Changes In Eye Velocity Research Articles

Learned Timing of Motor Behavior in the Smooth Eye Movement Region of the Frontal Eye Fields

Proper timing is a critical aspect of motor learning. We report a relationship between a representation of time and an expression of learned timing in neurons in the smooth eye movement region of the frontal eye fields (FEF(SEM)). During prelearning pursuit of target motion at a constant velocity, each FEF(SEM) neuron is most active at a distinct time relative to the onset of pursuit tracking. In response to an instructive change in target direction, a neuron expresses the most learning when the instruction occurs near the time of its maximal participation in prelearning pursuit. Different neurons are most active, and undergo the most learning, at distinct times during pursuit. We suggest that the representation of time in the FEF(SEM) drives learning that is temporally linked to an instructive change in target motion, and that this may be a general function of motor areas of the cortex.

Learning on Multiple Timescales in Smooth Pursuit Eye Movements

We commonly think of motor learning as a gradual process that makes small, adaptive steps in a consistent direction. We now report evidence that learning in pursuit eye movements could start with large, transient short-term alterations that stoke a more gradual long-term process. Monkeys tracked a target that started moving horizontally or vertically. After 250 ms of motion had produced a preinstruction eye velocity close to target velocity, an orthogonal component of target motion created an instructive change in target direction that was randomly in one of the two directions along the orthogonal axis. The preinstruction eye velocity in each trial expressed single-trial learning as a bias toward the direction of the instruction in the prior trial. The single-trial learning was forgotten within 4 to 10 s. Two observations implied that single-trial learning was not simply cognitive anticipation. First, the magnitude of the trial-over-trial change in eye velocity depended on the ongoing eye velocity at the time of the instruction in the prior trial. Single-trial learning was negligible if the prior trial had provided a well-timed cue without evoking any preinstruction eye velocity. Second, regular alternation of the direction of the instructive target motion caused reactive rather than anticipatory trial-over-trial changes in eye velocity. Humans showed very different responses that appeared to be based on cognitive anticipation rather than learning. We suggest that single-trial learning results from a low-level learning mechanism and may be a necessary prerequisite for longer-term modifications that are more permanent.

Spatial deployment of attention influences both saccadic and pursuit tracking

We examined the effects of changing spatial aspects of attention during oculomotor tracking. Human subjects were instructed to make a discrimination on either the small (0.8°) central or the large (8°) peripheral part of a compound stimulus (two counter-rotating concentric rings) while the stimulus either translated across the screen or was stationary. During this period, a transient perturbation with either step or ramp movement profile occurred. For perturbations leading to a change in position larger than the small ring, saccades occurred more frequently and had much shorter latencies (by 135 ms) when attention was directed to the small ring than when attention was directed to the large ring. These latency differences were sufficiently great that from a single saccade one can identify the attentional instruction with 94% accuracy. However, with target steps as small as the small ring, saccade latencies differed less. For pursuit, ramp perturbations caused larger changes in eye velocity with little change in latency when attention was directed to the small ring. Finally, when only the motion of the non-attended ring was perturbed, most subjects showed stronger saccadic responses to perturbations of the small than the large ring, and stronger pursuit responses to perturbations of the large than the small ring. By fitting the saccade latency distributions with the Reddi and Carpenter LATER model, we found that our subjects apparently employed at least two distinct strategies for changing latency when attending large vs. small. We propose that the timing of the saccade decision process depends on both the size of the attended object and the magnitude of the perturbation.

Role of the oculomotor vermis in generating pursuit and saccades: effects of microstimulation.

We studied the eye movements evoked by applying small amounts of current (2-50 microA) within the oculomotor vermis of two monkeys. We first compared the eye movements evoked by microstimulation applied either during maintained pursuit or during fixation. Smooth, pursuitlike changes in eye velocity caused by the microstimulation were directed toward the ipsilateral side and occurred at short latencies (10-20 ms). The amplitudes of these pursuitlike changes were larger during visually guided pursuit toward the contralateral side than during either fixation or visually guided pursuit toward the ipsilateral side. At these same sites, microstimulation also often produced abrupt, saccadelike changes in eye velocity. In contrast to the smooth changes in eye velocity, these saccadelike effects were more prevalent during fixation and during pursuit toward the ipsilateral side. The amplitude and type of evoked eye movements could also be manipulated at single sites by changing the frequency of microstimulation. Increasing the frequency of microstimulation produced increases in the amplitude of pursuitlike changes, but only up to a certain point. Beyond this point, the value of which depended on the site and whether the monkey was fixating or pursuing, further increases in stimulation frequency produced saccadelike changes of increasing amplitude. To quantify these effects, we introduced a novel method for classifying eye movements as pursuitlike or saccadelike. The results of this analysis showed that the eye movements evoked by microstimulation exhibit a distinct transition point between pursuit and saccadelike effects and that the amplitude of eye movement that corresponds to this transition point depends on the eye movement behavior of the monkey. These results are consistent with accumulating evidence that the oculomotor vermis and its associated deep cerebellar nucleus, the caudal fastigial, are involved in the control of both pursuit and saccadic eye movements. We suggest that the oculomotor vermis might accomplish this role by altering the amplitude of a motor error signal that is common to both saccades and pursuit.

システムニューロサイエンス教育講座 １４． いわゆる“Ｖｅｌｏｃｉｔｙ Ｓｔｏｒａｇｅ機構”

Substantial advances in understanding of oculomotor function have come from basing models of the oculomotor system on the control system theory. In this model, vestibular nystagmus, OKN and OKAN are produced by combined activation of two important pathways. One process, called the direct-pathway, produced rapid changes in eye velocity. A second process (indirect pathway) causes only slow changes in eye velocity and contains a non-ideal integrator. This integrator, labeled a “velocity-storage integrator”, appears to hold or store activity related to slow phase eye velocity. Activities in the direct and indirect pathways combine to form the velocity signal (This signal drives the “velocity-to-position integrator”, which drives the oculomotor plant). The velocity storage mechanism serves as a focus for superimposing a variety of sensory inputs that signal motion and provide the central nervous system with a coordinate basis for interpreting continuous movement of the head relative to the environment. However, neural circuits underlying these mechanism are still unknown. The recent studies suggest that the velocity-storage integrator appears to lie in the vestibular nuclei (mainly medial vestibular nucleus, MVN), while the velocity-to-position-integrator is probably closely associated with the prepositus hypoglossi nuclei. The recent extracellular recording study shows that activities of “vestibular only” and “vestibular, plus saccade” units in the rostral MVN are likely to carry an eye velocity signal related to velocity storage.

閉眼下頭部捻転時の一過性眼球偏位の偏位速度における年齢変化 老化の指標となり得るか

Active head turn with eyes closed may involuntarily induce transient saccadic eye deviation (TSD) in the direction of the head movement. This suspected of being provoked by activation of the lateral gaze center due to neck torsion.Using a computer, the maximal eye velocities of TSDs and visually elicited voluntary saccades of 20 degree were analyzed in 89 subjects aged 9 to 84. The mean velocity of TSD in subjects over 70 years of age was slower than that in the other age groups excluding the small number of subjects under age 20. In particular, a significant difference was noted between the elderly subjects and those in their 50s. Voluntary saccades, however, did not differ between age groups.In conclusion, age-related change in eye velocity was seen in involuntary TSD, but not in voluntary saccades. The velocity of TSD may be available for an assessment of aging.

Habituation and adaptation of the vestibuloocular reflex: a model of differential control by the vestibulocerebellum

We habituated the dominant time constant of the horizontal vestibuloocular reflex (VOR) of rhesus and cynomolgus monkeys by repeated testing with steps of velocity about a vertical axis and adapted the gain of the VOR by altering visual input with magnifying and reducing lenses. After baseline values were established, the nodulus and ventral uvula of the vestibulocerebellum were ablated in two monkeys, and the effects of nodulouvulectomy and flocculectomy on VOR gain adaptation and habituation were compared. The VOR time constant decreased with repeated testing, rapidly at first and more slowly thereafter. The gain of the VOR was unaffected. Massed trials were more effective than distributed trials in producing habituation. Regardless of the schedule of testing, the VOR time constant never fell below the time constant of the semicircular canals (approximately 5 s). This finding indicates that only the slow component of the vestibular response, the component produced by velocity storage, was habituated. In agreement with this, the time constant of optokinetic after-nystagmus (OKAN) was habituated concurrently with the VOR. Average values for VOR habituation were obtained on a per session basis for six animals. The VOR gain was adapted by natural head movements in partially habituated monkeys while they wore x 2.2 magnifying or x 0.5 reducing lenses. Adaptation occurred rapidly and reached about +/- 30%, similar to values obtained using forced rotation. VOR gain adaptation did not cause additional habituation of the time constant. When the VOR gain was reduced in animals with a long VOR time constant, there were overshoots in eye velocity that peaked at about 6-8 s after the onset or end of constant-velocity rotation. These overshoots occurred at times when the velocity storage integrator would have been maximally activated by semicircular canal input. Since the activity generated in the canals is not altered by visual adaptation, this finding indicates that the gain element that controls rapid changes in eye velocity in the VOR is separate from that which couples afferent input to velocity storage. Nodulouvulectomy caused a prompt and permanent loss of habituation, returning VOR time constants to initial values. VOR gain adaptation, which is lost after flocculectomy, was unaffected by nodulouvulectomy. Flocculectomy did not alter habituation of the VOR or of OKAN. Using a simplified model of the VOR, the decrease in the duration of vestibular nystagmus due to habituation was related to a decrement in the dominant time constant of the velocity storage integrator (1/h0).(ABSTRACT TRUNCATED AT 400 WORDS)

Visual tracking in monkeys: evidence for short-latency suppression of the vestibuloocular reflex

1. Monkeys normally use a combination of smooth head and eye movements to keep the eyes pointed at a slowly moving object. The visual inputs from target motion evoke smooth pursuit eye movements, whereas the vestibular inputs from head motion evoke a vestibuloocular reflex (VOR). Our study asks how the eye movements of pursuit and the VOR interact. Is there a linear addition of independent commands for pursuit and the VOR? Or does the interaction of visual and vestibular stimuli cause momentary, "parametric" modulation of transmission through VOR pathways? 2. We probed for the state of the VOR and pursuit by presenting transient perturbations of target and/or head motion under different steady-state tracking conditions. Tracking conditions included fixation at straight-ahead gaze, in which both the head and the target were stationary; "times-zero (X0) tracking," in which the target and head moved in the same direction at the same speed; and "times-two (X2) tracking," in which the target and head moved in opposite directions at the same speed. 3. Comparison of the eye velocities evoked by changes in the direction of X0 versus X2 tracking revealed two components of the tracking response. The earliest component, which we attribute to the VOR, had a latency of 14 ms and a trajectory that did not depend on initial tracking conditions. The later component had a latency of 70 ms or less and a trajectory that did depend on tracking conditions. 4. To probe the latency of pursuit eye movements, we imposed perturbations of target velocity imposed during X0 and X2 tracking. The resulting changes in eye velocity had latencies of at least 100 ms. We conclude that the effects of initial tracking conditions on eye velocity at latencies of less than 70 ms cannot be caused by visual feedback through the smooth-pursuit system. Instead, there must be another mechanism for short-latency control over the VOR; we call this component of the response "short-latency tracking." 5. Perturbations of head velocity or head and target velocity during X0 and X2 tracking showed that short-latency tracking depended only on the tracking conditions at the time the perturbation was imposed. The VOR appeared to be suppressed when the initial conditions were X0 tracking. 6. The magnitude of short-latency tracking depended on the speed of initial head and target movement. During X0 tracking at 15 deg/s, short-latency tracking was modest. When the initial speed of head and target motion was 60 deg/s, the amplitude of short-latency tracking was quite large and its latency became as short as 36 ms.(ABSTRACT TRUNCATED AT 400 WORDS)

Shared attentional control of smooth eye movement and perception.

Subjects performed a concurrent smooth pursuit and perceptual task to determine whether smooth pursuit eye movements and perception share the same attentional mechanism. Subjects pursued a pair of eccentric rows of moving characters while simultaneously attempting to identify and locate the single numeral in these target rows and the single numeral in a pair of untracked background rows, which moved at a different velocity. Average smooth pursuit gain (eye velocity/target velocity) was 0.7 to 1. Visual search was better for target rows (approximately 65% correct) than for background rows (approximately 22% correct). Superior search performance for the target was not due to its lower retinal speed: performance on the target was 2-3 times better than on the background when retinal speeds were the same. Superior performance for the pursuit target suggests that smooth eye movements and perception share the same selective attentional mechanism. A shared attentional mechanism was further supported by findings that subjects could not: (1) maintain a stable line of sight on a central stationary point while simultaneously attending to moving rows; and (2) pursue one pair of rows and attend the other, untracked rows. Attempts to attend untracked rows did, however, produce a partial improvement in search performance which was accompanied by only a very slight change in eye velocity. This demonstrates that the effects of decisions about how to apportion attention across the visual field depend on the task. Despite the common selective attentional mechanism, smooth eye movements do not provide accurate external indicators of attention unless the consequences of attentional decisions for performance are determined separately for oculomotor and for perceptual tasks.

The effect of central retinal lesions on optokinetic nystagmus in the monkey.

In alert monkeys (Macaca mulatta and fascicularis) the effect of central retinal lesions on 'fast' optokinetic responses was investigated during high velocity optokinetic and visual-vestibular conflict stimulation. The 'fast' component of the optokinetic response manifests itself as a rapid rise in the slow-phase eye velocity after light-on, during high velocity optokinetic stimulation; and a sudden drop in eye velocity after light-off. In contrast, the 'velocity storage' component leads only to gradual changes in eye velocity during continuous optokinetic stimulation and after light-off (optokinetic after-nystagmus). Retinal lesions were placed by laser coagulation in and around the fovea. Responses of the normal and lesioned eye were compared. It was found that central lesions up to 12 deg (fovea diameter 6 deg) had only a negligible effect on 'fast' optokinetic responses. With lesions of more than 25-30 deg diameter centered on the fovea definite 'fast' responses could still be obtained, on average reduced to about 50% of the responses of the normal eye. Some monkeys showed initially no 'fast' optokinetic responses and had, therefore, to be excluded from lesion experiments. The results demonstrate that 'fast' optokinetic responses also can be obtained from extrafoveal areas, i.e. areas which are not generally involved in smooth pursuit eye movements. These results are discussed in relation to reports that the 'smooth pursuit' eye movement system is also used to generate 'fast' optokinetic responses.

Role of the flocculus and paraflocculus in optokinetic nystagmus and visual-vestibular interactions: effects of lesions.

Optokinetic nystagmus (OKN), optokinetic after-nystagmus (OKAN), vestibular nystagmus and visual-vestibular interactions were studied in monkeys after surgical ablation of the flocculus and paraflocculus. After bilateral flocculectomy the initial rapid rise in slow phase eye velocity of horizontal and vertical OKN was severely attenuated, and maximum velocities fell to the preoperative saturation level of OKAN. There is generally little or no upward OKAN in the normal monkey, and upward OKN was lost after bilateral lesions. Unilateral flocculectomy affected the rapid rise in horizontal velocity to both sides. Consistent with the absence of a rapid response to steps of surround velocity, animals were unable to follow acceleration of the visual field with eye accelerations faster than about 3-5 degrees/s2. The slow rise in OKN slow phase velocity to a steady state level was prolonged after operation. However, rates of rise were approximately equal for the same initial retinal slips before and after operation. The similarity in the time course of OKN when adjusted for initial retinal slip, and in the gain, saturation level and time course of OKAN before and after flocculectomy indicates that the lesions had not significantly altered the coupling of the visual system to the velocity storage integrator or its associated time constant. When animals were rotated in a subject-stationary visual surround after flocculectomy, they could not suppress the initial jump in eye velocity at the onset of the step. Despite this, they could readily suppress the subsequent nystagmus. The time constant of decline in the conflict situations was almost as short as in the normal monkey and was in the range of the peripheral vestibular time constant. This suggests that although the animals were unable to suppress rapid changes in eye velocity due to activation of direct vestibulo-oculomotor pathways, they had retained their ability to discharge activity from the velocity storage mechanism. Consistent with this, animals had no difficulty in suppressing OKAN after flocculectomy. Visual-vestibular interactions utilizing the velocity storage mechanism were normal after flocculectomy, as was nystagmus induced by rotation about a vertical axis or about axes tilted from the vertical. Also unaffected were the discharge of nystagmus caused by tilting the head out of the plane of the response and visual suppression of nystagmus induced by off-vertical axis rotation. The flocculus does not appear to play an important role in mediating these responses. The data before and after flocculectomy were simulated by a model which is homeomorphic to that presented previously.(ABSTRACT TRUNCATED AT 400 WORDS)

Velocity storage in the vestibulo-ocular reflex arc (VOR).

Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 degrees/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 degrees/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression). These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.