Visually induced adaptive changes in primate saccadic oculomotor control signals

1985 ◽  
Vol 54 (4) ◽  
pp. 940-958 ◽  
Author(s):  
L. M. Optican ◽  
F. A. Miles

Saccades are the rapid eye movements used to change visual fixation. Normal saccades end abruptly with very little postsaccadic ocular drift, but acute ocular motor deficits can cause the eyes to drift appreciably after a saccade. Previous studies in both patients and monkeys with peripheral ocular motor deficits have demonstrated that the brain can suppress such postsaccadic drifts. Ocular drift might be suppressed in response to visual and/or proprioceptive feedback of position and/or velocity errors. This study attempts to characterize the adaptive mechanism for suppression of postsaccadic drift. The responses of seven rhesus monkeys were studied to postsaccadic retinal slip induced by horizontal exponential movements of a full-field stimulus. After several hours of saccade-related retinal image slip, the eye movements of the monkeys developed a zero-latency, compensatory postsaccadic ocular drift. This ocular drift was still evident in the dark, although smaller (typically 15% of the amplitude of the antecedent saccade, up to a maximum drift of 8 degrees). Retinal slip alone, without a net displacement of the image, was sufficient to elicit these adaptive changes, and compensation for leftward and rightward saccades was independent. It took several days to complete adaptation, but recovery (in the light) was much quicker. The decay of this adaptation in darkness was very slow; after 3 days the ocular drift was reduced by less than 50%. The time constants of single exponential curve fits to adaptation time courses of data from five animals were 35 h for acquisition, 4 h for recovery, and at least 40 h for decay in darkness. Descriptions of the central innervation for a saccade are usually simplified to only two components: a pulse and a step. It has been hypothesized that suppression of pathological postsaccadic drift is achieved by adjusting the ratio of the pulse to the step of innervation (19, 26). However, we show that the time constant of the ocular drift is influenced by the time constant of the adapting stimulus, which cannot be explained by the simple pulse-step model of saccadic innervation. A more realistic representation of the saccadic innervation has three components: a pulse, an exponential slide, and a step. Normal saccades were accurately simulated by a fourth-order, linear model of the ocular motor plant driven by such a pulse-slide-step combination. Saccades made after prolonged exposure to optically induced retinal image slip could also be simulated by properly adjusting the slide and step components.(ABSTRACT TRUNCATED AT 400 WORDS)

2006 ◽  
Vol 95 (3) ◽  
pp. 1588-1607 ◽  
Author(s):  
John S. Stahl ◽  
Robert A. James ◽  
Brian S. Oommen ◽  
Freek E. Hoebeek ◽  
Chris I. De Zeeuw

Mice carrying mutations of the gene encoding the ion pore of the P/Q calcium channel (Cacna1a) are an instance in which cerebellar dysfunction may be attributable to altered electrophysiology and thus provide an opportunity to study how neuronal intrinsic properties dictate signal processing in the ocular motor system. P/Q channel mutations can engender multiple effects at the single neuron, circuit, and behavioral levels; correlating physiological and behavioral abnormalities in multiple allelic strains will ultimately facilitate determining which alterations of physiology are responsible for specific behavioral aberrations. We used videooculography to quantify ocular motor behavior in tottering mutants aged 3 mo to 2 yr and compared their performance to data previously obtained in the allelic mutant rocker and C57BL/6 controls. Tottering mutants shared numerous abnormalities with rocker, including upward deviation of the eyes at rest, increased vestibuloocular reflex (VOR) phase lead at low stimulus frequencies, reduced VOR gain at high stimulus frequencies, reduced gain of the horizontal and vertical optokinetic reflex, reduced time constants of the neural integrator, and reduced plasticity of the VOR as assessed in a cross-axis training paradigm. Unlike rocker, young tottering mutants exhibited normal peak velocities of nystagmus fast phases, arguing against a role for neuromuscular transmission defects in the attenuation of compensatory eye movements. Tottering also differed by exhibiting directional asymmetries of the gains of optokinetic reflexes. The data suggest at least four pathophysiological mechanisms (two congenital and two acquired) are required to explain the ocular motor deficits in the two Cacna1a mutant strains.


Perception ◽  
1997 ◽  
Vol 26 (1_suppl) ◽  
pp. 228-228
Author(s):  
M T Leinonen ◽  
P Rinne

One of the main purposes of the oculomotor system is to keep the image projected on the retina stationary in spite of the continuous movement of the head. If the vestibulo-ocular and optokinetic reflexes are defective, the retinal image becomes blurred owing to the uncoordinated movements of the head and the eyes. It is well known that in children retinal blur caused by media opacities or large refraction errors results in amblyopia. In a similar way amblyopia could be caused by slip of the retinal image due to a defective oculomotor system. Our patient was a small for gestational age A-twin. He developed dystonic diplegia with poor head control. At the age of 7 months he was considered to have cortical visual impairment. In a magnetic resonance image of the brain there were diffuse periventricular changes in the white matter and hypoplasia of the corpus callosum and the cerebellar vermis. Binocular optokinetic reflexes to full-field stimuli were horizontally asymmetric and were missing vertically. The reflexes to rotation of the child were asymmetric in the same way. In order to stabilise the retinal image the head of the child was supported always when he was supposed to look at a target with fine details. Increase in visual acuity measured with a Teller acuity card procedure was apparent after head support. This suggests that retinal slip can cause amblyopia. It is usual practice not to support the head of a child who has cerebral palsy and poor head control. In the case of defective head - eye coordination this practice could be harmful to the normal development of vision.


1989 ◽  
Vol 61 (5) ◽  
pp. 879-891 ◽  
Author(s):  
Z. Kapoula ◽  
L. M. Optican ◽  
D. A. Robinson

1. Five human subjects viewed binocularly the interior of a full-field hemisphere filled with a random-dot pattern. During training, eye movements were recorded by the electrooculogram. A computer detected the end of every saccade and immediately moved the pattern horizontally either in the same or, in different experiments, the opposite direction as the saccade. The motion was exponential, its amplitude was 25% of the horizontal component of the antecedent saccade, and its time constant was either 25, 50, or 100 ms in different experiments. Before and after 2-3 h of this experience, movements of both eyes were measured simultaneously by the eye-coil/magnetic-field method while subjects made saccades across the moveable pattern, looked between stationary targets, or made saccades in the dark, to see the effect of such adaptation on postsaccadic eye movements. 2. After 2-3 h (10,000-20,000 saccades) subjects developed a zero-latency, postsaccadic, ocular drift in the dark in the direction of the pattern motion. Three subjects were trained to backward drift, two to onward drift. Drift amplitude in the dark changed by 6% of the saccade size (range: 2-11%). The drift was exponential with an overall time constant of 108 ms. 3. After training, while viewing the adapting pattern motion, the change in the amplitude of the zero-latency drift was approximately 10% (range: 6.5-14%). 4. Increasing the time constant of the pattern motion produced significant increases in the time constant of the ocular drift. 5. The incidence of dynamic overshoot (a tiny, backward saccade immediately following a main saccade) was idiosyncratic and went up in some subjects and down in others with adaptation. These changes did not seem related to modifications of postsaccadic drift. 6. Normal human saccades are characterized by essentially no postsaccadic drift in the abducting eye and a pronounced onward drift (approximately 4%) in the adducting eye. This adduction-adduction asymmetry is largely preserved through adaptation. Thus the changes in drift were conjugate and conformed to Hering's law of equal (change of) innervation. 7. These results agree with those previously demonstrated in the monkey and can similarly be explained by parametric changes in the pulse, slide, and step of normal saccadic innervation.


2019 ◽  
Vol 3 (2) ◽  
pp. 2514183X1988615
Author(s):  
Alexander A Tarnutzer ◽  
Marianne Dieterich

In the initial assessment of the patient with acute vertigo or dizziness, both structured history-taking and a targeted bedside neuro-otological examination are essential for distinguishing potentially life-threatening central vestibular causes from those of benign, self-limited peripheral labyrinthine origin and thus for deciding on further diagnostic testing. In this article, the key elements of the vestibular and ocular motor examination, which should be obtained at the bedside in these acutely dizzy patients, will be discussed. Specifically, this will include the following five domains: ocular stability for (I) nystagmus and for (II) eye position (skew deviation), (III) the head-impulse test (HIT), (IV) postural stability, and (V) ocular motor deficits of saccades, smooth pursuit eye movements, and optokinetic nystagmus. We will also discuss the diagnostic accuracy of specific combinations of these bedside tests (i.e. HIT, testing for nystagmus and vertical divergence, referred to as the H.I.N.T.S. three-step examination), emphasizing that the targeted neuro-otological bedside examination is more sensitive for identifying central causes in acute prolonged vertigo and dizziness than early MRI of the brain.


2003 ◽  
Vol 89 (5) ◽  
pp. 2516-2527 ◽  
Author(s):  
Laurent Petit ◽  
Michael S. Beauchamp

We used event-related fMRI to measure brain activity while subjects performed saccadic eye, head, and gaze movements to visually presented targets. Two distinct patterns of response were observed. One set of areas was equally active during eye, head, and gaze movements and consisted of the superior and inferior subdivisions of the frontal eye fields, the supplementary eye field, the intraparietal sulcus, the precuneus, area MT in the lateral occipital sulcus and subcortically in basal ganglia, thalamus, and the superior colliculus. These areas have been previously observed in functional imaging studies of human eye movements, suggesting that a common set of brain areas subserves both oculomotor and head movement control in humans, consistent with data from single-unit recording and microstimulation studies in nonhuman primates that have described overlapping eye- and head-movement representations in oculomotor control areas. A second set of areas was active during head and gaze movements but not during eye movements. This set of areas included the posterior part of the planum temporale and the cortex at the temporoparietal junction, known as the parieto-insular vestibular cortex (PIVC). Activity in PIVC has been observed during imaging studies of invasive vestibular stimulation, and we confirm its role in processing the vestibular cues accompanying natural head movements. Our findings demonstrate that fMRI can be used to study the neural basis of head movements and show that areas that control eye movements also control head movements. In addition, we provide the first evidence for brain activity associated with vestibular input produced by natural head movements as opposed to invasive caloric or galvanic vestibular stimulation.


2021 ◽  
pp. 194173812199411
Author(s):  
Rishi D. Patel ◽  
Cynthia R. LaBella

Background: Vestibular/ocular motor dysfunction can occur in pediatric concussions, which can impair reading, learning, and participation in athletics. This study evaluated 3 clinical tools for identifying postconcussion vestibular/ocular motor dysfunction: (1) Post-Concussion Symptom Scale (PCSS), (2) Convergence Insufficiency Symptom Survey (CISS), and (3) Vestibular/Ocular Motor Screening (VOMS). Hypothesis: Evaluating vestibular/ocular motor dysfunction with multiple clinical tools will capture more symptomatic patients than any 1 tool alone. Study Design: Cross-sectional data from a prospective cohort study. Level of Evidence: Level 4. Methods: Patients were between 8 and 17 years old and seen in a tertiary care pediatric sports medicine clinic between August 2014 and February 2018. Data were collected from initial visit and included VOMS, PCSS, and CISS. Descriptive statistics, Pearson’s correlations, and logistic regressions were used to describe relationships between clinical tools. Results: Of the 156 patients (55.1% female; 14.35 ± 2.26 years old) included, this study identified 129 (82.7%) with vestibular/ocular motor dysfunction. Of these 129, 65 (50.4%) reported “visual problems” on PCSS, 93 (72.1%) had abnormal CISS, and 99 (76.7%) had abnormal VOMS. Together, VOMS and CISS identified 64 (49.6%) patients without reported “visual problems” on PCSS. Higher total PCSS scores predicted abnormal CISS (odds ratio [OR], = 1.11; 95% CI, 1.07-1.17) and abnormal VOMS (OR, 1.03; 95% CI, 1.01-1.06). “Visual problems” on PCSS did not predict abnormal CISS or VOMS. Conclusions: Vestibular/ocular motor dysfunction were identified in nearly 83% of study subjects when PCSS, CISS, and VOMS are used together. Clinical Relevance: These results suggest adding CISS and VOMS to the clinical evaluation of concussions can help clinicians identify post-concussion vestibular/ocular motor dysfunction.


Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
John-Ross Rizzo ◽  
Todd Hudson ◽  
Briana Kowal ◽  
Michal Wiseman ◽  
Preeti Raghavan

Introduction: Visual abnormalities and manual motor control have been studied extensively after stroke, but an understanding of oculomotor control post-stroke has not. Recent studies have revealed that in visually guided reaches arm movements are planned during eye movement execution, which may contribute to increased task complexity. In fact, in healthy controls during visually guided reaches, the onset of eye movement is delayed, its velocity reduced, and endpoint errors are larger relative to isolated eye movements. Our objective in this experiment was to examine the temporal properties of eye movement execution for stroke patients with no diagnosed visual impairment. The goal is to improve understanding of oculomotor control in stroke relative to normal function, and ultimately further understand its coordination with manual motor control during joint eye and hand movements. We hypothesized that stroke patients would show abnormal initiation or onset latency for saccades made in an eye movement task, as compared to healthy controls. Methods: We measured the kinematics of eye movements during point-to-point saccades; there was an initial static, fixation point and the stimulus was a flashed target on a computer monitor. We used a video-based eye tracker for objective recording of the eye at a sampling frequency of 2000 Hz (SR Research, Eyelink). 10 stroke subjects, over 4 months from injury and with no diagnosed visual impairment, and 10 healthy controls completed 432 saccades in a serial fashion. Results: Stroke patients had significantly faster onset latencies as compared to healthy controls during saccades (99.5ms vs. 245.2ms, p=0.00058). Conclusion: A better understanding of the variations in oculomotor control post-stroke, which may go unnoticed during clinical assessment, may improve understanding of how eye control synchronizes with arm or manual motor control. This knowledge could assist in tailoring rehabilitative strategies to amplify motor recovery. For next steps, we will perform objective eye and hand recordings during visually guided reaches post-stroke to better understand the harmonization or lack thereof after neurologic insult.


2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Stefano Pensiero ◽  
Agostino Accardo ◽  
Paola Michieletto ◽  
Paolo Brambilla

It is not sure if persons with dyslexia have ocular motor deficits in addition to their deficits in rapid visual information processing. A 15-year-old boy afflicted by severe dyslexia was submitted to saccadic eye movement recording. Neurological and ophthalmic examinations were normal apart from the presence of an esophoria for near and slightly longer latencies of pattern visual evoked potentials. Subclinical saccadic alterations were present, which could be at the basis of the reading pathology: (1) low velocities (and larger durations) of the adducting saccades of the left eye with undershooting and long-lasting postsaccadic onward drift, typical of the internuclear ophthalmoplegia; (2) saccades interrupted in mid-flight and fixation instability, which are present in cases of brainstem premotor disturbances.


2021 ◽  
Author(s):  
Natalia Ladyka-Wojcik ◽  
Zhong-Xu Liu ◽  
Jennifer D. Ryan

Scene construction is a key component of memory recall, navigation, and future imagining, and relies on the medial temporal lobes (MTL). A parallel body of work suggests that eye movements may enable the imagination and construction of scenes, even in the absence of external visual input. There are vast structural and functional connections between regions of the MTL and those of the oculomotor system. However, the directionality of connections between the MTL and oculomotor control regions, and how it relates to scene construction, has not been studied directly in human neuroimaging. In the current study, we used dynamic causal modeling (DCM) to investigate this relationship at a mechanistic level using a scene construction task in which participants' eye movements were either restricted (fixed-viewing) or unrestricted (free-viewing). By omitting external visual input, and by contrasting free- versus fixed- viewing, the directionality of neural connectivity during scene construction could be determined. As opposed to when eye movements were restricted, allowing free viewing during construction of scenes strengthened top-down connections from the MTL to the frontal eye fields, and to lower-level cortical visual processing regions, suppressed bottom-up connections along the visual stream, and enhanced vividness of the constructed scenes. Taken together, these findings provide novel, non-invasive evidence for the causal architecture between the MTL memory system and oculomotor system associated with constructing vivid mental representations of scenes.


Sign in / Sign up

Export Citation Format

Share Document