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Biomedical subjects

D S Zee

Publications and source records attributed to D S Zee.

At least 145 records · Page 8Linked to original sources
PubMed1984

Signals used to compute errors in monkey vestibuloocular reflex: possible role of flocculus.

Adaptive changes were induced in the vestibuloocular reflex (VOR) of monkeys by oscillating them while they viewed the visual scene through optical devices ("spectacles") that required changes in the amplitude of eye movement during head turns. The "gain" of the VOR (eye velocity divided by head velocity) during sinusoidal oscillation in darkness underwent gradual changes that were appropriate to reduce the motion of images on the retina during the adapting procedures. Bilateral ablation of the flocculus and ventral paraflocculus caused a complete and enduring loss of the ability to undergo adaptive changes in the VOR. Partial lesions caused a substantial but incomplete loss of the adaptive capability. We conclude that the flocculus is necessary for adaptive changes in the monkey's VOR. Further experiments in normal animals determined the types of stimuli that were necessary and/or sufficient to cause changes in VOR gain. Full-field visual stimulation was not necessary to induce adaptive changes in the VOR. Monkeys tracked a small spot in conditions that elicited the same combination of eye and head movements seen during passive oscillation with spectacles. The gain of the VOR showed changes 50-70% as large as those produced by the same duration of oscillation with spectacles. Since the effective tracking conditions cause a consistent correlation of floccular output with vestibular inputs, these data are compatible with our previous suggestion that the flocculus may provide signals used by the central nervous system to compute errors in the gain of the VOR. Prolonged sinusoidal optokinetic stimulation with the head stationary caused only a slight increase in VOR gain. Left-right reversal of vision and eye movement during sinusoidal vestibular oscillation caused decreases in VOR gain. In rabbits, both of these stimulus conditions produced large increases in the gain of the VOR, which implied that eye velocity signals were used instead of vestibular inputs to compute errors in the VOR. Our different results argue that vestibular signals are necessary for computing errors in VOR gain in the monkey. The species difference may reflect the additional role that smooth pursuit eye movements play in stabilizing gaze during head turns in monkeys.

Animals↗
PubMed1984

Vestibulo-ocular and optokinetic deficits in albinos with congenital nystagmus.

Vestibular and optokinetic responses were recorded in three albino subjects with congenital nystagmus. Although an ice-water caloric stimulus did not elicit nystagmus, all patients showed a response to rotational stimuli containing high frequency components. Vestibular responses to a constant velocity rotation decremented with abnormally short time constants of 1-2 sec (normal 15-20 sec). For sinusoidal oscillation, in one subject, the cut-off frequency (where the amplitude of the response was 70% of maximum) was increased to 0.8 Hz (normal about 0.01 Hz). Full-field optokinetic stimulation generated no nystagmus response. These abnormalities may be due to defects in networks that act as mathematical integrators : either the final common neural gaze-holding network that converts velocity into position information for the ocular motor neurons or the "velocity-storage" mechanism that normally combines sensory inputs from both the labyrinths and visual system to generate appropriate (per-rotatory) nystagmus during rotation and to suppress inappropriate (post-rotatory) nystagmus after rotation.

Adult↗
PubMed1983

Blink-saccade synkinesis.

We studied two patients who could make saccades of normal velocity and amplitude only in association with a simultaneous blink. In one patient, the initiation of saccades was also facilitated by blinks. Both patients had signs of cerebellar or brainstem dysfunction, suggesting a posterior fossa localization for blink facilitation of saccadic velocity and amplitude.

Adult↗
PubMed1983

Downbeat nystagmus. A case report of herpetic brain stem encephalitis.

A 35-year-old man with aplastic anemia developed prominent downbeat nystagmus 80 days after receiving an allogeneic bone marrow transplant. A diagnosis of herpes simplex encephalitis was made which was confirmed by positive virus cultures at autopsy 1 week later. Routine pathologic examination of the brain stem revealed no lesions which would explain the downbeat nystagmus. Immunoperoxidase studies, however, revealed virus-infected neurones throughout the brain stem including the nuclei of the basis pontis, the superior olive, and nuclei of the spinal tracts of 5 and 10. The significance of "negative" pathologic brain stem findings in cases of downbeat nystagmus is discussed.

Adult↗
PubMed1983

Disorders of eye movements.

Eye movements serve the needs of our visual sense and can be classified into subtypes according to their specific functions. Main functions and dysfunctions are given, with an emphasis on nystagmus.

Abducens Nerve↗
PubMed1982

Visual following during stimulation of an immobile eye (the open loop condition).

We had the rare opportunity to examine a patient with a unilateral complete ophthalmoplegia in an eye with normal visual acuity. We recorded the movements of the covered, sound eye of the patient during full-field optokinetic stimulation of his seeing, immobile eye (open loop condition). The open loop gain for low velocity stimuli (less than 1 deg/sec) was high (greater than 50) but progressively fell with faster stimuli. This finding is inconsistent with the representation of the optokinetic system as a linear velocity servo. In a second experiment, the patient foveally fixated, with the immobile eye, a head-fixed target during sinusoidal, en block rotation. The vestibular movements of the sound eye were suppressed, even though no retinal image motion occurred in the seeing eye. This suggests that visual attention to a stable retinal image can be used to suppress the vestibulo-ocular reflex. Our results were from one patient only and any generalizations must be made cautiously. Nevertheless, our findings are comparable with previous "open loop" studies in normal human beings and patients.

Electrooculography↗
PubMed1981

The behavior of the vestibulo-ocular reflex at high velocities of head rotation.

The behavior of the vestibulo-ocular reflex (VOR) during both passive and active, high-velocity head movements was recorded in three normal subjects. We found that the VOR is compensatory for head velocities up to at least 350 deg . s-1, during both active and passive head rotation provided there is an attempt to visualize a real (or imagined) stationary object in space. Slow phase velocities, however, could reach values as high as 500 deg . s-1. Furthermore, during passive rotation at high velocities, the quick phase trajectory is modified--indicating an interaction between the slow phase and quick phase eye velocity commands.

Adult↗
PubMed1980

Cerebellar control of ocular gaze stability.

The ability to hold an eccentric position of gaze has been attributed to a brainstem network termed the ocular motor neural integrator. For this integrator to function properly, an intact cerebellum is necessary. This report describes a patient with cerebellar dysfunction who showed an unusual form of nystagmus: each slow phase had a waveform of increasing velocity. This contrasts with gaze paretic nystagmus, the more typical manifestation of cerebellar disorder, in which each slow phase has a waveform of decreasing velocity. Based on these observations and results from basic research, we propose that (1) the cerebellum controls neural integration in the brainstem by a positive feedback loop, and (2) pathological alterations in the strength of transmission (or gain) through the feedback loop cause the eyes to drift off target, with either an exponentially increasing (gain too high) or decreasing (gain too low) velocity.

Brain Stem↗
PubMed1980

Treatment of periodic alternating nystagmus.

Two patients with longstanding acquired periodic alternating nystagmus (PAN) were treated with baclofen, 30 mg/day. Baclofen abolished the PAN and relieved oscillopsia in both patients but was ineffective in another patient with congenital PAN.

Adult↗
PubMed1980

Eye movements of the blind.

We investigated a group of patients who were blind because of disease affecting the anterior visual pathways. All subjects showed an inability to maintain steady eye position, with a consequent jerk nystagmus. Blindness from birth was associated with an impaired vestibuloocular reflex and inability to voluntarily initiate saccades, although quick phases of nystagmus were maintained. Acquired blindness was associated with relatively preserved vestibulo-ocular responses and the ability to initiate voluntary saccades and smoothly track self-moved targets. Certain features of the eye movements of the blind are similar to those due to cerebellar dysfunction.

Adolescent↗
PubMed1979

A hypothetical explanation of saccadic oscillations.

Eye movements in a patient with saccadic oscillations (ocular flutter) were recorded and analyzed. Findings were related to recent microelectrode studies in the monkey pontine reticular formation which have identified three types of premotor neurons related to saccadic eye movements: burst, tonic, and pause cells. We incorporated these cell types into a hypothetical circuit that generates saccades by rapidly driving the eye to a designated orbital position rather than preprogramming a distance for movement. Physiological measurements suggest that this neural network is unstable and that the burst neurons must be tonically inhibited to prevent saccadic oscillations during periods of fixation. Pause cells, which discharge tonically except during saccades, when they pause, appear to inhibit burst cells and prevent such saccadic oscillations. Analysis of our patient's behavior indicates that many types of saccadic oscillations can be explained and classified by assuming an abnormality of pause cell control over saccadic burst neurons.

Adult↗