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Biomedical subjects

D S Zee

Publications and source records attributed to D S Zee.

At least 127 records · Page 7Linked to original sources
PubMed1988

Saccades in Huntington's disease: slowing and dysmetria.

Eye movements were recorded from 20 mildly affected patients with Huntington's disease (HD) who were divided into two groups, 10 patients with onset of symptoms before age 30 and 10 with onset of symptoms after age 30. In the younger onset group (HD less than 30), peak saccade velocities were low (less than 255 deg/sec for 20-deg saccades) in six of the 10 patients, whereas none of the 10 patients in the older onset group (HD greater than 30) had peak saccade velocities lower than 300 deg/sec. Latencies for volitional saccades were greater than normal in the HD greater than 30 group, but were normal for the HD less than 30 group. The ability to maintain steady fixation in the face of a distracting visual stimulus was decreased, to the same degree, in both groups of HD patients. In addition, 70% of the HD less than 30 group had an affected father, while 70% of the HD greater than 30 group had an affected mother. These findings suggest that the pathophysiology of the slow saccades, initiation deficit, and excessive distractibility in HD are different.

Adolescent↗
PubMed1987

Abduction nystagmus in internuclear ophthalmoplegia.

We tested the hypothesis that abnormalities of the abducting eye in internuclear ophthalmoplegia reflect an adaptive process that helps overcome the adduction weakness of the opposite eye. This response operates under the constraints of Hering's law of equal innervation: any attempt to increase the innervation to a weak muscle in one eye must be accompanied by a commensurate increase in innervation to the yoke muscle in the other eye. In 4 patients with internuclear ophthalmoplegia, we patched one eye for 1 to 5 days to allow time for the central nervous system to optimize innervation for the habitually viewing eye. We predicted that there would be a conjugate adjustment of innervation that would diminish the abduction overshoot and backward postsaccadic drift made by the habitually viewing eye. This was the case in 3 of our 4 patients. Our findings show that the abduction nystagmus is a manifestation of a normal adaptive response in some patients with INO.

Adaptation, Physiological↗
PubMed1987

Adaptive changes in post-saccadic drift induced by patching one eye.

A prior study showed that after horizontal saccades the abducting eye has little post-saccadic drift (about 0.5 deg/sec) while the abducting eye has considerable onward drift (about 1.7 deg/sec). To investigate this further, five subjects patched one eye for three days. This reduced the drift after adducting saccades in the viewing eye to the level of that after abducting saccades. The changes were a combination of conjugate and disconjugate alterations. Decreases in drift in the viewing eye did not cause increases in drift in the covered eye. These changes appear functional in that retinal image slip is decreased in the viewing eye but why this goal is not attained when both eyes habitually view is not understood. Also, post-saccadic drift could depend on which eye was used to view the target.

Adaptation, Ocular↗
PubMed1987

Effects of occipital lobectomy upon eye movements in primate.

1. Eye movements were recorded before and after bilateral occipital lobectomy in six rhesus monkeys trained to fixate and to follow small targets. Striate cortex was completely removed in two animals; small islands islands remained in the others. In all animals portions of extrastriate cortex were also removed but the medial superior temporal area in the superior temporal sulcus was largely spared. Optokinetic nystagmus (OKN) was markedly altered but not abolished in all animals. The immediate pursuit component of OKN was eliminated leading to a poor response to stimuli comprised of high frequencies. The velocity-storage component of OKN was present, but the maximum value of OKN that could be achieved was decreased to 6 and 16 degrees/s in the two most severely affected animals (preop, 65-116 degrees/s). The residual OKN was similar to that of afoveate animals with a diminished response to high velocities of retinal-image motion and a temporal to nasal predominance during monocular viewing. 2. In the initial postoperative period all animals appeared completely blind. Within 1-6 mo, however, they regained an ability to make visually guided saccades to, and smooth pursuit of, small targets. Saccades were nearly as accurate as preoperatively, but saccade amplitudes were more variable and saccade latencies increased. In the two animals with a complete removal of striate cortex, gains (eye velocity/target velocity) of smooth pursuit during sinusoidal tracking (60 degrees/s, 0.5 Hz) were 0.9 and 0.95. During tracking of step-ramp (Rashbass) stimuli with 60 degrees/s ramps, the average acceleration of the eyes during the first 120 ms of smooth pursuit was 189-278 degrees.s-1.s-1 (preop range, 154-418 degrees.s-1.s-1). In other respects, though, smooth pursuit was not normal. Latencies were increased two- to threefold, and tracking was more variable. 3. Paradoxically, as visually guided saccades and pursuit recovered, some other ocular motor functions deteriorated. Spontaneous and gaze-evoked nystagmus developed 3-6 mo after occipital lobectomy; the time constant of the neural eye-position integrator dropped to values as low as 2.6-4.8 s. The maximum slow-phase velocity of OKN also decreased. 4. The findings immediately after occipital lobectomy indicate that in normal primates occipital cortex is necessary for visually guided saccades and smooth pursuit as well as for the immediate component of OKN. Occipital cortex also makes the predominant contribution toward the generation of the velocity-storage component of OKN.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Saccades in Huntington's disease: initiation defects and distractibility.

We recorded saccadic eye movements in patients mildly affected with Huntington's disease. Most showed an increase in saccade latencies that was greater for saccades made on command than to the sudden appearance of a visual target. All patients showed excessive distractibility during attempted fixation. They had particular difficulty suppressing a saccade to a suddenly appearing visual target when simultaneously trying to initiate a saccade in the opposite direction. Our results are compatible with a posited role of the basal ganglia in both the initiation of volitional saccades and in the maintenance of fixation. Saccade abnormalities--especially distractibility--are sensitive but probably not specific indicators of Huntington's disease.

Adolescent↗
PubMed1986

Blink-induced saccadic oscillations.

A patient with a neurodegenerative disease had abnormal saccades only when he blinked. These saccades were hypermetric and were followed immediately, without any intersaccadic interval, by a large, oppositely directed saccade (dynamic overshoot). To explain these findings, we hypothesize that a blink-related neural signal can modulate the activity of pause cells that normally inhibit saccadic burst neurons during fixation. In pathological circumstances, abnormal function of pause cells could lead to large-amplitude saccadic oscillations. In normal subjects, blinks could induce short bursts of low-amplitude flutter.

Adult↗
PubMed1986

Influence of eye and head position on the vestibulo-ocular reflex.

For the vestibulo-ocular reflex (VOR) to function properly, namely to ensure a stable retinal image under all circumstances, it should be able to take into account varying eye positions in the orbit and varying orientations of the head with respect to the axis about which it is rotating. We tested this capability by quantifying the gain and the time constant of the horizontal component of the VOR during rotation about an earth vertical axis when the line of sight (optical axis) was moved out of the plane of head rotation--either by rotating the eyes up or down in the orbit or by pitching the head up or down with respect to earth-horizontal. In either case the gain of the horizontal component of the VOR was attenuated precisely by the cosine of the angle made between the optical axis and the plane of head rotation. Furthermore, if the head was pitched up or down but the eye rotated oppositely in the orbit so as to keep the line of sight in the plane of head rotation the gain of the horizontal component of the VOR was the same value as with the head and eyes both straight ahead. In contrast, the time constant of the VOR varied only as a function of the orientation of the head and not as a function of eye position in the orbit. During rotation about an earth vertical axis, the time constant was longest (about 18 s) when the head was pitched forward to place the lateral canals near earth-horizontal and shortest (about 11 s) when the head was pitched backward to place the vertical canals near earth-horizontal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Floccular lesions abolish adaptive control of post-saccadic ocular drift in primates.

After several days of exposure to optically-imposed post-saccadic retinal slip, the saccades of normal monkeys acquire an exponential ocular drift. This drift is in the direction of the imposed image motion, and persists in the dark. It has been argued that these changes result from the operation of a visually mediated adaptive mechanism that normally functions to minimize post-saccadic ocular drift. Adaptation to persistent post-saccadic retinal slip was assessed in two rhesus monkeys before and after bilateral ablations of the flocculi and portions of the paraflocculi ("flocculectomy"). After flocculectomy, both monkeys showed some post-saccadic ocular drift. Flocculectomized animals also failed to adapt to optically-imposed post-saccadic slip. We infer from this that the flocculi and/or paraflocculi are necessary for the successful suppression of post-saccadic ocular drift.

Adaptation, Ocular↗
PubMed1986

Effect of unilateral cerebral cortical lesions on ocular motor behavior in monkeys: saccades and quick phases.

Saccades and quick phases of vestibular and optokinetic nystagmus were quantitated using the magnetic-field search coil technique before and during 1 yr after unilateral decortication in three rhesus monkeys. Saccades were examined during several different behavioral conditions: spontaneous saccades made in the light and in the dark; intentional saccades including visually guided saccades to a target light, predictive saccades to a target light stepped to a predictable location, and target-searching saccades when the monkey was rewarded to find and fixate the target light located in the defective visual hemifield; and reflexive saccades made to novel visual, auditory, and tactile stimuli. Quick phases of nystagmus and spontaneous saccades could be initiated immediately postoperatively, although those initiated away from the side of the lesion were reduced in amplitude and rarely moved the eyes into contralateral craniotopic space. Intentional and reflexive saccades could not be initiated away from the side of the lesion during the first postoperative week. Visually guided saccades and reflexive saccades to stationary or moving visual stimuli in the defective visual hemifield never recovered. Target-searching and predictive saccades directed away from the lesioned side recovered but were generated in a staircase pattern; those saccades from orbital positions further into craniotopic space on the side opposite the lesion had progressively higher latencies and smaller amplitudes. The amplitudes of visually guided saccades to targets stepped into the normal visual hemifield were increased in amplitude by approximately 15% but slowly returned to near preoperative values by 20 wk. Pure vertical visually guided saccades to targets stepped or moved in the vertical direction were not generated throughout the postoperative period. Instead, the animals generated oblique saccades, tilted 10-15 degrees toward the side of the lesion. Velocities of saccades and quick phases were significantly reduced at all amplitudes both away from (approximately 37%) and toward (approximately 22%) the side of the lesion. This deficit diminished with time but velocities were still low one yr postoperatively. Our results suggest that cortical areas in one hemisphere are involved in the initiation of contralaterally directed intentional and reflexive saccades but not in the initiation of spontaneous saccades or quick phases. In time, other structures can initiate contralaterally directed intentional and reflexive saccades, except those guided by vision.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Brain stem and cerebellar deficits in eye movement control.

Recent experimental studies allow more precise functional-anatomical correlations in patients with ocular motor disorders. The abducens nucleus contains two groups of cells that together subserve ipsilateral horizontal conjugate gaze: Motoneurons with axons that innervate the lateral rectus and internuclear neurons with axons that cross the midline, ascend in the medial longitudinal fasciculus (MLF) and impinge upon medial rectus motoneurons. The pontine paramedian reticular formation (PPRF) contains burst neurons for horizontal saccades. The rostral interstitial nucleus of the MLF (riMLF) in the midbrain contains burst neurons for vertical saccades. The dorsal lateral pontine nuclei are important for relaying smooth pursuit commands from the cerebrum to the cerebellar flocculus. The medial vestibular nuclei contain neurons important for eccentric gaze-holding. The cerebellar flocculus is also important for gaze-holding as well as for smooth pursuit and the control of the amplitude and direction of vestibular responses. The cerebellar nodulus is important for controlling the duration of vestibular responses. The cerebellar dorsal vermis (and underlying deep nuclei) are important for controlling saccade accuracy.

Brain Stem↗
PubMed1985

Perspectives on the pharmacotherapy of vertigo.

Recent evidence from experiments in animals suggests a rationale for more effective pharmacologic and physical therapy in patients with vertigo. In particular, one must consider the possible effects of medications on the adaptive processes that naturally mediate recovery from vestibular lesions. The challenge now is for clinicians to devise medication and exercise regimens for patients with vestibular disturbances and critically (and quantitatively) evaluate their effects.

Animals↗
PubMed1985

Adaptive response to ocular muscle weakness in human pursuit and saccadic eye movements.

Eye movement deficits caused by ocular muscle weakness vary according to the position of the eye in the orbit and the direction of eye movement. We studied the ability of both the saccadic and pursuit eye-movement systems to compensate for these anisotropic deficits in four patients with ocular muscle weakness. The eye-position dependence of each patient's motor deficit was characterized by plotting the position of the weak eye against that of the normal eye (in various orbital positions) when fusion was prevented, thus giving a static eye-position curve from which relative muscle strength could be inferred. Movements of the weak eye were smaller and slower than those made by the normal eye, so that the weak eye required more time to acquire a visual target. When patients were forced to view monocularly with their weak eye for several days, both the saccadic and pursuit systems showed changes in the movements of the normal eye consistent with an increased central innervation designed to decrease the time it takes to bring the target's image onto the fovea of the weak eye and to keep it there. These adaptive changes varied with eye position and movement direction and compensated for the weak muscle in both its agonistic and antagonistic actions. Saccadic adaptation consisted of a change in the relationship between saccadic amplitude and retinal error (distance between the target's image and the fovea) to compensate for hypometria (undershoot) and a readjustment of the ratio of the phasic (pulse) and tonic (step) components of the saccadic innervation to suppress postsaccadic ocular drift. Pursuit adaptation consisted of an increase in the relationship between eye acceleration and the rate of motion of the image of the target on the retina during the initial phase of tracking as well as an increase in the velocity during tracking of a target moving at a constant velocity. These changes reflect an increase in pursuit innervation that would cause the weak eye's velocity to approach target velocity sooner. The average acceleration of the normal eye during the initial period of tracking (130 ms) increased by as much as threefold. The corresponding maximum smooth eye velocity increased so that, for example, the pursuit response to a 15 degree/s target movement could be over 50 degree/s in the normal eye.

Adaptation, Physiological↗
PubMed1985

Head shaking and vestibulo-ocular reflex in congenital nystagmus.

The authors investigated the mechanisms underlying the head shaking shown by some patients with congenital nystagmus (CN). In order to improve visual function by head shaking, a patient with CN must have some visual acuity loss due to retinal image motion created by the nystagmus; an abnormal vestibulo-ocular reflex (VOR); and the head shaking must be correlated with the nystagmus. The authors measured the VOR gain (eye velocity/head velocity) and examined eye-head coordination in five patients with CN with various combinations of these three factors. One patient met all three criteria and was able to increase his acuity by shaking his head. Other patients who shook their heads either had no loss of visual acuity due to the nystagmus or had a normal VOR. In either case, head shaking was of no apparent visual benefit and may represent, instead, an associated pathologic tremor in the cephalomotor control system.

Adult↗
PubMed1985

Mechanisms of nystagmus.

The slow phases of nystagmus can be divided into four types based on their wave forms: linear, exponentially decaying, exponentially increasing, and sinusoidal. The former three give risk to "jerk" nystagmus; the last to "pendular" nystagmus. The drift of the eyes that creates the slow phase of nystagmus can be analyzed by considering the mechanisms that normally hold the eyes still so that images are stable upon the retina for best visual acuity. Thus, we have a vestibular-optokinetic system to keep images of stationary objects stable on the retina during head rotation; a pursuit system to keep images of moving objects stable on the fovea during smooth trackings; and a gaze-holding network (neural integrator) to provide the appropriate tonic innervation to the ocular motor neurons to hold positions of gaze. It is disorders of these systems that create nystagmus.

Biomechanical Phenomena↗
PubMed1984

Alexander's law: its behavior and origin in the human vestibulo-ocular reflex.

Alexander's law refers to the phenomenon in which the spontaneous nystagmus of a patient with a vestibular lesion is more intense when the patient looks in the quick-phase than in the slow-phase direction. Alexander's law was investigated in normal subjects as well as patients with vestibular lesions. During sinusoidal rotations of normal subjects, there was no trace of this phenomenon when subjects looked 25 degrees left and right in the dark. The phenomenon of Alexander's law is therefore created centrally and is not due to any mechanical properties of the orbit. During rotation at constant velocity in the dark, normal subjects did weakly demonstrate Alexander's law because of a mild gaze-evoked nystagmus present in normal subjects in the dark. Gaze-evoked nystagmus from a cerebellar lesion involved a pronounced demonstration of Alexander's law during rotatory nystagmus. In patients with a vestibular lesion and a mild spontaneous nystagmus in the dark that obeyed Alexander's law, the nystagmus reversed upon far gaze in the slow-phase direction. We propose that in patients with a vestibular lesion, the phenomenon of Alexander's law is created by the sum of vestibular nystagmus and an abnormally large gaze-evoked nystagmus that is consequent to the vestibular lesion. This conclusion has a number of neurological implications concerning the ways in which the nervous system attempts to compensate for vestibular lesions.

Adult↗
PubMed1984

A hypothetical explanation of congenital nystagmus.

Congenital nystagmus (CN) is a conjugate, rhythmic, eye movement disorder characterized by a wide variety of waveforms ranging from jerk to pendular types. No detailed mechanisms have been proposed to explain the generation of the CN waveform. This paper proposes a hypothetical mechanism for CN, and shows with computer simulations that a model based on this hypothesis can account for a variety of disparate waveforms. The basis of this model is a gaze-holding network, or neural integrator, that has both position and velocity feedback loops. The signals carried in these loops could arise from either afference or efference . In normal subjects, the position feedback would be positive and the velocity feedback would be negative. Both would help to increase the time constant of an imperfect neural integrator in the brain stem. We propose that in patients with CN the sign of the velocity pathway is reversed, making the neural integrator unstable. This instability could manifest as many different CN waveforms, depending on the direction and velocity of post-saccadic ocular drift and actions of nonlinearities within the position and velocity feedback loops. Thus a single underlying abnormality may be responsible for a variety of CN waveforms.

Brain↗
PubMed1984

Graphic analysis of paralytic strabismus with the Lancaster red-green test.

We used the Lancaster red-green test to monitor changes in ocular alignment in patients with paralytic strabismus. By inferring the position of the right eye and that of the left eye at many different positions of gaze and then plotting the data on a graph, one can derive a static eye position curve. The location of the curve relative to the line depicting normal ocular alignment ( orthophoria ) indicates whether there is an esodeviation or an exodeviation . The slope of a line drawn tangent to the curve indicates, for that particular point, whether the deviation is concomitant or not and which eye is relatively weak or restricted and by how much. This graphic technique provides a simple, sensitive, and quantitative measure of ocular alignment that may be especially useful for detecting subtle changes in the relative positions of the two eyes. This method may be a useful adjunct in the planning and evaluation of therapy for patients with paralytic strabismus.

Humans↗