Computer Simulation of Eye Movements for Teaching and Training in Ocular Motor Pathology

2015 ◽  
pp. 81-84
Author(s):  
P.L.M. Huygen
Keyword(s):  
Computer Simulation ◽  
Eye Movements ◽  
Ocular Motor ◽  
Motor Pathology ◽  
And Training

Disorders of Ocular Motility with Disease Affecting the Basal Ganglia, Cerebral Cortex, and in Systemic Conditions

2015 ◽  
pp. 916-1024
Author(s):  
R. John Leigh ◽  
David S. Zee
Keyword(s):  
Eye Movements ◽  
Basal Ganglia ◽  
Bipolar Affective Disorder ◽  
Ocular Motility ◽  
Ocular Motor ◽  
Psychiatric Illnesses ◽  
Tay Sachs Disease ◽  
Motor Apraxia ◽  
Niemann Pick ◽  
Eye Movement Disorders

This chapter reviews (with illustrative videos) disorders of gaze in diseases involving the basal ganglia, including Parkinson’s disease, progressive supranuclear palsy (PSP), hyperkinetic movement syndromes such as oculogyric crisis, and Huntington’s disease. Ocular motor syndromes caused by lesions in the cerebral hemispheres are discussed, including gaze deviations. Distinctive features of ocular motor apraxia, both acquired and congenital, are highlighted. Eye movements during epilepsy, and abnormal eye movements in patients with dementia, including Alzheimer’s disease, frontotemporal dementia, and amyotrophic lateral sclerosis are reviewed. Eye movement disorders in psychiatric illnesses, including schizophrenia, bipolar affective disorder, and autism are summarized. Eye movements in stupor and coma are discussed. The range of ocular motor disturbances in multiple sclerosis (MS) is reviewed as well as the ocular motor manifestations of metabolic and deficiency disorders, including Niemann-Pick disease, Tay-Sachs disease, Gaucher’s disease, and Wernicke’s encephalopathy. Disorders of eye movements induced by drugs or toxins are tabulated.

Eye Movements of the Murine P/Q Calcium Channel Mutant Tottering, and the Impact of Aging

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
Keyword(s):  
Eye Movements ◽  
Calcium Channel ◽  
Motor Behavior ◽  
Motor Deficits ◽  
Ocular Motor ◽  
Gene Encoding ◽  
Optokinetic Reflex ◽  
Behavioral Abnormalities ◽  
Cross Axis ◽  
The Impact

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.

Aetiological Factors in Dyslexia: II. Ocular-Motor Programming

1978 ◽  
Vol 47 (2) ◽  
pp. 667-672 ◽  
Author(s):  
Gerald Leisman ◽  
Maureen Ashkenazi ◽  
Lance Sprung ◽  
Joddy Schwartz
Keyword(s):  
Eye Movements ◽  
Saccadic Eye Movements ◽  
Motor Programming ◽  
Ocular Motor

A study is presented in which the preprogramming of saccadic eye movements is examined in normal (16 boys, 4 girls) and dyslexic subjects (19 boys, 1 girl), as well as the patterning of ocular-motor differences between subjects, which is consistent with the previous study in which no differences in saccadic control are demonstrated between groups of subjects.

Disconjugate Eye Movements during Electronystagmographic Testing in Patients with Known Central Nervous System Lesions

1975 ◽  
Vol 84 (3) ◽  
pp. 368-373
Author(s):  
Joseph Kimm ◽  
James B. MacLean
Keyword(s):  
Central Nervous System ◽  
Eye Movements ◽  
Eye Movement ◽  
Motor System ◽  
Treatment Plan ◽  
Medial Longitudinal Fasciculus ◽  
Ocular Motor ◽  
Measuring Techniques ◽  
Ocular Motor System ◽  
Cns Lesions

A tacit assumption underlying current ENG testing is that the eyes move conjugately. However, considering the intricate neuroanatomical pathways within the ocular motor system in addition to the elaborate vestibulo-ocular connections, we think it reasonable that disconjugate eye movements may result with certain CNS lesions. Recently we have employed independent eye movement measuring techniques in order to assess the movement of each eye separately during our ENG valuations. The preliminary work has revealed that disconjugate eye movements occurred even with extra-axial lesions which spared the medial longitudinal fasciculus. These data may be valuable for the neurotologist with regard to differential diagnosis and prescription of a treatment plan for the patient. The eye movement patterns of patients with confirmed CNS lesions and other interesting findings are presented.

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
Keyword(s):  
Eye Movements ◽  
Time Constant ◽  
Retinal Image ◽  
Prolonged Exposure ◽  
Oculomotor Control ◽  
Motor Deficits ◽  
Ocular Motor ◽  
Retinal Slip ◽  
Full Field ◽  
Adaptive Changes

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)

Eye movements and balance

2020 ◽  
pp. 5922-5931
Author(s):  
Michael Strupp ◽  
Thomas Brandt
Keyword(s):  
Eye Movements ◽  
Systematic Approach ◽  
Correct Diagnosis ◽  
Special Importance ◽  
Reciprocal Effects ◽  
Ocular Motor ◽  
Motor Systems ◽  
Vestibular Vertigo

The disorders underlying vertigo and dizziness are often combined with disturbances of eye movements; reciprocal effects occur because of the anatomical and functional overlap of the vestibular and ocular motor systems. Therefore, both systems must always be tested in patients complaining of vertigo and dizziness. Using a systematic approach it is possible to make a correct diagnosis in more than 90% of patients. The history is of special importance and one should already have an idea, from the symptoms reported by the patient, what the underlying cause of the vertigo is in order to differentiate the different forms of peripheral, central and functional vestibular vertigo/dizziness and non-vestibular forms.

scholarly journals T71. A DIRECT COMPARISON OF ADHD, ASD AND SCHIZOPHRENIA ON FOUR BASIC OCULAR-MOTOR TASKS: TOWARDS A MODEL OF NEURODEVELOPMENTAL CONTINUUM

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S258-S259
Author(s):  
Daniela Canu ◽  
Chara Ioannou ◽  
Katarina Müller ◽  
Matthias Martin ◽  
Stephan Bender ◽  
...  
Keyword(s):  
Eye Movements ◽  
Functional Impairment ◽  
Continuum Hypothesis ◽  
Autism Spectrum ◽  
Diagnostic Process ◽  
Ocular Motor ◽  
Response Preparation ◽  
Motor Tasks ◽  
Psychomotor Slowing ◽  
Neurodevelopmental Impairment

Abstract Background According to the Neurodevelopmental continuum hypothesis, neurodevelopmental disorders such as ADHD, Autism and Schizophrenia, should be conceptualised as lying on a continuum of neurodevelopmental impairment, with the individual disorders reflecting different degrees of abnormal brain development and resulting functional impairment. The model also hypothesizes that these disorders lie on a gradient of severity, suggesting that they might differ to some extent quantitatively but also qualitatively. The severity of neurodevelopmental impairment is also expressed by the severity of cognitive impairment and persistence of functional impairment. The main objective of the present study was therefore to investigate commonalities and differences among the three conditions in various cognitive subdomains using standard ocular-motor paradigms. Methods Four groups of young adults were included: 21 with Early-Onset Schizophrenia (“SCZ”, 19.7±1.7, 15 males), 26 with Autism Spectrum Disorder (“ASD”, 19.7±1.9, 25 males), 28 with Attention-Deficit/Hyperactivity Disorder (“ADHD”, 19.9±1.4, 15 males), 29 typically developing participants (“TD”, 19.8±1.6, 12 males). Participants were matched on age and full-scale IQ. Eye movements were recorded binocularly at 1000 Hz using the Eye Link 1000+ system while four basic ocular-motor tasks (prosaccade (PRO), antisaccade (ANT), memory-guided saccade (MEM), fixation (FIX)) were administered in counterbalanced order. Eye movements were analysed with Data Viewer 3.2, SPSS 2.3 and MorePower 6.1. Results With respect to standard deviation of saccadic reaction times (SRTSD), ASD and ADHD did not differ from TD for PRO, ANTI, MEM. Conversely, SCZ were significantly more variable in all tasks than TD, but not compared to ASD and ADHD. Furthermore, SCZ were significantly slower than TD and ASD, but not ADHD, in PRO and ANT. Compared to TD, increased percentage of anticipatory saccades was found for MEM in ASD and ADHD, only marginally for PRO in ASD, again for all tasks in SCZ, when compared to both TD and ASD and, in less extent, to ADHD in ANT. A significantly higher percentage of direction errors during ANT was common to all clinical groups, this inhibitory deficit being significantly more severe in SCZ than ASD, but not compared to ADHD. Increased frequency of intrusive saccades during FIX was found in SCZ and ASD, and marginally in ADHD, when compared to TD. As for microsaccades, SCZ and ASD showed a higher frequency of microsaccades for FIX (condition without distractors) and PRO (preceding correct saccades), only SCZ for ANT (both preceding correct saccades and direction errors), compared to TD. Discussion Results suggest psychomotor slowing, unique for SCZ, as compared to ASD and ADHD, as indicated by increased mean RT in PRO. Conversely, increased anticipatory saccades and direction errors support the presence of inhibition deficits across groups, suggesting a common (pre-)frontal functional impairment. Of note, mean RT discriminates the clinical groups better than ISV, thus emerging as a trans-diagnostic process to the three conditions and, uniquely for SCZ as a deficit independent of the specific tasks administered here. Finally, atypical microsaccadic frequency might suggest common abnormalities in motor response preparation in SCZ and ASD. Across all tasks, participants with SCZ appear more impaired than those with ADHD and ASD, while the performance of ADHD was often in between SCZ and ASD, possibly in line with the idea of a continuum of neurodevelopmental impairment.

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