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Biomedical subjects

D S Zee

Publications and source records attributed to D S Zee.

At least 55 records · Page 3Linked to original sources
PubMed1999

Hyperventilation-induced nystagmus in patients with vestibular schwannoma.

OBJECTIVE: To analyze the nystagmus evoked by hyperventilation in patients with unilateral vestibular schwannoma and to use this information to predict the effects of hyperventilation on individual ampullary nerves. METHODS: Three-dimensional scleral search coil eye movement recording techniques were used to record the magnitude and time course of eye movements in six patients with unilateral vestibular schwannoma and hyperventilation-induced nystagmus. The presenting complaints in five of these patients were vertigo or dysequilibrium. RESULTS: The eye movement response to hyperventilation was a "recovery" nystagmus with slow-phase components corresponding to excitation of the affected vestibular nerve. Projection of the eye velocity vector into the plane of the semicircular canals revealed that fibers arising from the ampulla of the horizontal canal were most affected by hyperventilation with lesser activation of fibers to the superior canal and smaller, more variable responses from posterior canal fibers. CONCLUSIONS: The three-dimensional characteristics of the nystagmus evoked by hyperventilation in patients with vestibular schwannoma provide insight into the vestibular end organs affected by the tumor and the mechanism responsible for the nystagmus. This finding indicates that hyperventilation resulted in a transient increase in activity from these partially demyelinated axons.

Adult↗
PubMed1999

The effect of hyperventilation on downbeat nystagmus in cerebellar disorders.

Hyperventilation can affect nystagmus in patients with vestibular disorders. However, the effects on nystagmus in patients with cerebellar disease have not been systematically studied. Using the magnetic field search coil technique, we studied the effects of hyperventilation on nystagmus in a series of cerebellar patients. In four of eight patients, hyperventilation produced an increase in the slow-phase velocity of downbeat nystagmus. We speculate that this effect may be mediated through metabolic effects on cerebellar calcium channels.

Adult↗
PubMed1999

Directional abnormalities of vestibular and optokinetic responses in cerebellar disease.

Directional abnormalities of vestibular and optokinetic responses in patients with cerebellar degeneration are reported. Three-axis magnetic search-coil recordings of the eye and head were performed in eight cerebellar patients. Among these patients, examples of directional cross-coupling were found during (1) high-frequency, high-acceleration head thrusts; (2) constant-velocity chair rotations with the head fixed; (3) constant-velocity optokinetic stimulation; and (4) following repetitive head shaking. Cross-coupling during horizontal head thrusts consisted of an inappropriate upward eye-velocity component. In some patients, sustained constant-velocity yaw-axis chair rotations produced a mixed horizontal-torsional nystagmus and/or an increase in the baseline vertical slow-phase velocity. Following horizontal head shaking, some patients showed an increase in the slow-phase velocity of their downbeat nystagmus. These various forms of cross-coupling did not necessarily occur to the same degree in a given patient; this suggests that different mechanisms may be responsible. It is suggested that cross-coupling during head thrusts may reflect a loss of calibration of brainstem connections involved in the direct vestibular pathways, perhaps due to dysfunction of the flocculus. Cross-coupling during constant-velocity rotations and following head shaking may result from a misorientation of the angular eye-velocity vector in the velocity-storage system. Finally, responses to horizontal optokinetic stimulation included an inappropriate torsional component in some patients. This suggests that the underlying organization of horizontal optokinetic tracking is in labyrinthine coordinates. The findings are also consistent with prior animal-lesion studies that have shown a role for the vestibulocerebellum in the control of the direction of the VOR.

Adult↗
PubMed1999

Disconjugate adaptation of saccades: contribution of binocular and monocular mechanisms.

We studied the effects of prism-induced disparity on static and intrasaccadic alignment in six normal human subjects. A ten diopter base-out prism, calling for convergence, was placed in front of the central field of the right eye, so that at the center the eye viewed through the prism; at left and right, outside the prism. During 15 min of training, subjects made repetitive saccades solely in the right field of vision (C-R-C sequence). This paradigm required relative divergence for centrifugal (C-R) saccades and relative convergence for centripetal (R-C) saccades, as well as increase of the amplitude for all saccades made by the right eye. We found that during training, all subjects incorporated the necessary change in alignment into the saccades. After training the resultant intrasaccadic disconjugacy persisted when tested during monocular viewing, indicating that motor learning had occurred. Subjects demonstrated increased divergence for C-R and increased convergence for R-C saccades, in accordance with the change acquired during adaptation to the prism. In addition, five subjects developed increased divergence for C-L saccades, for which they did not train. Smaller and less consistent divergence was also observed for L-C saccades. Changes in intrasaccadic alignment were accompanied by changes in the relative velocities of the two eyes' saccades and slowing of the peak velocities in both eyes during training. Static alignment showed a general tendency toward convergence that did not parallel the changes in the intrasaccadic alignment, suggesting that saccade adaptation is system-specific. The pattern of transfer of the intrasaccadic disconjugacy to saccades in the untrained field and the changes in the relative speeds of the two eyes cannot be explained by monocular adjustment of the saccades. Our results indicate that both a binocular mechanism--saccade-vergence interaction--and monocular adaptation contribute to disconjugate adaptation of saccades.

Adaptation, Psychological↗
PubMed1999

Eye-movement recordings in the evaluation of ophthalmologic and neurologic disorders.

This review focuses on the use of quantitative eye-movement recordings in the diagnosis of ophthalmologic and neurologic disorders and in the investigation of the pathophysiologic mechanisms of and possible treatments for these disorders. Recently developed methods for measuring eye movements about all three axes of rotation (horizontal, vertical, and torsion) are emphasized. These techniques are providing important insights into the basic physiology of eye-movement control and into the mechanisms of ocular motor disturbances in which torsion plays a significant role.

Diagnosis, Differential↗
PubMed1999

Proprioceptive and retinal afference modify postsaccadic ocular drift.

Drift of the eyes after saccades produces motion of images on the retina (retinal slip) that degrades visual acuity. In this study, we examined the contributions of proprioceptive and retinal afference to the suppression of postsaccadic drift induced by a unilateral ocular muscle paresis. Eye movements were recorded in three rhesus monkeys with a unilateral weakness of one vertical extraocular muscle before and after proprioceptive deafferentation of the paretic eye. Postsaccadic drift was examined in four visual states: monocular viewing with the normal eye (4-wk period); binocular viewing (2-wk period); binocular viewing with a disparity-reducing prism (2-wk period); and monocular viewing with the paretic eye (2-wk period). The muscle paresis produced vertical postsaccadic drift in the paretic eye, and this drift was suppressed in the binocular viewing condition even when the animals could not fuse. When the animals viewed binocularly with a disparity-reducing prism, the drift in the paretic eye was suppressed in two monkeys (with superior oblique pareses) but generally was enhanced in one animal (with a tenotomy of the inferior rectus). When drift movements were enhanced, they reduced the retinal disparity that was present at the end of the saccade. In the paretic-eye-viewing condition, postsaccadic drift was suppressed in the paretic eye and was induced in the normal eye. After deafferentation in the normal-eye-viewing state, there was a change in the vertical postsaccadic drift of the paretic eye. This change in drift was idiosyncratic and variably affected the amplitude and velocity of the postsaccadic drift movements of the paretic eye. Deafferentation of the paretic eye did not affect the postsaccadic drift of the normal eye nor did it impair visually mediated adaptation of postsaccadic drift. The results demonstrate several new findings concerning the roles of visual and proprioceptive afference in the control of postsaccadic drift: disconjugate adaptation of postsaccadic drift does not require binocular fusion; slow, postsaccadic drift movements that reduce retinal disparity but concurrently increase retinal slip can be induced in the binocular viewing state; postsaccadic drift is modified by proprioception from the extraocular muscles, but these modifications do not serve to minimize retinal slip or to correct errors in saccade amplitude; and visually mediated adaptation of postsaccadic drift does not require proprioceptive afference from the paretic eye.

Adaptation, Physiological↗
PubMed1998

Sound- and/or pressure-induced vertigo due to bone dehiscence of the superior semicircular canal.

OBJECTIVES: To present symptoms, patterns of nystagmus, and computed tomographic scan identification of patients with sound- and/or pressure-induced vertigo due to dehiscence of bone overlying the superior semicircular canal. To describe anatomical findings and outcome in 2 patients undergoing plugging of the superior semicircular canal for treatment of these symptoms. DESIGN AND SETTING: Prospective study of a case series in a tertiary care referral center. PATIENTS AND RESULTS: Eight patients with vertigo, oscillopsia, and/or disequilibrium related to sound, changes in middle ear pressure, and/or changes in intracranial pressure were identified in a 2-year period. Seven of these patients also had vertical-torsional eye movements induced by these sound and/or pressure stimuli. The direction of the evoked eye movements could be explained by excitation or inhibition of the superior semicircular canal in the affected ear. Computed tomographic scans of the temporal bones identified dehiscence of bone overlying the affected superior semicircular canal in each case. Disabling disequilibrium in 2 patients prompted plugging of the dehiscent superior canal through a middle cranial fossa approach. Symptoms were improved in each case. One patient developed recurrent symptoms requiring an additional plugging procedure and developed sensorineural hearing loss several days after this second procedure. CONCLUSIONS: We have identified patients with a syndrome of vestibular symptoms induced by sound in an ear or by changes in middle ear or intracranial pressure. These patients can also experience chronic disequilibrium. Eye movements in the plane parallel to that of the superior semicircular canal were evoked by stimuli that have the potential to cause ampullofugal or ampullopetal deflection of this canal's cupula in the presence of a dehiscence of bone overlying the canal. The existence of such deshiscences was confirmed with computed tomographic scans of the temporal bones. Surgical plugging of the affected canal may be beneficial in patients with disabling symptoms.

Adult↗
PubMed1998

Context-specific short-term adaptation of the phase of the vestibulo-ocular reflex.

The phase of the angular vestibulo-ocular reflex (VOR) is subject to adaptive control. We had previously found that adapting the phase of the VOR also produced changes in drift on eccentric gaze-holding, implying a change in the time constant of the velocity-to-position neural integrator. Here we attempted to dissociate changes in gaze-holding drift from changes in the phase of the VOR. In normal human subjects, for 2 h, we alternated 5 min of VOR phase adaptation (sinusoids, 0.2 Hz) with 5 min of making saccades in the light with the head stationary. Afterwards, changes in VOR phase were the same (32% of requested) as those obtained with 1 h of phase adaptation alone, but changes in drift following saccades were much smaller than those found after phase adaptation alone (0.8 degrees/s compared with 5 degrees/s). When measuring drift after VOR steps, however, the changes were closer to those found after phase adaptation alone (3.8 degrees/s). To test the relationship between gaze-holding drift after VOR steps and adaptive changes in VOR phase, we alternated sinusoidal VOR phase adaptation with normal VOR steps in the light. In this paradigm, the adaptive change in VOR phase was about the same as with phase-adaptation alone (35%), but there was now little drift after saccades (1.9 degrees/s) or after VOR steps (0.7 degrees/s). We conclude that the state of the velocity-to-position neural integrator can be altered selectively and rapidly depending upon the task required. Such context-specific adaptation is advantageous, because it allows adjustment of the phase of the VOR without degrading the ability to hold eccentric fixation.

Adaptation, Physiological↗
PubMed1998

Short-term vestibulo-ocular adaptation: influence of context.

A number of mechanisms and strategies are used to help an individual compensate for loss of labyrinthine function. One important example is the ability to produce a preplanned motor response that anticipates the motion of the head and so compensates for it. Closely tied to this phenomenon is the gating, in or out, of a learned response on the basis of the context in which it must occur. This issue is particularly relevant to designing programs of physical therapy that optimize performance for natural behavior. Here we discuss a model of short-term vestibulo-ocular adaptation-adjustment of vestibulo-ocular phase (timing)-and how it can be used to study context-dependent vestibulo-ocular learning. We will show how vestibulo-ocular phase can be adjusted by selectively altering the common velocity-to-position ocular motor neural integrator for one type of eye movement (vestibular) and not for another (saccades), or for one type of head movement (sinusoidal) and not for another (step). These results are another example of the remarkable flexibility of the vestibulo-ocular adaptive mechanism and further show that the fundamental process of integration for eye movements can be modified according to the pattern of afferent information.

Adaptation, Physiological↗
PubMed1998

Effects of lesions of the oculomotor vermis on eye movements in primate: saccades.

We studied the effects on saccades of ablation of the dorsal cerebellar vermis (lesions centered on lobules VI and VII) in three monkeys in which the deep cerebellar nuclei were spared. One animal, with a symmetrical lesion, showed bilateral hypometric horizontal saccades. Two animals, with asymmetrical lesions, showed hypometric ipsilateral saccades, and saccades to vertically positioned targets were misdirected, usually deviating away from the side to which horizontal saccades were hypometric. Postlesion, all animals showed an increase (2- to 5-fold) in trial-to-trial variability of saccade amplitude. They also showed a change in the ratio of the amplitudes of centripetal to centrifugal saccades (orbital-position effect); usually centrifugal saccades became smaller. In the two animals with asymmetrical lesions, for saccades in the hypometric direction, latencies were markedly increased (up to approximately 500 ms). There was also an absence of express and anticipatory saccades in the hypometric direction. When overall saccade latency was increased, centrifugal saccades became relatively more delayed than centripetal saccades. The dynamic characteristics of saccades were affected to some extent in all monkeys with changes in peak velocity, eye acceleration, and especially eye deceleration. There was relatively little effect of orbital position on saccade dynamics, however, with the exception of one animal that showed an orbital position effect for eye acceleration. In a double-step adaptation paradigm, animals showed an impaired ability to adaptively adjust saccade amplitude, though increased amplitude variability postlesion may have played a role in this deficit. During a single training session, however, the latency to corrective saccades-which had been increased postlesion-gradually decreased and so enabled the animal to reach the final position of the target more quickly. Overall, both in the early postlesion period and during recovery, changes in saccade amplitude and latency tended to vary together but not with changes in saccade dynamics or adaptive capability, both of which behaved relatively independently. These findings suggest that the cerebellum can adjust saccade amplitude and saccade dynamics independently. Our results implicate the cerebellar vermis directly in every aspect of the on-line control of saccades: initiation (latency), accuracy (amplitude and direction), and dynamics (velocity and acceleration) and also in the acquisition of adaptive ocular motor behavior.

Adaptation, Physiological↗
PubMed1998

Dissociated vertical deviation: an exaggerated normal eye movement used to damp cyclovertical latent nystagmus.

PURPOSE: Dissociated vertical deviation (DVD) has eluded explanation for more than a century. The purpose of this study has been to elucidate the etiology and mechanism of DVD. METHODS: Eye movement recordings of six young adults with DVD were made with dual-coil scleral search coils under various conditions of fixation, illumination, and head tilt. Horizontal, vertical, and torsional eye movements were recorded for both eyes simultaneously. Analyses of the simultaneous vertical and torsional movements occurring during the DVD response were used to separate and identify the component vergence and version eye movements involved. RESULTS: Typically, both horizontal and cyclovertical latent nystagmus developed upon occlusion of either eye. A cycloversion then occurred, with the fixing eye intorting and tending to depress, the covered eye extorting and elevating. Simultaneously, upward versions occurred for the maintenance of fixation, consisting variously of saccades and smooth eye movements, leading to further elevation of the eye behind the cover. The cyclovertical component of the latent nystagmus became partially damped as the DVD developed. CONCLUSIONS: In patients with an early-onset defect of binocular function, the occlusion of one eye, or even concentration on fixing with one eye, produces unbalanced input to the vestibular system. This results in latent nystagmus, sometimes seen only with magnification. The cyclovertical component of the latent nystagmus, when present, is similar to normal vestibular nystagmus induced by dynamic head tilting about an oblique axis. Such vestibular nystagmus characteristically produces a hyperdeviation of the eyes. In the case of cyclovertical latent nystagmus, the analogous hyperdeviation will persist unless corrected by a vertical vergence. A normal, oblique-muscle-mediated, cycloversion/vertical vergence is called into play. This occurs in the proper direction to correct the hyperdeviation, but it occurs in an exaggerated form in the absence of binocular vision, probably as a learned response. The cycloversion/vertical vergence helps damp the cyclovertical nystagmus (a cyclovertical "nystagmus block-age" phenomenon), aiding vision in the fixing eye. But this mechanism also produces unavoidable and undesirable elevation and extortion of the fellow eye, which we call DVD.

Adaptation, Physiological↗
PubMed1998

Effect of horizontal vergence on the motor and sensory components of vertical fusion.

PURPOSE: To compare motor and sensory capabilities for fusion of vertical disparities at different angles of horizontal vergence in healthy humans. METHODS: Eye movements were recorded from both eyes of 12 healthy subjects using three-axis search coils. The stimulus was a cross (+) (3.4 x 3.2 degrees , vertically and horizontally, respectively) presented to each eye with a stereoscopic display. Vertical disparities were introduced by adjusting the vertical position of the cross in front of one eye. The disparity was increased in small increments (0.08 degrees ) every 8 seconds. Viewing was defined as "near" if there was a horizontal disparity that elicited 6 degrees to 15 degrees convergence, depending on the subject's capability for horizontal fusion; viewing was defined as "far" at 1 degrees convergence. Maximum motor (measured), sensory (stimulus minus motor), and total (motor plus sensory) vertical fusion were compared. RESULTS: In 9 (75%) of 12 subjects the maximum total vertical fusion was more in near than in far viewing. The three who did not show this effect had relatively weak horizontal fusion. For the entire group, the motor component differed significantly between far (mean, 1.42 degrees ) and near (mean, 2.13 degrees). Total vertical fusion capability (motor plus sensory) also differed significantly between far (mean, 1.68 degrees ) and near (mean, 2.39 degrees ). For the sensory component there was no difference between between far (mean, 0.268 degrees ) and near (mean, 0.270 degrees ). As vertical disparity increased in a single trial, however, there was a small gradual increase of the contribution of the sensory component to vertical fusion. CONCLUSIONS: Vertical fusion capability usually increases with convergence. This increase is caused primarily by an increase in the motor component. There is a gradual but small increase in the sensory component as target disparity slowly increases.

Adult↗
PubMed1997

Spinocerebellar ataxia type 6: gaze-evoked and vertical nystagmus, Purkinje cell degeneration, and variable age of onset.

Spinocerebellar ataxia type 6 (SCA6) was recently identified as a form of autosomal dominant cerebellar ataxia associated with small expansions of the trinucleotide repeat (CAG)n in the gene CACNL1A4 on chromosome 19p13, which encodes the alpha1 subunit of a P/Q-type voltage-gated calcium channel. We describe clinical, genetic, neuroimaging, neuropathological, and quantitative oculomotor studies in four kindreds with SCA6. We found strong genetic linkage of the disease to the CACNL1A4 locus and strong association with the expanded (CAG)n alleles in two large ataxia kindreds. The expanded alleles were all of a single size (repeat number) within the two large kindreds, numbering 22 and 23 repeat units. It is noteworthy that the age of onset of ataxia ranged from 24 to 63 years among all affected individuals, despite the uniform repeat number. Radiographically and pathologically, there was selective atrophy of the cerebellum and extensive loss of Purkinje cells in the cerebellar cortex. In addition, clinical and quantitative measurement of extraocular movements demonstrated a characteristic pattern of ocular motor and vestibular abnormalities, including horizontal and vertical nystagmus and an abnormal vestibulo-ocular reflex. These studies identify a distinct phenotype associated with this newly recognized form of dominant SCA.

Adult↗
PubMed1997

Ocular motor abnormalities in Huntington's disease.

We review here the eye movements in patients with Huntington's disease (HD), concentrating upon saccades as they show the most prominent abnormalities. Inability to suppress reflexive glances to suddenly appearing novel visual stimuli and delayed initiation of voluntary saccades, including predictive saccades, are early and consistent findings. These two abnormalities can be interpreted in the context of a model, based upon the idea that the frontal lobes and basal ganglia contribute more to the control of voluntary than to reflexive types of saccades. Most patients eventually also show slow saccades but they are most prominent when the disease is early-onset. Slowing of saccades may reflect involvement of both the higher-level cerebral centers that trigger saccades and the areas in the brain stem that produce premotor saccade commands. The study of eye movements in HD has led to a fruitful interaction between basic science and clinical investigation, and has served as a paradigm for examining higher-level defects in saccadic eye movement control in patients with various degenerative, neurological diseases or with focal cerebral hemispheral lesions.

Humans↗
PubMed1996

Validity of Listing's law during fixations, saccades, smooth pursuit eye movements, and blinks.

In its original formulation, Listing's law referred only to eye positions during steady fixation. In recent years, however, several studies have suggested that Listing's law can be extended to the movements of the eyes, including during saccades and smooth pursuit. A major problem in deciding whether or not Listing's law is obeyed during eye movements is the influence of any spontaneous fluctuations in torsional eye position. To try to settle this question, the three-dimensional position of the eyes (around the three axes: horizontal, vertical, and torsional) was recorded with dual search coils in five normal subjects during fixations, 20 degrees saccades, blinks, and 20 degrees pursuit movements with a 20 degrees/s stimulus velocity. Eye movements across a wide range of horizontal positions were measured at different elevations of gaze during 11 min. Variability (as reflected in the standard deviation of torsional eye position) was used as a measure of the validity of Listing's law. After linear detrending single trials, each lasting 21.5 s, to remove the effects of drift over minutes, the reduction in the standard deviation of torsional position in tertiary eye positions was 54% assuming a planar and 58% assuming a second-order curved Listing's surface. We attributed this long-term fluctuation of the torsional signal to slippage of the coil on the eye. The remaining variability was mainly due to short-term fluctuation of eye torsion over seconds. The impact of hysteresis, associated with consecutive centrifugal-centripetal horizontal movements, on the variability of torsional eye position appeared negligible. Peak increases in the standard deviation from the fixation baseline after fitting individual Listing's planes for each trial were 348% during blinks, 141% during saccades, and 72% during pursuit movements (median value of five subjects). In conclusion, Listing's law during blinks, saccades, and pursuit is less valid than during fixations, which raises doubts about the existence of an internal "Listing's law operator" for eye movements. Possibly, central eye velocity commands do not comply with Listing's law.

Blinking↗