By comparing the visuomotor performance of 10 adult, normal subjects in three tasks, we investigated whether errors in pointing movements reflect biased estimations of the hand starting position. In a manual pointing task with no visual feedback, subjects aimed at 48 targets spaced regularly around two starting positions. Nine subjects exhibited a similar pattern of systematic errors across targets, i.e., a parallel shift of the end points that accounted, on average, for 49% of the total variability. The direction of the shift depended on the starting location. Systematic errors decreased dramatically in the second condition where subjects were allowed to see their hand before movement onset. The third task was to use a joystick held by the left hand to estimate the location of their (unseen) right hand. The systematic perceptual errors in this condition were found to be highly correlated with the motor errors in the first condition. The results support the following conclusions. 1) Kinesthetic estimation of hand position may be consistently biased. Some of the mechanisms responsible for these biases are always active, irrespective of whether position is estimated overtly (e.g., with a matching paradigm), or covertly as part of the motor planning for aimed movements. 2) Pointing errors reflect to a significant extent the erroneous estimation of initial hand position. This suggests that aimed hand movements are planned vectorially, i.e., in terms of distance and direction, rather than in terms of absolute position in space.

Three hypotheses concerning the control variables in visuomanual pointing were tested. Participants pointed to a visual target presented briefly in total darkness on the horizontal plane. The starting position of the hand alternated randomly among 4 points arranged as a diamond. Results show that during the experiment, movement drifted from hypometric to hypermetric. Final positions depended on the starting position. Their average pattern reproduced the diamond of the starting points, either in same orientation (hypometric trials), or with a double inversion (hypermetric trials). The distribution of variable errors was elliptical, with the major axis aligned with the direction of the movement. Statistical analysis and Monte Carlo simulations showed that the results are incompatible with the final point control hypothesis (A. Polit & E. Bizzi, 1979). Better, but not fully satisfactory, agreement was found with the view that pointing involves comparing initial and desired postures (J. F. Soechting & M. Flanders, 1989a). The hypothesis that accounted best for the results is that final hand position is coded as a vector represented in an extrinsic frame of reference centered on the hand.

Recent models based, in part on a study of Huntington's disease, suggest that the basal ganglia are involved in on-line movement guidance. Two experiments were conducted to investigate this idea. First, we studied advanced Parkinson's disease patients performing a reaching task known to depend on on-line guidance. The task was to 'look and point' in the dark at visual targets displayed in the peripheral visual field. In some trials, the target location was slightly modified during saccadic gaze displacement (when vision is suppressed). In both patient and control groups, the target jump induced a gradual modification of the movement which diverged smoothly from its original path to reach the new target location. No deficit was found in the patients, except for an increased latency to respond to the target jump (Parkinson's disease: 243 ms; controls: 166 ms). A computational simulation indicated that this response slowing was likely to be a by-product of bradykinesia. The unexpected inconsistency between this result and previous reports was investigated in a second experiment. We hypothesized that the relevant factor was the characteristics of the corrections to be performed. To test this prediction, we investigated a task requiring corrections of the same type as investigated in Huntington's disease, namely large, consciously detected errors induced by large target jumps at hand movement onset. In contrast with the smooth adjustments observed in the first experiment, the subjects responded to the target jump by generating a discrete corrective sub-movement. While this iterative response was relatively rapid in the control subjects (220 ms), Parkinson's disease patients exhibited either dramatically late (>730 ms) or totally absent on-line corrections. When on-line corrections were absent, the initial motor response was completed before a second corrective response was initiated (the latency of the corrective response was the same as the latency of the initial response). Considered together, these results suggest that basal ganglia dependent circuits are not critical for feedback loops involving a smooth modulation of the ongoing command. These circuits may rather contribute to the generation of discrete corrective sub-movements. This deficit is in line with the general impairment of sequential and simultaneous actions in patients with basal ganglia disorders.

An experiment investigated systematic pointing errors in horizontal movements performed without visual feedback toward 48 targets placed symmetrically around two initial hand positions. Our main goal was to provide evidence in favor of the hypothesis that amplitude and direction of the movements are planned independently on the basis of the hand-target vector (vectorial parametric hypothesis, VP). The analysis was carried out mainly at the individual level. By screening a number of formal models of the potential error components, we found that only models compatible with the VP hypothesis provide an accurate description of the error pattern. A quantitative analysis showed that errors are explained mostly by a bias in the represented initial hand position (46% of the sum of squared errors) and a visuomotor gain bias (26%). Range effect (3%), directional biases (3%), and inertia-dependent amplitude modulations (1%) also provided significant contributions. The error pattern was incompatible with the view that movements are planned by specifying either a final posture or a final position. Instead, the results fully supported the view that, at least in the horizontal plane, amplitude, and direction of pointing movements are planned independently in a hand- or target-centered frame of reference.

This study addresses the hypothesis that the basal ganglia (BG) are involved speci®cally in the planning of movement amplitude (or covariates). Although often advanced, based on observations that Parkinson's disease (PD) patients exhibit hypokinesia in the absence of signi®cant directional errors, this hypothesis has been challenged by a recent alternative, that parkinsonian hypometria could be caused by dysfunction of on-line feedback loops. To re-evaluate this issue, we conducted two successive experiments. In the ®rst experiment we assumed that if BG are involved in extent planning then PD patients (who exhibit a major dysfunction within the BG network) should exhibit a preserved ability to use a direction precue with respect to normals, but an impaired ability to use an amplitude precue. Results were compatible with this prediction. Because this evidence did not prove conclusively that the BG is involved in amplitude planning (functional de®cits are not restricted to the BG network in PD), a second experiment was conducted using positron emission tomography (PET). We hypothesized that if the BG is important for planning movement amplitude, a task requiring increased amplitude planning should produce increased activation in the BG network. In agreement with this prediction, we observed enhanced activation of BG structures under a precue condition that emphasized extent planning in comparison with conditions that emphasized direction planning or no planning. Considered together, our results are consistent with the idea that BG is directly involved in the planning of movement amplitude or of factors that covary with that parameter.