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Biomedical subjects

L M Optican

Publications and source records attributed to L M Optican.

At least 55 records · Page 3Linked to original sources
PubMed1987

Optically induced changes in the couplings between vergence and accommodation.

Vergence-induced accommodation (V-A) and accommodation-induced vergence (A-V) were measured in human subjects before and after they had worn various optical devices for 30 min. Laterally displacing periscopic spectacles, which increase the required change in vergence per unit change in accommodation, caused decreases and increases in the gain of V-A and A-V responses, respectively. These observations are consistent with the view that the gain of the neural cross-linkages between vergence and accommodation are subject to adaptive regulation. However, there were strong asymmetries: Medially displacing periscopes (cyclopean spectacles), which reduce the required change in vergence per unit change in accommodation to zero, were almost totally without effect. Base-out prisms, which increase the required convergence by an amount that is constant for all viewing distances, caused downward and upward shifts in the V-A and A-V response curves, respectively. Base-in prisms, which reduce the required convergence by a constant amount for all viewing distances, caused downward shifts of A-V curves but had no significant effect on V-A curves. These effects of prisms are in essential agreement with the work of others and confirm the existence of adaptive elements that regulate the bias in the vergence and/or accommodation control systems. Secondary effects of wearing periscopes and prisms indicated a certain lack of specificity in the sensing of gain and bias errors: vertical shifts of V-A and A-V curves (resembling those seen with base-out prisms) often occurred with the laterally displacing periscopes, and gain changes (generally resembling those seen with laterally displacing periscopes) often occurred with the base-out prisms.

Accommodation, Ocular↗
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

Short-latency ocular following responses of monkey. I. Dependence on temporospatial properties of visual input.

The ocular following responses elicited by brief unexpected movements of the visual scene were studied in 10 rhesus monkeys. Test patterns were either random dots or sine-wave gratings [spatial frequency (Fs) 0.046-1.06 cycles per degree (c/degree)]. Test stimuli were velocity steps [speed (V) 5-400 degrees/s] of 100-ms duration, applied 50 ms after spontaneous saccades to avoid saccadic intrusions. Eye velocity response profiles were nonmonotonic and idiosyncratic, but consistent and closely time-locked to stimulus onset. Two measures of response amplitude were used: initial peak in eye velocity (ei), and average final eye velocity over the period of 110-140 ms measured from stimulus onset (ef). Using random dot patterns, response latencies were short, e.g., when the criterion for onset was an eye acceleration of 100 degrees/s2, mean latency (+/- SE) for eight monkeys with a 40 degrees/s test ramp was 51.5 +/- 0.6 ms. Using gratings of low spatial frequency (Fs less than 0.5 c/degree), latency was inversely related to, and solely a function of, contrast and temporal frequency, Ft (where Ft = V X Fs). We conclude from the latter that ocular following is triggered by local changes in luminance, and propose a model of the detection mechanism that reproduces all the essential features of these data. Moderate low-pass spatial filtering ("blurring") of the random dot pattern, by interposing a sheet of ground glass between the animal and the scene, progressively increased the response latency and decreased ef, but ei was either little affected or increased. When used with gratings, the ground glass simply reduced the contrast (range: 0.5-0.003), with very similar consequences for ocular following: latency increased and ef decreased, but ei changed little over the first decade of contrast reduction, increased over the second, and began to show attenuation (often pronounced) only at the lowest contrast. We suggest that these anomalous increases in ei with reductions in contrast are secondary to the delay in response onset and might be explained if the motion detectors responsible for triggering ocular following act as a gate for integrated retinal slip inputs to the tracking system proper: the delay in detection causes a buildup in the error signal driving the tracking response. En masse movement of the visual field was not the optimal stimulus for ocular following.(ABSTRACT TRUNCATED AT 400 WORDS)

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

Visually induced adaptive changes in primate saccadic oculomotor control signals.

Saccades are the rapid eye movements used to change visual fixation. Normal saccades end abruptly with very little postsaccadic ocular drift, but acute ocular motor deficits can cause the eyes to drift appreciably after a saccade. Previous studies in both patients and monkeys with peripheral ocular motor deficits have demonstrated that the brain can suppress such postsaccadic drifts. Ocular drift might be suppressed in response to visual and/or proprioceptive feedback of position and/or velocity errors. This study attempts to characterize the adaptive mechanism for suppression of postsaccadic drift. The responses of seven rhesus monkeys were studied to postsaccadic retinal slip induced by horizontal exponential movements of a full-field stimulus. After several hours of saccade-related retinal image slip, the eye movements of the monkeys developed a zero-latency, compensatory postsaccadic ocular drift. This ocular drift was still evident in the dark, although smaller (typically 15% of the amplitude of the antecedent saccade, up to a maximum drift of 8 degrees). Retinal slip alone, without a net displacement of the image, was sufficient to elicit these adaptive changes, and compensation for leftward and rightward saccades was independent. It took several days to complete adaptation, but recovery (in the light) was much quicker. The decay of this adaptation in darkness was very slow; after 3 days the ocular drift was reduced by less than 50%. The time constants of single exponential curve fits to adaptation time courses of data from five animals were 35 h for acquisition, 4 h for recovery, and at least 40 h for decay in darkness. Descriptions of the central innervation for a saccade are usually simplified to only two components: a pulse and a step. It has been hypothesized that suppression of pathological postsaccadic drift is achieved by adjusting the ratio of the pulse to the step of innervation (19, 26). However, we show that the time constant of the ocular drift is influenced by the time constant of the adapting stimulus, which cannot be explained by the simple pulse-step model of saccadic innervation. A more realistic representation of the saccadic innervation has three components: a pulse, an exponential slide, and a step. Normal saccades were accurately simulated by a fourth-order, linear model of the ocular motor plant driven by such a pulse-slide-step combination. Saccades made after prolonged exposure to optically induced retinal image slip could also be simulated by properly adjusting the slide and step components.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Ocular↗
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↗
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↗
PubMed1983

Frequency-selective adaptation: evidence for channels in the vestibulo-ocular reflex?

The vestibulo-ocular reflex (VOR) is under long-term adaptive regulation to minimize retinal image slip during head movement; normally this process keeps VOR gain (eye velocity divided by head velocity) near 1.0. It has been common to think of the adaptive mechanism as a single pure gain element, although some properties of the system (e.g., frequency-selective changes in the gain of the VOR) argue that it must be more complex. We now report new observations on the frequency selectivity of the adaptive mechanism. Our data suggest a new model in which the VOR operates as a series of parallel, temporal frequency channels, each of which has an independently adjustable gain element. Adaptive changes were produced by oscillating monkeys sinusoidally at a single temporal frequency (0.2 or 2.0 Hz) in visual conditions that cause either increases (toward two) or decreases (toward zero) in VOR gain. When tested in darkness at the adapting frequency, the VOR showed large changes in gain and little or no change in phase. When tested at frequencies other than the adapting frequency, the VOR showed less pronounced changes in gain and unexpected changes in phase. The phase changes were orderly but depended in a complex way on adapting frequency, testing frequency, and VOR gain. We have tested the channels concept by calculating the response properties of a mathematical model that processed its inputs in parallel pathways. The model reproduced our data when we assumed that the vestibular primary afferents were distributed in an orderly way to parallel brain channels that had differing dynamics: vestibular inputs with more phase lead projected to higher frequency channels, which themselves had faster dynamics than their low frequency counterparts. Such an organization, when regulated by an adaptive controller that can selectively alter the gain of one channel, could play a key role in establishing and maintaining the frequency-independent performance seen in the adult VOR.

Adaptation, Physiological↗
PubMed1980

Cerebellar-dependent adaptive control of primate saccadic system.

1. The ability of the central nervous system to compensate for saccadic dysmetria was demonstrated in rhesus monkeys. The behavior of this adaptive mechanism after cerebellar ablations was examined. 2. Monkeys were trained to fixate small target lights. Eye movements were monitored while the animals were seated, with their heads fixed, in a rotating magnetic field. The horizontal recti muscles of one eye were weakened by tenectomy. Saccades made by this weakened eye were hypometric and followed by postsaccadic drift. 3. When the patch was switched so that the weak eye was viewing, the hypometric saccades made by the weak eye gradually became larger, until after 3 days they were essentially orthometric. This indicated that the central nervous system could compensate for a peripheral weakness. 4. The tenectomy operation reduced the strength of the muscles, creating hypometria, and upset the ratio of viscosity to elasticity in the orbit, creating postsaccadic drift in the weak eye. The innervation required to make a saccade has both phasic and tonic components, the so-called pulse and step. The sacccadic repair mechanism increased both the pulse and the step to compensate for the hypometria and also adjusted the ratio of the pulse to the step to eliminate postsaccadic drift. 5. Total cerebellectomies were performed on two monkeys, each of which had one tenectomized eye. These ablations created an enduring saccadic hypermetria and postsaccadic drift in the unoperated eye of both animals. The total cerebellectomy abolished all adaptive repair of the saccadic system. 6. Partial cerebellectomies were performed on two monkeys, each of which had one tenectomized eye. Lesions of the vermis and paravermis (lobes IV-IX) and the fastigial nuclei created an enduring saccadic hypermetria without postsaccadic drift in the unoperated eye of both animals. These lesions abolished adaptive control of the pulse of innervation. Adaptive changes in the step of innervation still occurred, so that postsaccadic drift was always eliminated in the experienced, viewing eye. Thus the midline cerebellum (vermis, paravermis, and fastigial nuclei) appears to be important for repair of saccadic dysmetria, but not for repair of postsaccadic drift. Additional evidence that postsaccadic retinal slip cannot be compensated for in flocculectomized monkeys suggest that the adaptive control of the step may depend on the flocculus. 7. After cerebellar lesions the monkeys were able to make saccades of all amplitudes and directions. The principal deficit in these animals seemed to be that the pulse and step of innervation were no longer appropriate to the target displacement. We conclude that the cerebellum's principal contribution to saccadic eye movements is the adjustment of the gains of the pulse- and step-generating mechanisms. Hence this study supports the hypothesis that repair of dysmetria is a general function of the cerebellum.

Adaptation, Physiological↗
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↗
PubMedDate not supplied

Age-related differences in visual perception: a PET study.

To assess age-related differences in cortical activation during form perception, two classes of visual textures were shown to young and older subjects undergoing positron emission tomography (PET). Subjects viewed even textures that were rich in rectangular blocks and extended contours and random textures that lacked these organized form elements. Within-group significant increases in regional cerebral blood flow (rCBF) during even stimulation relative to random stimulation in young subjects were seen in occipital, inferior and medial temporal regions, and cerebellum, and in older subjects, in posterior occipital and frontal regions. Group by texture type interactions revealed significantly smaller rCBF increases in older subjects relative to young in occipital and medial temporal regions. These results indicate that young subjects activate the occipitotemporal pathway during form perception, whereas older subjects activate occipital and frontal regions. The between-group differences suggest that age-related reorganization of cortical activation occur during early visual processes in humans.

Adult↗