Biomedical subjects

Lance M Optican

Publications and source records attributed to Lance M Optican.

12 recordsLinked to original sources

PubMed2006

What clinical disorders tell us about the neural control of saccadic eye movements.

Saccades are rapid eye movements that redirect the fovea from one object to another. A great deal has been learned about the anatomy and physiology of saccades, making them an ideal system for studying the neural control of movement. Basic research on normal eye movements has greatly increased our understanding of saccadic performance, anatomy and physiology, and led to a large number of control system models. These models simulate normal saccades well, but are challenged by clinical disorders because they often do not incorporate the specific anatomical and physiological substrates needed to model clinically important abnormalities. Historically, studies of saccadic abnormalities in patients have played a critical role in understanding the neural control of saccades because they provide information that complements basic research and thus restricts hypotheses to those that are biologically plausible. This review presents four examples of clinical disorders (slow saccades, interrupted saccades, high-frequency saccadic oscillations and macrosaccadic oscillations) that have provided insights into the neurobiology of saccades, have driven the development of new models, and have suggested an explanation or treatment for these disorders. We raise general questions for both scientists and clinicians that will assist in their efforts to understand the neural control of movement, improve diagnostic criteria and develop new treatments.

Brain↗

PubMed2006

Saccade-related spread of activity across superior colliculus may arise from asymmetry of internal connections.

The superior colliculus (SC) receives a retinotopic projection of the contralateral visual field in which the representation of the central field is expanded with respect to the peripheral field. The visual projection forms a nonlinear, approximately logarithmic, map on the SC. Models of the SC commonly assume that the function defining the strength of neuronal connections within this map (the kernel) depends only on the distance between two neurons, and is thus isotropic and homogeneous. However, if the connection strength is based on the distance between two stimuli in sensory space, the kernel will be asymmetric because of the nonlinear projection onto the brain map. We show, using a model of the SC, that one consequence of these asymmetric intrinsic connections is that activity initiated at one point spreads across the map. We compare this simulated spread with the spread observed experimentally around the time of saccadic eye movements with respect to direction of spread, differing effects of local and global inhibition, and the consequences of localized inactivation on the SC map. Early studies suggested that the SC spread was caused by feedback of eye displacement during a saccade, but subsequent studies were inconsistent with this feedback hypothesis. In our new model, the spread is autonomous, resulting from intrinsic connections within the SC, and thus does not depend on eye movement feedback. Other sensory maps in the brain (e.g., visual cortex) are also nonlinear and our analysis suggests that the consequences of asymmetric connections in those areas should be considered.

Algorithms↗

PubMed2006

A model that integrates eye velocity commands to keep track of smooth eye displacements.

Past results have reported conflicting findings on the oculomotor system's ability to keep track of smooth eye movements in darkness. Whereas some results indicate that saccades cannot compensate for smooth eye displacements, others report that memory-guided saccades during smooth pursuit are spatially correct. Recently, it was shown that the amount of time before the saccade made a difference: short-latency saccades were retinotopically coded, whereas long-latency saccades were spatially coded. Here, we propose a model of the saccadic system that can explain the available experimental data. The novel part of this model consists of a delayed integration of efferent smooth eye velocity commands. Two alternative physiologically realistic neural mechanisms for this integration stage are proposed. Model simulations accurately reproduced prior findings. Thus, this model reconciles the earlier contradictory reports from the literature about compensation for smooth eye movements before saccades because it involves a slow integration process.

Animals↗

PubMed2006

Membrane channel properties of premotor excitatory burst neurons may underlie saccade slowing after lesions of omnipause neurons.

Chemical lesions of the brain stem region containing glycinergic omnipause neurons (OPNs) cause saccade slowing with no change in latency. To explore the mechanisms responsible for this deficit, simulation studies were performed with a conductance-based model of premotor excitatory burst neurons (EBNs) that incorporated multiple membrane channels, including the T-type calcium channel. The peak speed of a normal saccade was determined by the T- and NMDA currents in EBNs after the OPNs shut off. After OPN lesions, the model made slow saccades, because the EBN activity was lower than normal due to a reduced T-current (caused by the loss of hyperpolarization), and a reduced NMDA current (caused by a reduced glycine concentration around the receptors). Thus, we propose that two biophysical mechanisms are responsible for saccade slowing after OPN lesions: reduced T-current and reduced NMDA current, both of which are caused by the loss of glycine from OPNs.

Action Potentials↗

PubMed2005

Ocular oscillations generated by coupling of brainstem excitatory and inhibitory saccadic burst neurons.

The human saccadic system is potentially unstable and may oscillate if the burst neurons, which generate saccades, are not inhibited by omnipause neurons. A previous study showed that combined saccade vergence movements can evoke oscillations in normal subjects. We set out to determine: 1) whether similar oscillations can be recorded during other paradigms associated with inhibition of omnipause neurons; 2) whether lesions of the fastigial nuclei disrupt such oscillations; and 3) whether such oscillations can be reproduced using a model based on the coupling of excitatory and inhibitory burst neurons. We recorded saccadic oscillations during vergence movements, combined saccade-vergence movements, vertical saccades, pure vergence and blinks in three normal subjects, and in a patient with saccadic hypermetria due to a surgical lesion affecting both fastigial nuclei. During combined saccade-vergence, normal subjects and the cerebellar patient developed small-amplitude (0.1 - 0.5 degrees), high-frequency (27-35 Hz), conjugate horizontal saccadic oscillations. Oscillations of a similar amplitude and frequency occurred during blinks, pure vergence and vertical saccades. One normal subject could generate saccadic oscillations voluntarily (approximately 0.7 degrees amplitude, 25 Hz) during sustained convergence. Previous models proposed that high-frequency eye oscillations produced by the saccadic system (saccadic oscillations), occur because of a delay in a negative feedback loop around high-gain, excitatory burst neurons in the brainstem. The feedback included the cerebellar fastigial nuclei. We propose another model that accounts for saccadic oscillations based on 1) coupling of excitatory and inhibitory burst neurons in the brainstem and 2) the hypothesis that burst neurons show post-inhibitory rebound discharge. When omnipause neurons are inhibited (as during saccades, saccade-vergence movements and blinks), this new model simulates oscillations with amplitudes and frequencies comparable to those in normal human subjects. The finding of saccadic oscillations in the cerebellar patient is compatible with the new model but not with the recent models including the fastigial nuclei in the classic negative-feedback loop model. Our model proposes a novel mechanism for generating oscillations in the oculomotor system and perhaps in other motor systems too.

Adult↗

PubMed2005

Properties of saccades in Duane retraction syndrome.

PURPOSE: To improve understanding of the binocular control of saccades by making high-resolution eye movement recordings in patients with unilateral Duane retraction syndrome (DRS) type I (marked by congenital absence of the sixth cranial nerve). METHODS: Binocular eye movements were recorded in four patients in binocular viewing conditions during a saccade task. RESULTS: Affected-side gaze showed normal saccades of the sound eye and undershooting saccades of the affected eye-evidence of intact interneurons, but deficient motoneurons, in the sixth-nerve nucleus on the affected side. Postsaccadic smooth onward drift followed undershooting saccades of the affected eye. Sound-side gaze, in the centripetal direction, showed relatively accurate saccades despite large offsets in initial position between the two eyes. In the centrifugal direction, there was a consistent undershoot of the affected eye. The sound eye showed unexpected overshoot. Postsaccadic drifts in opposite directions in the two eyes brought both eyes onto the target in an optimal time course. CONCLUSIONS: Studying the characteristics of the saccadic system in this oculomotor disorder gives new insight into binocular control of saccades and adaptation. In these patients, the oculomotor system was not capable of adapting the pulse command to the two eyes separately, even though DRS offers clear advantages of independent control. In contrast, independent adaptation of the saccadic step command was sent to the two eyes. This supports the idea that the rapid part of the saccadic command is common to both eyes.

Duane Retraction Syndrome↗

PubMed2005

Sensorimotor transformation for visually guided saccades.

Visually guided movements require the brain to perform a sensorimotor transformation. The key to understanding this transformation is to understand the different roles of the superior colliculus (SC) and cerebellum (CB). The SC has a three-layered structure. Cells in the top layer have visual, but not motor, responses. However, cells in the deeper layers have both visual and motor responses. Thus, for a long time it was thought that the SC encoded both the retinal location of a sensory stimulus and the desired change in eye movement needed to acquire it. However, copious evidence has accumulated that shows that the SC encodes only the retinal location of a visual target, and not the movement needed to foveate it. Thus, the information needed to make accurate movements must come from another part of the brain, which is proposed to be the cerebellum. Here it is shown how the cerebellum could perform the sensorimotor transformation.

Brain↗

PubMed2004

Recovery of saccadic dysmetria following localized lesions in monkey superior colliculus.

Damage to the monkey superior colliculus (SC) produces deficits in the generation of saccadic eye movements. Recovery of the accuracy of saccades is rapid, but saccadic latency and peak velocity recover slowly or not at all. In the present experiments we revisited the issue of recovery of function following localized lesions of the SC using three methodological advances: implantation of wire recording electrodes into the SC for the duration of the experiment to ensure that we were recording from the same site on the SC map on successive days; quantification of changes in saccadic accuracy, latency, and velocity using a standard grid of target points in the visual field contralateral to the SC lesion; measurement of movement field size to quantitatively determine any changes following the lesion. We confirmed a decrease in saccadic accuracy following electrolytic lesions of the SC, and we found that this dysmetria recovered within about 4 days. Saccadic latency increased for saccades to the lesion area and this deficit persisted. Peak saccadic velocity decreased immediately after the lesion and decreased further during the 10 days to 2 weeks of the experiment. We found no indication of an expansion of the movement fields of neurons adjacent to the lesion area. This lack of reorganization suggests that movement field changes within the SC cannot mediate the recovery in accuracy of the saccade. The persistence of the latency and velocity deficits despite the recovery of amplitude deficits indicates that saccadic latency and peak velocity are dependent upon the SC whereas saccadic amplitude is not.

Animals↗

PubMed2003

Effects of tenotomy surgery on congenital nystagmus waveforms in adult patients. Part I. Wavelet spectral analysis.

Congenital nystagmus (CN) is an aperiodic oscillatory eye movement disorder. Horizontal rectus tenotomy with simple re-attachment has been proposed as a therapy for CN. This therapy might affect vision and/or eye movements. Another paper deals with improvements in visual acuity. This and the companion paper examine changes in eye movements. In this study, we examined the effect of tenotomy on nystagmus waveforms using wavelet spectral analysis. No common effect was found across the patients on the wavelet spectra of the CN beat, suggesting that tenotomy surgery has no effect, or only a quite small effect, on the waveform structure of CN.

Adult↗

PubMed2003

Effects of tenotomy surgery on congenital nystagmus waveforms in adult patients. Part II. Dynamical systems analysis.

Congenital nystagmus (CN) is an aperiodic oscillatory eye movement disorder of unknown etiology. We examined the effect of horizontal rectus tenotomy with simple re-attachment on the dimensionality of the dynamical mechanism underlying CN. The correlation dimensions (CDs) were calculated from eight patients who had tenotomy surgery. We found no significant differences in the CDs that could be associated with the surgery. The change in dimensionality was less than 5% on average. The results suggest that the tenotomy has no effect, or only a quite small effect, on the underlying mechanism of the CN beats.

Adult↗

PubMed2003

Dynamic eye plant models and the control of eye movements.

Models of the oculomotor plant (globe, muscles, pulleys, and orbital tissues) fall into three categories: 1). one-dimensional dynamic with lumped plant elements, 2). three-dimensional dynamic with lumped plant elements, or 3). three-dimensional static with distinct plant elements. The second class of models is most often used when studying the neural control of 3-D eye movement, because they best represent the plant dynamics. However, they are often faulted because they make two unrealistic assumptions: 1). muscle pairs act along the three orthogonal axes (symmetry assumption); and 2). the force generated by the muscles depends only on their innervation (force assumption). It turns out that the symmetry assumption is quite benign, because in a realistic model of the plant the deviations from orthogonal axes can be easily accounted for by simple adjustments to the innervation. In contrast, the force assumption introduces some serious problems. In the present paper, the authors show that a realistic, dynamic model of the geometry of the orbit, with independent muscles, makes different predictions than a similar model with lumped muscles. This difference arises because muscle force is a function of both innervation and muscle length.

Biomechanical Phenomena↗

PubMed2002

Distributed model of collicular and cerebellar function during saccades.

How does the brain tell the eye where to go? Classical models of rapid eye movements are lumped control systems that compute analogs of physical signals such as desired eye displacement, instantaneous error, and motor drive. Components of these lumped models do not correspond well with anatomical and physiological data. We have developed a more brain-like, distributed model (called a neuromimetic model), in which the superior colliculus (SC) and cerebellum (CB) play novel roles, using information about the desired target and the movement context to generate saccades. It suggests that the SC is neither sensory nor motor; rather it encodes the desired sensory consequence of the saccade in retinotopic coordinates. It also suggests a non-computational scheme for motor control by the cerebellum, based on context learning and a novel spatial mechanism, the pilot map. The CB learns to use contextual information to initialize the pilot signal that will guide the saccade to its goal. The CB monitors feedback information to steer and stop the saccade, and thus replaces the classical notion of a displacement integrator. One consequence of this model is that no desired eye movement signal is encoded explicitly in the brain; rather it is distributed across activity in both the SC and CB. Another is that the transformation from spatially coded sensory information to temporally coded motor information is implicit in the velocity feedback loop around the CB. No explicit spatial-to-temporal transformation with a normalization step is needed.

Cerebellum↗