Gaze Holding and the Neural Integrator

2015 ◽  
pp. 360-385 ◽  
Author(s):  
R. John Leigh ◽  
David S. Zee
Keyword(s):  
Tonic Contraction ◽  
Laboratory Evaluation ◽  
Neural Integrator ◽  
Compensatory Mechanisms ◽  
Interstitial Nucleus Of Cajal ◽  
The Neural Network ◽  
Clinical Disorders ◽  
Gaze Holding ◽  
Prepositus Hypoglossi ◽  
Alexander’S Law

This chapter reviews the neural network that temporally integrates premotor, velocity-coded signals to achieve tonic contraction of the extraocular muscles to hold the eyes at an eccentric position in the orbits. The mechanical properties of the eye and its supporting tissues are quantified and related to the pulse-slide-step neural command for a saccadic change in eye position. The anatomical substrate and neuropharmacology of the neural integrator is reviewed, including nucleus prepositus hypoglossi, interstitial nucleus of Cajal and cerebellum. Mathematical and animal models for the neural integrator are discussed, addressing points about how a leaky or unstable integrator may arise. Clinical and laboratory evaluation of gaze holding is summarized. Effects of experimentally inactivating the neural integrator are compared with clinical disorders affecting gaze holding, including a discussion of the pathogenesis of gaze-evoked nystagmus and Alexander’s law. Compensatory mechanisms for a leaky neural integrator are discussed, including centripetal, rebound, and gaze-evoked nystagmus.

Effect of muscimol microinjections into the prepositus hypoglossi and the medial vestibular nuclei on cat eye movements

1994 ◽  
Vol 72 (2) ◽  
pp. 785-802 ◽  
Author(s):  
P. Mettens ◽  
E. Godaux ◽  
G. Cheron ◽  
H. L. Galiana
Keyword(s):  
Eye Movements ◽  
Transient Analysis ◽  
Medial Vestibular Nucleus ◽  
Neural Integrator ◽  
Vestibular Nystagmus ◽  
Vestibular Input ◽  
Complete Darkness ◽  
Gaze Holding ◽  
Prepositus Hypoglossi ◽  
Rostral Part

1. For horizontal eye movements, previous observations led to the hypothesis that the legendary neural integrator necessary for correct gaze holding, adequate vestibuloocular reflex (VOR), and optokinetic nystagmus, was located in the region of the complex formed by the nucleus prepositus hypoglossi (NPH) and the medial vestibular nucleus (MVN). 2. The aim of the present study was to test the respective contributions of the NPH, of the rostral part of the MVN, which contains most second-order vestibular neurons, and of the central part of the MVN to the horizontal integrator. 3. An injection of muscimol was used to inactivate each of these three zones in the cat's brain. Muscimol is a gamma-aminobutyric acid (GABA) agonist. By binding to GABAA receptors, it induces a hyperpolarization of the neurons that nullifies their activity. Muscimol was injected into the brain stem of the alert cat through a micropipette by an air pressure system. 4. The search coil technique was used to record spontaneous eye movements and the VOR induced by rotating a turntable at a constant velocity. VOR was analyzed by a new method: transient analysis of vestibular nystagmus. 5. A unilateral injection of muscimol into the NPH induced a bilateral gaze-holding failure: saccades were followed by a centripetal postsaccadic drift. A vestibular imbalance was also present but it was moderate and variable. The VOR responses were distorted drastically. Through transient analysis of vestibular nystagmus, that distortion was revealed to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator. The responses to a rotation either toward the injected side or in the opposite direction were asymmetrical. The direction of that asymmetry was variable. 6. A unilateral injection of muscimol into the rostral part of the MVN caused a vestibular imbalance: in complete darkness, a nystagmus appeared, whose linear slow phases were directed toward the side of injection. 7. A unilateral injection of muscimol into the central part of the MVN induced a syndrome where a severe bilateral gaze-holding failure was combined with a vestibular imbalance. In the light, saccades were followed by a bilateral centripetal postsaccadic drift. In complete darkness, a nystagmus was observed, whose curved slow phases were directed towards the side of injection. The VOR responses were distorted drastically. Here again, that distortion was revealed by our analysis to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator.(ABSTRACT TRUNCATED AT 400 WORDS)

Hereditary congenital nystagmus and gaze-holding failure: The role of the neural integrator

Neurology ◽  
1993 ◽  
Vol 43 (9) ◽  
pp. 1741-1741 ◽  
Author(s):  
L. F. Dell'Osso ◽  
B. M. Weissman ◽  
R. J. Leigh ◽  
L. A. Abel ◽  
N. V. Sheth
Keyword(s):  
Congenital Nystagmus ◽  
Neural Integrator ◽  
Gaze Holding

Eye Movement Deficits After Ibotenic Acid Lesions of the Nucleus Prepositus Hypoglossi in Monkeys. I. Saccades and Fixation

1997 ◽  
Vol 78 (4) ◽  
pp. 1753-1768 ◽  
Author(s):  
Chris R. S. Kaneko
Keyword(s):  
Eye Movement ◽  
Rhesus Macaques ◽  
Ibotenic Acid ◽  
Feedback Signal ◽  
Neural Integrator ◽  
Nucleus Prepositus Hypoglossi ◽  
System A ◽  
Classical Models ◽  
Prepositus Hypoglossi ◽  
Made In

Kaneko, Chris R. S. Eye movement deficits after ibotenic acid lesions of the nucleus prepositus hypoglossi in monkeys. I. Saccades and fixation. J. Neurophysiol. 78: 1753–1768, 1997. It has been suggested that the function of the nucleus prepositus hypoglossi (nph) is the mathematical integration of velocity-coded signals to produce position-coded commands that drive abducens motoneurons and generate horizontal eye movements. In early models of the saccadic system, a single integrator provided not only the signal that maintained steady gaze after a saccade but also an efference copy of eye position, which provided a feedback signal to control the dynamics of the saccade. In this study, permanent, serial ibotenic acid lesions were made in the nph of three rhesus macaques, and their effects were studied while the alert monkeys performed a visual tracking task. Localized damage to the nph was confirmed in both Nissl and immunohistochemically stained material. The lesions clearly were correlated with long-lasting deficits in eye movement. The animals' ability to fixate in the dark was compromised quickly and uniformly so that saccades to peripheral locations were followed by postsaccadic centripetal drift. The time constant of the drift decreased to approximately one-tenth of its normal values but remained 10 times longer than that attributable to the mechanics of the eye. In contrast, saccades were affected minimally. The results are more consistent with models of the neural saccade generator that use separate feedback and position integrators than with the classical models, which use a single multipurpose element. Likewise, the data contradict models that rely on feedback from the nph. In addition, they show that the oculomotor neural integrator is not a single neural entity but is most likely distributed among a number of nuclei.

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.

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.

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.

Discharge Dynamics of Oculomotor Neural Integrator Neurons During Conjugate and Disjunctive Saccades and Fixation

2003 ◽  
Vol 90 (2) ◽  
pp. 739-754 ◽  
Author(s):  
Pierre A. Sylvestre ◽  
Julia T. L. Choi ◽  
Kathleen E. Cullen
Keyword(s):  
Eye Movements ◽  
Vestibular Nucleus ◽  
Vestibular Nuclei ◽  
Medial Vestibular Nucleus ◽  
Eye Position ◽  
Neural Integrator ◽  
Abducens Nucleus ◽  
Nucleus Prepositus Hypoglossi ◽  
Prepositus Hypoglossi ◽  
Eye Velocity

Burst-tonic (BT) neurons in the prepositus hypoglossi and adjacent medial vestibular nuclei are important elements of the neural integrator for horizontal eye movements. While the metrics of their discharges have been studied during conjugate saccades (where the eyes rotate with similar dynamics), their role during disjunctive saccades (where the eyes rotate with markedly different dynamics to account for differences in depths between saccadic targets) remains completely unexplored. In this report, we provide the first detailed quantification of the discharge dynamics of BT neurons during conjugate saccades, disjunctive saccades, and disjunctive fixation. We show that these neurons carry both significant eye position and eye velocity-related signals during conjugate saccades as well as smaller, yet important, “slide” and eye acceleration terms. Further, we demonstrate that a majority of BT neurons, during disjunctive fixation and disjunctive saccades, preferentially encode the position and the velocity of a single eye; only few BT neurons equally encode the movements of both eyes (i.e., have conjugate sensitivities). We argue that BT neurons in the nucleus prepositus hypoglossi/medial vestibular nucleus play an important role in the generation of unequal eye movements during disjunctive saccades, and carry appropriate information to shape the saccadic discharges of the abducens nucleus neurons to which they project.

Numbness matters: A clinical review of trigeminal neuropathy

Cephalalgia ◽  
2011 ◽  
Vol 31 (10) ◽  
pp. 1131-1144 ◽  
Author(s):  
Jonathan H Smith ◽  
F Michael Cutrer
Keyword(s):  
Sensory Neurons ◽  
Facial Pain ◽  
Laboratory Evaluation ◽  
Trigeminal Neuropathy ◽  
First Order ◽  
Clinical Disorders ◽  
Secondary Pathology ◽  
Periodic Evaluation ◽  
Trigeminal Nerves ◽  
Management Issues

Aim: Trigeminal neuropathies are a group of clinical disorders that involve injury to primary first-order neurons within the trigeminal nerve. We review the spectrum of etiologies underlying both painful and non-painful trigeminal neuropathies, with attention to particularly dangerous processes that may elude the clinician in the absence of a meticulous evaluation. Complications and management issues specific to patients with trigeminal neuropathy are discussed. Methods: Retrospective literature review. Results: Facial or intraoral numbness, the hallmark of trigeminal neuropathy, may represent the earliest symptomology of malignancy or autoimmune connective tissue disease as sensory neurons are destroyed. Such numbness, especially if progressive, necessitates periodic evaluation and vigilance even years after presentation if no diagnosis can be made. Conclusions: In the routine evaluation of patients with facial pain, the clinician will inevitably be confronted with secondary pathology of the trigeminal nerves and nuclei. The appearance of numbness, even when pain continues to be the most pressing complaint, necessitates clinical assessment of the integrity of all aspects of the trigeminal pathways, which may also include neurophysiologic, radiographic, and laboratory evaluation.

Alexander's Law and the Oculomotor Neural Integrator: Three-Dimensional Eye Velocity in Patients With an Acute Vestibular Asymmetry

2008 ◽  
Vol 100 (6) ◽  
pp. 3105-3116 ◽  
Author(s):  
Christopher J. Bockisch ◽  
Stefan Hegemann
Keyword(s):  
Order Term ◽  
Second Order ◽  
Slow Phase ◽  
Vertical Position ◽  
Horizontal Position ◽  
Neural Integrator ◽  
Fast Phase ◽  
Alexander’S Law ◽  
Phase Direction ◽  
Vestibular Asymmetry

According to Alexander's law (AL), the slow phase velocity of nystagmus of vestibular origin is dependent on horizontal position, with lower velocity when gaze is directed in the slow compared with the fast phase direction. Adaptive changes in the velocity-to-position neural integrator are thought to cause AL. Although these changes have been described for the horizontal neural integrator, nystagmus often includes vertical and torsional components, but the adaptive abilities of the vertical and torsional integrators have not been investigated. We measured 11 patients with a peripheral vestibular asymmetry and used second-order equations to describe how velocity varied with position. Horizontal velocity changed with horizontal position in accordance with AL and the second-order term for horizontal position was also significant. Whereas velocity decreased in the slow phase direction, it was relatively unchanged >10° into the fast phase direction. Vertical velocity was also highest in the vertical fast phase direction and the second-order term for vertical position was also significant, in that vertical velocity increased in the vertical fast phase direction, but was unchanging in the slow phase direction. Torsional velocity varied linearly with horizontal, but not vertical, position. These results show that the horizontal and vertical oculomotor neural integrators react to altered vestibular input by maintaining different integrating time constants depending on gaze direction.

scholarly journals A Unifying Model-Based Hypothesis for the Diverse Waveforms of Infantile Nystagmus Syndrome

2011 ◽  
Vol 4 (1) ◽  
Author(s):  
Zhong I. Wang ◽  
Louis F. Dell'Osso
Keyword(s):  
Slow Phase ◽  
Neural Integrator ◽  
Ocular Motor ◽  
The Gaze ◽  
Infantile Nystagmus Syndrome ◽  
Infantile Nystagmus ◽  
Pursuit System ◽  
Alexander’S Law ◽  
Ocular Motor System ◽  
Braking Saccades

We expanded the original behavioral Ocular Motor System (OMS) model for Infantile Nystagmus Syndrome (INS) by incorporating common types of jerk waveforms within a unifying mechanism. Alexander’s law relationships were used to produce desired INS null positions and sharpness. At various gaze angles, these relationships influenced the IN slow-phase amplitudes differently, thereby mimicking the gaze-angle effects of INS patients. Transitions from pseudopendular with foveating saccades to jerk waveforms required replacing braking saccades with foveating fast phases and adding a resettable neural integrator in the pursuit pre-motor circuitry. The robust simulations of accurate OMS behavior in the presence of diverse INS waveforms demonstrate that they can all be generated by a loss of pursuit-system damping, supporting this hypothetical origin.

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