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Results for “Nystagmus, Physiologic”

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30 records · Page 2
All sourcesNASA NTRSDOE OSTI
NASA NTRS1992

Plasticity of the human otolith-ocular reflex

The eye movement response to earth vertical axis rotation in the dark, a semicircular canal stimulus, can be altered by prior exposure to combined visual-vestibular stimuli. Such plasticity of the vestibulo-ocular reflex has not been described for earth horizontal axis rotation, a dynamic otolith stimulus. Twenty normal human subjects underwent one of two types of adaptation paradigms designed either to attenuate or enhance the gain of the semicircular canal-ocular reflex prior to undergoing otolith-ocular reflex testing with horizontal axis rotation. The adaptation paradigm paired a 0.2 Hz sinusoidal rotation about a vertical axis with a 0.2 Hz optokinetic stripe pattern that was deliberately mismatched in peak velocity. Pre- and post-adaptation horizontal axis rotations were at 60 degrees/s in the dark and produced a modulation in the slow component velocity of nystagmus having a frequency of 0.17 Hz due to putative stimulation of the otolith organs. Results showed that the magnitude of this modulation component response was altered in a manner similar to the alteration in semicircular canal-ocular responses. These results suggest that physiologic alteration of the vestibulo-ocular reflex using deliberately mismatched visual and semicircular canal stimuli induces changes in both canal-ocular and otolith-ocular responses. We postulate, therefore, that central nervous system pathways responsible for controlling the gains of canal-ocular and otolith-ocular reflexes are shared.

Non-NASA Center↗
NASA NTRS1963

PILOT REACTION TO HIGH SPEED ROTATION

Ten pilots subjected to high speed rotation to determine their susceptibility to motion sickness, vestibular nystagmus and performance of complex functions

ROTATING VEHICLE↗
NASA NTRS1995

Investigations of the pathogenesis of acquired pendular nystagmus

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.

NASA Program Space Physiology and Countermeasures↗
NASA NTRS1981

Vestibular and oculomotor physiology; Proceedings of the International Meeting, New York, NY, September 22-25, 1980

Papers are presented showing recent progress in the understanding of the processing of visual and vestibular signals by the central nervous system to produce eye movements and postural responses. Specific topics include the directional sensitivity of hair cells to hair bundle deflection, the effects of gravity on rotatory nystagmus, the reticulovestibular organization associated with horizontal fast eye movement, the pathways controlling the extraocular eye muscles, the organization of visual-vestibular interaction in vestibular neurons, motion sickness due to vision reversal in stroboscopic light, and vestibular habituation during sinusoidal rotation. Attention is also given to vestibulo-ocular, vestibulocollic and cervicocollic reflexes, visual mossy fiber inputs to the flocculus, directional plasticity of the vestibulo-ocular reflex, the relation of active head rotation with eye-head coordination, instability in the optokinetic-vestibular system as an explanation for periodic alternating nystagmus, the effects of visual and nonvisual fixation on vestibular nystagmus, interaction of saccades with the vestibulo-ocular reflex, and the role of the plantar mechanoreceptor in equilibrium control.

Cohen, B.↗
NASA NTRS1975

Motor activity of astronauts in unsupported state

The performance quality of movements away and approaches to an airlock by astronauts was tested during parabolic flights for weightlessness simulation. Coordination of movement, orientation and performance capacity of the astronauts were not singificantly disrupted. Observed physiological shifts are characterized by an increase in pulse and respiration rate and an increase in arterial pressure under g-forces, a gradual decrease in these indices during repeated stays in weightlessness or during the prolonged effect of it, by a reduction of the length of postrotational nystagmus and counterrotation illusions under weightless conditions.

Kasyan, I. I.↗
NASA NTRS1993

A reevaluation of the vestibulo-ocular reflex: new ideas of its purpose, properties, neural substrate, and disorders

Conventional views of the vestibulo-ocular reflex (VOR) have emphasized testing with caloric stimuli and by passively rotating patients at low frequencies in a chair. The properties of the VOR tested under these conditions differ from the performance of this reflex during the natural function for which it evolved--locomotion. Only the VOR (and not visually mediated eye movements) can cope with the high-frequency angular and linear perturbations of the head that occur during locomotion; this is achieved by generating eye movements at short latency (< 16 msec). Interpretation of vestibular testing is enhanced by the realization that, although the di- and trisynaptic components of the VOR are essential for this short-latency response, the overall accuracy and plasticity of the VOR depend upon a distributed, parallel network of neurons involving the vestibular nuclei. Neurons in this network variously upon a distributed, parallel network of neurons involving the vestibular nuclei. Neurons in this network variously encode inputs from the labyrinthine semicircular canals and otoliths, as well as from the visual and somatosensory systems. The central vestibular pathways branch to contact vestibular cortex (for perception) and the spinal cord (for control of posture). Thus, the vestibular nuclei basically coordinate the stabilization of gaze and posture, and contribute to the perception of verticality and self-motion. Consequently, brainstem disorders that disrupt the VOR cause not just only nystagmus, but also instability of posture (eg, increased fore-aft sway in patients with downbeat nystagmus) and disturbance of spatial orientation (eg, tilt of the subjective visual vertical in Wallenberg's syndrome).

Review↗
NASA NTRS1993

Human vertical eye movement responses to earth horizontal pitch

The vertical eye movements in humans produced in response to head-over-heels constant velocity pitch rotation about a horizontal axis resemble those from other species. At 60 degrees/s these are persistent and tend to have non-reversing slow components that are compensatory to the direction of rotation. In most, but not all subjects, the slow component velocity was well characterized by a rapid build-up followed by an exponential decay to a non-zero baseline. Super-imposed was a cyclic or modulation component whose frequency corresponded to the time for one revolution and whose maximum amplitude occurred during a specific head orientation. All response components (exponential decay, baseline and modulation) were larger during pitch backward compared to pitch forward runs. Decay time constants were shorter during the backward runs, thus, unlike left to right yaw axis rotation, pitch responses display significant asymmetries between paired forward and backward runs.

NASA Program Space Physiology and Countermeasures↗
NASA NTRS1990

International Union of Physiological Sciences Commission on Gravitational Physiology, Annual Meeting, 11th, Lyons, France, Sept. 25-27, 1989, Proceedings

Topics discussed include recent space flight results in gravitational physiology, cardiovascular changes, current concepts in gravitational physiology, musculoskeletal changes, gravity and the cardiovascular system, hypergravic conditions, and head-down tilt. Papers are presented on the effect of space flight on the ultrastructure of the rat cerebellar and hemisphere cortex, a comparative study of cardiovascular responses in primates exposed to tilt test and lower body positive pressure, catecholamines during short- and long-term head-down bedrest, and effects of a 40-day tail-suspension on rat weight-bearing bones. Attention is also given to otolith versus vertical semicircular canal input in the inhibition of horizontal postrotatory nystagmus, cardiovascular responses to sustained acceleration, effects of high sustained hypergravity on plasma catecholamines, and the carotid baroreceptor cardiac-vagal reflex responses during 10 days of head-down tilt.

Reynolds, Orr E.↗
NASA NTRS1980

Physiological response to hyper- and hypogravity during rollercoaster flight

Twenty-six healthy male subjects were flown in a Lear jet aircraft through rollercoaster and parabolic weightlessness flight. Eye movements, respiration, and blood volume pulse were recorded on magnetic tape. The same subjects underwent a battery of five vestibular tests in the laboratory on the ground. One subject in each flight was flown in an upright position, the other in a 90 deg forward tilted head position. The forward tilted subjects always reported motion sickness earlier and after fewer rollercoaster maneuvers than the upright-sitting subjects. It is concluded that the susceptibility to changes of X-axis acceleration is higher than to changes of Z-axis acceleration. Correlation was found between the ability to estimate the subjective vertical (modified Mueller-Aubert-test), optokinetic nystagmus asymmetries, and susceptibility to rollercoaster flight sickness.

Von Baumgarten, R. J.↗
NASA NTRS1996

Adaptation of primate vestibuloocular reflex to altered peripheral vestibular inputs. I. Frequency-specific recovery of horizontal VOR after inactivation of the lateral semicircular canals

1. The adaptive plasticity of the vestibuloocular reflex (VOR) following a selective lesion of the peripheral vestibular organs was investigated in rhesus monkeys whose lateral semicircular canals were inactivated by plugging of the canal lumen in both ears. Gain and phase of horizontal, vertical, and torsional slow-phase eye velocity were determined from three-dimensional eye movement recordings obtained acutely after the plugging operation, as well as in regular intervals up to 10 mo later. 2. Acutely after plugging, horizontal VOR was minimal during yaw rotation with gains of < 0.1 at all frequencies. Horizontal VOR gain gradually increased over time, reaching gains of 0.4-0.5 for yaw oscillations at 1.1 Hz approximately 5 mo after lateral canal inactivation. This response recovery was strongly frequency dependent: horizontal VOR gains were largest at the highest frequency tested and progressively decreased for lower frequencies. Below approximately 0.1 Hz, no consistent horizontal VOR could be elicited even 10 mo after plugging. 3. The frequency-dependent changes in gain paralleled changes in horizontal VOR phase. Below approximately 0.1-0.05 Hz large phase leads were present, similarly as in semicircular canal primary afferents. Smaller phase leads were also present at higher frequencies, particularly at 1.1 Hz (the highest frequency tested). 4. Consistent with the afferent-like dynamics of the adapted horizontal VOR, per- and postrotatory horizontal responses to constant-velocity yaw rotations were short lasting. Time constants of the slow-phase eye velocity envelope of the horizontal postrotatory nystagmus were approximately 2 s. Nonetheless, a consistent horizontal optokinetic afternystagmus was evoked in plugged animals. 5. A torsional component that was absent in intact animals was consistently present during yaw rotation acutely after lateral canal inactivation and remained approximately constant thereafter. The frequency response characteristics of this torsional component resembled those of the adapted horizontal slow-phase responses: gain decreased and large phase leads were introduced at frequencies below approximately 0.05-0.1 Hz. Torsional responses elicited by roll oscillations in supine position, on the other hand, were indistinguishable in their dynamics from intact animals. No consistent vertical nystagmus was elicited during yaw rotation. 6. Our results show that there is a slow, frequency-specific recovery of horizontal VOR after selective inactivation of the lateral semicircular canals. Both the spatial organization and the dynamic properties of the adapted VOR responses are distinctly different from responses in intact animals, suggesting complex changes in the underlying vestibuloocular circuitry.

NASA Program Space Physiology and Countermeasures↗
NASA NTRS1998

Vestibular influences on autonomic cardiovascular control in humans

There is substantial evidence that anatomical connections exist between vestibular and autonomic nuclei. Animal studies have shown functional interactions between the vestibular and autonomic systems. The nature of these interactions, however, is complex and has not been fully defined. Vestibular stimulation has been consistently found to reduce blood pressure in animals. Given the potential interaction between vestibular and autonomic pathways this finding could be explained by a reduction in sympathetic activity. However, rather than sympathetic inhibition, vestibular stimulation has consistently been shown to increase sympathetic outflow in cardiac and splanchnic vascular beds in most experimental models. Several clinical observations suggest that a link between vestibular and autonomic systems may also exist in humans. However, direct evidence for vestibular/autonomic interactions in humans is sparse. Motion sickness has been found to induce forearm vasodilation and reduce baroreflex gain, and head down neck flexion induces transient forearm and calf vasoconstriction. On the other hand, studies using optokinetic stimulation have found either very small, variable, or inconsistent changes in heart rate and blood pressure, despite substantial symptoms of motion sickness. Furthermore, caloric stimulation severe enough to produce nystagmus, dizziness, and nausea had no effect on sympathetic nerve activity measured directly with microneurography. No effect was observed on heart rate, blood pressure, or plasma norepinephrine. Several factors may explain the apparent discordance of these results, but more research is needed before we can define the potential importance of vestibular input to cardiovascular regulation and orthostatic tolerance in humans.

Review↗
NASA NTRS1992

Stabilization of gaze during circular locomotion in light. I. Compensatory head and eye nystagmus in the running monkey

1. A rhesus and cynomolgus monkey were trained to run around the perimeter of a circular platform in light. We call this "circular locomotion" because forward motion had an angular component. Head and body velocity in space were recorded with angular rate sensors and eye movements with electrooculography (EOG). From these measurements we derived signals related to the angular velocity of the eyes in the head (Eh), of the head on the body (Hb), of gaze on the body (Gb), of the body in space (Bs), of gaze in space (Gs), and of the gain of gaze (Gb/Bs). 2. The monkeys had continuous compensatory nystagmus of the head and eyes while running, which stabilized Gs during the slow phases. The eyes established and maintained compensatory gaze velocities at the beginning and end of the slow phases. The head contributed to gaze velocity during the middle of the slow phases. Slow phase Gb was as high as 250 degrees/s, and targets were fixed for gaze angles as large as 90-140 degrees. 3. Properties of the visual surround affected both the gain and strategy of gaze compensation in the one monkey tested. Gains of Eh ranged from 0.3 to 1.1 during compensatory gaze nystagmus. Gains of Hb varied around 0.3 (0.2-0.7), building to a maximum as Eh dropped while running past sectors of interest. Consistent with predictions, gaze gains varied from below to above unity, when translational and angular body movements with regard to the target were in opposite or the same directions, respectively. 4. Gaze moved in saccadic shifts in the direction of running during quick phases. Most head quick phases were small, and at times the head only paused during an eye quick phase. Eye quick phases were larger, ranging up to 60 degrees. This is larger than quick phases during passive rotation or saccades made with the head fixed. 5. These data indicate that head and eye nystagmus are natural phenomena that support gaze compensation during locomotion. Despite differential utilization of the head and eyes in various conditions, Gb compensated for Bs. There are various frames of reference in which an estimate of angular velocity that drives the head and eyes could be based. We infer that body in space velocity (Bs) is likely to be represented centrally to provide this signal.

Non-NASA Center↗