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Biomedical subjects

D S Zee

Publications and source records attributed to D S Zee.

At least 109 records · Page 6Linked to original sources
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1990

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↗
PubMed1989

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↗
PubMed1989

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↗
PubMed1989

Unilateral pursuit-induced congenital nystagmus.

We describe two patients with a lifelong history of oscillopsia only when following objects moving toward their left side. Neurologic examination was normal except for eye movements. The patients showed nystagmus during any tasks that required visual following toward the left (ie, smooth pursuit, optokinetic nystagmus, and vestibulo-ocular-reflex-suppression), but had no nystagmus during fixation of stationary targets or visual following tasks to the right. Eye-movement recordings showed waveforms during pursuit to the left that were typical of congenital nystagmus.

Adult↗
PubMed1989

Vergence.

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Convergence, Ocular↗
PubMed1989

Neurological aspects of vergence eye movements.

This review of vergence eye movements emphasizes the importance of performing a more rigorous examination of vergence at the bedside. Furthermore, recent experimental studies have better defined the physiological organization of brain-stem neurons that generate immediate premotor vergence commands. We emphasize analogies with the saccadic system and suggest that there are common organizational features of models for the generation of saccadic and of vergence movements. Finally, using the paradigm of spectacle-corrected anisometropia, we have demonstrated a remarkable adaptive capability that assures proper ocular alignment with changes of gaze.

Animals↗
PubMed1988

Smooth pursuit eye movements in schizophrenics: quantitative measurements with the search-coil technique.

Eye movements of five schizophrenic and five normal subjects were measured with the magnetic-field search-coil technique. Subjects followed targets moving smoothly at various speeds, either unpredictably in a step-ramp fashion or predictably in a triangular wave. The tracking stimulus was either a small dot or a large, richly-textured image that occupied a large portion of the visual field. Tracking by schizophrenics was abnormal; it was punctuated by catch-up saccades that corrected for smooth following movements of inadequate velocity. We did not, however, find saccadic intrusions, such as square wave jerks. Under all tracking conditions steady-state gains (eye velocity/target velocity) and, in the case of step-ramps, average acceleration in the first 120 ms were lower in patients than in normal subjects. The differences were most pronounced for tracking of the small target, moving at the highest speed tested (30 degree/s), in the nonpredictable, step-ramp waveform. With this stimulus mean steady-state gain was 0.36 (SD +/- 0.12) for the schizophrenic patients and 0.73 (SD +/- 0.11) for the normal subjects. When the target was changed to the large-field stimulus or moved in a predictable (triangular-wave) fashion, tracking improved in both patients and normal subjects, and even more so when these features were combined.

Adult↗
PubMed1988

Recovery from unilateral labyrinthectomy in rhesus monkey.

1. We recorded eye movements in six rhesus monkeys before and after unilateral labyrinthectomy and quantified the compensation for both the static and the dynamic disturbances of the vestibuloocular reflex (VOR). 2. When first recorded after labyrinthectomy (18-20 h postlesion), all animals had a spontaneous nystagmus with mean slow-phase velocities ranging from 24 to 54 degrees/s measured in darkness and 0-4 degrees/s measured in the light. The level of nystagmus diminished quickly, and by postoperative day 25 mean values ranged from 4 to 22 degrees/s, measured in darkness. The waveform of individual slow phases was variable, but in the first postoperative week its trajectory usually showed an increasing, or an increasing then decreasing, velocity. This finding indicates that peripheral vestibular lesions can alter the function of the ocular motor eye-position integrator. 3. The VOR gain (eye velocity/head velocity, corrected for spontaneous nystagmus) during rotations (30-300 degrees/s) in the dark was diminished from nearly 1.0 preoperatively to approximately 0.5 when first measured after labyrinthectomy, except for rotations toward the lesioned side at high speeds for which the gain was even lower. Within the first few postoperative days, for rotations toward the intact side, the VOR gain increased rapidly, to approximately 0.8. For rotations toward the lesioned side similar behavior was noted for stimuli of 30-60 degrees/s, but at higher velocities compensation proceeded more slowly. By 3 mo postoperatively gains had reached values ranging from 0.77 to 1.03 for rotations toward the intact side and from 0.61 to 0.98 for rotations toward the lesioned side. Values were higher for lower-velocity stimuli. 4. Caloric testing with ice water in the unoperated ear elicited nystagmus with a mean value of maximum slow-phase velocity of 129 degrees/s preoperatively and 195 degrees/s 3 mo postoperatively. There was no caloric response on the lesioned side. From the increase in caloric responses from the intact ear we infer considerable restoration of spontaneous activity of vestibular neurons on the deafferented side. 5. The time constant of the VOR was a function of stimulus speed preoperatively with a maximum mean value of 35 s for a 60 degrees/s stimulus. After labyrinthectomy the VOR time constant was low (6.0-9.1 s) at all speeds. Subsequently, in three animals only, there was a small increase (2-3 s) in VOR time constant during the 3-mo period following labyrinthectomy. These results indicate that labyrinthectomy profoundly and persistently impairs the action of the vestibular velocity-storage mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1988

Effect of lack of vision and of occipital lobectomy upon recovery from unilateral labyrinthectomy in rhesus monkey.

1. We investigated the influence of visual experience upon vestibular compensation in monkeys. Two paradigms were used to elicit vestibular adaptation: artificially imposed motion of images upon the retina during head rotation and unilateral labyrinthectomy. Two groups of animals were investigated: monkeys that underwent a bilateral occipital lobectomy and intact monkeys without a cortical lesion. Occipital lobectomy alone caused only a minor change in the vestibuloocular reflex (VOR); the gain (eye vel/head vel) decreased slightly (10-15%) for high speeds of rotation (180-300 degrees/s). 2. In response to a 4-h period of continuous oscillation of the head (0.25 Hz, 30 degrees/s) with the visual scene made to move in phase with the head (X0 viewing) or out of phase with the head (X2 viewing), intact monkeys showed an average 40% decrease or increase, respectively, of the VOR gain measured in darkness. After occipital lobectomy this adaptive capability was diminished, primarily for increasing the VOR gain after X2 viewing (42% preop to 13% postop). 3. Unilateral labyrinthectomy in either occipital-lobectomized or in otherwise intact monkeys led to a static imbalance with initial (18- to 20-h postlesion) values of spontaneous nystagmus of 22-62 degrees/s measured in darkness and to a dynamic disturbance with an approximately 50% decrease of VOR gain. Compensation for both abnormalities was studied in three groups of animals: previously occipital-lobectomized monkeys kept in the light after labyrinthectomy, intact monkeys kept in the light after labyrinthectomy, and intact monkeys kept in the dark for 4 days after labyrinthectomy and then exposed to light. Spontaneous nystagmus disappeared at the same rate in each group of animals. VOR gain increased in the intact monkeys kept in the light after labyrinthectomy but not in the intact monkeys kept in the dark after labyrinthectomy until they were exposed to light. The occipital-lobectomized monkeys showed some recovery of VOR gain (approximately 25-40%), but only at low speeds of rotation (30-60 degrees/s). Occipital lobectomy performed in monkeys after they had already compensated for a labyrinthectomy caused the VOR gain to drop to values approximately 0.5 but without any recurrence of spontaneous nystagmus. 4. Our results indicate that visual experience after labyrinthectomy is essential for recovery of VOR gain but not for resolution of spontaneous nystagmus. Furthermore, geniculostriate pathways play a major role in providing information about high velocities of retinal image motion that is necessary for the acquisition of VOR gain adaptation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗