Biomedical subjects

D Pélisson

Publications and source records attributed to D Pélisson.

At least 19 recordsLinked to original sources

PubMed2005

Ipsidirectional impairment of prism adaptation after unilateral lesion of anterior cerebellum.

In a patient with damage of the left cerebellar cortex (SCA territory), the authors tested four combinations of exposure to optical shift (leftward prisms, right hand; rightward prisms, right hand; leftward prisms, left (ataxic) hand; rightward prisms, left (ataxic) hand). He adapted to rightward but not leftward prisms, independent of which hand was used during exposure. This suggests a role of anterior cerebellar cortex in the computation or compensation of ipsidirectional visual error.

Adaptation, Physiological↗

PubMed2001

Early head movements elicited by visual stimuli or collicular electrical stimulation in the cat.

During the course of previous recordings of visually-triggered gaze shifts in the head-unrestrained cat, we occasionally observed small head movements which preceded the initiation of the saccadic eye/head gaze shift toward a visual target. These early head movements (EHMs) were directed toward the target and occurred with a probability varying between animals from 0.4% to 16.4% (mean=5.2%, n=11 animals). The amplitude of EHM ranged from 0.4 degrees to 8.3 degrees (mean=1.9 degrees ), their latency from 66 to 270 ms (median=133 ms) and the delay from EHM onset to gaze shift onset averaged 183+/-108 ms (n=240). Their occurrence did not depend on visual target eccentricity in the studied range (7-35 degrees ), but influenced the metrics and dynamics of the ensuing gaze shifts (gain and velocity reduced). We also found in the two tested cats that low intensity microstimulation of the superior colliculus deeper layers elicited a head movement preceding the gaze shift. Altogether, these results suggest that the presentation of a visual target can elicit a head movement without triggering a saccadic eye/head gaze shift. The visuomotor pathways triggering these early head movements can involve the deep superior colliculus.

Animals↗

PubMed2001

Gaze shifts evoked by electrical stimulation of the superior colliculus in the head-unrestrained cat. II. Effect of muscimol inactivation of the caudal fastigial nucleus.

The medioposterior cerebellum [vermian lobules VI and VII and caudal fastigial nucleus (cFN)] is known to play a major role in the control of saccadic gaze shifts toward a visual target. To determine the relative contribution of the cFN efferent pathways to the brainstem reticular formation and to the superior colliculus (SC), we recorded in the head-unrestrained cat the effects of cFN unilateral inactivation on gaze shifts evoked by electrical microstimulation of the deeper SC layers. Gaze shifts evoked after muscimol injection still exhibited the typical qualitative features of normal saccadic gaze shifts. Nevertheless, consistent modifications in amplitude and latency were observed. For ipsiversive movements (evoked by the SC contralateral to the inactivated cFN), these changes depended on the locus of stimulation on the motor map: for the anterior 2/3 of the SC, amplitude increased and latency tended to decrease; for the posterior 1/3 of the SC, amplitude decreased and latency increased. For the contraversive direction, amplitude moderately decreased and latency tended to increase for all but the caudal-most stimulated SC site. These modifications of SC-evoked gaze shifts during cFN inactivation differed from the ipsiversive hypermetria/contraversive hypometria pattern observed for visually triggered gaze shifts recorded during the same recording sessions. We conclude that (i) the topographical organization of gaze shift amplitude in the deeper SC layers is influenced by the cerebellum and is either severely distorted or demonstrates an amplitude reduction during inactivation of the contralateral or ipsilateral cFN, respectively; (ii) gaze shifts evoked by SC microstimulation and visually triggered gaze shifts either rely on distinct cerebellar-dependent control processes or differ by the location of the caudal-most active SC population. We present a functional scheme providing several predictions regarding the modulatory influence of the cerebellum on SC neuronal activities and on the topographical organization of fastigial-SC projections.

Acceleration↗

PubMed2001

Gaze shifts evoked by electrical stimulation of the superior colliculus in the head-unrestrained cat. I. Effect of the locus and of the parameters of stimulation.

Several studies have suggested that the pattern of neuronal activity in the superior colliculus (SC) interacts with the well-known topographical coding of saccades (motor map). To further describe this interaction, we recorded gaze saccades evoked by electrical microstimulation of SC deeper layers in the head-unrestrained cat and systematically varied the collicular locus (25 sites) and parameters (intensity, frequency) of the stimulation. Long stimulation trains were used to avoid saccade truncation. We found that the direction and amplitude of evoked gaze shifts were related to the stimulation locus, describing a gaze shift map. For 18 out of 20 sites the amplitude, but not the direction, also strongly depended on stimulation strength. Indeed, gaze amplitude continuously increased when raising current intensity up to several times the threshold value T (the largest intensity tested was 6 x T), whereas varying pulse frequency from 150 to 750 pulses per second (p.p.s.) revealed an optimal frequency range (300 and 500 p.p.s.) eliciting the largest gaze shifts. Moreover, the intensity effect on amplitude increased in an orderly fashion with the rostro-caudal stimulation locus. Gaze shift amplitude was not related to the number of delivered stimulation pulses. Concerning movement initiation, increasing either intensity or frequency led to an exponential decrease in gaze latency until minimal values near 30 ms were reached, but the number of pulses delivered during the corresponding latency period remained constant within a 300-500 p.p.s. frequency range. These findings indicate that the pattern of collicular discharge evoked by electrical stimulation strongly interacts with the gaze shift map and provide evidence for a summation of collicular activities by downstream premotor neurons.

Animals↗

PubMed2000

Functional adaptation of reactive saccades in humans: a PET study.

It is known that the saccadic system shows adaptive changes when the command sent to the extraocular muscles is inappropriate. Despite an abundance of supportive psychophysical investigations, the neurophysiological substrate of this process is still debated. The present study addresses this issue using H2(15)O positron emission tomography (PET). We contrasted three conditions in which healthy human subjects were required to perform saccadic eye movements toward peripheral visual targets. Two conditions involved a modification of the target location during the course of the initial saccade, when there is suppression of visual perception. In the RAND condition, intra-saccadic target displacement was random from trial-to-trial, precluding any systematic modification of the primary saccade amplitude. In the ADAPT condition, intra-saccadic target displacement was uniform, causing adaptive modification of the primary saccade amplitude. In the third condition (stationary, STAT), the target remained at the same location during the entire trial. Difference images reflecting regional cerebral-blood-flow changes attributable to the process of saccadic adaptation (ADAPT minus RAND; ADAPT minus STAT) showed a selective activation in the oculomotor cerebellar vermis (OCV; lobules VI and VII). This finding is consistent with neurophysiological studies in monkeys. Additional analyses indicated that the cerebellar activation was not related to kinematic factors, and that the absence of significant activation within the frontal eye fields (FEF) or the superior colliculus (SC) did not represent a false negative inference. Besides the contribution of the OCV to saccadic adaptation, we also observed, in the RAND condition, that the saccade amplitude was significantly larger when the previous trial involved a forward jump than when the previous trial involved a backward jump. This observation indicates that saccade accuracy is constantly monitored on a trial-to-trial basis. Behavioral measurements and PET observations (RAND minus STAT) suggest that this single-trial control of saccade amplitude may be functionally distinct from the process of saccadic adaptation.

Adaptation, Physiological↗

PubMed1999

Effects of short-term adaptation of saccadic gaze amplitude on hand-pointing movements.

We investigated whether and how adaptive changes in saccadic amplitudes (short-term saccadic adaptation) modify hand movements when subjects are involved in a pointing task to visual targets without vision of the hand. An experiment consisted of the pre-adaptation test of hand pointing (placing the finger tip on a LED position), a period of adaptation, and a post-adaptation test of hand pointing. In a basic task (transfer paradigm A), the pre- and post-adaptation trials were performed without accompanying eye and head movements: in the double-step gaze adaptation task, subjects had to fixate a single, suddenly displaced visual target by moving eyes and head in a natural way. Two experimental sessions were run with the visual target jumping during the saccades, either backwards (from 30 to 20 degrees, gaze saccade shortening) or onwards (30 to 40 degrees, gaze saccade lengthening). Following gaze-shortening adaptation (level of adaptation 79+/-10%, mean and s.d.), we found a statistically significant shift (t-test, error level P<0.05) in the final hand-movement points, possibly due to adaptation transfer, representing 15.2% of the respective gaze adaptation. After gaze-lengthening adaptation (level of adaptation 92+/-17%). a non-significant shift occurred in the opposite direction to that expected from adaptation transfer. The applied computations were also performed on some data of an earlier transfer paradigm (B, three target displacements at a time) with gain shortening. They revealed a significant transfer relative to the amount of adaptation of 18.5< or = 17.5% (P<0.05). In the coupling paradigm (C), we studied the influence of gaze saccade adaptation of hand-pointing movements with concomitant orienting gaze shifts. The adaptation levels achieved were 59+/-20% (shortening) and 61+/-27% (lengthening). Shifts in the final fingertip positions were congruent with internal coupling between gaze and hand, representing 53% of the respective gaze-amplitude changes in the shortening session and 6% in the lengthening session. With an adaptation transfer of less than 20% (paradigm A and B), we concluded that saccadic adaptation does not "automatically" produce a functionally meaningful change in the skeleto-motor system controlling hand-pointing movements. In tasks with concomitant gaze saccades (coupling paradigm C), the modification of hand pointing by the adapted gaze comes out more clearly, but only in the shortening session.

Adaptation, Physiological↗

PubMed1998

From eye to hand: planning goal-directed movements.

The nature of the neural mechanisms involved in movement planning still remains widely unknown. We review in the present paper the state of our knowledge of the mechanisms whereby a visual input is transformed into a motor command. For the sake of generality, we consider the main problems that the nervous system has to solve to generate a movement, that is: target localization, definition of the initial state of the motor apparatus, and hand trajectory formation. For each of these problems three questions are addressed. First, what are the main results presented in the literature? Second, are these results compatible with each other? Third, which factors may account for the existence of incompatibilities between experimental observations or between theoritical models? This approach allows the explanation of some of the contradictions existing within the movement-generation literature. It also suggests that the search for general theories may be in vain, the central nervous system being able to use different strategies both in encoding the target location with respect to the body and in planning hand displacement. In our view, this conclusion may advance the field by both opening new lines of research and bringing some sterile controversies to an end.

Animals↗

PubMed1998

Functional anatomy of saccadic adaptation in humans.

Positron emission tomography (PET) was used to investigate the neurophysiological substrate of human saccadic adaptation. Subjects made saccadic eye movements toward a visual target that was displaced during the course of the initial saccade, a time when visual perception is suppressed. In one condition, displacement was random from trial to trial, precluding any systematic modification of the initial saccade amplitude. In the second condition, the direction and magnitude of displacement were consistent, causing adaptative modification of the initial saccade amplitude. PET difference images reflecting metabolic changes attributable to the process of saccadic adaptation showed selective activation of the medioposterior cerebellar cortex. This localization is consistent with neurophysiological findings in monkeys and brain-lesioned humans.

Adaptation, Physiological↗

PubMed1998

Orienting gaze shifts during muscimol inactivation of caudal fastigial nucleus in the cat. I. Gaze dysmetria.

The cerebellar control of orienting behavior toward visual targets was studied in the head-unrestrained cat by analyzing the deficits of saccadic gaze shifts after unilateral injection of muscimol in the caudal part of the fastigial nucleus (cFN). Gaze shifts are rendered strongly inaccurate by muscimol cFN inactivation. The characteristics of gaze dysmetria are specific to the direction of the movement with respect to the inactivated cFN. Gaze shifts directed toward the injected side are hypermetric. Irrespective of their starting position, all these ipsiversive gaze shifts overshoot the target by a constant horizontal error (or bias) to terminate at a "shifted goal" location. In particular, when gaze is directed initially at the future target's location, a response with an amplitude corresponding to the bias moves gaze away from the actual target. Additionally, when gaze is initially in between the target and this shifted goal location, the response again is directed toward the latter. This deficit of ipsiversive gaze shifts is characterized by a consistent increase in the y intercept of the relationship between horizontal gaze amplitude and horizontal retinal error. Slight increases in the slope sometimes are observed as well. Contraversive gaze shifts are markedly hypometric and, in contrast to ipsiversive responses, they do not converge onto a shifted goal but rather underestimate target eccentricity in a proportional way. This is reflected by a decrease in the slope of the relationship between horizontal gaze amplitude and horizontal retinal error, with, for some experiments, a moderate change in the y-intercept value. The same deficits are observed in a different setup, which permits the control of initial gaze position. Correction saccades rarely are observed when visual feedback is eliminated on initiation of the primary orienting response; instead, they occur frequently when the target remains visible. Like the primary contraversive saccades, they are hypometric and the ever-decreasing series of three to five correction saccades reduces the gaze fixation error but often does not completely eliminate it. We measured the position of gaze after the final correction saccade and found that fixation of a visible target is still shifted toward the inactivated cFN by 4.9 +/- 2.4 degrees. This fixation offset is correlated to, but on average 54% smaller than, the hypermetric bias of ipsiversive responses measured in the same experiments. In conclusion, the cFN contributes to the control of saccadic shifts of the visual axis toward a visual target. The hypometria of contraversive gaze shifts suggests a cFN role in adjusting a gain in the translation of retinal signals into gaze motor commands. On the basis of the convergence of ipsiversive gaze shifts onto a shifted goal, the straightness of gaze trajectory during these responses and the production of misdirected or inappropriately initiated responses toward this shifted goal, we propose that the cFN influences the processes that specify the goal of ipsiversive gaze shifts.

Animals↗

PubMed1998

Orienting gaze shifts during muscimol inactivation of caudal fastigial nucleus in the cat. II. Dynamics and eye-head coupling.

We have shown in the companion paper that muscimol injection in the caudal part of the fastigial nucleus (cFN) consistently leads to dysmetria of visually triggered gaze shifts that depends on movement direction. Based on the observations of a constant error and misdirected movements toward the inactivated side, we have proposed that the cFN contributes to the specification of the goal of the impending ipsiversive gaze shift. To test this hypothesis and also to better define the nature of the hypometria that affects contraversive gaze shifts, we report in this paper on various aspects of movement dynamics and of eye/head coordination patterns. Unilateral muscimol injection in cFN leads to a slight modification in the dynamics of both ipsiversive and contraversive gaze shifts (average velocity decrease = 55 degrees/s). This slowing in gaze displacements results from changes in both eye and head. In some experiments, a larger gaze velocity decrease is observed for ipsiversive gaze shifts as compared with contraversive ones, and this change is restricted to the deceleration phase. For two particular experiments testing the effect of visual feedback, we have observed a dramatic decrease in the velocity of ipsiversive gaze shifts after the animal had received visual information about its inaccurate gaze responses; but virtually no change in hypermetria was noted. These observations suggest that there is no obvious causal relationship between changes in dynamics and in accuracy of gaze shifts after muscimol injection in the cFN. Eye and head both contribute to the dysmetria of gaze. Indeed, muscimol injection leads to parallel changes in amplitude of both ocular and cephalic components. As a global result, the relative contribution of eye and head to the amplitude of ipsiversive gaze shifts remains statistically indistinguishable from that of control responses, and a small (1.6 degrees) increase in the head contribution to contraversive gaze shifts is found. The delay between eye and head movement onsets is increased by 7.3 +/- 7.4 ms for contraversive and decreased by 8.3 +/- 10.1 ms for ipsiversive gaze shifts, corresponding respectively to an increased or decreased lead time of head movement initiation. The modest changes in gaze dynamics, the absence of a link between eventual dynamics changes and dysmetria, and a similar pattern of eye-head coordination to that of control responses, altogether are compatible with the hypothesis that the hypermetria of ipsiversive gaze shifts results from an impaired specification of the metrics of the impending gaze shift. Regarding contraversive gaze shifts, the weak changes in head contribution do not seem to reflect a pathological coordination between eye and head but would rather result from the tonic deviations of gaze and head toward the inactivated side. Hence, our data suggest that the hypometria of contraversive gaze shifts also might result largely from an alteration of processes that specify the goal rather than the on-going trajectory, of saccadic gaze shifts.

Analysis of Variance↗

PubMed1998

Contribution of the rostral fastigial nucleus to the control of orienting gaze shifts in the head-unrestrained cat.

The implication of the caudal part of the fastigial nucleus (cFN) in the control of saccadic shifts of the visual axis is now well established. In contrast a possible involvement of the rostral part of the fastigial nuceus (rFN) remains unknown. In the current study we investigated in the head-unrestrained cat the contribution of the rFN to the control of visually triggered saccadic gaze shifts by measuring the deficits after unilateral muscimol injection in the rFN. A typical gaze dysmetria was observed: gaze saccades directed toward the inactivated side were hypermetric, whereas those with an opposite direction were hypometric. For both movement directions, gaze dysmetria was proportional to target retinal eccentricity and could be described as a modified gain in the translation of visual signals into eye and head motor commands. Correction saccades were triggered when the target remained visible and reduced the gaze fixation error to 2.7 +/- 1.3 degrees (mean +/- SD) on average. The hypermetria of ipsiversive gaze shifts resulted predominantly from a hypermetric response of the eyes, whereas the hypometria of contraversive gaze shifts resulted from hypometric responses of both eye and head. However, even in this latter case, the eye saccade was more affected than the motion of the head. As a consequence, for both directions of gaze shift the relative contributions of the eye and head to the overall gaze displacement were altered by muscimol injection. This was revealed by a decreased contribution of the head for ipsiversive gaze shifts and an increased head contribution for contraversive movements. These modifications were associated with slight changes in the delay between eye and head movement onsets. Inactivation of the rFN also affected the initiation of eye and head movements. Indeed, the latency of ipsiversive gaze and head movements decreased to 88 and 92% of normal, respectively, whereas the latency of contraversive ones increased to 149 and 145%. The deficits induced by rFN inactivation were then compared with those obtained after muscimol injection in the cFN of the same animals. Several deficits differed according to the site of injection within the fastigial nucleus (tonic orbital eye rotation, hypermetria of ipsiversive gaze shifts and fixation offset, relationship between dysmetria and latency of contraversive gaze shifts, postural deficit). In conclusion, the present study demonstrates that the rFN is involved in the initiation and the control of combined eye-head gaze shifts. In addition our findings support a functional distinction between the rFN and cFN for the control of orienting gaze shifts. This distinction is discussed with respect to the segregated fastigiofugal projections arising from the rFN and cFN.

Animals↗

PubMed1998

Compensation for gaze perturbation during inactivation of the caudal fastigial nucleus in the head-unrestrained cat.

Muscimol injection in the caudal part of the fastigial nucleus (cFN) leads, in the head-unrestrained cat, to a characteristic dysmetria of saccadic gaze shifts toward visual targets. The goal of the current study was to test whether this pharmacological cFN inactivation impaired the ability to compensate for unexpected perturbations in gaze position during the latency period of the saccadic response. Such perturbations consisted of moving gaze away from the target by a transient electrical microstimulation in the deep layers of the superior colliculus simultaneously with extinction of the visual target. After injection of muscimol in the cFN, targets located in the contralesional hemifield elicited gaze shifts that fell short of the target in both "perturbed" and "unperturbed" trials. The amplitude of the compensatory contraversive gaze shifts in perturbed trials coincided with the predicted amplitude of unperturbed responses starting from the same position. Targets located in the opposite hemifield elicited hypermetric gaze shifts in both trial types, and the error of compensatory responses was not statistically different from that of unperturbed gaze shifts. These results indicate that inactivation of the cFN does not interfere with the ability of the head-unrestrained cat to compensate for ipsiversive or contraversive perturbations in gaze position. Thus the gaze-related feedback signals that are used to compute a reference signal of desired gaze displacement are not impaired by cFN inactivation.

Animals↗

PubMed1997

Changes in initiation of orienting gaze shifts after muscimol inactivation of the caudal fastigial nucleus in the cat.

1. The production of a goal-directed saccadic gaze shift involves the specification of movement amplitude and direction, and the decision to trigger the movement. Behavioural and neurophysiological data suggest that these two functions involve separate processes which may interact. 2. The medio-posterior cerebellar areas are classically assigned a major contribution to the control of saccade metrics, and previous cerebellar lesion studies have revealed marked dysmetria of visually triggered gaze shifts. In contrast, these studies did not provide evidence for a cerebellar role in saccadic initiation. 3. In the present study, we investigated in the head-unrestrained cat the deficits in both the initiation and the metrics control of saccadic gaze shifts following pharmacological inactivation of the caudal part of the fastigial nucleus (cFN). 4. After cFN inactivation, latencies for contraversive gaze shifts increased to about 137 +/- 28% of normal, and latencies for ipsiversive gaze shifts decreased to about 84 +/- 8% of normal. Similar changes in head movement latency were observed, such that the temporal coupling between eye and head components remained largely unaffected. 5. Contraversive gaze shifts were more hypometric as their latency increased. In contrast, the degree of hypermetria in ipsiversive gaze shifts was unrelated to latency. 6. These results suggest a functional role of the medio-posterior cerebellum in gaze shift initiation and in storing information about the target location and/or the desired gaze shift amplitude.

Animals↗

PubMed1996

The caudo ventral pontine tegmentum is involved in the generation of high velocity eye saccades in bursts during paradoxical sleep in the cat.

Cat eye movements were recorded in the head restrained condition, with the technique of the scleral search coil in a magnetic field, and the maximum velocity/amplitude relationships were analyzed for saccades in the following conditions, (1) during waking (W); (2) during paradoxical sleep (PS); and (3) during W following carbachol microinjections in the medioventral part of the caudal pontine tegmentum. These findings indicate that (1) the neurophysiological mechanisms underlying carbachol induced events are similar to those acting during PS and that the caudal pontine tegmentum might be the generator of high velocity eye saccades in bursts accompanied by ponto geniculo occipital waves (PGOw) during PS, and (2) caudal pontine tegmentum neurons show 'state-dependent' responsiveness to cholinergic inputs, suggesting that a change in the synaptic inputs and/or the membrane properties of these neurons during PS may be responsible for the induction of saccadic eye movements in bursts and associated PGOw.

Animals↗

PubMed1996

On the short-term adaptation of eye saccades and its transfer to head movements.

During a sequence of eye saccades toward a target that is systematically displaced during initiation of the saccade, the oculomotor system adjusts saccadic amplitude and direction in less than 100 trials to directly reach the second target position. The goal of the present work was to test whether and under which conditions these short-term, adaptive modifications in eye movements are transferred from horizontal eye saccades to horizontal head-pointing movements. In the first series of experiments subjects had to execute head yaw rotations to an extent defined by verbal command (assessed movements). These head movements were not part of visually elicited gaze shifts. They were recorded before and after a period of saccadic adaptation. Saccades were adapted to reduced amplitudes by using target displacements from 30 to 20 degrees and from 40 to 30 degrees. After 40-50 trials per target displacement, the amount of eye saccade adaptation was 79% (30-20 degrees) and 97% (40-30 degrees) of the displacement amplitude. In the second series of experiments, visually triggered head movements to briefly illuminated targets (100 ms) were measured before and after adaptation. The data obtained from both series did not reveal a functionally significant transfer of saccadic adaptation to head movements. The amount of possible transfer given as a percentage of the amount of achieved adaptation was: assessed head movements, 40 degrees, 1.9%, 20 degrees, -8.6%; visually triggered movements, 40 degrees, 5.1%, 20 degrees, 10.0%. No values significantly deviated from zero.

Adaptation, Physiological↗

PubMed1995

Modifications in end positions of arm movements following short-term saccadic adaptation.

We investigated whether short-term saccadic adaptation modifies hand pointing. Subjects were presented with double-step targets, the second target jump occurring during the saccade to the first one and bringing the target back to 66% of the first target eccentricity, in order to reduce the gain of their gaze saccades. Before and after this adaptation phase, they pointed with their hand to single step targets while keeping their gaze straight ahead. The results show that the hand movements terminated at positions that were significantly less eccentric following the adaptation phase, resembling the adaptive modification seen in the gaze movements. These results suggest that the motor systems controlling gaze and hand use common information about target position.

Adaptation, Physiological↗

PubMed1995

On-line compensation of gaze shifts perturbed by micro-stimulation of the superior colliculus in the cat with unrestrained head.

Prior studies have led to the gaze feedback hypothesis, which states that quick orienting movements of the visual axis (gaze shifts) are controlled by a feedback system. We have previously provided evidence for this hypothesis by extending the original study of Mays and Sparks (1980) to the cat with unrestrained head (Pélisson et al. 1989). We showed that cats compensated for a stimulation-induced perturbation of initial gaze position by generating, in the dark, an accurate gaze shift towards the remembered location of a flashed target. In the present study, we investigate goal-directed gaze shifts perturbed "in flight" by a brief stimulation of the superior colliculus. The microstimulation parameters were tuned such that significant perturbations were induced without halting the movement. The ambient light was turned off at the onset of the gaze shift, suppressing any visual feedback. We observed that, following stimulation offset, the gaze shift showed temporal and spatial changes in its trajectory to compensate for the transient perturbation. Such compensations, which occurred "on-line" before gaze shift termination, involved both eye and head movements and had dynamic characteristics resembling those of unperturbed saccadic gaze shifts. These on-line compensations maintained gaze accuracy when the stimulation was applied during the early phase of large and medium (about 60 and 40 degrees) movements. These results are compatible with the notion of a gaze feedback loop providing a dynamic gaze error signal.

Animals↗

PubMed1993

Error processing in pointing at randomly feedback-induced double-step stimuli.

Two experiments were conducted to determine the spatial and temporal organization of the arm trajectory in human subjects as they pointed to single- and double-step target displacements. Subjects pointed either without (Experiment 1) or with (Experiment 2) vision of their moving hand throughout the trial. In both experiments, target perturbation occurring in double-step trials was clearly perceived by the subjects and was randomly introduced either at the onset or at peak velocity of hand movement. Regardless of whether or not visual reafference from the pointing hand was available, subjects corrected the trajectory of their moving hand to accommodate the double-step. Moreover, asymmetrical velocity profiles were observed for responses to both types of target, with or without vision of the moving hand. The acceleration phase was a fixed pattern independent of the type of step stimulation. However, a clear dissociation, both in the deceleration phase and accuracy of responses to double-step targets, emerged according to the timing of target perturbation. When targets were perturbed at the onset of hand movement, subjects modulated the deceleration phase of their response to compensate for 88 to 100% of the second target displacement. In contrast, when targets were perturbed at peak velocity of hand movement, subjects were unable to modulate the deceleration phase adequately and compensated for only 20 to 40% of the perturbation. These results suggest that motor error is dynamically evaluated during the acceleration phase of a movement toward a perturbed target, allowing amendments to the trajectory to be performed during the deceleration phase. This main corrective process appears to be basically independent of visual reafference from the moving hand.

Journal Article↗