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1. The discharge of neurons in the deeper layers of the monkey superior colliculus was recorded during saccades made to stationary and to smoothly moving visual targets. 2. All neurons that discharged for saccades made to stationary targets also discharged during saccades made to moving targets, but there was a systematic shift in the saccade vector yielding maximal activity (i.e. center of the movement field) of collicular neurons for the latter class of movements. The shift moved the center of the movement fields toward larger-amplitude pursuit saccades for target motion away from the fovea, in comparison with saccades made to stationary targets. However, the discharge at the center of the movement field for pursuit saccades was 14% lower when averaged over the sample of recorded cells. 3. The saccades made during pursuit tracking of moving visual stimuli have different dynamics than saccades made to stationary targets. At similar amplitudes pursuit saccades are slower, and their velocity profiles often show secondary velocity peaks or inflection points and have longer-duration decelerating phases. 4. The combined experimental observations of a change in saccade dynamics and the shift in movement fields in collicular neurons for pursuit saccades are compatible with the hypothesis that saccades made to moving targets are controlled by neural processing in two partially separate pathways. In this theory, one path is concerned with correction of a presaccadic retinal position error (a path that includes the colliculus) and another path is concerned with position extrapolations based on the velocity of the moving target (a path that does not include the colliculus).

Electrical stimulation of the omnipause neuron region (OPN) at saccade onset results in interrupted saccades (IS)- eye movements which pause in midflight, resume after a brief period, and end near the target location. Details on the endpoint accuracy of IS do not exist, except for a brief report by Becker et al. (1981). Their analysis emphasized the accuracy of IS relative to the visual target which remained on during the interrupted period. We instead quantified the metric properties of IS relative to nonstimulated saccades during a target flash paradigm. Our results show that IS tend to be slightly hypermetric relative to the nonstimulated saccades to the same target location. The amount of overshoot is not correlated with target eccentricity. Detailed analyses also indicate that the standard deviations of the endpoint in IS are not significantly larger than those for nonstimulated saccades, although there was a much larger variability produced in eye position during the interruption. Both these latter observations support the notion that saccades are controlled by an internal negative feedback system. Also, the size of the remaining motor error during the interrupted period is one factor influencing when an IS resumes, but the variability in this measure is large particularly for smaller motor errors. Recent results have suggested that the resettable neural integrator involved in the feedback loop may be reset after each saccade through an exponential decay process. To probe the properties of the neural integrator, we varied the duration of interruption between the initial and resumed saccades and sought a systematic overshoot in the final eye position with increasing interruption period and variable initial saccade size. Our results showed the neural integrator does not decay during the pause period of interrupted saccades.

1. We recorded visuomotor burst neurons in the deeper layers of the superior colliculus while two monkeys (Macaca fascicularis) made short-latency saccades known as express saccades to visual targets in order to determine whether the visual discharge normally seen for these cells served as the premotor burst during express saccades. We then compared saccade-related activity during express saccades with that recorded during regular latency saccades and delayed saccades. 2. Saccade latency histograms for two monkeys during trials with a temporal gap between fixation-point offset and target onset showed a distinct peak of saccades around 70-80 ms. One monkey also showed an additional peak around 125 ms. 3. Express saccades were found on the average to have the same relationship of saccade peak velocity to saccade amplitude as regular latency saccades and delayed saccades. Express saccades tended to be somewhat more hypometric than the other classes of saccades. However, express saccades were clearly visually guided and not anticipatory responses. 4. For most cells studied (33/40), express saccades were accompanied by a single, uninterrupted burst of activity beginning 40-50 ms after target onset and continuing until sometime around the end of the saccade. For a smaller group of cells (7/40), two peaks of burst activity were seen, although the second peak was smaller and tended to occur late, after saccade onset. Across all cells, the peak of visuomotor cell activity during express saccades correlated just as well with target onset as it did with saccade onset. 5. When considered as discharge temporally aligned to the onset of the saccade, bursts accompanying express saccades tended to begin at approximately the same time as that for regular and delayed saccades. However, this discharge generally peaked earlier for express than for regular and delayed saccades. Also, the magnitude of discharge for express saccades was higher than that for delayed saccades throughout the burst. 6. When considered as discharge temporally aligned to the appearance of the target, bursts began earlier for express and regular saccade trials than for delayed saccade trials. Peak discharge tended to be greater for express saccades than for the other classes of saccades. 7. The results of this investigation are consistent with the suggestion that the visual burst of visuomotor neurons in the deeper layers of the superior colliculus plays a role in the initiation of express saccades similar to that played by the premotor burst for saccades of longer latency. The elevated discharge for express saccades supports the idea that the superior colliculus plays a more critical role in express saccade generation than in the generation of longer-latency saccades. The elevated discharge also suggests that visuomotor bursters do not code one-to-one for saccade velocity nor for saccade dynamic motor error.

The cerebellum is known to participate in visually guided eye movements. The cerebellar uvula receives projections from pontine nuclei that have been implicated in visual motion processing and the generation of smooth pursuit. Single-unit and lesion studies were conducted to determine how the uvula might further process these input signals. Purkinje cells and input fibers were recorded during a variety of visual and oculomotor paradigms. Most Purkinje cells were modulated in either an excitatory or inhibitory fashion by prolonged, horizontal optokinetic drum rotation. A small proportion of cells responded during smooth tracking of a small spot of light. As a paradox to the physiological data, lesions of the uvula produced a profound effect on smooth-pursuit eye movements. Initial eye velocity for pursuit in the direction contraversive to the lesion site was increased substantially following lesions in comparison with prelesion controls. The lesions also affected optokinetic nystagmus in the direction contraversive to the lesion, but not as drastically as they did pursuit. Overall the results suggest that the uvula is not in the neuronal pathway that directly controls pursuit, but instead serves to adjust the gain of this system as a result of abnormal periods of motion of the visual world.

Saccade-related burst neurons (SRBNs) in the monkey superior colliculus (SC) have been hypothesized to provide the brainstem saccadic burst generator with the dynamic error signal and the movement initiating trigger signal. To test this claim, we performed two sets of open-loop simulations on a burst generator model with the local feedback disconnected using experimentally obtained SRBN activity as both the driving and trigger signal inputs to the model. First, using neural data obtained from cells located near the middle of the rostral to caudal extent of the SC, the internal parameters of the model were optimized by means of a stochastic hill-climbing algorithm to produce an intermediate-sized saccade. The parameter values obtained from the optimization were then fixed and additional simulations were done using the experimental data from rostral collicular neurons (small saccades) and from more caudal neurons (large saccades); the model generated realistic saccades, matching both position and velocity profiles of real saccades to the centers of the movement fields of all these cells. Second, the model was driven by SRBN activity affiliated with interrupted saccades, the resumed eye movements observed following electrical stimulation of the omnipause region. Once again, the model produced eye movements that closely resembled the interrupted saccades produced by such simulations, but minor readjustment of parameters reflecting the weight of the projection of the trigger signal was required. Our study demonstrates that a model of the burst generator produces reasonably realistic saccades when driven with actual samples of SRBN discharges.

Several phenomenological models of the oculomotor mechanics that produce saccadic eye movements have been developed. These models have been based on measurements of macroscopic muscle and orbital tissue properties and measurements of eye kinematics during saccades. We recorded the forces generated by the medial and lateral recti during saccades in an alert, behaving monkey using chronically implanted force transducers. With this new data, we tested the ability of the classic saccade models to generate realistic muscle force profiles. Errors in the predictions of the classic saccade models led to a reexamination of the current models of extraocular muscle. Both a phenomenological, Hill-type muscle model and an approximation to Huxley's molecular level muscle model based on the cross-bridge mechanism of contraction (distribution moment model) were derived and studied for monkey extraocular muscle. Simulations of the distribution moment model led to insights suggesting (i) specific modifications in the lumped force/velocity relationship in the Hill-type model that resulted in this type of phenomenological model being able to generate realistic dynamics in extraocular muscle during saccades; (ii) the distribution of activity in the different fiber types in extraocular muscle may be central to the characteristics exhibited by the muscle during saccades; (iii) the transient properties of lengthening muscle such as yielding are not significant during saccades; and (iv) the series elastic component in active muscle may be predominantly generated by the elastic properties of the cross-bridges.

To define predictive behavior and mechanisms in visual smooth pursuit, various target motions were presented to 2 monkeys. Target stimuli included: single sinusoids (1's), triangle waves (T's), sums of 4 nonharmonically related sinusoids (4's), bandpass limited white noise (B's), and wideband white noise (N's). Velocity error was least for 1's, greatest for N's, and intermediate for T's, 4's, and B's. For the bandlimited 4's and B's, monkeys demonstrated the greatest relative amplitude response at the highest frequencies. Predictive mechanisms are classified as short- and long-term, depending on how much past target motion information is employed. The T's and a modification of this stimulus pattern involving a random perturbation were used to test the hypothesis that prediction is based exclusively on short-term signal processing related to target position and its derivatives. The existence of long-term predictive mechanisms in monkey smooth pursuit was unequivocally demonstrated with the use of the latter stimulus.

1. We recorded the spatial and temporal dynamics of saccade-related burst neurons (SRBNs) found in the intermediate layers of the superior colliculus (SC) in the alert, behaving monkey. These burst cells are normally the first neurons recorded during radially directed microelectrode penetrations of the SC after the electrode has left the more dorsally situated visual layers. They have spatially delimited movement fields whose centers describe the well-studied motor map of the SC. They have a rather sharp, saccade-locked burst of activity that peaks just before saccade onset and then declines steeply during the saccade. Many of these cells, when recorded during saccade trials, also have an early, transient visual response and an irregular prelude of presaccadic activity. 2. Because saccadic eye movements normally have very stereotyped durations and velocity trajectories that vary systematically with saccade size, it has been difficult in the past to establish quantitatively whether the activity of SRBNs temporally codes dynamic saccadic control signals, e.g., dynamic motor error or eye velocity, where dynamic motor error is defined as a signal proportional to the instantaneous difference between desired final eye position and the actual eye position during a saccade. It has also not been unequivocally established whether SRBNs participate in an organized spatial shift of ensemble activity in the intermediate layers of the SC during saccadic eye movements. 3. To address these issues, we studied the activity of SRBNs using an interrupted saccade paradigm. Saccades were interrupted with pulsatile electrical stimulation through a microelectrode implanted in the omnipauser region of the brain stem while recordings were made simultaneously from single SRBNs in the SC. 4. Shortly after the beginning of the stimulation (which was electronically triggered at saccade onset), the eyes decelerated rapidly and stopped completely. When the high-frequency (typically 300-400 pulses per second) stimulation was terminated (average duration 12 ms), the eye movement was reinitiated and a resumed saccade was made accurately to the location of the target. 5. When we recorded from SRBNs in the more caudal colliculus, which were active for large saccades, cell discharge was powerfully and rapidly suppressed by the stimulation (average latency = 3.8 ms). Activity in the same cells started again just before the onset of the resumed saccade and continued during this saccade even though it has a much smaller amplitude than would normally be associated with significant discharge for caudal SC cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Electrical stimulation in the monkey vestibulocerebellum has previously been shown to produce ocular nystagmus, but large stimulating current values were used. Using long duration (< or = 10-second) stimulus pulse trains and low current values (< 50 microA), we studied the nystagmus evoked by microstimulation in the uvular/nodular regions of the cerebellum. In doing this, we found quantitative differences in the nystagmus evoked from these two regions. Stimulation of the nodulus typically produced a vigorous nystagmus with a contralateral slow phase and a prolonged afternystagmus in the same direction. In contrast, stimulation of the uvula typically produced a regular ipsilateral nystagmus pattern with a very short, if any, afternystagmus in the same direction. In addition, at some stimulation sites in the uvula we observed an adaptation in the slow phase eye velocity during the time that the stimulation remained on. This effect could result in a secondary nystagmus, with a slow phase velocity direction opposite to that first evoked by the stimulation, followed by a prolonged afternystagmus in the direction of the secondary nystagmus at stimulus offset. The nystagmus evoked by these cerebellar stimulations differs from both natural nystagmus produced by large field visual motion and from the nystagmus produced by electrical stimulation of the nucleus of the optic tract. The nystagmus produced by uvular and nodular stimulation shows a shorter latency and a more rapid slow phase eye velocity buildup. The uvula stimulations also showed a much shorter afternystagmus. Also, the same nystagmus was evoked whether the animal was in a lighted or dark surround. These characteristics and recent single-unit recording studies in the uvula seem to suggest that the uvula acts not as a direct input to the velocity storage mechanism, but instead perhaps as part of an internal regulator for balance between the bilateral vestibular nuclei which are normally part of the nystagmus response. On the other hand, the nodulus, with its prolonged afternystagmus in the same direction as the evoked nystagmus, may be involved as a part of the velocity storage mechanism.

This article reviews the current state of knowledge of the primate smooth-pursuit system. The emphasis is on the neuronal mechanisms and pathways that control pursuit eye movements in the monkey. The review covers the neuronal structures believed to be involved in pursuit generation from striate cortex to the final premotoneuron structures in the brainstem. Information gathered from physiological and anatomical work is stressed.

1. In this study we sought to characterize the visual motion processing that exists in the dorsolateral pontine nucleus (DLPN) and make a comparison with the reported visual responses of the middle temporal (MT) and medial superior temporal (MST) areas of the monkey cerebral cortex. The DLPN is implicated as a component of the visuomotor interface involved with the regulation of smooth-pursuit eye movements, because it is a major terminus for afferents from MT and MST and also the source of efferents to cerebellar regions involved with eye-movement control. 2. Some DLPN cells were preferentially responsive to discrete (spot and bar) visual stimuli, or to large-field, random-dot pattern motion, or to both discrete and large-field visual motion. The results suggest differential input from localized regions of MT and MST. 3. The visual-motion responses of DLPN neurons were direction selective for 86% of the discrete visual responses and 95% of the large-field responses. Direction tuning bandwidths (full-width at 50% maximum response amplitude) averaged 107 degrees and 120 degrees for discrete and large-field visual motion responses, respectively. For the two visual response types, the direction index averaged 0.95 and 1.02, indicating that responses to stimuli moving in preferred directions were, on average, 20 and 50 times greater than responses to discrete or large-field stimulus movement in the opposite directions, respectively. 4. Most of the DLPN visual responses to movements of discrete visual stimuli exhibited increases in amplitude up to preferred retinal image speeds between 20 and 80 degrees/s, with an average preferred speed of 39 degrees/s. At higher speeds, the response amplitude of most units decreased, although a few units exhibited a broad saturation in response amplitude that was maintained up to at least 150 degrees/s before the response decreased. Over the range of speeds up to the preferred speeds, the sensitivity of DLPN neurons to discrete stimulus-related, retinal-image speed averaged 3.0 spikes/s per deg/s. The responses to large-field visual motion were less sensitive to retinal image speed and exhibited an average sensitivity of 1.4 spikes/s per deg/s before the visual response saturated. 5. DLPN and MT were quantitatively comparable with respect to degree of direction selectivity, retinal image speed tuning, and distribution of preferred speeds. Many DLPN receptive fields contained the fovea and were larger than those of MT and more like MST receptive fields in size.(ABSTRACT TRUNCATED AT 400 WORDS)

1. Anatomical and single-unit recording studies suggest that the dorsolateral pontine nucleus (DLPN) in monkey is a major link in the projection of descending visual motion information to the cerebellum. Such studies coupled with cortical and cerebellar lesion results suggest a major role for this basilar pontine region in the mediation of smooth-pursuit eye movements. 2. To provide more direct evidence that this pontine region is involved in the control of smooth-pursuit eye movements, focal chemical lesions were made in DLPN in the vicinity of previously recorded visual motion and pursuit-related neurons. Eye movement responses were subsequently recorded in these lesioned animals under several behavioral paradigms. 3. A major deficit in smooth-pursuit performance was produced after unilateral DLPN lesions generated either reversibly with lidocaine or more permanently with ibotenic acid. Pursuit impairments were observed during steady-state tracking of sinusoidal target motion as well as during the initiation of pursuit tracking to sudden ramp target motion. Through the use of the latter technique, initial eye acceleration was reduced to less than one-half of normal for animals with large lesions of the dorsolateral and lateral pontine nuclei. 4. The pursuit deficit in all animals was directional in nature and was not dependent on the visual hemifield in which the motion stimulus occurred. The largest effect for horizontal tracking occurred in all animals for pursuit directed ipsilateral to the lesion. Animals also showed major deficits in one or both directions of vertical pursuit, although the primary direction of the vertical impairment was variable from animal to animal. 5. Chemical lesions in the DLPN also produced comparable deficits in the initiation of optokinetic-induced smooth eye movements in the ipsilateral direction. In contrast to this effect on the initial optokinetic response, in the one lesioned animal studied during prolonged constant velocity optokinetic drum rotation, smooth eye speed increased slowly over a 10- to 15-s period to reach a level that closely matched drum speed. These results suggest that pathways outside the DLPN can generate the steady-state optokinetic response. 6. Saccades to stationary targets were normal after DLPN lesions, but corrective saccades made to targets moving in the direction ipsilateral to the lesion were much more hypometric than similar prelesion control saccades. 7. The pursuit deficits produced by lidocaine injections recovered within 30 min. The ibotenic acid deficits were maximal approximately 1 day after the injection and recovered rapidly thereafter over a time period of 3-7 days.(ABSTRACT TRUNCATED AT 400 WORDS)

Intracisternal injections of 6-hydroxydopamine were used to deplete brain catecholamines in cats. These animals were then subjected to a prolonged period of lateral head rotations while viewing a visual scene that always rotated with them. In contrast to their predepletion behavior, these cats showed very little decrease in the gain of their vestibuloocular reflex. These results suggest that brain catecholamines may play a role in regulating neural plasticity in the vestibuloocular system just as they appear to do in the visual cortex.

Many children who roller skate sustain injuries. To determine the type and severity of these mishaps, the medical records of 76 children less than 16 years of age with roller skating injuries presenting to two pediatric emergency departments were reviewed. Seventy-five percent were girls, and 25% were boys. The upper extremity was the most common body part injured (74%) (P less than 0.0001). Lower extremity injuries occurred in 12%, head and face injuries in 10%, and chest injuries in 4%. The most common type of injury was a fracture (69%), with the wrist and forearm being most frequently fractured (53%). Hospitalization and long-term sequelae were infrequent. Younger children (less than or equal to 9) had an increased frequency of fracture injury (P less than 0.02). This is most likely because maturation of lower and upper extremity speed, strength, agility, coordination, balance, and reaction time and morphologically stronger bones combine to afford relative protection to the older child. Physicians and parents need to be aware of a child's skill level before the child is encouraged to roller skate. Measures which may decrease the likelihood of injury include protective gear, instruction in roller skating technique, learning to skate in an uncongested area on level, familiar terrain, and learning to fall properly.

The cerebellar vermal cortex in monkey was electrically stimulated through a microelectrode with brief pulse strains synchronized to the onset of selected saccadic eye movements. The delivery of these intrasaccadic microstimuli were randomly interposed in groups of saccadic eye movements made by trained monkeys to known target locations. The trajectory of the saccades with intrasaccadic stimuli were then compared to those made to the same target without stimulation. Contralaterally directed saccades were consistently slowed from their normal trajectory (normally at 12 ms after stimulus onset) and were made hypometric. Ipsilaterally directed saccades were not affected. Vertical eye movement components were also affected at some stimulating sites. Changing the stimulus train duration from 10 to 80 ms had no effect on the change in velocity or amount of dysmetria produced in contralateral saccades. Taken together these results suggest that a different set of cerebellar elements were being stimulated by the intrasaccadic mode as contrasted to stimulation at the same site at random times. Furthermore, the short period of time during an ongoing saccade presents a unique instant in which to test the relationship of various central structures to the saccadic system. Based on current concepts of the organization of the brainstem saccadic pulse generators, these data are interpreted to suggest that: (1) the cerebellar vermis has a rather direct influence on the contralateral saccade generator, (2) this influence can act to recode (diminish) the generator's representation of the size of motor error, (3) the effect occurs at a point in the generator where motor error is spatially coded.

A small region in the dorsal midline portion of the nucleus reticularis tegmenti pontis (NRTP) in monkeys contains neurons that respond to focal visual stimuli or during saccadic eye movements or both. None of these cells or any others in this region respond to the motion of large visual fields (optokinetic stimulation), although such responses were specifically sought. Thus, this group of NRTP neurons forms a completely different set of cells than those previously described in more rostral but closely adjacent portions of the pontine nuclei which respond well to optokinetic stimulation. The most frequently encountered cell type in this region of NRTP (153 neurons) produced a high-frequency burst of discharges during saccadic eye movements. Neural discharge (burst intensity or duration) was not related to saccade metrics. Instead, peak burst frequency and/or the number of spikes in a unit's burst reached a maximum when the saccade moved the eyes to a circumscribed region (movement field) of the animal's visual field. There were two subtypes of these burst neurons. In one type (44%) the movement fields were smaller and entirely contained within the oculomotor range. In the other type (56%) the movement fields consisted of a whole sector (some as wide as 180 degrees) of the entire oculomotor range. All the neurons in this sample that we were able to test in total darkness continued to produce bursts of discharges of similar profile during spontaneous saccades into their movement field. All the movement fields were retinotopically organized, although a few cells (22%) showed a marked variation of burst metrics with initial eye position. Another small group of cells in NRTP (8 neurons) responded to small spots of light turned on within a circumscribed region of the visual field while the animal maintained fixation on a separate spot of light. These visual neurons produced no saccade-related discharge. A larger group of neurons (24 out of 52 tested cells) produced both a visual response and a saccadic burst. The visual field of this type of cell was always smaller and was contained within the movement field of the cell. The response of both types of NRTP visual neurons was enhanced when the visual stimulus was to be the target for a saccadic eye movement. On double-saccade trials the visual stimulus was never present in the hemifield containing the cell's visual field.(ABSTRACT TRUNCATED AT 400 WORDS)

The behavior of single vestibular nerve fibers from the lateral semicircular canal was recorded during sinusoidal oscillations of the head, during optokinetic stimulation with the head stationary, and during spontaneous oculomotor behavior in the alert monkey. The response of similar fibers to adequate vestibular stimulation was also studied in some of the animals under deeply anesthetized conditions. In the alert animals all units were spontaneously active and their discharge was modulated only by adequate vestibular stimulation. Ipsilateral horizontal rotations of the head were excitatory for all units. No modification of this basic vestibular response by visual stimulation including full-field striped drum rotation was observed. Furthermore no correlation of unit activity with oculomotor function including voluntary saccadic and pursuit eye movements was found in any of the units. The regularity of spontaneous discharge was the most consistent characteristic that differentiated the unit response into types. Most units were very regular in discharge, but a few were very irregular. The averaging of unit discharge over several cycles of oscillatory head rotation showed that the irregular type units were also consistently modulated by adequate vestibular stimulation. Both regular and irregular type units were found in the anesthetized animals. Unimodal distributions of the quantitative values for unit resting discharge rate, sensitivity, and phase relationship were found. The distributions for these three parameters were similar in the units recorded in the anesthetized animals. Thus at least these characteristics of semicircular canal response seem not to be affected by the vestibular efferent system which should be altered or eliminated in the case of the anesthetized animals.

Smooth pursuit eye movements in the monkey were studied by measuring the average eye acceleration in the first 100 msec of the ocular response to suddenly moving constant velocity discrete visual targets. The tracking target's motion was initiated on or eccentric to the fovea against a very dimly lit homogeneous background or an illuminated, highly textured, large-field background. The effect of the textured background was always to reduce the initial eye acceleration as compared to that present in the homogeneous background case. Movement of the background in the opposite direction to target spot movement also reduced the initial eye acceleration. In contrast, steady-state tracking measured several hundred msec after the onset of pursuit under the same conditions was only marginally reduced by the presence of the textured background.

The cerebellar vermis (lobules V to VII) was focally stimulated (maximum current = 300 microA) through microelectrodes in alert monkeys trained to fixate on visual targets located at different positions in the eye movement field. Microstimulation of this area evoked saccades whose direction and amplitude were dependent on the spatial locus of the vermal point stimulated and on the position of the eye at the time of stimulation. Stimulation evoked saccades on most (70%) of the electrode penetrations. By alternatively stimulating and recording through the electrode as it advanced through the depth of the vermis, it was possible to map the threshold for evoking saccades along a penetration as well as to ascertain the type of tissue (white matter or Purkinje cell layer) situated at the stimulation points. On penetrations where saccades were evoked, there was generally one (90%) and sometimes two (10%) low-threshold region(s). These low-threshold regions were located in fiber tracks and not in the Purkinje or other cellular layers of the cerebellar cortex. The direction and size of the evoked saccades were dependent on position of the eye in the orbit. At a few sites, even the presence or the absence of an evoked saccade depended on the initial eye position. Postsaccadic drifts after termination of evoked saccades were also a common feature (50% of the tracks) associated with vermal microstimulation. The presence or absence as well as the direction of the postsaccadic drift were also dependent on initial eye position. These observations suggest that the vermal stimulations evoked saccades by the antidromic activation of mossy fiber afferent inputs that emanate from the brain stem saccadic burst generator. Furthermore, stimulation in this manner would actually bypass the cerebellar circuitry and produce saccades without the usual modifying influence of the cerebellum.

Responses to pure visual stimuli and visual-vestibular interactions similar to those reported in other vertebrates were found in single vestibular nucleus neurons in cat. Contrary to prevailing hypotheses, the cerebellum is not an essential part of the pathway mediating these visual responses.

The vestibulo-ocular reflex (VOR) was measured in congenitally blind, adventitiously blind, and normally sighted adults to determine how it was affected by loss of vision. VOR gain and phase were measured in subjects rotated sinusoidally in total darkness, while concentrating on an imaginary earth-fixed target. Gain was lower in adventitiously blind subjects than in sighted subjects. The gain reduction in blind subjects was accompanied by an increase in the amount of phase lead at low frequencies. The dominant time constant was typically 3 sec for adventitiously blind subjects and 16 sec for sighted subjects. No convincing vestibulo-ocular responses were measured in congenitally blind subjects except at the highest test frequencies. These findings demonstrate that vision is necessary early in life for development of the VOR, and that vision is also necessary throughout life for ongoing maintenance of the VOR.

Head velocity-related modulations in Purkinje cell activity were observed in lobules VI and VII of the cerebellar vermis. The sensitivities and phase shifts with respect to head velocity of Purkinje cells were comparable with vestibular responses observed in the fastigial nuclei. The results support the hypothesis of a vermal target velocity correlate and necessitate the inclusion of vermal lobules VI and VII among the cerebellar regions involved with vestibular information processing.

1. The observation of smooth-pursuit eye and retinal image velocity signals in lobules VI and VII of the vermis has given rise to the hypothesis that a neural correlate of a target velocity signal exists in this region of the cerebellum (29). However, activity signaling head velocity is also required to regenerate a target velocity signal. Vermal Purkinje cell activity was, therefore, recorded during the performance of paradigms designed to dissociate head movement-related responses. 2. The activity of 107 Purkinje cells was found to be related to horizontal head velocity. Of these, 52% increased their discharge rate for ipsilaterally directed passive head movement (type I), and 48% were excited by contralateral head movements (type II). 3. In five Purkinje cells in which sufficient data were obtained, cell discharge rate increased monotonically with head velocity over the range of 5-40 deg/s. The sensitivity to head velocity at 0.4 Hz +/- 25 deg/s averaged approximately 0.5 spikes.s-1/deg.s-1 in a larger sample of cells (n = 39). The sensitivities to head velocity, at this same frequency and velocity, of type I and type II Purkinje cells were comparable at 0.44 and 0.51 spikes.s-1/deg.s-1, respectively. 4. The Purkinje cell responses led head velocity by an average of 12 degrees at 0.4 Hz +/- 25 deg/s of passive head rotation. The phase shifts associated with type I and II responses were similar with phase leads of 13 and 9 degrees with respect to head velocity, respectively. 5. A linear interaction of smooth-pursuit eye and head velocity signals was observed during the performance of a variety of antiphase and inphase eye and head movement paradigms. The results support the conclusion that some Purkinje cells in lobules VI and VII of the cerebellar vermis encode a gaze velocity signal. Contributions of the head velocity signal to the regeneration of target velocity are considered in a companion paper (32).

Poisoning continues to be one of the major causes of mortality and morbidity in young children. The Product Safety Packaging Act needs to be expanded to cover toxic agents and drugs known to be involved in the majority of ingestions. Those agents that are particularly toxic will require more stringent measures than safety packaging. The primary physician is in the position to institute rapid and appropriate therapy for most poisoning. Consideration of poisoning in making a presumptive diagnosis and early institution of general supportive measures are critical. Familiarity with techniques of gastric emptying and with use of activated charcoal and naloxone as antidotes is essential, as is s knowledge of when to refer patients for specialized care. By educating parents about poison proofing the home and about appropriate first aid measures, the primary physician can play an important role in poison prevention.

1. Purkinje cell activity was recorded from lobules VI and VII of the cerebellar vermis during the performance of visuooculomotor tasks designed to dissociate the signals related to head, smooth-pursuit eye, and retinal image movements. Task-related modulations in the simple spike discharge rates of 157 cells were observed in three alert monkeys. 2. Of 65 Purkinje cells that were completely tested for all three signals, all exhibited smooth-pursuit eye movement-related activity. An additional vestibular or visual response was observed in 17 and 11% of the cells, respectively. Eye, head, and retinal image velocity signals were all recorded in the same unit in 52% of the Purkinje cells. The responses of 5% of the fully tested cells were associated with changes in the direction of eye, head, and retinal image movement. 3. The observed sensorioculomotor responses were direction selective in 98% of the Purkinje cells. For the Purkinje cells that were fully tested, 60% of the cells exhibited peak discharge rates for ipsilateral and 40% for contralateral eye velocity. Of these Purkinje cells, 45% exhibited eye, head, and retinal image velocity signals with equivalent direction preferences. 4. Of 42 Purkinje cells tested, 88% demonstrated some kinds of interactive responses during combined eye and sensory stimulation. The interaction of eye and head velocity signals has been discussed in a companion paper (38). The modulation in discharge rate observed during tracking in the presence of a random dot background pattern could be predicted from the dissociated responses to smooth pursuit in the dark and to movements of the background pattern during suppression of eye movements. 5. The sensitivity to smooth-pursuit eye velocity averaged 1.4 times the sensitivity to head velocity. In 80% of the Purkinje cells, however, the sensitivity to eye velocity exceeded the sensitivity to head velocity by an average of only 10%. The sensitivity to smooth-pursuit eye velocity averaged 1.6 times the sensitivity to retinal image velocity. 6. An increase in Purkinje cell discharge rate was observed during the open-loop period of the initiation of smooth-pursuit eye movements. This open-loop response was consistent with the presence of a visual signal during ocular pursuit, since these cells were also shown to be responsive to a dissociated retinal image velocity signal. Furthermore, the magnitude of the open-loop response indicated an enhancement of the sensitivity to retinal image velocity when visual information became behaviorally significant.(ABSTRACT TRUNCATED AT 400 WORDS)

Visual evoked potentials (VEP's) recorded from the scalp are sensitive to retinal image sharpness and thus to changes in the refractive state of the eye. Initially the responses to checkerboard flash or reversal stimuli were computer-averaged in order to raise the signal above the noise, primarily the electroencephalogram (EEG). Recently analogue Fourier signal analysis has been proposed for using the VEP for rapid clinical refraction. We have confirmed that this method can measure the spherical refractive state to within +/- 0.50D. However, because of large slow-wave fluctuations, measurements of changes within +/- 1.00D are not always clear. Despite its promise the method does not appear to be clinically useful at present.

The central nervous system is a parallel dynamical system which connects sensory input with motor output for the performance of visual tracking. This paper applies elementary control system tools to extend dynamical neural network models to the visual smooth pursuit system. Observed eye position responses to target motions and characteristics of the plant (eye muscles and orbital mechanics) place dynamical constraints on the interposed neural network controller. In the process of constructing a model for the controller, we show two previous pursuit system models, using efference copy and feedforward compensation, are equivalent from an input-output standpoint. We introduce a controller model possessing a potentially highly parallel implementation and offer an example with supporting neural firing rate data. Changes in time delays or other system dynamics are expected to lead to compensatory adaptive changes in the controller. A scheme to noninvasively simulate such changes in system dynamics was developed. Actual physiologic data of adaptive responses to increased time delay is presented as an example of the utility of this parallel controller. Compensatory changes in our parallel controller model are easily predicted. These results suggest a productive interaction between neural network modeling, neurophysiology, and control systems engineering.