The primary manifestations of Parkinson's disease are abnormalities of movement, including movement slowness, difficulties with gait and balance, and tremor. We know a considerable amount about the abnormalities of neuronal and muscle activity that correlate with these symptoms. Motor symptoms can also be described in terms of motor control, a level of description that explains how movement variables, such as a limb's position and speed, are controlled and coordinated. Understanding motor symptoms as motor control abnormalities means to identify how the disease disrupts normal control processes. In the case of Parkinson's disease, movement slowness, for example, would be explained by a disruption of the control processes that determine normal movement speed. Two long-term benefits of understanding the motor control basis of motor symptoms include the future design of neural prostheses to replace the function of damaged basal ganglia circuits, and the rational design of rehabilitation strategies. This type of understanding, however, remains limited, partly because of limitations in our knowledge of normal motor control. In this article, we review the concept of motor control and describe a few motor symptoms that illustrate the challenges in understanding such symptoms as motor control abnormalities.T he effects of Parkinson's disease (PD) can be described at different levels. Within the brain, the major pathological change is progressive degeneration of neurons in the pars compacta of the substantia nigra, one of the nuclei that constitute the basal ganglia (BG). These neurons normally transmit dopamine to another BG nucleus, the striatum, but their degeneration leads to dysfunction of these neuronal circuits that include the BG and motor cortical areas. At the level of an individual's behavior, these changes result in movement abnormalities, which are the major manifestations of the disease. These difficulties, in turn, cause major disruptions that range from an individual's quality of life to society-wide economics. Our goal in this article is to describe motor symptoms of PD at the level of motor control. We briefly review what is meant by "motor control" and describe the process of understanding a symptom as a motor control abnormality. We then focus on selected symptoms that, among the many and varied motor symptoms of PD, have been most studied from a motor control perspective.

Visuomotor adaptation is mediated by errors between intended and sensory-detected arm positions. However, it is not clear whether visual-based errors that are shown during the course of motion lead to qualitatively different or more efficient adaptation than errors shown after movement. For instance, continuous visual feedback mediates online error corrections, which may facilitate or inhibit the adaptation process. We addressed this question by manipulating the timing of visual error information and task instructions during a visuomotor adaptation task. Subjects were exposed to a visuomotor rotation, during which they received continuous visual feedback (CF) of hand position with instructions to correct or not correct online errors, or knowledge-of-results (KR), provided as a static hand-path at the end of each trial. Our results showed that all groups improved performance with practice, and that online error corrections were inconsequential to the adaptation process. However, in contrast to the CF groups, the KR group showed relatively small reductions in mean error with practice, increased inter-trial variability during rotation exposure, and more limited generalization across target distances and workspace. Further, although the KR group showed improved performance with practice, after-effects were minimal when the rotation was removed. These findings suggest that simultaneous visual and proprioceptive information is critical in altering neural representations of visuomotor maps, although delayed error information may elicit compensatory strategies to offset perturbations.

This study was designed to differentiate between two models of motor lateralization: "feedback corrections" and dynamic dominance. Whereas the feedback correction hypothesis suggests that handedness reflects a dominant hemisphere advantage for visual-mediated correction processes, dynamic dominance proposes that each hemisphere has become specialized for distinct aspects of control. This model suggests that the dominant hemisphere is specialized for controlling task dynamics, as required for coordinating efficient trajectories, and the nondominant hemisphere is specialized for controlling limb impedance, as required for maintaining stable postures. To differentiate between these two models, we examined whether visuomotor corrections are mediated differently for the nondominant and dominant arms. Participants performed targeted reaches in a virtual reality environment in which visuomotor rotations occurred in two directions that elicited corrections with different coordination requirements. The feedback correction model predicts a dominant arm advantage for the timing and accuracy of corrections in both directions. Dynamic dominance predicts that correction timing and accuracy will be similar for both arms, but that interlimb differences in the quality of corrections will depend on the coordination requirements, and thus, direction of corrections. Our results indicated that correction time and accuracy did not depend on arm. However, correction quality, as reflected by trajectory curvature, depended on both arm and rotation direction. Nondominant trajectories were systematically more curvilinear than dominant trajectories for corrections with the highest coordination requirement. These results support the dynamic dominance hypothesis.

This study was designed to determine how visual feedback mediates error corrections during reaching. We used visuomotor rotations to dissociate a cursor, representing finger position, from the actual finger location. We then extinguished cursor feedback at different distances from the start location to determine whether corrections were based on error extrapolation from prior cursor information. Results indicated that correction amplitude varied with the extent of cursor feedback. A second experiment tested specific aspects of error information that might mediate corrections to visuomotor rotations: rotation angle, distance between the finger and cursor positions and the duration of cursor exposure. Results showed that corrections did not depend on the amplitude of the rotation angle or the amount of time the cursor was shown. Instead, participants corrected for the cursor–finger distance, at the point where cursor feedback was last-seen. These findings suggest that within-trial corrections and inter-trial adaptation might employ different mechanisms.

The basal ganglia are known to play a crucial role in movement execution, but their importance for motor skill learning remains unclear. Obstacles to our understanding include the lack of a universally accepted definition of motor skill learning (definition confound), and difficulties in distinguishing learning deficits from execution impairments (performance confound). We studied how healthy subjects and subjects with a basal ganglia disorder learn fast accurate reaching movements. We addressed the definition and performance confounds by: (1) focusing on an operationally defined core element of motor skill learning (speed-accuracy learning), and (2) using normal variation in initial performance to separate movement execution impairment from motor learning abnormalities. We measured motor skill learning as performance improvement in a reaching task with a speed-accuracy trade-off. We compared the performance of subjects with Huntington's disease (HD), a neurodegenerative basal ganglia disorder, to that of premanifest carriers of the HD mutation and of control subjects. The initial movements of HD subjects were less skilled (slower and/or less accurate) than those of control subjects. To factor out these differences in initial execution, we modeled the relationship between learning and baseline performance in control subjects. Subjects with HD exhibited a clear learning impairment that was not explained by differences in initial performance. These results support a role for the basal ganglia in both movement execution and motor skill learning.

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