Effect of head orientation and position on vestibuloocular reflex adaptation.
Explore the source record for details and available documents.
Acclimatization↗
Biomedical subjects
D S Zee
Publications and source records attributed to D S Zee.
Velocity storage in labyrinthine disorders.
We studied 13 patients with unilateral peripheral vestibular lesions following removal of acoustic neurinomas. The time constant of the VOR after surgery was 6.4 +/- 2.6 seconds (normal is 18.5 +/- 7.7 seconds). The time constant of OKAN after surgery was 7.2 +/- 1.8 seconds (normal is 11.3 +/- 3.2 seconds). The mean initial velocity of OKAN after surgery was 9.7 +/- 2.4 deg/second (normal is 11.7 +/- 5.9 deg/second). These data suggest that unilateral peripheral vestibular loss is associated with a complete loss of velocity storage for canal input but only a partial loss of velocity storage for visual input. These results can be accounted for by current mathematical models of the velocity storage mechanism.
Humans↗
Disconjugate ocular motor adaptation in rhesus monkey.
We report a model for inducing disconjugate, orbital-position dependent, ocular motor adaptation in the rhesus monkey. Animals wore a combination of laterally-displacing prisms placed in front of one eye calling for a discrete change in ocular alignment when the eyes reached particular orbital positions. After wearing the prism combination the animals developed adaptive changes both in static alignment during fixation and in dynamic alignment during eye movements. These changes persisted with only one eye viewing and so became independent of the immediate presence of disparity cues. There were, however, imperfections in the adaptive responses; the changes in the innervation were gradual across the prism edge, not abrupt as required. This finding may reflect inherent limitations in the capability for disconjugate adaptation.
Adaptation, Ocular↗
Abnormalities of predictive saccades in hemi-Parkinson's disease.
We studied reflexive and predictive saccades by direct current electro-oculography in nine patients with mild hemi-Parkinson's disease (hemi-PD) and in 16 age-matched controls. In five patients, the neurological syndrome was predominant on the right side of the body (RPD) and in four patients, on the left side (LPD). Reflexive saccades were elicited in response to the random appearance (timing and location) of a light-emitting diode (LED). Predictive saccades were elicited by alternatively illuminating LEDs at 10 degrees right and left, at various fixed frequencies (0.25-1 Hz). In the reflexive task, latency and amplitude of the saccades were normal in both PD groups. In the predictive task, mean saccade latency was not significantly different between patients and normals but there were two significant abnormalities in timing: first, but only in LPD, a directional asymmetry in latency (left greater than right, e.g. at 0.25 Hz, mean difference of 90 ms); secondly, especially in RPD, an abnormal tracking pattern, reflected by more variability of the mean value (for each group of patients) of saccade latency at each point in time, throughout a period of tracking at a given frequency. Predictive saccades were also strongly hypometric in both PD groups but especially in LPD (e.g. for rightwards saccades: controls = 19 degrees, SD = 1.6; LPD = 14 degrees, SD = 2.7; RPD = 15.7 degrees, SD = 2.3). These defects in saccadic timing and amplitude during predictive tracking were most salient at low frequencies. While these defects were largely bilateral, our findings suggest slightly different contributions of the right and left cerebral hemispheres to the spatial and timing components, respectively, that comprise optimal predictive saccadic behaviour.
Adult↗
Saccade-vergence interactions in humans.
1. We recorded eye movements in four normal human subjects during refixations between targets calling for various combinations of saccades and vergence. We confirmed and extended prior observations of 1) transient changes in horizontal ocular alignment during both pure horizontal saccades (relative divergence followed by relative convergence) and pure vertical saccades (usually divergence for upward and convergence for downward saccades); 2) occasional, high-frequency (20-25 Hz), conjugate oscillations along the axis orthogonal to the main saccade; and 3) the speeding up of horizontal vergence by both horizontal and vertical saccades. 2. To interpret these findings, we developed a hypothesis for the generation of vergence to step changes in target depth, both with and without associated saccades. The essential features of this hypothesis are 1) the transient changes in horizontal ocular alignment during pure horizontal saccades reflect asymmetries in the mechanical properties of the lateral and medial rectus muscles causing adduction to lag abduction; 2) pure vergence movements in response to step changes in target depth are generated by a neural network that uses a desired change in vergence position as its input command and instantaneous vergence motor error (the difference between the desired change and the actual change in vergence) to drive vergence premoter neurons; and 3) the facilitation of horizontal vergence by saccades arises from nonlinear interactions in central premotor circuits. 3. The hypothetical network for generating pure vergence to step changes in target depth is analogous in structure to the local feedback model for the generation of saccades and has the same conceptual appeal. With the assumption of a single nonlinearity describing the relationship between a vergence motor error signal and the output of the neurons that generate promoter vergence velocity commands, this model generates pure vergence movements with peak velocity-amplitude relationships and trajectories that closely match those of experimental data. 4. Several types of models are proposed for the central, nonlinear interaction that occurs when saccades and vergence are combined. Common to all models is the idea that omnidirectional pause neurons (OPN), which are thought to gate activity for saccade burst neurons, also gate activity for saccade-related vergence. In one model we hypothesize the existence of a separate class of saccade-related vergence burst neurons, which generate premotor horizontal vergence commands but only during saccades. In a second model we hypothesize separate right eye and left eye saccadic burst neurons that receive not only conjugate, but also equal but oppositely directed vergence error signals.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Postural stability in patients with Huntington's disease.
We characterized postural stability in patients with Huntington's disease (HD) by examining their ability to use different sensory cues to maintain balance and by recording their automatic postural responses to externally applied perturbations. Our HD patients, like normal subjects, depended more on proprioceptive than on visual cues to maintain balance. HD patients, however, developed more sway than normal subjects when proprioceptive cues, or when proprioceptive cues and vision, were altered. Thus, HD patients showed a defect in using vestibular information alone to maintain normal postural stability. The onset of compensatory motor responses in the lower extremities following sudden translations of the support surface was delayed by 30 to 60 msec in HD patients as compared with normal subjects. HD patients also had more sway and falls during unexpected rotations of the support surface, although they could appropriately reduce their motor responses on the next trial.
Adult↗
Internuclear ophthalmoplegia: pathophysiology and diagnosis.
The main findings in unilateral INO are paresis of adduction in the eye on the side of the lesion (for conjugate but not vergence eye movements) and abduction nystagmus in the eye on the side opposite to the lesion. A skew deviation (eye usually higher on the side of the lesion) or a dissociated, mixed vertical-torsional nystagmus, with the eye beating down on the side of the lesion, may also occur. The main findings in bilateral INO are paresis of adduction in both eyes, bilateral abduction nystagmus and, in the vertical plane, impaired gaze-holding, vestibular responses and smooth tracking. Abduction nystagmus in INO may have a number of causes; probably most common are a gaze-evoked nystagmus superimposed on adduction weakness and adaptation to adduction weakness. Most of the findings in INO can be explained by interruption of projections from abducens internuclear neurones, mediating adduction, and from the vestibular nuclei, mediating both canal- and otolith-induced reflexes as well as vertical gaze holding and pursuit. Extension of the lesion to structures near but outside the MLF, or involvement of cell bodies intermixed with MLF fibres, may also be important in the pathogenesis of the abduction nystagmus and the occasional slowing of abducting saccades.
Eye Movements↗
Clinical implications of otolith-ocular reflexes.
While difficult to test clinically, otolith-induced vestibular responses play an important role in both vestibulo-ocular and vestibulo-spinal reflexes, and are likely a source of symptoms in patients with vestibular disorders. Here we review basic aspects of otolith-induced vestibulo-ocular reflexes and consider some clinical implications of disordered otolith function. Emphasis is placed on ocular responses to translation and to tilt and the influence of gravity on vestibulo-ocular responses induced during head rotation.
Adaptation, Physiological↗
Microsaccadic flutter.
Microsaccadic flutter is a rare symptomatic saccadic oscillation that has been reported only twice previously. Here we describe 5 patients with this disorder. The oscillation is horizontal, has a frequency of 15-30 Hz, an amplitude of 0.1-0.5 degrees, and cannot be seen with the unaided eye. It is usually not associated with any underlying neurological disorder. We hypothesize that microsaccadic flutter is due to malfunction of the brainstem omnipause neurons.
Abducens Nerve↗
Abolition of optokinetic afternystagmus by aminoglycoside ototoxicity.
We studied optokinetic afternystagmus in eight subjects with loss of or impairment of vestibular function due to ototoxic antibiotics. We found that the initial amplitude, the time constant, and the slow-phase cumulative eye position of optokinetic afternystagmus were significantly reduced in the patients. Slow-phase cumulative eye position most reliably distinguished our patients' responses from those of a normal group.
Adult↗
Acquired pendular nystagmus in toluene addiction.
We studied the ocular motor abnormalities in 4 patients chronically addicted to sniffing glue containing toluene. They showed acquired pendular nystagmus with horizontal and vertical components. One patient also showed saccadic oscillations. The pendular nystagmus may be a manifestation of a disturbance in brainstem-cerebellar connections secondary to the toxic effect of toluene on white matter.
Adult↗
Saccades in Huntington's disease: predictive tracking and interaction between release of fixation and initiation of saccades.
We compared saccadic eye movements in 21 patients with Huntington's disease (HD) and 21 normal subjects. In a predictive tracking task, HD patients were unable to anticipate normally the timing and location of a visual target that alternated its position predictably (+/- 10 degrees, 0.5 Hz; mean latency of +170 msec in HD and -78 msec in normal subjects). HD patients and normal subjects, however, showed comparable decreases in saccade latency (110 msec in HD, 124 msec in normal subjects) when the fixation target was turned off 200 msec before (gap task) versus 200 msec after (overlap task) the appearance of an unexpected peripheral stimulus. Taken together, these findings support the idea that HD patients show greater defects in initiating internally generated than in initiating externally triggered saccades. This dichotomy is likely due to involvement of frontal lobe--basal ganglia structures in HD, with relative sparing of parietal--superior collicular pathways.
Adult↗
Postural control in Huntington's disease (HD).
We studied postural control, using quantitative moving-platform posturography, in 20 patients with Huntington's Disease (HD) and in 20 age-matched controls. HD patients showed considerably more anterior-posterior sway than normals, even when a correction for chorea was attempted. This increase in sway was especially true when, by eliminating visual and by attenuating proprioceptive cues, patients were forced to rely primarily on vestibular cues for balance. HD patients also showed increased latencies (30-50 ms) but normal amplitude, in response to translational perturbations of the platform. HD patients showed increased amplitude of responses to rotational perturbations of the platform but a normal decrease in response on successive trials. Thus, patients with HD show a consistent pattern of abnormality on posturography suggesting a role for the basal ganglia in a number of aspects of postural control.
Cognition↗
Adaptation to vestibular disturbances: some clinical implications.
A knowledge of the mechanisms used in adaptation to vestibular lesions is important for both diagnostic and therapeutic purposes. Here we discuss commonly encountered circumstances--habitual wearing of spectacles, unilateral or bilateral labyrinthine dysfunction--that call for adaptation. The context specificity of vestibular adaptation is emphasized because of its crucial role in designing programs of physical therapy. The pharmacological manipulation of plasticity, either purposeful facilitation, or inadvertent retardation, is an area of current investigation of direct clinical importance. Finally, the wide range of adaptive responses and strategies available to participate in the compensatory process is emphasized, so that they can be marshalled together to optimize vision and balance.
Adaptation, Ocular↗
Disconjugate adaptation to long-standing, large-amplitude, spectacle-corrected anisometropia.
A 12-yr-old anisometropic patient had worn corrective eyeglasses (right eye, -0.50 +1.50 x 125; LE, -9.75 +2.50 x 60) for 7 yr, and then changed to contact lenses. Eye movements were recorded before and after the change to contact lenses using binocular search coils. In habitual spectacle viewing, the patient showed disconjugate adaptation. During monocular viewing, for example, ocular alignment changed by as much as 4 degrees during a 20 degrees saccade. Also, during monocular viewing, with either eye, placing the spectacle lens in front of the eye caused an increase in the disconjugate adaptive response compared with viewing without lenses. This finding emphasizes the context specificity of adaptive responses. After switching to contact lenses, the patient still wore his spectacles for 20-40 min each day. Although there was little residual disconjugate adaptation for vertical saccades, he showed considerable adaptation for horizontal saccades, especially for gaze changes that required divergence. The persistence of a partial state of disconjugate adaptation allowed the patient to use immediate, disparity-induced, horizontal vergence to aid ocular alignment in either the contact-lens-viewing or the spectacle-viewing condition. A more complete reversion to conjugacy occurred after nine days of exclusive use of his contact lenses. Then, in a short-term experiment, two minutes of binocular viewing through the eyeglasses induced a considerable reversion toward the previous state of disconjugate adaptation (up to 1.25 degrees of vergence change during monocular viewing). Finally, the waveform of the adapted (to spectacles) intrasaccadic vergence change with monocular viewing was similar to the waveform of the unadapted intrasaccadic vergence change during binocular refixations between targets that required a combined saccade and vergence. This finding suggests a common mechanism for adaptation to spectacle-corrected anisometropia and for normal binocular vergence-saccade interactions.
Adaptation, Ocular↗
Optokinetic nystagmus and afternystagmus in human beings: relationship to nonlinear processing of information about retinal slip.
In four normal human subjects we measured eye movements during full-field optokinetic stimulation (10-220 deg/s) and determined the relationship among retinal-slip velocity (drum velocity minus slow-phase eye velocity), the slow-phase velocity of optokinetic nystagmus (OKN) and the initial value of the slow-phase velocity of optokinetic afternystagmus (OKAN) measured in darkness. OKN and OKAN were maximum (63-84 and 11-19 deg/s, respectively) when retinal slip ranged from 30-100 deg/s. For higher values of retinal slip, OKN and OKAN fell (in 3 subjects) or reached a plateau (in the fourth). The amplitude of OKAN in human beings was much less than that reported in monkeys. The shape, however, of the curve relating retinal slip to the amplitude of OKAN was similar to that of monkeys. Furthermore, in both cases the curve resembles that obtained by plotting the results of experimental recordings of neural discharge in the nucleus of the optic tract as a function of retinal slip. These results imply that the processing of visual information for generation of OKAN is similar in monkeys and human beings but that the gain of the system is much less in human beings. We also found that fixation of a small target during optokinetic stimulation nearly completely prevented the development of OKAN while fixation of a small target for short periods after optokinetic stimulation did not alter the pattern of decay of OKAN. Thus, fixation may actively prevent the coupling of visual information into the velocity-storage mechanism.
Adult↗
Vestibular testing in comatose patients.
The analysis of vestibular responses in a comatose patient often provides the critical information for making a correct preliminary diagnosis and directing the subsequent laboratory evaluation. Because of some uncertainties about what is being tested with the various bedside maneuvers that are used to elicit vestibular responses, we review the physiologic basis for the oculomotor responses that occur with head rotation or with caloric stimuli. We further urge precise and unambiguous terminology to describe both stimulus and response. We suggest using physiologically well-defined terms such as vestibulo-ocular reflex and cervico-ocular reflex and avoiding potentially misleading terms such as the doll's head and the oculocephalic maneuvers.
Coma↗
Optokinetic afternystagmus in humans: normal values of amplitude, time constant, and asymmetry.
It has been suggested that the appearance of directional asymmetry and/or a reduced time constant of optokinetic afternystagmus (OKAN) might be a clinical index of vestibular imbalance. However, we do not know the limits for OKAN parameters in normal humans. Accordingly, we studied OKAN in 30 normal subjects using a "sampling" method, in which a number of values of OKAN are obtained by turning out the lights periodically during optokinetic stimulation. We found that the initial velocity of OKAN has a large intrasubject variability. Accordingly, if precision is desired so as to obtain 95% confidence that the measured mean of the initial velocity of OKAN is within 25% of the true mean in an individual subject, at least eight measurements of the initial OKAN velocity must be taken. When 12 measurements are made, all subjects had a minimum value of 5 degrees/s initial OKAN, and there was little directional asymmetry (mean of -0.47 degree/s +/- 3.13 degrees/s). The intrasubject variability of the time constant of OKAN was similar to the variability of initial OKAN velocity. However, because it is not possible to obtain repeated measures of the time constant in a short period of time, the time constant of OKAN is less likely to be useful in clinical testing.
Adult↗