Michel Desmurget

Although slowness of movement is a typical feature of Parkinson's disease (PD), it has been suggested that severely disabled patients remained able to produce normal motor responses in the context of urgent or externally driven situations. To investigate this phenomenon (often designated “paradoxical kinesis”), we required PD patients and healthy subjects to press a large switch under three main conditions: Self Generated, produce the fastest possible movement; External Cue, same as Self Generated but in response to an acoustic cue; Urgent External Cue, same as External Cue with the switch controlling an electromagnet that prevented a ball falling at the bottom of a tilted ramp. Task difficulty was equalized for the two experimental groups. Results showed that external cues and urgent conditions decreased movement duration (Urgent External Cue < External Cue < Self Generated) and reaction time (Urgent External Cue < External Cue). The amount of reduction was identical in PD patients and healthy subjects. These observations show that paradoxical kineses are not a hallmark of PD or a byproduct of basal ganglia dysfunctions, but a general property of the motor system. © 2006 Movement Disorder Society

The gain of reactive saccades was manipulated in 17 subjects using a target–jump paradigm. Following adaptation three sub-groups were formed: (1) rest 15 min in the dark, eyes closed; (2) perform self-generated saccades for 15 min; (3) perform reactive saccades for 15 min. The series of saccades were the same in groups 2 and 3 (amplitude, sequence), except that group 3 performed fewer saccades (same number as the lowest number of saccades performed by one subject in group 2). Neither the rest period nor the series of self-generated saccades affected the adapted gain. The series of reactive saccades generated, by contrast, quick de-adaptation. These results support the conclusion that the gain of self-generated and reactive saccades is independently controlled.

Six results are reported. (a) Reaching accuracy increases when visual capture of the target is allowed (e.g., target on vs. target off at saccade onset). (b) Whatever the visual condition, trajectories diverge only after peak acceleration, suggesting that accuracy is improved through feedback mechanisms. (c) Feedback corrections are smoothly implemented, causing the corrected and uncorrected velocity profiles to exhibit similar shapes. (d) Initial kinematics poorly predict final accuracy whatever the condition, indicating that target capture is not the only critical input for feedback control. (e) Hand and eye final variability are unrelated, suggesting that gaze direction is not a target signal for arm control. (f) Extent errors are corrected without modification of movement straightness; direction errors cause path curvature to increase. Together these data show that movements with straight paths and bell-shaped velocity profiles are not necessarily ballistic.

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.

We address three issues that might be important in evaluating the validity of the planning–control model: (1) It could be artificial to distinguish between control and planning when control involves the re-planning of a new corrective submovement that overlaps with the initial response; (2) experiments involving illusions are not totally compelling; (3) selectively implicating the superior parietal lobe in movement control and the basal ganglia in movement planning, appears questionable.

We briefly address three issues that might be important to evaluate the validity of the “emulation theory”: (1) Does it really say something new? (2) Are similar processes engaged in action, imagery, and perception? (3) Does a brain amodal emulator exist?