that will require further investigation and management. This article reviews the terminology, pathophysiology, causes and treatment of acquired nystagmus.

Adaptation of the phase of the human linear vestibulo-ocular reflex (LVOR) and effects on the oculomotor neural integrator

2000 ◽  
Vol 10 (4-5) ◽  
pp. 239-247
Author(s):  
Stefan Hegemann ◽  
Mark Shelhamer ◽  
Phillip D. Kramer ◽  
David S. Zee
Keyword(s):  
Visual Display ◽  
Phase Changes ◽  
Dark Phase ◽  
Phase Lag ◽  
Neural Integrator ◽  
Ocular Reflex ◽  
Before And After ◽  
Vestibulo Ocular Reflex ◽  
The Subject

The phase of the translational linear VOR (LVOR) can be adaptively modified by exposure to a visual-vestibular mismatch. We extend here our earlier work on LVOR phase adaptation, and discuss the role of the oculomotor neural integrator. Ten subjects were oscillated laterally at 0.5 Hz, 0.3 g peak acceleration, while sitting upright on a linear sled. LVOR was assessed before and after adaptation with subjects tracking the remembered location of a target at 1 m in the dark. Phase and gain were measured by fitting sine waves to the desaccaded eye movements, and comparing sled and eye position. To adapt LVOR phase, the subject viewed a computer-generated stereoscopic visual display, at a virtual distance of 1 m, that moved so as to require either a phase lead or a phase lag of 53 deg. Adaptation lasted 20 min, during which subjects were oscillated at 0.5 Hz/0.3 g. Four of five subjects produced an adaptive change in the lag condition (range 4–45 deg), and each of five produced a change in the lead condition (range 19–56 deg), as requested. Changes in drift on eccentric gaze suggest that the oculomotor velocity-to-position integrator may be involved in the phase changes.

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