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Biomedical subjects

D S Zee

Publications and source records attributed to D S Zee.

At least 163 records · Page 9Linked to original sources
PubMed1979

Rebound nystagmus: EOG analysis of a case with a floccular tumour.

Eye movements were recorded and quantitatively analysed in a patient with a tumour initially involving the cerebellar flocculus. Ocular motor abnormalities included (1) impaired smooth pursuit, (2) impaired cancellation of the vestibulo-ocular reflex when fixating an object rotating with the head, and (3) gaze paretic and rebound nystagmus. Comparable findings have been reported in monkeys with experimental floccular lesions. The rebound nystagmus (but not the other ocular motor abnormalities) disappeared when the tumour appeared to invade the brain stem in the region near the vestibular nuclei. This finding suggests that the floccular lesion unmasked a bias which created rebound nystagmus and that the bias probably arose in the vestibular nuclei.

Adolescent↗
PubMed1978

Eye-head coordination in labyrinthine-defective human beings.

(1) Eye-head coordination was studied in three human beings with absent labyrinthine function. Each subject adopted a unique pattern of adaptive responses to achieve optimal gaze stability. (2) One subject used saccades (even in darkness) to help stabilize gaze. In addition, during rotation of the body with the head stationary in darkness, he made slow and quick phases of nystagmus in the same direction. This subject apparently used quick phases to help stabilize gaze rather than to redirect the center of visual attention. (3) One subject, to help prevent gaze overshoot, showed a decrease in the saccadic amplitude-retinal error relationship selectively during active combined eye-head movements. (4) One subject showed a significant amount of preprogramming of compensatory slow phases independent of actual head motion. (5) In all subjects, the passively induced cervico-ocular reflex was moderately potentiated, accounting for about 25% of compensation for head motion during active target seeking. (6) In all subjects, 'effort of spatial localization', as shown by imagining targets in total darkness, increased the velocity of compensatory slow phases to near that of head movements during both active and passively induced head rotations. (7) In all subjects, gaze stability was enhanced during tracking of targets jumping in a predictable fashion. (8) The choice of strategies used by each subject may depend, in part, upon the latency of the cervico-ocular reflex during active head movements.

Adaptation, Physiological↗
PubMed1977

Abnormal saccades in paralytic strabismus.

Saccadic eye movements were measured in ten patients with unilateral limitation of function of an extraocular muscle. With the paretic eye fixating, there were a series of saccades when refixating in the direction opposite to the paralysis. Between each saccade, the eye drifted back toward the starting position; the drift rate decreased as the eye moved into the field of action of the strong agonist muscle. In one patient, the normal (covered) eye was immobilized during attempted refixations. In this case, the abnormal pattern of saccades made by the paretic eye persisted. Thus, the central nervous system uses innervation or efference to calculate the position of the eye in the orbit for saccadic eye movements.

Eye Movements↗
PubMed1976

Slow saccades in spinocerebellar degeneration.

Two patients with spinocerebellar degeneration made abnormally slow horizontal refixations. One patient produced quick phases of nystagmus with identical maximum velocities, suggesting her refixations were abnormal saccades and not voluntary pursuit movements. In response to double target jumps, neither patient showed an obligatory refractory period after each saccade; they responded to every target movement after one reaction time. Their slow refixations were not preprogrammed since they could be modified in flight. To reconcile these observations with normal saccadic behavior, we hypothesized a neural network that made saccades by driving the eyes to an orbital position rather than preprogramming a distance for movement. Computer simulation of this model produced both realistically appearing normal saccades and, when appropriately "lesioned" to simulate a loss of saccadic "burst" neurons in the pontine reticular formation, slow saccades that could be modified in flight.

Adolescent↗
PubMed1976

Ophthalmoplegia and dissociated nystagmus in adetalipoproteinemia.

A characteristic pattern of acquired exotropia, progressive paresis of the medial rectus muscles, and dissociated nystagmus on lateral gaze was found in three patients with abetalipoproteinemia. Study with electronystagmography of the eye movements of one patient revealed abnormally slow voluntary saccades and slow or absent fast components of vestibular nystagmus, optokinetic nystagmus, and jerk-type, disassociated nystagmus. Defects in central nervous system centers generating saccadic eye movements are postulated.

Abetalipoproteinemia↗
PubMed1976

Rapid eye movements in myasthenia gravis. II. Electro-oculographic analysis.

Voluntary saccades were studied by electro-oculography in ten patients with myasthenia gravis (MG) and in eight patients with other types of ophthalmoplegia. Despite limited range of eye movements, maximum velocities of 20 degree and 40 degree saccades in patients with MG were not significantly different from those in normal individuals, whereas maximum velocities in patients with other types of ophthalmoplegia were significantly decreased. In some myasthenic patients, small amplitude saccades were hypermetric and had high velocities, appearing clinically as "quiver" movements characteristic of MG. In MG the preservation of saccades with high initial velocities, even in the presence of severe ophthalmoplegia, suggests that muscle fibers generating rapid movements during saccades (twitch fibers) can be relatively spared when muscle fibers responsible for maintenance of excentric gaze (tonic fibers) are severely affected.

Adolescent↗
PubMed1976

Ocular manifestations of acute pandysautonomia.

A 33-year-old white man developed premature presbyopia and anisocoria as initial manifestations of acute pandysautonomia. Nine months later signs and symptoms of generalized, severe autonomic dysfunction developed, and six years later only paralysis of pupillary reactions, presbyopia, and orthostatic hypotension were unresolved. Pharmacologic testing of the pupils demonstrated no mydriasis to cocaine 4% or hydroxyamphetamine 1% and hypersensitivity to epinephrine 0.1%, methacholine 2.5%, and pilocarpine 0.0625%, suggesting the presence of sympathetic and parasympathetic, postganglionic blockage of autonomic innervation of the iris.

Adult↗
PubMed1976

Ocular motor abnormalities in hereditary cerebellar ataxia.

Twelve members of a family with hereditary cerebellar ataxia of late onset were examined and, in 5, quantitative recording of eye movements were obtained. The initial and most severe symptom in all patients was ataxia of gait, followed by dysarthria and later by dysmetria of the limbs. Clinical examination did not reveal involvement of structures other than the cerebellum. Ocular motor examination showed: (1) inability to hold eccentric gaze resulting in gaze-paretic nystagmus; (2) downward beating nystagmus, accentuated on lateral gaze; (3) defective smooth pursuit, with relative preservation of optokinetic nystagmus induced by full-field stimulation; (4) rebound nystagmus; (5) enhanced gain (eye velocity/head velocity) of the vestibulo-ocular reflex during rotation in darkness; (6) decreased ability to suppress the vestibulo-ocular reflex during fixation of an object rotating with the patient; (7) saccadic dysmetria, especially downward overshoot; and (8) square wave-jerks. Although each of these signs can probably occur with lesions elsewhere in the brain, in combination they are highly suggestive of cerebellar involvement. With the reservation that we do not yet have pathological confirmation of the location of our patients' lesions, our results support the suggestion that the cerebellum specifically: (1) helps maintain eccentric gaze; (2) produces smooth pursuit eye movements; and (3) modulates the amplitude of saccadic eye movements. Many of the characteristics of the altered vestibulo-ocular responses and rebound nystagmus could be explained by the underlying anomaly in the smooth pursuit system.

Adult↗