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PubMed2006

Development of saccadic suppression in children.

We measured saccadic suppression in adolescent children and young adults using spatially curtailed low spatial frequency stimuli. For both groups, sensitivity for color-modulated stimuli was unchanged during saccades. Sensitivity for luminance-modulated stimuli was greatly reduced during saccades in both groups but far more for adolescents than for young adults. Adults' suppression was on average a factor of about 3, whereas that for the adolescent group was closer to a factor of 10. The specificity of the suppression to luminance-modulated stimuli excludes generic explanations such as task difficulty and attention. We suggest that the enhanced suppression in adolescents results from the immaturity of the ocular-motor system at that age.

Adolescent↗
PubMed1977

Deep ocular socket reconstruction.

A technique to reconstruct totally contracted sockets forms spacious, deep ocular fornices to accommodate ocular prostheses. Fixation of the midperiphery of mucous-membrane-lined, custommade conformers to the superior and inferior orbital rims secures the posterior periphery of the conformer deep in the orbit. The method restores the normal anatomy of the ocular fornices that not only extends to the orbital rims but also penetrates deeply into the orbit along its roof and floor. The procedure contrasts with conventional, frequently unsuccessful methods of socket reconstruction that form fornices only to the superior and inferior orbital rims without extending posteriorly into the orbit. Using this technique, we reconstructed deep, spacious sockets in five patients with serious socket contracture, allowing the patients to retain cosmetically acceptable artificial eyes. The principles advocated apply to all contracted sockets.

Adolescent↗
PubMed1991

[Rebound nystagmus in normal subjects].

Rebound nystagmus represents a disorder of ocular movement in patients with cerebellar lesions. It was reported, however, that it occurred in normal subjects in darkness. Jerk nystagmus, amplitude of 0.5-2 deg and frequency of less than 2Hz, was evoked after prolonged eccentric fixation and fatigue within about 5 to 15 seconds in 7 normal subjects of the experiment. The nystagmus increased depending on the eccentricity and duration of gaze holding. It also depended on the orbital position 10deg left, 0 deg, 10 deg right after eccentric gaze. It is suggested that rebound nystagmus resulted from the leaky neural integrator of the brainstem, and a shift of the null position in the direction of the eccentric gaze. These two components may cause different types of nystagmus by various combinations.

Adult↗
PubMed1981

Nystagmus, gaze shift, and self-motion perception during sinusoidal head and neck rotation.

Report on eye movements and perceived horizontal head rotation in 26 healthy students during sinusoidal vestibular, visual, cervical, congruent vestibular-plus-visual, or vestibular-plus-cervical stimulation. Circularvection occurred more often during neck afferent than during full-field optokinetic stimuli. In contrast, the cervico-ocular response had a low average velocity. As first noted by Frenzel (1928), a greater gaze shift distinguished the normal cervical from the normal labyrinthine response. The cervico-ocular and vestibulo-ocular responses were found to add up. Clinically, the results imply that ocular movements may be a poor measure of dizziness in cervical syndromes.

Adult↗
PubMed1974

Strabismus.

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Accommodation, Ocular↗
PubMed2005

The origin of downbeat nystagmus: an asymmetry in the distribution of on-directions of vertical gaze-velocity Purkinje cells.

Various hypotheses on the origin of cerebellar downbeat nystagmus (DBN) have been presented; the exact pathomechanism, however, is still not known. Based on previous anatomical and electrophysiological studies, we propose that an asymmetry in the distribution of on-directions of vertical gaze-velocity Purkinje cells leads to spontaneous upward ocular drift in cerebellar disease, and therefore, to DBN. Our hypothesis is supported by a computational model for vertical eye movements.

Fixation, Ocular↗
PubMed1971

Strabismus.

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Accommodation, Ocular↗
PubMed1987

Abnormal ocular motor function predicts clinical diagnosis of familial ataxia.

Ocular motor performance was significantly impaired in familial ataxia patients as compared with normal controls. Ataxic patients showed prolonged saccadic latencies, longer saccadic refixation times, reduced visual tracking performance, and increased hypermetria. Cutoff values were derived and applied to 15 subjects at risk for developing familial ataxia. Three of 15 showed abnormal values in three or more of four categories of ocular motor performance. Within 3 years, all three subjects were diagnosed on clinical grounds as having familial ataxia. We conclude that ocular motor performance is impaired in familial ataxia and may prove useful for earlier diagnosis.

Eye Movements↗
PubMed1979

Relation between perceived depth and perceived motion in uniform flow fields.

Three experiments are reported that examined the nature of the perceptual linkage between perceived depth and perceived motion in bidirectional uniform velocity fields. In such displays there is systematic misperception of both the speeds and directions of motion of visual objects. It was found that the speed and the direction of perceived motion were related to objective velocity by the addition of a uniform velocity component across the visual field. It is proposed that this uniform component may be the result of compensation for incorrectly registered ocular rotation and that such an account may also apply to classical center-surround induced motion effects.

Depth Perception↗
PubMed1988

Effects of visual and non-visual mechanisms on the vestibulo-ocular reflex during pseudo-random head movements in man.

1. The behaviour of the vestibulo-ocular reflex (VOR) in man was examined using pseudo-random and sinusoidal whole-body angular-motion stimuli applied about the yaw axis by a servo-controlled turn-table. 2. The VOR response was assessed in four conditions; during fixation on a head-fixed target (HFT); during attempted fixation in the dark of an imagined head-fixed (IHFT) or earth-fixed target (IEFT) and in darkness (DRK) whilst performing an auditory discrimination task. 3. When the pseudo-random stimulus was composed of four sinusoids, the three lowest frequencies (0.11, 0.24 and 0.37 Hz) were maintained constant whilst the highest frequency (F4) was varied from 0.39 to 2.08 Hz. In darkness (DRK condition) and when imagining a head-fixed target (IHFT condition) the gain of slow-phase eye velocity was not significantly affected by the frequency of the highest-frequency component, although there were significant changes in the phase for the IHFT condition. 4. During fixation of a real head-fixed target (HFT condition), both the gain and phase of eye velocity were significantly modified by the frequency (F4) of the highest-frequency component. When F4 was 0.39 Hz, all frequency components had a low gain (mean 0.05), but as F4 was increased there was a significant (P less than 0.001) increase in gain for all three low-frequency components which reached a maximum (mean 0.17) when F4 was 2.08 Hz. However, the gain for the highest frequency component always remained comparable to that obtained in response to a single discrete sinusoid of the same frequency. 5. When the stimulus was composed of only two sinusoids a similar increase in gain of the lower-frequency (0.22 Hz) component was observed in the head-fixed target condition as the frequency of the higher-frequency component was increased from 0.39 to 2.78 Hz. However, VOR gain was not significantly modified by the frequency of the higher-frequency component when subjects imagined a head-fixed or earth-fixed target in darkness. 6. The findings indicate that high levels of VOR suppression can be achieved in the head-fixed target condition with pseudo-random stimuli when all frequency components are below 0.4 Hz. But if the highest-frequency component rises above 0.8 Hz, optimum suppression is confined to the highest-frequency component, whilst suppression of the low-frequency components is significantly reduced.(ABSTRACT TRUNCATED AT 400 WORDS)

Darkness↗
PubMed2004

Specificity of "peering at the tip of the nose" for a diagnosis of thalamic hemorrhage.

BACKGROUND: Tonic inward and downward deviation of the eyes ("peering at the tip of the nose") is regarded as a unique feature of thalamic hemorrhage, but the mechanisms of this ocular finding remain obscure. OBJECTIVES: To describe 4 patients who showed tonic inward and downward deviation of the eyes from brainstem or thalamic lesions and to discuss the possible mechanisms involved. DESIGN: Case report. SETTING: Secondary and tertiary referral hospitals. RESULTS: One patient developed alternating esotropia with downward ocular deviation from thalamic hemorrhage compressing the midbrain. Two patients showed multiple infarctions in the territory of the posterior circulation with or without the involvement of the thalamus. Another patient had lateral pontine hemorrhage extending up to the midbrain tegmentum. Ocular bobbing preceded or accompanied tonic ocular deviation in 3 patients. CONCLUSIONS: Tonic inward and downward deviation of the eyes may develop in thalamic or brainstem lesions. Irritation or destruction of the neural structures involved in the vergence and vertical gaze may cause this ocular sign in mesodiencephalic lesions. Skew deviation and esotropia from abduction deficit may be involved in some patients. Ocular bobbing and tonic downward deviation may share a common pathogenesis.

Aged↗
PubMed2005

Saccade-contingent spatial and temporal errors are absent for saccadic head movements.

Psychophysical studies extending over a thirty-year period have repeatedly demonstrated that visual stimuli presented close to the onset of a saccadic eye movement are mislocalised both spatially and temporally. When post-saccadic visual references are available, this spatial distortion is best characterised by a compression of visual space toward the target of the saccadic eye movement. An important but unresolved issue, concerns the specificity of saccade-dependent visual mislocalisation phenomena. We investigated this by examining whether saccade-dependent spatial and temporal mislocalisation are observed in an individual (A.I.) who cannot make any form of eye movement (opthalamoplegia), but compensates when reading or scanning visual scenes by making saccadic head movements. We demonstrate that saccade-dependent spatial and temporal mislocalisation are absent in subject A.I. and suggest that spatiotemporal mislocalisation may be specific to rapid forms of movement, such as ocular saccades, that necessitate predictive re-mapping to maintain space constancy.

Adult↗
PubMed1981

A new neurotological test for detecting cerebellar dysfunction.

The adaptation of the vestibulo-ocular reflex (VOR) was studied in 26 normal subjects and 26 patients with cerebellar lesions, using horizontal vision-reversal prisms. In normal subjects, the adaptation of gain after wearing prisms for one hour was approximately 50% of the VOR value in the dark. In contrast to this, patients with cerebellar lesions showed less adaptation--approximately 20% after a one-hour forced adaptation task. These were type A, higher gain in the initial level and abnormal adaptation (10 cases); type B, higher gain in the initial level and normal adaptation (5 cases); and type C, normal initial level and abnormal adaptation (11 cases). The cases showing the typical type-A responses tended to have severe widespread or midline lesions of the cerebellum. Typical type-B cases had mild cerebellar lesions, and typical type-C cases tended to have lesions restricted to one side of the cerebellum. From these results, it can be speculated that reduction of VOR adaptation occurs when one side of the cerebellum has severe lesions, but it is sufficient to produce a normal vestibulo-ocular reflex if at least half of the cerebellum is intact.

Adult↗
PubMed2006

Priming of head premotor circuits during oculomotor preparation.

Large, rapid gaze shifts necessitate intricate coordination of the eyes and head. Brief high-frequency bursts of activity within the intermediate and deeper layers of the superior colliculus (dSC) encode desired gaze shifts regardless of component movements of the eyes and head. However, it remains unclear whether low-frequency activity emitted by oculomotor neurons within the dSC and elsewhere has any role in eye-head gaze shifts. Here we test the hypothesis that such low-frequency activity contributes to eye-head coordination by selectively priming head premotor circuits. We exploited the capacity for short-duration (10 ms, 4 pulses) dSC stimulation to evoke neck muscle responses without compromising ocular stability, stimulating at various intervals of a "gap-saccade" task. Low-frequency neural activity in many oculomotor areas (including the dSC) is known to increase during the progression of the gap-saccade task. Stimulation was passed during either a fixation-interval while a central fixation point was illuminated, a 200-ms gap-interval between fixation point offset and target onset, or a movement-interval following target onset. In the two monkeys studied, the amplitude of evoked responses on multiple neck muscles tracked the known increases in low-frequency oculomotor activity during the gap-saccade task, being greater following stimulation passed at the end of the gap- versus the fixation-interval, and greater still when the location of stimulation during the movement interval coincided with the area of the dSC generating the ensuing saccade. In one of these monkeys, we obtained a more detailed timeline of how these results co-varied with low-frequency oculomotor activity by stimulating, across multiple trials, at different times within the fixation-, gap- and movement-intervals. Importantly, in both monkeys, baseline levels of neck EMG taken immediately prior to stimulation onset did not co-vary with the known pattern of low-frequency oculomotor activity up until the arrival of a transient burst associated with visual target onset. These baseline results demonstrate that any priming of the head premotor circuits occurs without affecting the output of neck muscle motoneurons, We conclude that low-frequency oculomotor activity primes head premotor circuits well in advance of gaze shift initiation, and in a manner distinct from its effects on the eye premotor circuits. Such distinctions presumably aid the temporal coordination of the eyes and head despite fundamentally different biomechanics.

Action Potentials↗
PubMed2004

Deficits in ocular and manual tracking due to episodic ataxia type 2.

Four patients with a novel mutation leading to episodic ataxia type 2 were studied in a task that required them to track target motion either with the eyes or with the index finger of the right hand. The target initially moved in a straight line and then changed direction at an unpredictable time by an unpredictable amount. On the day of testing, 3 of the patients were evaluated as normal on a neurological exam, whereas the fourth was severely ataxic. Nevertheless, all 4 showed deficits in tracking behavior with common features. Ocular tracking tended to result in hypermetric saccades at longer than normal latencies. Smooth pursuit tracking was absent in 1 patient and had lower than normal gain in the others. Deficits in manual tracking showed similarities to the deficits in ocular tracking, with hypermetric compensations for changes in target direction. The similarities in the deficits in manual and ocular tracking suggest that they are subject to similar control by the cerebellar structures.

Adult↗
PubMed1979

Otolithic-acoustic interaction in the control of eye movement.

In order to examine otolithic contribution to eye movements ten subjects were asked to track either a moving acoustic target or a stationary target during subject linear motion on a cart. The relative displacement between the subject and the target was the same in the two situations. Recordings of eye movements during subject lateral acceleration in the dark without any task, or with the task of tracking an imagined stationary target were made as a control. The frequencies ranged between 0.15 and 0.3 Hz and peak acceleration between 0.55 and 1.2 m/s2. No lateral eye movements (L-nystagmus) were recorded in the dark. Only saccadic eye movements were recorded during the tracking of a moving acoustic target. Slow eye movements interspersed by saccades were observed when the moving subject tracked an imagined or an acoustic stationary target. Contribution of the slow phase to tracking was more important in the presence of an acoustic target than in the presence of imagined target. The results are interpreted in terms of an otolithic contribution to the central reconstruction of the acoustic target velocity, or in terms of an adaptive control of the otolithic-ocular reflex gain. A conceptual model accounting for these interpretations is proposed.

Acoustic Maculae↗