Lidocaine-induced unilateral internuclear ophthalmoplegia: effects on convergence and conjugate eye movements

1989 ◽  
Vol 62 (1) ◽  
pp. 82-95 ◽  
Author(s):  
P. D. Gamlin ◽  
J. W. Gnadt ◽  
L. E. Mays
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Open Loop ◽  
Medial Longitudinal Fasciculus ◽  
Slow Phase ◽  
Internuclear Ophthalmoplegia ◽  
Unaffected Side ◽  
Affected Side ◽  
Position Signal ◽  
Slow Drift

1. To characterize the vergence signal carried by the medial longitudinal fasciculus (MLF), it was subjected to reversible blockade by small injections of 10% lidocaine hydrochloride. The effects of these blockades on both conjugate and vergence eye movements were studied. 2. With this procedure, experimentally induced internuclear ophthalmoplegia (INO) and its effects on conjugate eye movements could be studied acutely, without possible contamination from long-term oculomotor adaptation. In the eye contralateral to the MLF blockade, saccadic and horizontal smooth-pursuit eye movements were normal. Horizontal abducting nystagmus, often seen in patients with INO, was not observed in this eye. 3. As previously reported for INO, profound oculomotor deficits were seen in the eye ipsilateral to the MLF blockade. During maximal blockade, adducting saccades and horizontal smooth-pursuit movements in this eye did not cross the midline. Adducting saccades were reduced in amplitude and peak velocity and showed significantly increased durations. Abducting saccades, which were slightly hypometric, displayed a marked postsaccadic centripetal drift. 4. The eye ipsilateral to the blockade displayed a pronounced, upward, slow drift, whereas the eye contralateral to the blockade showed virtually no drift. Furthermore, although vertical saccades to visual targets remained essentially conjugate, the size of the resetting quick phases in each eye was related to the amplitude of the slow phase movement in that eye. Thus the eye on the affected side displayed large quick phases, whereas the eye on the unaffected side showed only slight movements. On occasion, unilateral downbeating nystagmus was seen. This strongly suggests that the vertical saccade generators for the two eyes can act independently. 5. The effect of MLF blockade on the vergence gain of the eye on the affected side was investigated. As a measure of open-loop vergence gain, the relationship of accommodative convergence to accommodation (AC/A) was measured before, during, and after reversible lidocaine block of the MLF. After taking conjugate deficits into account, the net vergence signal to the eye ipsilateral to the injection was found to increase significantly during the reversible blockade. 6. The most parsimonious explanation for this increased vergence signal is suggested by the accompanying single-unit study. This study showed that abducens internuclear neurons, whose axons course in the MLF, provide medial rectus motoneurons with an appropriate horizontal conjugate eye position signal but an inappropriate vergence signal. Ordinarily, this incorrect vergence signal is overcome by another, more potent, v

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.

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.

Central Ocular Motor Disorders: Clinical and Topographic Anatomical Diagnosis, Syndromes and Underlying Diseases

2021 ◽  
Vol 238 (11) ◽  
pp. 1197-1211
Author(s):  
Michael Leo Strupp ◽  
Dominik Straumann ◽  
Christoph Helmchen
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Time Course ◽  
Metabolic Diseases ◽  
Spontaneous Nystagmus ◽  
Medial Longitudinal Fasciculus ◽  
Motor Disorders ◽  
Ocular Motor ◽  
Ocular Motor Disorders ◽  
Underlying Diseases

AbstractThe key to the diagnosis of ocular motor disorders is a systematic clinical examination of the different types of eye movements, including eye position, spontaneous nystagmus, range of eye movements, smooth pursuit, saccades, gaze-holding function, vergence, optokinetic nystagmus, as well as testing of the function of the vestibulo-ocular reflex (VOR) and visual fixation suppression of the VOR. This is like a window which allows you to look into the brain stem and cerebellum even if imaging is normal. Relevant anatomical structures are the midbrain, pons, medulla, cerebellum and rarely the cortex. There is a simple clinical rule: vertical and torsional eye movements are generated in the midbrain, horizontal eye movements in the pons. For example, isolated dysfunction of vertical eye movements is due to a midbrain lesion affecting the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), with impaired vertical saccades only or vertical gaze-evoked nystagmus due to dysfunction of the Interstitial nucleus of Cajal (INC). Lesions of the lateral medulla oblongata (Wallenberg syndrome) lead to typical findings: ocular tilt reaction, central fixation nystagmus and dysmetric saccades. The cerebellum is relevant for almost all types of eye movements; typical pathological findings are saccadic smooth pursuit, gaze-evoked nystagmus or dysmetric saccades. The time course of the development of symptoms and signs is important for the diagnosis of underlying diseases: acute: most likely stroke; subacute: inflammatory diseases, metabolic diseases like thiamine deficiencies; chronic progressive: inherited diseases like Niemann-Pick type C with typically initially vertical and then horizontal saccade palsy or degenerative diseases like progressive supranuclear palsy. Treatment depends on the underlying disease. In this article, we deal with central ocular motor disorders. In a second article, we focus on clinically relevant types of nystagmus such as downbeat, upbeat, fixation pendular, gaze-evoked, infantile or periodic alternating nystagmus. Therefore, these types of nystagmus will not be described here in detail.

Cranial Neuropathies & Brainstem Syndromes

Neuroanatomy ◽  
2017 ◽  
pp. 206-244
Author(s):  
Adam J Fisch
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Facial Palsy ◽  
Internuclear Ophthalmoplegia ◽  
Smooth Pursuit Eye Movements ◽  
Pupillary Reflex ◽  
Pursuit Eye Movements ◽  
Gag Reflex ◽  
Cranial Neuropathies ◽  
Specific Disorders

This chapter addresses the various cranial neuropathies and brainstem syndromes and their respective anatomical components. Included among these disorders are pupillary reflex pathologies, oral-palatal deviations, gag reflex, facial palsy, Bell’s palsy, internuclear ophthalmoplegia, midbrain syndromes, pontine syndromes, and medullary syndromes. Instructions are presented on how to draw the elements of the neuropathies and syndromes, as well as the trigeminal nerve, central pathways, central somatotopic maps, and smooth pursuit eye movements. Finally, case histories of specific disorders are presented along with discussion of the elements involved in making the diagnosis.

Nystagmus

2008 ◽  
Author(s):  
Agnes Wong
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
The Other ◽  
Whipple’S Disease ◽  
Internuclear Ophthalmoplegia ◽  
Optokinetic System ◽  
Gaze Holding ◽  
Slow Eye Movements ◽  
Ocular System ◽  
System 1

Nystagmus is involuntary eye oscillations initiated by slow eye movements that drive the eye away from the target. In contrast, saccadic dyskinesia consists of involuntary, fast eye movements that take the fovea off target. Nystagmus usually arises from lesions in the 1. Vestibulo-ocular system (VOR) 2. Gaze-holding system 3. Smooth pursuit and optokinetic system. 1. Pendular versus jerk ■ Pendular (see A in the figure below): both phases are slow eye movements. ■ Jerk (see B, C, and D in the figure below): one phase consists of fast eye movements (quick phase), and the other consists of slow eye movements. By convention, the direction of nystagmus is named after the direction of quick phases that return the eye to the target. 2. Plane: horizontal, vertical, torsional, or combined form (e.g., rotary, elliptical) 3. Conjugacy ■ Conjugate: Both eyes move in the same direction with similar amplitude and frequency. ■ Disconjugate: Both eyes move in the same direction with different amplitude and frequency (e.g., internuclear ophthalmoplegia). ■ Disjunctive: The eyes move in opposite directions (e.g., oculomasticatory myorhythmia seen in Whipple’s disease).

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)

Effects of Lesions of the Oculomotor Cerebellar Vermis on Eye Movements in Primate: Smooth Pursuit

2000 ◽  
Vol 83 (4) ◽  
pp. 2047-2062 ◽  
Author(s):  
Mineo Takagi ◽  
David S. Zee ◽  
Rafael J. Tamargo
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Dynamic Properties ◽  
Critical Role ◽  
Open Loop ◽  
Cerebellar Vermis ◽  
Peak Acceleration ◽  
Triangular Wave ◽  
Oculomotor Vermis ◽  
Eye Velocity

We studied the effects on smooth pursuit eye movements of ablation of the dorsal cerebellar vermis (lesions centered on lobules VI and VII) in three monkeys in which the cerebellar nuclei were spared. Following the lesion the latencies to pursuit initiation were unchanged. Monkeys showed a small decrease (up to 15%) in gain during triangular-wave tracking. More striking were changes in the dynamic properties of pursuit as determined in the open-loop period (the 1st 100 ms) of smooth tracking. Changes included a decrease in peak eye acceleration (e.g., in one monkey from ∼650°/s2, prelesion to ∼220–380°/s2, postlesion) and a decrease in the velocity at the end of the open-loop period [e.g., in another monkey from a gain (eye velocity/target velocity at 100 ms of tracking) of 0.93, prelesion to 0.53, postlesion]. In individual monkeys, the pattern of deficits in the open-loop period of pursuit was usually comparable to that of saccades, especially when comparing the changes in the acceleration of pursuit to the changes in the velocity of saccades. These findings support the hypothesis that saccades and the open-loop period of pursuit are controlled by the cerebellar vermis in an analogous way. Saccades could be generated by eye velocity commands to bring the eyes to a certain position and pursuit by eye acceleration commands to bring the eyes toward a certain velocity. On the other hand, changes in gain during triangular-wave tracking did not correlate with either the saccade or the open-loop pursuit deficits, implying different contributions of the oculomotor vermis to the open loop and to the sustained portions of pursuit tracking. Finally, in a pursuit adaptation paradigm (×0.5 or ×2, calling for a halving or doubling of eye velocity, respectively) intact animals could adaptively adjust eye acceleration in the open-loop period. The main pattern of change was a decrease in peak acceleration for ×0.5 training and an increase in the duration of peak acceleration for ×2 training. Following the lesion in the oculomotor vermis, this adaptive capability was impaired. In conclusion, as for saccades, the oculomotor vermis plays a critical role both in the immediate on-line and in the short-term adaptive control of pursuit.

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)

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