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Sensory factors are insufficient to define the ocular saccade goal in complex visual fields.

In most normal visual search situations, the environment is filled with a variety of stimuli, and selection among possible saccade targets is necessary. Current theories of visuomotor mechanisms must take into account not only the classical 'retinal error' input signal, but also perceptual and decisional factors as well as task-specific strategies adopted by the subjects. Experiments are reported in which eye movements are recorded in tasks requiring ocular saccades to be made onto target letters indicated by a peripherally visible mark or embedded within lines of homogeneous background letters. The results show how nonsensory factors interact with visual determinants in the preparation of the exploratory saccades. Expectations concerning the visibility of the sought-for target influence the spatial and temporal parameters of the eye movement which will be executed.

Attention↗

Ptosis and supranuclear downgaze paralysis.

A patient developed the unusual combination of a supranuclear downward gaze paralysis and bilateral ptosis. It was caused by a single midbrain glioma. Other ocular motor functions were intact. The neuropathologic examination showed a tumor growing mainly around the third ventricle and the aqueduct. The findings agree with recent experimental evidence that a network of neural elements involved in eyelid control lies in the supraoculomotor area immediately dorsal to the oculomotor nucleus.

Aged↗

Abnormal ocular head postures: Part III.

All patients exhibiting the various types of abnormal head postures of ocular origin that were seen during the last two years are presented in order to determine the relative frequency of the different causes of these postures, and the purposes they serve. The treatment modality and results are also discussed. The manuscript is divided into four parts: Parts I, II, and III concern head postures in incomitant strabismus. In Part IV, head postures in Ciancia's syndrome, restrictions, and refractive errors are described.

Fixation, Ocular↗

[Problems on expert classification in cases of traumatic disturbances of ocular motility (author's transl)].

The classification of reduction in ability to earn a livelihood in cases of traumatical disturbances of ocular motility is still mainly based on antiquated values which no longer do justice to the real sensomotor situations. Today new diagnostic methods, most of them developed by Cüppers, give a better and more certain base as to the objectivation of the disturbances and the subjective troubles of the subjet. Moreover, new operative indications and techniques can cure them. Four cases are demonstrated as examples for an equivalent and adequate classification.

Accidents, Traffic↗

Volitional control of anticipatory ocular smooth pursuit after viewing, but not pursuing, a moving target: evidence for a re-afferent velocity store.

Although human subjects cannot normally initiate smooth eye movements in the absence of a moving target, previous experiments have established that such movements can be evoked if the subject is required to pursue a regularly repeated, transient target motion stimulus. We sought to determine whether active pursuit was necessary to evoke such an anticipatory response or whether it could be induced after merely viewing the target motion. Subjects were presented with a succession of ramp target motion stimuli of identical velocity and alternating direction in the horizontal axis. In initial experiments, the target was exposed for only 120 ms as it passed through centre, with a constant interval between presentations. Ramp velocity was varied from +/- 9 to 45 degrees/s in one set of trials; the interval between ramp presentations was varied from 640 to 1920 ms in another. Subjects were instructed either to pursue the moving target from the first presentation or to hold fixation on another, stationary target during the first one, two or three presentations of the moving display. Without fixation, the first smooth movement was initiated with a mean latency of 95 ms after target onset, but with repeated presentations anticipatory smooth movements started to build up before target onset. In contrast, when the subjects fixated the stationary target for three presentations of the moving target, the first movement they made was already anticipatory and had a peak velocity that was significantly greater than that of the first response without prior fixation. The conditions of experiment 1 were repeated in experiment 3 with a longer duration of target exposure (480 ms), to allow higher eye velocities to build up. Again, after three prior fixations, the anticipatory velocity measured at 100 ms after target onset (when visual feedback would be expected to start) was not significantly different to that evoked after the subjects had made three active pursuit responses to the same target motion, reaching a mean of 20 degrees/s for a 50 degrees/s target movement. In a further experiment, we determined whether subjects could use stored information from prior active pursuit to generate anticipatory pursuit in darkness if there was a high expectancy that the target would reappear with identical velocity. Subjects made one predictive response immediately after target disappearance, but very little response thereafter until the time at which they expected the target to reappear, when they were again able to re-vitalize the anticipatory response before target appearance. The findings of these experiments provide evidence that information related to target velocity can be stored and used to generate future anticipatory responses even in the absence of eye movement. This suggests that information for storage is probably derived from a common pre-motor drive signal that is inhibited during fixation, rather than an efference copy of eye movement itself. Furthermore, a high level of expectancy of target appearance can facilitate the release of this stored information in darkness.

Afferent Pathways↗

Neuropharmacologic aspects of the ocular motor system and the treatment of abnormal eye movements.

Neuropharmacology is aiding our understanding of the control of eye movements in at least three ways. First, neurotransmitters have been identified in the pathways that coordinate gaze. Second, the technique of pharmacologic inactivation has provided a powerful method to determine the contributions of populations of neurons to specific behaviors, such as steady gaze holding. Finally, the results of basic neuropharmacologic studies have been used to identify candidate drugs for therapeutic trials of abnormal eye movements.

Abducens Nerve↗

A non-linear model for visual-vestibular interaction during body rotation in man.

A mathematical model for visual-vestibular interaction during body rotation in an illuminated visual surround is obtained by combining a previous model of the optokinetic reflex (OKR) with a simplified model of the vestibulo-ocular reflex (VOR). OKR is activated by the slip of the image of the external world on the retina, and represents a negative feedback loop around VOR. For large retinal slip velocities OKR behaves as a basically non-linear system. The validity of the model is proved via computer simulation by comparing predicted responses with the experimental results obtained in man by Koenig et al. (1978) in different situations of visual-vestibular interaction.

Eye Movements↗

Eye-head coordination in labyrinthine-defective humans.

Eye-head coordination during saccadic gaze shifts normally relies on vestibular information. A vestibulo-saccadic reflex (VSR) is thought to reduce the eye-in-head saccade to account for current head movement, and the vestibulo-ocular reflex (VOR) stabilizes postsaccadic gaze while the head movement is still going on. Acute bilateral loss of vestibular function is known to cause overshoot of gaze saccades and postsaccadic instability. We asked how patients suffering from chronic vestibular loss adapt to this situation. Eye and head movements were recorded from six patients and six normal control subjects. Subjects tracked a random sequence of horizontal target steps, with their heads (1) fixed in primary position, (2) free to move, or (3) preadjusted to different head-to-target offsets (to provoke head movements of different amplitudes). Patients made later and smaller head movements than normals and accepted correspondingly larger eye eccentricities. Targeting accuracy, in terms of the mean of the signed gaze error, was better in patients than in normals. However, unlike in normals, the errors of patients exhibited a large scatter and included many overshoots. These overshoots cannot be attributed to the loss of VSR because they also occurred when the head was not moving and were diminished when large head movements were provoked. Patients' postsaccadic stability was, on average, almost as good as that of normals, but the individual responses again showed a large scatter. Also, there were many cases of inappropriate postsaccadic slow eye movements, e.g., in the absence of concurrent head movements, and correction saccades, e.g., although gaze was already on target. Performance in patients was affected only marginally when large head movements were provoked. Except for the larger lag of the head upon the eye, the temporal coupling of eye and head movements in patients was similar to that in normals. Our findings show that patients with chronic vestibular loss regain the ability to make functionally appropriate gaze saccades. We assume, in line with previous work, three main compensatory mechanisms: a head movement efference copy, an active cervico-ocular reflex (COR), and a preprogrammed backsliding of the eyes. However, the large trial-to-trial variability of targeting accuracy and postsaccadic stability indicates that the saccadic gaze system of patients does not regain the high precision that is observed in normals and which appears to require a vestibular head-in-space signal. Moreover, this variability also permeates their gaze performance in the absence of head movements.

Adaptation, Physiological↗

Amplitude of human head movements associated with horizontal saccades.

Human saccades may or may not be associated with head movements. To date, little attention has been devoted to the mechanisms determining head movement recruitment and scaling. Normal human subjects made horizontal, centrifugal saccades along an encircling array of light-emitting diodes. Measurements of gaze, head, and eye-in-head angle were made at the conclusion of the head movement (or at the end of the eye movement in eye-only saccades). We found that head movement amplitude (deltaH) related in a simple fashion to the eye eccentricity that would have resulted if the gaze shift had been performed without a head movement. Plots of deltaH vs this predicted eye eccentricity (E(PRED)) had a central flat region in which gaze shifts were unaccompanied by head movements (the eye-only range) and two flanking lobes in which deltaH was a linear function of E(PRED) (the eye-head ranges). DeltaH correlated with EPRED better than with gaze shift amplitude, as would be expected if head movements were controlled so as to keep eye eccentricity within a particular range. Head movement tendencies were quantified by the width of the eye-only range, the slope of the eye-head range, and the width of the region within which the eye was likely to be found at the conclusion of the completed gaze-shifting behavior (the customary ocular motor range). The measures ranged widely in these normal subjects: 35.8+/-31.9 degrees for the eye-only range (mean+/-SD), 0.77+/-0.16 for the slope of the eye-head range, and 44.0+/-23.8 degrees for the customary ocular motor range. Yet for a given subject, the measurements were reproducible across experimental sessions, with the customary ocular motor range being the most consistent measure of the three. The form of the deltaH vs E(PRED) plots suggests that the neural circuitry underlying eye-head coordination carries out two distinct functions--gating the head movement and scaling the head movement. The reason for the large intersubject variability of head movement tendencies is unknown. It does not parallel intersubject differences in full-scale eye (in orbit) range or full-scale neck range.

Adult↗

Torsional optokinetic nystagmus after unilateral vestibular loss: asymmetry and compensation.

The aim of this study was to analyse torsional optokinetic nystagmus (tOKN) in 17 patients with Menière's disease before and after (1 week, 1 month and 3 months) a curative unilateral vestibular neurotomy (UVN). The tOKN was investigated during optokinetic stimulations around the line of sight directed towards either the lesioned or the healthy side, at various constant angular velocities. Dynamic properties of tOKN and static ocular cyclotorsion were analysed using videonystagmography. Patients' performances were compared with those of 10 healthy subjects. The results indicate that, in the acute stage after UVN, patients exhibited drastic impairment of tOKN velocity that depended on the direction of stimulation: tOKN velocity increased for ipsilesional stimulations and decreased for contralesional stimulations. These changes were responsible for a dramatic tOKN asymmetry, with ipsilesional directional preponderance of torsional slow-phase eye velocity. The changes were associated with static ocular cyclotorsion towards the operated side. Despite progressive compensation of tOKN deficits over time, tOKN velocity still differed from that recorded preoperatively, and tOKN asymmetry remained uncompensated 3 months after UVN. A static ocular cyclotorsion remained up to 3 months after lesion. These results are the first description of tOKN deficits and recovery after unilateral vestibular loss. They show that vestibular cues contribute to gaze stabilization during optokinetic stimulation around the line of sight. They also strongly suggest that tOKN impairment could be part of the long-term asymmetrical functions reported after unilateral loss of vestibular functions.

Adult↗

Paroxysmal tonic upgaze: a reappraisal of outcome.

Paroxysmal tonic upgaze (PTU) of childhood is a distinctive neuro-ophthalmological syndrome of unknown etiology and pathogenesis that is characterized by episodes of sustained upward deviation of the eyes, often with incomplete downward saccades on attempted downgaze. It is generally regarded as having a benign outcome. We observed 16 children with PTU, from 10 months to 11 years from onset (mean, 5.4 years), to study the natural history and possible etiology. Five cases were from two unrelated families. Onset of PTU occurred either during or after an intercurrent infection or vaccination in 5 children. No antecedent was identifiable in the rest. PTU had completely resolved in 10 children (62%) (mean age at offset, 2.5 years), whereas 2 children intermittently manifest a modified form of the disorder. At follow-up, 11 children (69%) had developmental delay, intellectual disability, or language delay and 9 (56%) had ocular motility problems other than PTU. Only 3 children (19%) had normal development and neurological findings. PTU is a heterogeneous syndrome with respect to associations and outcome and may simply be an age-dependent manifestation of a variety of disorders affecting corticomesencephalic control of vertical eye movement. This disorder may be an early sign of more widespread neurological dysfunction.

Adolescent↗

Video recording system for the measurement of eyelid movements during classical conditioning of the eyeblink response in the rabbit.

Classical conditioning of the eyeblink response in the rabbit is a popular model for studying the neural substrates of associative learning. Most of the common eyeblink recording techniques require invasive procedures. To perform experiments in intact animals, a non-invasive, high-speed video recording system was developed to measure eyeblink responses of rabbits during classical conditioning experiments. Besides being non-invasive, this method does not require excessive restraint of the animal. The PC-based system combines a Pulnix video camera with National Instruments video capture and timing hardware to control the experiment and acquire images of the peri-ocular region. The software developed for controlling these experiments also detects the eyeblink by measuring the movement of the upper and lower eyelids, the area of the exposed surface of the eye, and head movements in the sagittal plane. The time resolution of this relatively inexpensive system is 8.33 ms, and at a working distance of 0.8 m, it can detect movements as small as 0.11 mm.

Animals↗

Effects of the vestibular system on human development, Part I. Overview of functions and effects of stimulation.

Studies concerned with the effects of vestibular stimulation on human development and function are reviewed and some implications for therapy are suggested in this paper. Studies are included that relate to changes in the vestibulo-ocular reflex with age, effects of vestibular stimulation on smiling, crying, general activity, and visual attentiveness of infants; and studies that show that typical sequelae to vestibular stimulation are reduced following long-term stimulation. The importance of reviews of the literature and transference of research results to therapeutic use are stressed, with the implication that vestibular-based therapy will improve as occupational therapists become more aware of related research.

Adolescent↗

Temporal influences on retinal correspondence: ocular motor findings in paradoxical spatial projection.

BACKGROUND: Paradoxical diplopia is a condition in which objective eye position contradicts subjective localization in visual space. The term "paradoxical" is usually reserved for instances when known sensory adaptations cannot explain the contradiction. The development of this condition begins with infantile or childhood strabismus, followed by the development of a common sensory adaptation, anomalous retinal correspondence (ARC). ARC causes a reduction in the subjective angle of strabismus compared with the objective angle, and in its completed form the subjective angle decreases to zero. There is no "adaptive" mechanism that would increase the subjective angle such that it would be greater than the objective. In cases of treatment by corrective surgery, the anatomically based motor correction leads to a contradiction between eye position and binocular perception. In this event, the objective angle is less than the subjective, and the result is a paradoxical perception. We encountered a 25-year-old woman who experiences paradoxical localization on cover testing in the absence of a manifest strabismus and with no previous surgical intervention. METHODS: Using a magnetic search coil technique, we evaluated eye movements during fixation, smooth pursuit, saccades, and during cover test conditions to determine how these eye movements correlated to the subjective perception in space. RESULTS: Although smooth pursuit and saccades were normal, there were two elements during cover test that could explain the paradoxical projection. One was the phenomenon that during the cover test the paradoxical projection appeared only when the eye was covered for >4 s. The second was that there was a regression from the full exophoria position toward the midline while the eye was under cover that correlated with a possible paradoxical projection situation. DISCUSSION: ARC, usually associated with a beneficial sensorimotor adaptation, can express itself as a detrimental sensorimotor manifestation. Paradoxical perception also can exist without previous surgical intervention and without the influence of prisms and instrumentation such as the synoptophore. Further studies are indicated to explore the sensorimotor feedback mechanism between eye position and spatial perception.

Adult↗

Nonvisual eye position control in a patient with ocular lateropulsion.

For elucidating the nonvisual eye position control system, we studied the accuracy of saccades toward the remembered position (memory-guided saccades) in a patient with ocular lateropulsion having tonic bias of the eye position. Although the saccadic dysmetria caused by ocular lateropulsion was recorded during memory-guided saccades in the same manner as visually guided saccades, the eyes reached precisely the intended position by corrective saccades. The mean latency of corrective saccades was significantly longer than that of corrective saccades observed for visually guided saccades. This long latency of corrective saccades supports the assumption that feedback information of the eye position is a signal generated by orbital afferents rather than a copy of the motor command.

Eye Movements↗

Abnormal ocular head postures: Part IV.

All patients exhibiting the various types of abnormal head postures of ocular origin that were seen during the last two years are presented in order to determine the relative frequency of the different causes of these postures, and the purposes they serve. The treatment modality and results are also discussed. This manuscript is divided into four parts: Parts I, II, and III concern head postures in incomitant strabismus. In Part IV, head postures in Ciancia's syndrome, restrictions, and refractive errors are described.

Adolescent↗

Smooth pursuit eye movements and otolith-ocular responses are differently impaired in cerebellar ataxia.

Horizontal and vertical smooth pursuit was compared with otolith-ocular responses in 11 patients with cerebellar ataxia and 21 normal subjects using three-dimensional magnetic search coil eye movement recordings. Otolith-ocular responses were investigated during off-vertical axis rotation. This stimulus induces nystagmus consisting of the exponentially decaying canalicular response, and an eye-velocity modulation and offset which arise from the excitation of the otoliths by the gravity vector, which lasts as long as the rotation continues. Otolith-ocular reflexes are intimately interrelated with visual tracking when real targets are viewed during linear motion. The responses of both the translational vestibulo-ocular reflex and the pursuit system have been shown to be linearly dependent on the inverse of the viewing distance, so that a common central pathway for the two systems has been suggested, probably travelling through the cerebellum. Thus, the aim of the study was to evaluate to what extent these reflexes are disturbed in cerebellar disease. The results confirm the earlier notion that in normal subjects pursuit performance is better for horizontal than for vertical tracking, and that it is better for upward than for downward tracking. This pattern is also found in patients. In addition, smooth pursuit performance is clearly degraded in patients, but the modulation of eye-velocity during off-vertical axis rotation is enhanced. Since the amount of this enhancement does not correlate with the amount of pursuit impairment, degradation of smooth pursuit and pathological enhancement of otolith-ocular responses seem to be independent effects of cerebellar degeneration. Thus, the increase in the otolith-ocular response in patients cannot be attributed to adaptational mechanisms trying to overcome the smooth pursuit deficiency; it is more likely to represent pathological disinhibition of otolith derived responses. The absence of compensatory eye-velocity offset during off-vertical axis rotation may reflect the fact that in patients the otolith signals are not utilized in computations thought to be important for spatial orientation mechanisms arising from the interaction of vestibular, visual and somatosensory signals.

Adult↗

Caloric stimulation and unilateral visual neglect.

We studied performance on tests of visual neglect and left lateral gaze after caloric stimulation in 18 patients with left-sided visual neglect after strokes. Except for one patient with absent vestibulo-ocular responses, all improved during caloric stimulation on the left by cold (LC) or on the right by warm water (RW). Improvement seemed to depend on the facilitation of left lateral gaze and on past-pointing to the left. During LC and RW caloric stimulation, patients worked from left to right instead of their usual right to left. Caloric stimulation may be of use in training patients with hemispatial neglect to orient toward the affected hemispatial field.

Adult↗