(1/194) Eye movement deficits following ibotenic acid lesions of the nucleus prepositus hypoglossi in monkeys II. Pursuit, vestibular, and optokinetic responses.

The eyes are moved by a combination of neural commands that code eye velocity and eye position. The eye position signal is supposed to be derived from velocity-coded command signals by mathematical integration via a single oculomotor neural integrator. For horizontal eye movements, the neural integrator is thought to reside in the rostral nucleus prepositus hypoglossi (nph) and project directly to the abducens nuclei. In a previous study, permanent, serial ibotenic acid lesions of the nph in three rhesus macaques compromised the neural integrator for fixation but saccades were not affected. In the present study, to determine further whether the nph is the neural substrate for a single oculomotor neural integrator, the effects of those lesions on smooth pursuit, the vestibulo-ocular reflex (VOR), vestibular nystagmus (VN), and optokinetic nystagmus (OKN) are documented. The lesions were correlated with long-lasting deficits in eye movements, indicated most clearly by the animals' inability to maintain steady gaze in the dark. However, smooth pursuit and sinusoidal VOR in the dark, like the saccades in the previous study, were affected minimally. The gain of horizontal smooth pursuit (eye movement/target movement) decreased slightly (<25%) and phase lead increased slightly for all frequencies (0.3-1.0 Hz, +/-10 degrees target tracking), most noticeably for higher frequencies (0.8-0.7 and approximately 20 degrees for 1.0-Hz tracking). Vertical smooth pursuit was not affected significantly. Surprisingly, horizontal sinusoidal VOR gain and phase also were not affected significantly. Lesions had complex effects on both VN and OKN. The plateau of per- and postrotatory VN was shortened substantially ( approximately 50%), whereas the initial response and the time constant of decay decreased slightly. The initial OKN response also decreased slightly, and the charging phase was prolonged transiently then recovered to below normal levels like the VN time constant. Maximum steady-state, slow eye velocity of OKN decreased progressively by approximately 30% over the course of the lesions. These results support the previous conclusion that the oculomotor neural integrator is not a single neural entity and that the mathematical integrative function for different oculomotor subsystems is most likely distributed among a number of nuclei. They also show that the nph apparently is not involved in integrating smooth pursuit signals and that lesions of the nph can fractionate the VOR and nystagmic responses to adequate stimuli.  (+info)

(2/194) Ocular responses to radial optic flow and single accelerated targets in humans.

Self-movement in a structured environment induces retinal image motion called optic flow. Optic flow on one hand provides information about the direction of self-motion. On the other hand optic flow presents large field visual motion which will elicit eye movements for the purpose of image stabilization. We investigated oculomotor behavior in humans during the presentation of radial optic flow fields which simulated forward or backward self-motion. Different conditions and oculomotor tasks were compared. In one condition, subjects had to actively pursue single dots in a radial flow pattern. In a second condition, subjects had to pursue single dots over a dark background. These dots accelerated or decelerated similar to single dots in radial optic flow. In a third condition, subjects were asked to passively view the entire optic flow stimulus. Smooth pursuit eye movements with high gain were observed when dots were actively pursued. This was true for single dots moving over a homogeneous background and for single dots in the optic flow. Passive viewing of optic flow stimuli evoked eye movements that resembled an optokinetic nystagmus. Slow phase eye movements tracked the motion of elements in the optic flow. Gain was low for simulated forward self-motion (expanding optic flow) and high for simulated backward movement self-motion (contracting optic flow). Thus, voluntary pursuit and passive optokinetic responses yielded different gain for the tracking of elements of an expanding optic flow pattern. During passive viewing of the optic flow stimulus, gaze was usually at or near the focus of radial flow. Our results give insights into the oculomotor performances and needs for image stabilization during self-motion and in the role of gaze strategy for the detection of the direction of heading.  (+info)

(3/194) Asymmetric responses in cortical visually evoked potentials to motion are not derived from eye movements.

PURPOSE: Normal neonates and many adults after abnormal visual development have directional preferences for visual stimulus motions; i.e., they give better responses for optokinetic nystagmus (OKN) and visually evoked potentials (VEPs) in one direction than to those in the opposite direction. The authors tested whether the VEP responses were asymmetrical because of abnormal eye movements. METHODS: VEPs were recorded from the visual cortices of five macaque monkeys: one normal, one neonate, and three reared with alternating monocular occlusion (AMO). They were lightly anesthetized, followed by paralysis to prevent eye movements. They then had "jittered" vertical grating patterns presented in their visual fields. The steady state VEPs were analyzed with discrete Fourier transforms to obtain the amplitudes and phases of the asymmetries. RESULTS: The normal, control monkey had small, insignificant amplitudes of its asymmetrical Fourier component and random phases that were not 180 degrees out of phase across the left and right eyes. The neonatal monkey and the AMO monkeys all had large, significant asymmetries that were approximately 180 degrees out of phase between the left and right eyes. CONCLUSIONS: The neonate and abnormally reared monkeys continued to have asymmetrical responses even after their eyes were paralyzed. Therefore, eye movements cannot be the source of the asymmetrical amplitudes of the VEPs, and the visual cortex is at least one source responsible for asymmetries observed in neonates and adults reared under abnormal visual inputs.  (+info)

(4/194) Genetic disorders of vision revealed by a behavioral screen of 400 essential loci in zebrafish.

We examined optokinetic and optomotor responses of 450 zebrafish mutants, which were isolated previously based on defects in organ formation, tissue patterning, pigmentation, axon guidance, or other visible phenotypes. These strains carry single point mutations in >400 essential loci. We asked which fraction of the mutants develop blindness or other types of impairments specific to the visual system. Twelve mutants failed to respond in either one or both of our assays. Subsequent histological and electroretinographic analysis revealed unique deficits at various stages of the visual pathway, including lens degeneration (bumper), melanin deficiency (sandy), lack of ganglion cells (lakritz), ipsilateral misrouting of axons (belladonna), optic-nerve disorganization (grumpy and sleepy), inner nuclear layer or outer plexiform layer malfunction (noir, dropje, and possibly steifftier), and disruption of retinotectal impulse activity (macho and blumenkohl). Surprisingly, mutants with abnormally large or small eyes or severe wiring defects frequently exhibit no discernible behavioral deficits. In addition, we identified 13 blind mutants that display outer-retina dystrophy, making this syndrome the single-most common cause of inherited blindness in zebrafish. Our screen showed that a significant fraction (approximately 5%) of the essential loci also participate in visual functions but did not reveal any systematic genetic linkage to particular morphological traits. The mutations uncovered by our behavioral assays provide distinct entry points for the study of visual pathways and set the stage for a genetic dissection of vertebrate vision.  (+info)

(5/194) Motor dynamics encoding in cat cerebellar flocculus middle zone during optokinetic eye movements.

We investigated the relationship between eye movement and simple-spike (SS) frequency of Purkinje cells in the cerebellar flocculus middle zone during the optokinetic response (OKR) in alert cats. The OKR was elicited by a sequence of a constant-speed visual pattern movement in one direction for 1 s and then in the opposite direction for 1 s. Quick-phase-free trials were selected. Sixty-six cells had direction-selective complex spike (CS) activity that was modulated during horizontal (preferring contraversive) but not vertical stimuli. The SS activity was modulated during horizontal OKR, preferring ipsiversive stimuli. Forty-one cells had well-modulated activity and were suitable for the regression model. In these cells, an inverse dynamics approach was applied, and the time course of the SS rate was reconstructed, with mean coefficient of determination 0.76, by a linear weighted superposition of the eye acceleration (mean coefficient, 0.056 spikes/s per deg/s(2)), velocity (5.10 spikes/s per deg/s), position (-2.40 spikes/s per deg), and constant (mean 34.3 spikes/s) terms, using a time delay (mean 11 ms) from the unit response to the eye response. The velocity and acceleration terms contributed to the increase in the reconstructed SS rates during ipsilateral movements, whereas the position term contributed during contralateral movements. The standard regression coefficient analyses revealed that the contribution of the velocity term (mean coefficient 0.81) was predominant over the acceleration (0.03) and position (-0.17) terms. Forward selection analysis revealed three cell types: Velocity-Position-Acceleration type (n = 27): velocity, position, and acceleration terms are significant (P < 0.05); Velocity-Position type (n = 12): velocity and position terms are significant; and Velocity-Acceleration type (n = 2): velocity and acceleration terms are significant. Using the set of coefficients obtained by regression of the response to a 5 deg/s stimulus velocity, the SS rates during higher (10, 20, and 40 deg/s) stimulus velocities were successfully reconstructed, suggesting generality of the model. The eye-position information encoded in the SS firing during the OKR was relative but not absolute in the sense that the magnitude of the position shift from the initial eye position (0 deg/s velocity) contributed to firing rate changes, but the initial eye position did not. It is concluded that 1) the SS firing frequency in the cat middle zone encodes the velocity and acceleration information for counteracting the viscosity and inertia forces respectively, during short-duration horizontal OKR and 2) the apparent position information encoded in the SS firing is not appropriate for counteracting the elastic force during the OKR.  (+info)

(6/194) Three-dimensional kinematics of ocular drift in humans with cerebellar atrophy.

One of the signs of the cerebellar ocular motor syndrome is the inability to maintain horizontal and vertical fixation. Typically, in the presence of cerebellar atrophy, the eyes show horizontal gaze-evoked and vertical downbeat nystagmus. We investigated whether or not the cerebellar ocular motor syndrome also includes a torsional drift and, specifically, if it is independent from the drift in the horizontal-vertical plane. The existence of such a torsional drift would suggest that the cerebellum is critically involved in maintaining the eyes in Listing's plane. Eighteen patients with cerebellar atrophy (diagnosis confirmed by magnetic resonance imaging) were tested and compared with a group of normal subjects. Three-dimensional eye movements (horizontal, vertical, and torsional) during attempted fixations of targets at different horizontal and vertical eccentricities were recorded by dual search coils in a three-field magnetic frame. The overall ocular drift was composed of an upward drift that increased during lateral gaze, a horizontal centripetal drift that appeared during lateral gaze, and a torsional drift that depended on horizontal eye position. The vertical drift consisted of two subcomponents: a vertical gaze-evoked drift and a constant vertical velocity bias. The increase of upward drift velocity with eccentric horizontal gaze was caused by an increase of the vertical velocity bias; this component did not comply with Listing's law. The horizontal-eye-position-dependent torsional drift was intorsional in abduction and extorsional in adduction, which led to an additional violation of Listing's law. The existence of torsional drift that is eye-position-dependent suggests that the cerebellum is critically involved in the implementation of Listing's law, perhaps by mapping a tonic torsional signal that depends on the direction of the line of sight. The magnitude of this signal might reflect the difference in torsional eye position between the torsional resting position determined by the mechanics of the eye plant and the torsional position required by Listing's law.  (+info)

(7/194) Abnormal vertical optokinetic nystagmus in infants and children.

AIMS: To determine if testing vertical optokinetic nystagmus (VOKN) has a role in the clinical assessment of infants and children. METHODS: A large field projection system was developed with which optokinetic nystagmus (OKN) could be stimulated in any direction. Gross abnormalities in the response were detected simply by observation. RESULTS: VOKN was tested in 144 children using this OKN projection system. 26 of these children had abnormal VOKN; 13 had a vertical saccade initiation failure "ocular motor apraxia" (in either direction, up/down, or in both) and 13 had absent VOKN (in either direction, up/down, or in both). Nine of the children with an up and/or down vertical saccade initiation failure (VSIF) had a neurometabolic disease (two had Niemann-Pick disease type C, five had Gaucher disease type III, one had Gaucher disease type II, and one had Gaucher disease type I). Five children with a VSIF had an abnormality identified by a magnetic resonance imaging (MRI) scan of the brain. In two of these children there was a focal lesion of the rostral midbrain. In 11 of the children with absent up and/or down VOKN an MRI scan revealed an abnormality. This involved the brainstem and/or the cerebellum in 10. Absent up and/or down VOKN was found in association with Joubert syndrome, Leigh disease, and cerebral palsy. CONCLUSION: VOKN testing has a useful role in detecting neurological abnormalities in infants and children. Detection of abnormal VOKN should indicate further investigations for a neurometabolic disease or an abnormality involving the cortex, brainstem, and/or cerebellum. Abnormal VOKN but normal horizontal OKN is highly suggestive of a rostral midbrain lesion.  (+info)

(8/194) Functions of the nucleus of the optic tract (NOT). II. Control of ocular pursuit.

Ocular pursuit in monkeys, elicited by sinusoidal and triangular (constant velocity) stimuli, was studied before and after lesions of the nucleus of the optic tract (NOT). Before NOT lesions, pursuit gains (eye velocity/target velocity) were close to unity for sinusoidal and constant-velocity stimuli at frequencies up to 1 Hz. In this range, retinal slip was less than 2 degrees. Electrode tracks made to identify the location of NOT caused deficits in ipsilateral pursuit, which later recovered. Small electrolytic lesions of NOT reduced ipsilateral pursuit gains to below 0.5 in all tested conditions. Pursuit was better, however, when the eyes moved from the contralateral side toward the center (centripetal pursuit) than from the center ipsilaterally (centrifugal pursuit), although the eyes remained in close proximity to the target with saccadic tracking. Effects of lesions on ipsilateral pursuit were not permanent, and pursuit gains had generally recovered to 60-80% of baseline after about 2 weeks. One animal had bilateral NOT lesions and lost pursuit for 4 days. Thereafter, it had a centrifugal pursuit deficit that lasted for more than 2 months. Vertical pursuit and visually guided saccades were not affected by the bilateral NOT lesions in this animal. We also compared effects of these and similar NOT lesions on optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN). Correlation of functional deficits with NOT lesions from this and previous studies showed that rostral lesions of NOT in and around the pretectal olivary nucleus, which interrupted cortical input through the brachium of the superior colliculus (BSC), affected both smooth pursuit and OKN. In two animals in which it was tested, NOT lesions that caused a deficit in pursuit also decreased the rapid and slow components of OKN slow-phase velocity and affected OKAN. It was previously shown that slightly more caudal NOT lesions were more effective in altering gain adaptation of the angular vestibulo-ocular reflex (aVOR). The present findings suggest that cortical pathways through rostral NOT play an important role in maintenance of ipsilateral ocular pursuit. Since lesions that affected ocular pursuit had similar effects on ipsilateral OKN, processing for these two functions is probably closely linked in NOT, as it is elsewhere.  (+info)