Two devices for analysis of nystagmus.
Electromechanical slope computer and electronic summation device for measurement of nystagmus and analysis of nystagmus data
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Electromechanical slope computer and electronic summation device for measurement of nystagmus and analysis of nystagmus data
Results of a previous metric analysis and an electronic simulation of acceleratory nystagmus are given. On this basis, a tentative mathematical model for describing acceleratory nystagmus is reported. The essential content of the model is Lorente de No's neuron circuit, to which the two-factor theory of excitation has been applied.
The asymmetry of reflex activity of labyrinths and directional preponderance of the reaction were studied on healthy persons subjected to caloric tests. Calorization with hot water was accompanied by less pronounced reactions in all parameters of nystagmus than analogous indices at cold water stimulation. The symmetry of labyrinth function shifted to the right in individuals with greater activity of the left central vestibular formations, analogous to right handedness behavior. It is concluded that asymmetry of reflex nystagmus in healthy persons can be due to a certain preponderance of functional activity in structures of the left hemisphere of the brain.
A digital computer program, MITNYS-II, has been developed for on-line analysis of nystagmus which results from visual, vestibular or caloric stimulation. The program accepts sampled records of eye position and yields cumulative slow phase position, slow phase velocity, instantaneous fast phase frequency and other parameters in 25 ms. In this paper the algorithms by which fast phases are detected, and by which slow phase cumulative eye position is extrapolated across the fast phase interval are described. Extensive tests with vestibular, optokinetic and caloric nystagmus yield reliability figures of the order of 2% for false identification of fast phases and missed fast phases. MITNYS-II has been successfully employed to interpret clinical EOG records, examples of which are presented.
A current literature review of the analog and digital process of vestibular and optical kinetic nystagmus reveals little agreement in the methods used by various labs. The strategies for detection of saccade (fast phase velocity component of nystagmus) vary between labs, and most of the process have not been evaluated and validated with a standard database. A survey was made of major vestibular labs in the U.S. that perform computer analyses of vestibular and optokinetic reflexes to stimuli, and a baseline was established from which to standardize data acquisition and analysis programs. The concept of an Error Index was employed as the criterium for evaluating the performance of the vestibular analysis software programs. The performance criterium is based on the detection of saccades and is the average of the percentages of missed detections and false detections. Evaluation of the programs produced results for lateral gaze with saccadic amplitude of one, two, three, five, and ten degrees with various signal-to-noise ratios. In addition, results were obtained for sinusoidal pursuit of 0.05, 0.10, and 0.50 Hz with saccades from one to ten degrees at various signal-to-noise ratios. Selection of the best program was made from the performance in the lateral gaze with three degrees of saccadic amplitude and in the 0.10 Hz sinusoid with three degrees of saccadic amplitude.
The extent to which the slow phase velocity (SPV) of nystagmus elicited by a vertical optokinetic stimulation with constant velocity could be modulated by sinusoidal angular motion in the vertical plane was investigated under normal gravity condition and during the microgravity period of parabolic flight. In normal gravity, when the angular head motion and the optokinetic stimulation were in the same direction, the peak SPV was slower than the velocity of the optokinetic display. When the head motion and the optokinetic stimulation were in opposite directions, the peak SPV was equal to the velocity of the optokinetic display. In microgravity, the peak SPV was approximately equal to the velocity of the optokinetic display when head rotation and optokinetic stimulation were in the same direction, and was faster than the velocity of the optokinetic dispaly when head rotation and optokinetic stimulation were in opposite directions. In addition, the interaction of vestibular and optokinetic nystagmus was found to be nonlinear in microgravity, especially when the optokinetic stimulation was directed downward. These results suggest an interaction between the vestibular and the optokinetic systems modulated as a function of the gravitational state, and support the observation that visual input is more effective in reducing sensory conflict experienced in microgravity.
Compensatory nystagmus as a conditioned response in adaptation to a rotating environment
Study of reduction of nystagmus, disorientation and nausea in human subjects living for several days in slowly rotating room
Human performance - nystagmus fluctuation during adaptation to living in rotating room
Effect of changing resultant linear acceleration relative to human subject on nystagmus generated by angular acceleration
Relationships between blood alcohol, positional alcohol nystagmus, and postural equilibrium
Centripetal acceleration effect on nystagmus for various orientations relative to rotation center, noting otolith modulation of sensory input from semicircular canals
Additional effect of centripetal acceleration on nystagmus in humans already exposed to angular acceleration
Influence of otoliths on duration of post-caloric nystagmus in cats
Horizontal nystagmus elicitation in man by periodic linear acceleration
Nystagmus in normal and labyrinthine defectives as related to orientation of rotation axis relative to gravity
Nystagmus response to linear and angular accelerations
We investigated the pathogenesis of acquired pendular nystagmus (APN) in six patients, three of whom had multiple sclerosis. First, we tested the hypothesis that the oscillations of APN are due to a delay in visual feedback secondary, for example, to demyelination of the optic nerves. We manipulated the latency to onset of visually guided eye movements using an electronic technique that induces sinusoidal oscillations in normal subjects. This manipulation did not change the characteristics of the APN, but did superimpose lower-frequency oscillations similar to those induced in normal subjects. These results are consistent with current models for smooth (non-saccadic) eye movements, which predict that prolongation of visual feedback could not account for the high-frequency oscillations that often characterize APN. Secondly, we attempted to determine whether an increase in the gain of the visually-enhanced vestibulo-ocular reflex (VOR), produced by viewing a near target, was accompanied by a commensurate increase in the amplitude of APN. Increases in horizontal or vertical VOR gain during near viewing occurred in four patients, but only two of them showed a parallel increase in APN amplitude. On the other hand, APN amplitude decreased during viewing of the near target in the two patients who showed no change in VOR gain. Taken together, these data suggest that neither delayed visual feedback nor a disorder of central vestibular mechanisms is primarily responsible for APN. More likely, these ocular oscillations are produced by abnormalities of internal feedback circuits, such as the reciprocal connections between brainstem nuclei and cerebellum.