Interventions to alleviate anxiety and pain during venipuncture in children with chronic gastrointestinal and/or liver disease: A single-center prospective observational study.

Objectives: The goal of this longitudinal study was to reduce anxiety and pain in children with chronic conditions from the gastrointestinal tract during venipuncture. These children undergo regular venipuncture as part of their medical management and the procedure is often accompanied with anxiety and pain. In addition, children as well as their parents and health care professionals (HCPs) often suffer "compassionate pain" because of emotional interference. Method: In a realistic clinical setting, different psychological and medical interventions were examined: (1) Psychoeducational brochures and (2) four different medical-technical interventions during venipuncture. In a large hospital in Germany, 169 children, their parents, and HCPs were asked to rate anxiety and pain during venipuncture before and after the intervention. Results: Children showed a clear preference for some of the medical-technical interventions. Using Linear Mixed Models anxiety and pain rated by the children themselves showed no significant reduction. However, parents and HCPs reported a significant reduction. Age, gender, and status of liver transplantation were associated with a reduction in anxiety and pain in most of the analyses. Conclusion: Both psychoeducational brochures and medical-technical interventions had a positive impact on anxiety and pain. However, effectivity for the medical-technical interventions was lower than in previous studies utilizing individual interventions. Reasons for this difference as well as possibilities to improve the intervention are discussed. In addition, this study provides practical day-to-day information about the implementation of interventions for the work in pediatric units such as when and how to provide psychoeducational materials.

A Sorrow Shared Is a Sorrow Halved? Patient and Parental Anxiety Associated with Venipuncture in Children before and after Liver Transplantation.

Taking blood via venipuncture is part of the necessary surveillance before and after liver transplantation. The spectrum of response from children and their parents is variable, ranging from a short and limited aversion to paralyzing phobia. The aim of this retrospective, cross-sectional study was to determine the level of anxiety amongst children during venipuncture, to compare the anxiety reported by children and parents, and to identify the factors affecting the children's and parents' anxiety in order to develop therapeutic strategies. In total, 147 children (aged 0-17 years, 78 female) and their parents completed questionnaires. Statistical analysis was performed using qualitative and quantitative methods. Results showed that the majority of children reported anxiety and pain during venipuncture. Younger children had more anxiety (self-reported or assessed by parents). Children and parental reports of anxiety were highly correlated. However, the child's anxiety was often reported as higher by parents than by the children themselves. The child's general anxiety as well as the parents' perceived stress from surgical interventions (but not the number of surgical interventions) prompted parental report of child anxiety. For children, the main stressors that correlated with anxiety and pain were factors during the blood collection itself (e.g., feeling the puncture, seeing the syringe). Parental anxiety was mainly related to circumstances before the blood collection (e.g., approaching the clinic, sitting in the waiting room). The main stressors mentioned by parents were the child's discomfort and their inability to calm the child. Results indicate that the children's fear of factors during the blood collection, along with the parents' perceived stress and helplessness as well as their anticipatory anxiety are important starting points for facilitating the drawing of blood from children before and after liver transplantation, thereby supporting a better disease course in the future.

How cerebellar motor learning keeps saccades accurate.

The neuronal substrate underlying the learning of a sophisticated task has been difficult to study. However, the advent of a behavioral paradigm that deceives the saccadic system into thinking it is making an error has allowed the mechanisms of the adaptation that corrects this error to be revealed in a primate. The neural elements that fashion the command signal for the generation of accurate saccades involve subcortical structures in the brain stem and cerebellum. In this review we show that sites in both those structures also are involved with the gradual adaptation of saccade size, a form of motor learning. Pharmacological manipulation of the oculomotor vermis (lobules VIc and VII) impairs mechanisms that either increase or decrease saccade size during adaptation. The net saccade-related simple spike (SS) activity of its Purkinje cells is correlated with the changes in saccade characteristics that occur during adaptation. These changes in SS activity are driven by an error signal delivered over climbing fibers, which create complex spikes whose probability of occurrence reflects the motor error between the actual and desired saccade size. These climbing fibers originate in the part of the inferior olive that receives projections from the superior colliculus (SC). Disabling the SC prevents adaptation and stimulation of the SC just after a normal saccade produces a surrogate error signal that drives adaptation without an actual visual error. Therefore, the SC provides not only the initial command that generates a saccade, as shown by others, but also the error signal that ensures that saccades remain accurate.

Adaptation and adaptation transfer characteristics of five different saccade types in the monkey.

Shifts in the direction of gaze are accomplished by different kinds of saccades, which are elicited under different circumstances. Saccade types include targeting saccades to simple jumping targets, delayed saccades to visible targets after a waiting period, memory-guided (MG) saccades to remembered target locations, scanning saccades to stationary target arrays, and express saccades after very short latencies. Studies of human cases and neurophysiological experiments in monkeys suggest that separate pathways, which converge on a common locus that provides the motor command, generate these different types of saccade. When behavioral manipulations in humans cause targeting saccades to have persistent dysmetrias as might occur naturally from growth, aging, and injury, they gradually adapt to reduce the dysmetria. Although results differ slightly between laboratories, this adaptation generalizes or transfers to all the other saccade types mentioned above. Also, when one of the other types of saccade undergoes adaptation, it often transfers to another saccade type. Similar adaptation and transfer experiments, which allow inferences to be drawn about the site(s) of adaptation for different saccade types, have yet to be done in monkeys. Here we show that simian targeting and MG saccades adapt more than express, scanning, and delayed saccades. Adaptation of targeting saccades transfers to all the other saccade types. However, the adaptation of MG saccades transfers only to delayed saccades. These data suggest that adaptation of simian targeting saccades occurs on the pathway common to all saccade types. In contrast, only the delayed saccade command passes through the adaptation site of the MG saccade.

An experimental vestibular neural prosthesis: design and preliminary results with rhesus monkeys stimulated with modulated pulses.

A vestibular neural prosthesis was designed on the basis of a cochlear implant for treatment of Meniere's disease and other vestibular disorders. Computer control software was developed to generate patterned pulse stimuli for exploring optimal parameters to activate the vestibular nerve. Two rhesus monkeys were implanted with the prototype vestibular prosthesis and they were behaviorally evaluated post implantation surgery. Horizontal and vertical eye movement responses to patterned electrical pulse stimulations were collected on both monkeys. Pulse amplitude modulated (PAM) and pulse rate modulated (PRM) trains were applied to the lateral canal of each implanted animal. Robust slow-phase nystagmus responses following the PAM or PRM modulation pattern were observed in both implanted monkeys in the direction consistent with the activation of the implanted canal. Both PAM and PRM pulse trains can elicit a significant amount of in-phase modulated eye velocity changes and they could potentially be used for efficiently coding head rotational signals in future vestibular neural prostheses.

Auditory outcomes following implantation and electrical stimulation of the semicircular canals.

We measured auditory brainstem responses (ABRs) in eight Rhesus monkeys after implantation of electrodes in the semicircular canals of one ear, using a multi-channel vestibular prosthesis based on cochlear implant technology. In five animals, click-evoked ABR thresholds in the implanted ear were within 10 dB of thresholds in the non-implanted control ear. Threshold differences in the remaining three animals varied from 18 to 69 dB, indicating mild to severe hearing losses. Click- and tone-evoked ABRs measured in a subset of animals before and after implantation revealed a comparable pattern of threshold changes. Thresholds obtained five months or more after implantation--a period in which the prosthesis regularly delivered electrical stimulation to achieve functional activation of the vestibular system--improved in three animals with no or mild initial hearing loss and increased in a fourth with a moderate hearing loss. These results suggest that, although there is a risk of hearing loss with unilateral vestibular implantation to treat balance disorders, the surgery can be performed in a manner that preserves hearing over an extended period of functional stimulation.

Effect of inactivation and disinhibition of the oculomotor vermis on saccade adaptation.

The ability to adapt a variety of motor acts to compensate for persistent natural or artificially induced errors in movement accuracy requires the cerebellum. For adaptation of the rapid shifts in the direction of gaze called saccades, the oculomotor vermis (OMV) of the cerebellum must be intact. We disrupted the neural circuitry of the OMV by manipulating gamma aminobutyric acid (GABA), the transmitter used by many neurons in the vermis. We injected either muscimol, an agonist of GABA, to inactivate the OMV or bicuculline, an antagonist, to block GABA inhibition. Our previous study showed that muscimol injections cause ipsiversive saccades to fall short of their targets, whereas bicuculline injections cause most ipsiversive saccades to overshoot. Once these dysmetrias had stabilized, we tested the monkey's ability to adapt saccade size to intra-saccadic target steps that produced a consistent saccade under-shoot (amplitude increase adaptation required) or overshoot (amplitude decrease adaptation required). Injections of muscimol abolished the amplitude increase adaptation of ipsiversive saccades, but had either no effect, or occasionally facilitated, amplitude decrease adaptation. In contrast, injections of bicuculline impaired amplitude decrease adaptation and usually facilitated amplitude increase adaptation. Neither drug produced consistent effects on the adaptation of contraversive saccades. Taken together, these data suggest that OMV activity is necessary for amplitude increase adaptation, whereas amplitude decrease adaptation may involve the inhibitory circuits within the OMV.

Behavior of the oculomotor vermis for five different types of saccade.

Single unit and lesion studies have implicated the oculomotor vermis of the cerebellum in the control of targeting saccades to jumping visual targets. However, saccades can be made in a variety of other target situations where they can occur with different reaction times (express or delayed saccades) in response to a remembered target location (memory-guided saccades) or between several targets that are always visible (scanning saccades). Here we ask whether the oculomotor vermis contributes to generating all these types of saccades by examining the simple spike discharge of its Purkinje cells. Twenty-six of 32 P-cells (81%) exhibited qualitatively similar phasic firing patterns for targeting, express, scanning, delayed, and memory-guided saccades. The remaining six exhibited a different pattern for just scanning saccades. Although a sensitive test of discharge patterns revealed significant differences for some pairs of saccade types in ∼29% of P-cells, there was no cell-to-cell consistency as to which pairs were associated with different patterns. Also, a less sensitive comparison identified substantially fewer cells (∼15%) with different patterns. Thus the lack of any consistent difference in firing for different saccade types leads us to conclude that the oculomotor vermis is not likely to contribute differently to targeting, express, scanning, delayed, or memory-guided saccades.

Effects of GABA agonist and antagonist injections into the oculomotor vermis on horizontal saccades.

The oculomotor vermis (OMV) of the cerebellum is necessary for the generation of the accurate rapid eye movements called saccades. Large lesions of the midline cerebellar cortex involving the OMV cause saccades to become hypometric and more variable. However, saccades were not examined immediately after these lesions so the interpretation of the resulting deficits might have been contaminated by some adaptation to the saccade dysmetria. Therefore, to better understand the contribution of the OMV to normal saccades, we impaired its operation locally by injecting small amounts of either an agonist or antagonist of γ-aminobutyric acid (GABA), which is a ubiquitous neurotransmitter throughout the cerebellar cortex. Muscimol, a GABA agonist, inactivated part of the OMV, whereas bicuculline, an antagonist, disinhibited it. Muscimol caused all ipsiversive horizontal saccades from 5 to 30° to become hypometric. In contrast, bicuculline produced an amplitude-dependent dysmetria: ipsiversive horizontal saccades elicited by target steps <10° became hypometric, whereas those in response to larger steps became hypermetric. At the transition target amplitude, saccade amplitudes were quite variable with some being hypo- and others hypermetric. After most injections of either agent, saccades had lower peak velocities and longer durations than pre-injection saccades of the same amplitude. The longer durations were associated with a prolongation of the deceleration phase. Both agents produced inconsistent effects on contraversive saccades. These results establish that the oculomotor vermis helps control the characteristics of normal ipsiversive saccades and that GABAergic inhibitory processes are a crucial part of this process.

Changes in simple spike activity of some Purkinje cells in the oculomotor vermis during saccade adaptation are appropriate to participate in motor learning.

Adaptation of saccadic eye movements provides an excellent motor learning model to study theories of neuronal plasticity. When primates make saccades to a jumping target, a backward step of the target during the saccade can make it appear to overshoot. If this deception continues for many trials, saccades gradually decrease in amplitude to go directly to the back-stepped target location. We used this adaptation paradigm to evaluate the Marr-Albus hypothesis that such motor learning occurs at the Purkinje (P)-cell of the cerebellum. We recorded the activity of identified P-cells in the oculomotor vermis, lobules VIc and VII. After documenting the on and off error directions of the complex spike activity of a P-cell, we determined whether its saccade-related simple spike (SS) activity changed during saccade adaptation in those two directions. Before adaptation, 57 of 61 P-cells exhibited a clear burst, pause, or a combination of both for saccades in one or both directions. Sixty-two percent of all cells, including two of the four initially unresponsive ones, behaved differently for saccades whose size changed because of adaptation than for saccades of similar sizes gathered before adaptation. In at least 42% of these, the changes were appropriate to decrease saccade amplitude based on our current knowledge of cerebellum and brainstem saccade circuitry. Changes in activity during adaptation were not compensating for the potential fatigue associated with performing many saccades. Therefore, many P-cells in the oculomotor vermis exhibit changes in SS activity specific to adapted saccades and therefore appropriate to induce adaptation.

Head-free gaze shifts provide further insights into the role of the medial cerebellum in the control of primate saccadic eye movements.

This study examines how signals generated in the oculomotor cerebellum could be involved in the control of gaze shifts, which rapidly redirect the eyes from one object to another. Neurons in the caudal fastigial nucleus (cFN), the output of the oculomotor cerebellum, discharged when monkeys made horizontal head-unrestrained gaze shifts, composed of an eye saccade and a head movement. Eighty-seven percent of our neurons discharged a burst of spikes for both ipsiversive and contraversive gaze shifts. In both directions, burst end was much better timed with gaze end than was burst start with gaze start, was well correlated with eye end, and was poorly correlated with head end or the time of peak head velocity. Moreover, bursts accompanied all head-unrestrained gaze shifts whether the head moved or not. Therefore we conclude that the cFN is not part of the pathway that controls head movement. For contraversive gaze shifts, the early part of the burst was correlated with gaze acceleration. Thereafter, the burst of the neuronal population continued throughout the prolonged deceleration of large gaze shifts. For a majority of neurons, gaze duration was correlated with burst duration; for some, gaze amplitude was less well correlated with the number of spikes. Therefore we suggest that the population burst provides an acceleration boost for high acceleration (smaller) contraversive gaze shifts and helps maintain the drive required to extend the deceleration of large contraversive gaze shifts. In contrast, the ipsiversive population burst, which is less well correlated with gaze metrics but whose peak rate occurs before gaze end, seems responsible primarily for terminating the gaze shift.

Identifying sites of saccade amplitude plasticity in humans: transfer of adaptation between different types of saccade.

To view different objects of interest, primates use fast, accurate eye movements called saccades. If saccades become inaccurate, the brain adjusts their amplitudes so they again land on target, a process known as saccade adaptation. The different types of saccades elicited in different behavioral circumstances appear to utilize different parts of the oculomotor circuitry. To gain insight into where adaptation occurs in different saccade pathways, we adapted saccades of one type and examined how that adaptation affected or transferred to saccades of a different type. If adaptation of one type of saccade causes a substantial change in the amplitude of another, that adaptation may occur at a site used in the generation of both types of saccade. Alternatively, if adaptation of one type of saccade transfers only partially, or not at all, to another, adaptation occurs at least in part at a location that is not common to the generation of both types of saccade. We produced significant amplitude reductions in memory-guided, delayed, targeting and express saccades by moving the target backward during the saccade. After memory-guided saccades were adapted, the amplitude of express, targeting and delayed saccades exhibited only a partial reduction. In contrast, when express, targeting, or delayed saccades were adapted, amplitude transfer to memory-guided saccades was more substantial. These results, combined with previously published data, suggest that there are at least two sites of adaptation within the saccadic system. One is used communally in the generation of express, targeting, delayed and memory-guided saccades, whereas the other is specific for the generation of memory-guided saccades.

Subthreshold activation of the superior colliculus drives saccade motor learning.

How the brain learns and maintains accurate precision movements is currently unknown. At times throughout life, rapid gaze shifts (saccades) become inaccurate, but the brain makes gradual adjustments so they again stop on target. Previously, we showed that complex spikes (CSs) in Purkinje cells of the oculomotor cerebellum report the direction and amplitude by which saccades are in error. Anatomical studies indicate that this error signal could originate in the superior colliculus (SC). Here, we deliver subthreshold electrical stimulation of the SC after the saccade lands to signal an apparent error. The size of saccades in the same direction as the simulated error gradually increase; those in the opposite direction decrease. The electrically adapted saccades endure after stimulation is discontinued, exhibit an adaptation field, can undergo changes in direction, and depend on error timing. These electrically induced adaptations were virtually identical with those produced by the visually induced adaptations that we report here for comparable visual errors in the same monkeys. Therefore, our experiments reveal that an additional role for the SC in the generation of saccades is to provide a vector error signal that drives dysmetric saccades to adapt. Moreover, the characteristics of the electrically induced adaptation reflect those of error-related CS activity in the oculomotor cerebellum, suggesting that CS activity serves as the learning signal. We speculate that CS activity may serve as the error signal that drives other kinds of motor learning as well.

Complex spike activity signals the direction and size of dysmetric saccade errors.

The cerebellar oculomotor vermis (OMV) receives inputs from both the superior colliculus (SC) via the nucleus reticularis tegmenti pontis as mossy fibres and the inferior olive as climbing fibres. Lesion studies show that the OMV is necessary for the saccade amplitude adaptation that corrects persistent motor errors. In this study, we examined whether the complex spike (CS) activity due to climbing fibre inputs could serve as an error signal to drive saccade adaptation. When there was an error during behaviourally induced saccade dysmetrias, the probability of CS occurrence depended on the direction and size of the error. If this CS activity actually drives saccade adaptation, we speculate that adaptation should be equally efficient in all directions and that the course of adaptation could have two operating modes.

Complex spike activity in the oculomotor vermis of the cerebellum: a vectorial error signal for saccade motor learning?

Brain stem signals that generate saccadic eye movements originate in the superior colliculus. They reach the pontine burst generator for horizontal saccades via short-latency pathways and a longer pathway through the oculomotor vermis (OMV) of the cerebellum. Lesion studies implicate the OMV in the adaptation of saccade amplitude that occurs when saccades become inaccurate because of extraocular muscle weakness or behavioral manipulations. We studied the nature of the possible error signal that might drive adaptation by examining the complex spike (CS) activity of vermis Purkinje (P-) cells in monkeys. We produced a saccade error by displacing the target as a saccade was made toward it; a corrective saccade approximately 200 ms later eliminated the resulting error. In most P-cells, the probability of CS firing changed, but only in the error interval between the primary and corrective saccade. For most P-cells, CSs occurred in a tight cluster approximately 100 ms after error onset. The probability of CS occurrence depended on both error direction and size. Across our sample, all error directions were represented; most had a horizontal component. In more than one half of our P-cells, the probability of CS occurrence was greatest for error sizes<5 degrees and less for larger errors. In the remaining cells, there was a uniform increased probability of CS occurrence for all errors

Effects of initial eye position on saccade-related behavior of abducens nucleus neurons in the primate.

Previous work suggests that when the eye starts at different orbital initial positions (IPs), the saccade control system is faced with significant nonlinearities. Here we studied the effects of IP on saccade-related firing of monkey abducens neurons by either isolating saccade variables behaviorally or applying a multiple linear regression analysis. Over a 50 degrees range of IPs, we could select 10 degrees horizontal saccades with identical velocity profiles, which would require identical control signals in a linear system. The bursts accompanying ipsiversive saccades for IPs above the threshold for steady firing were quite similar. The excess burst rate above steady firing was either constant or decreased with ipsiversive IP, and both the number of excess spikes in the burst and burst duration were nearly constant. However, for ipsiversive saccades from IPs below threshold, both peak burst rate (6.82 +/- 1.38 spikes.s(-1).deg(-1)) and burst duration (0.67 +/- 0.28 ms/deg) increased substantially with ipsiversive IPs. Moreover, the pause associated with contraversive saccades shortened considerably with ipsiversive IPs (mean 1.2 ms/deg). This pattern of results for pauses and for bursts below threshold suggests the presence of a significant nonlinearity. Abducting saccades are produced by the net force of agonist lateral rectus (LR) and antagonist medial rectus (MR) muscles. We suggest that the decreasing force in the MR muscle with IPs in the abducting direction requires a more vigorous burst in LR motoneurons, which appears to be generated by a combination of saturating and nonsaturating burst commands and the recruitment of additional abducens neurons.

Activity changes in monkey superior colliculus during saccade adaptation.

Saccades are eye movements that are used to foveate targets rapidly and accurately. Their amplitude must be adjusted continually, throughout life, to compensate for movement inaccuracies due to maturation, pathology, or aging. One possible locus for such saccade adaptation is the superior colliculus (SC), the relay for cortical commands to the premotor brain stem generator for saccades. However, previous stimulation and recording studies have disagreed as to whether saccade adaptation occurs up- or downstream of the SC. Therefore we have reexamined the behavior of SC burst neurons during saccade adaptation under conditions that were optimized to produce the biggest possible change in neuronal activity. We show that behavioral adaptation of saccade amplitude was associated with significant increases or decreases, in the number of spikes in the burst and/or changes in the shape of the movement field in 35 of 43 SC neurons tested. Of the 35, 29 had closed movement fields and 14 were classified indeterminate because the movement field could not be definitively diagnosed. Changes in the number of spikes occurred gradually during adaptation and resulted from correlated changes in burst lead and duration without consistent changes in peak burst rate. These data indicate that the great majority of SC neurons show a change in discharge in association with saccade amplitude adaptation. Based on these and previous results, we speculate that the site for saccade adaptation resides in the SC or that the SC is the final common pathway for adaptive changes that occur elsewhere in the saccade system.

Contribution of the frontal eye field to gaze shifts in the head-unrestrained monkey: effects of microstimulation.

The role of the primate frontal eye field (FEF) has been inferred primarily from experiments investigating saccadic eye movements with the head restrained. Three recent reports investigating head-unrestrained gaze shifts disagree on whether head movements are evoked with FEF stimulation and thus whether the FEF participates in gaze movement commands. We therefore examined the eye, head, and overall gaze movement evoked by low-intensity microstimulation of the low-threshold region of the FEF in two head-unrestrained monkeys. Microstimulation applied at 200 or 350 Hz for 200 ms evoked large gaze shifts with substantial head movement components from most sites in the dorsomedial FEF, but evoked small, predominantly eye-only gaze shifts from ventrolateral sites. The size and direction of gaze and eye movements were strongly affected by the eye position before stimulation. Head movements exhibited little position dependency, but at some sites and initial eye positions, head-only movements were evoked. Stimulus-evoked gaze shifts and their eye and head components resembled those elicited naturally by visual targets. With stimulus train durations >200 ms, the evoked gaze shifts were more likely to be accomplished with a substantial head movement, which often continued for the entire stimulus duration. The amplitude, duration and peak velocity of the evoked head movement were more strongly correlated with stimulus duration than were those of the gaze or eye movements. We conclude that the dorsomedial FEF generates a gaze command signal that can produce eye, head, or combined eye-head movement depending on the initial orbital position of the eye.

Complex spike activity of purkinje cells in the oculomotor vermis during behavioral adaptation of monkey saccades.

Throughout life, the oculomotor system can correct itself when saccadic eye movements become inaccurate. This adaptation mechanism can be engaged in the laboratory by displacing the target when the saccade toward it is in flight. Forward and backward target displacements cause gradual increases and decreases in saccade amplitude, respectively. Equipped with this paradigm, we asked whether Purkinje cells (P-cells) in the vermis of the oculomotor cerebellum, lobules VIc and VII, changed their complex spike (CS) discharge during the behavioral adaptation of horizontal saccades. We tested the hypothesis that CS activity would change only when a targeting saccade caused an error in eye position relative to the target, i.e., during the error interval between the primary and corrective saccades. We examined only those P-cells whose simple spike activity exhibited either a burst or pause with saccades in several directions. Approximately 80% of such P-cells exhibited an increase in CS activity during the error interval when the adaptation paradigm imposed horizontal eye-position errors in one direction and a decrease in activity for errors in the other. As adaptation progressed and errors were reduced, there was no consistent change in the CS activity. These data suggest that the CS activity of P-cells in the oculomotor vermis signals the direction but not the magnitude of eye-position error during saccade adaptation. Our results are consistent with cerebellar learning models that have been proposed to explain adaptation of the vestibulo-ocular reflex so similar mechanisms may also underlie plasticity of this precision voluntary oculomotor behavior.

Amplitude adaptation occurs where a saccade is represented as a vector and not as its components.

When saccades become inaccurate, their amplitude is adapted. We examined, in humans, whether this adaptation occurs where the saccade is represented as a vector or as its horizontal and vertical components. In one experiment, we behaviorally reduced the amplitude of clockwise oblique saccades and examined the transfer to saccades made to other target amplitudes and directions. In a second, we adapted rightward saccades of the same size as the rightward component of the clockwise oblique saccades and examined the effect on oblique saccades. The results of both experiments imply that adaptation occurs where the saccade command is represented as a vector.