A Unifying Model-Based Hypothesis for the Diverse Waveforms of Infantile Nystagmus Syndrome

We expanded the original behavioral Ocular Motor System (OMS) model for Infantile Nystagmus Syndrome (INS) by incorporating common types of jerk waveforms within a unifying mechanism. Alexander’s law relationships were used to produce desired INS null positions and sharpness. At various gaze angles, these relationships influenced the IN slow-phase amplitudes differently, thereby mimicking the gaze-angle effects of INS patients. Transitions from pseudopendular with foveating saccades to jerk waveforms required replacing braking saccades with foveating fast phases and adding a resettable neural integrator in the pursuit pre-motor circuitry. The robust simulations of accurate OMS behavior in the presence of diverse INS waveforms demonstrate that they can all be generated by a loss of pursuit-system damping, supporting this hypothetical origin

The sub-clinical see-saw nystagmus embedded in infantile nystagmus

AbstractA transient, decompensated vertical phoria in an individual with infantile nystagmus syndrome (INS) resulted in two images that oscillated vertically—a diplopic oscillopsia. Ocular motor studies during the vertical oscillopsia recreated by vertical prisms, led to the identification of a sub-clinical see-saw nystagmus (SSN), present under the prism-induced diplopic condition. Retrospective analysis of ocular motor recordings made prior to the above episode of vertical diplopia revealed the presence of that same sub-clinical SSN. The SSN had not been detected previously despite extensive observations and recordings of this subject’s pendular IN over a period of forty years. Three- dimensional search-coil data from fourteen additional INS subjects (with pendular and jerk waveforms) confirmed the existence of sub-clinical SSN embedded within the clinically detectable horizontal-torsional IN in seven of the fifteen and a sub-clinical, conjugate, vertical component in the remaining eight. Unlike the clinically visible SSN found in achiasma, the cause of this sub-clinical SSN is hypothesized to be due to a failure of the forces of the oblique muscles (responsible for the torsional component of the IN) to balance out the associated forces of the vertical recti; the net result is a small, sub-clinical SSN. Thus, so-called “horizontal” IN is actually a horizontal-torsional oscillation with a secondary, sub-clinical SSN or conjugate vertical component. The suppression of oscillopsia by efference copy in INS appears to be accomplished for each eye individually, even in a binocular individual. However, failure to fuse the two images results in oscillopsia of one of them

Biologically Relevant Models of Infantile Nystagmus Syndrome: The Requirement for Behavioral Ocular Motor System Models

ABSTRACT Infantile nystagmus syndrome (I NS) is a combination of several types of nystagmus, each representing dysfunction in one subsystem of the oc ular motor system (OMS) and having characteristic waveforms. Eye-movement recordings are the only certain way to identifY IN and differentiate it from other types. The waveform classification scheme in use for 30 years is both accurate, inclusive, and suggests the underlying subsystem instabilities. In dif ferent individuals, they may appear at birth (hard wired) or in early infancy (developmental). The primary subsystem instability in IN is hypothesized to lie in the normally underdamped smooth pursuit system; vestibular dysfunction (imbalance) may also be present. Less often, the nucleus of the optic tract may be involved. Ocular motility studies over the past 40 years have demonstrated that saccades and gaze holding are normal in the INS and saccades contained within IN waveforms are always corrective; i.e., they cannot be the initiating movement responsible for IN. Because there are an infinite number of solu tions to simulating specific waveforms, models that merely generate waveforms that resemble IN in isolation are of little use, either clinically or to increase our understanding of the underlying mechanisms of IN. A biologically relevant model of the INS should be part of, and operate within, a complete OMS model, capable of reproducing the normal ocular motor behavior of these in dividuals while still oscillating; i.e., the model, like the patient, must not have oscillopsia and be able to respond correctly to various target inputs

Quantifying perception and oculomotor instability in infantile nystagmus

The purpose of the studies described herein was to better understand the impact of involuntary eye movements on oculomotor control and perception in infantile nystagmus. Therapeutic interventions that result in slowed nystagmus oscillations often fail to elicit significant quantifiable improvements in visual function, despite patients reporting subjective benefits. It is difficult to justify surgical or pharmacological intervention when the only outcome measures are subjective. Objective quantification of nystagmus eye movements per se usually involves time-consuming manual marking of recordings to both calibrate and analyse data. As a result, analyses are rarely (if ever) performed in the clinical setting. Software was therefore developed to automate calibration and assessment. Psychophysical experiments were undertaken to quantify the spatiotemporal constraints of vision in infantile nystagmus. Visual acuity was measured in the absence of retinal image motion to reveal the maximum improvement to spatial vision that might be expected if nystagmus were halted altogether. The results indicate that poor spatial vision underlies infantile nystagmus, even in cases without comorbid pathology. Gaze acquisition time was compared to stimulus recognition time. The results indicate that infantile nystagmus does not increase visual processing time; rather, redeploying gaze takes longer. An incidental finding revealed a temporal relationship between voluntary saccades and involuntary nystagmus quick phases. Both typically occur together, presumably to maximise efficiency and minimise saccadic suppression. Clinical tests of gaze acquisition time must now be developed, to be used in conjunction with the software developed here, as objective outcome measures of therapeutic interventions

Longitudinal investigation of disparity vergence in young adult convergence insufficiency patients

Vergence is a form of eye movement in which the eyes move in opposite directions to minimize retinal disparity. It allows an object at different distances from a viewer to appear single during binocular vision by centering the image on the fovea of each retina. Convergence insufficiency (CI) is a binocular disfunction in which blurry and double vision is a symptom. Office-based Vergence/Accommodative Therapy (OBVAT) has been shown to be effective in treating CI. A randomized clinical trial was designed to study fifty participants with CI before and after therapy using randomized therapy treatment (active and placebo), standardized clinical definitions, and a masked clinician to measure clinical outcomes. A haploscope was used to independently show stimuli to the left and right eye of the participants. A video-based eye tracker was used to capture eye-movement data, and a custom MATLAB program was used to analyze the following data parameters: latency, time to peak velocity, peak velocity, and final amplitude. Eye-movement data parameters significantly improved post OBVAT when comparing baseline and post treatment results. The results after Office-Based Placebo Therapy (OBPT) were compared to OBVAT results, and a statically significant difference was found. Results support that OBVAT leads to a significant improvement in vergence dynamics post therapy compared to baseline measurements

Aerospace medicine and biology, an annotated bibliography. volume xi- 1962-1963 literature

Aerospace medicine and biology - annotated bibliography for 1962 and 196

The computational neurology of active vision

In this thesis, we appeal to recent developments in theoretical neurobiology – namely, active inference – to understand the active visual system and its disorders. Chapter 1 reviews the neurobiology of active vision. This introduces some of the key conceptual themes around attention and inference that recur through subsequent chapters. Chapter 2 provides a technical overview of active inference, and its interpretation in terms of message passing between populations of neurons. Chapter 3 applies the material in Chapter 2 to provide a computational characterisation of the oculomotor system. This deals with two key challenges in active vision: deciding where to look, and working out how to look there. The homology between this message passing and the brain networks solving these inference problems provide a basis for in silico lesion experiments, and an account of the aberrant neural computations that give rise to clinical oculomotor signs (including internuclear ophthalmoplegia). Chapter 4 picks up on the role of uncertainty resolution in deciding where to look, and examines the role of beliefs about the quality (or precision) of data in perceptual inference. We illustrate how abnormal prior beliefs influence inferences about uncertainty and give rise to neuromodulatory changes and visual hallucinatory phenomena (of the sort associated with synucleinopathies). We then demonstrate how synthetic pharmacological perturbations that alter these neuromodulatory systems give rise to the oculomotor changes associated with drugs acting upon these systems. Chapter 5 develops a model of visual neglect, using an oculomotor version of a line cancellation task. We then test a prediction of this model using magnetoencephalography and dynamic causal modelling. Chapter 6 concludes by situating the work in this thesis in the context of computational neurology. This illustrates how the variational principles used here to characterise the active visual system may be generalised to other sensorimotor systems and their disorders

Handbook on clinical neurology and neurosurgery

HANDBOOKNEUROLOGYNEUROSURGERYКЛИНИЧЕСКАЯ НЕВРОЛОГИЯНЕВРОЛОГИЯНЕЙРОХИРУРГИЯThis handbook includes main parts of clinical neurology and neurosurgery