Motor program

Abstract: Although current knowledge attributes movement disorders to a dysfunction of the basal ganglia-motor cortex circuits, abnormalities in the peripheral afferent inputs or in their central processing may interfere with motor program execution. We review the abnormalities of sensorimotor integration described in the various types of movement disorders. Several observations, including those of parkinsonian patients' excessive reliance on ongoing visual information during movement tasks, suggest that proprioception is defective in Parkinson's disease (PD). The disturbance of proprioceptive regulation, possibly related to the occurrence of abnormal muscle-stretch reflexes, might be important for generating hypometric or bradykinetic movements. Studies with somatosensory evoked potentials (SEPs), prepulse inhibition, and event-related potentials support the hypothesis of central abnormalities of sensorimotor integration in PD. In Huntington's disease (HD), changes in SEPs and long-latency stretch reflexes suggest that a defective gating of peripheral afferent input to the brain might impair sensorimotor integration in cortical motor areas, thus interfering with the processing of motor programs. Defective motor programming might contribute to some features of motor impairment in HD. Sensory symptoms are frequent in focal dystonia and sensory manipulation can modify the dystonic movements. In addition, specific sensory functions (kinaesthesia, spatial-temporal discrimination) can be impaired in patients with focal hand dystonia, thus leading to a "sensory overflow." Sensory input may be abnormal and trigger focal dystonia, or defective "gating" may cause an input-output mismatch in specific motor programs. Altogether, several observations strongly support the idea that sensorimotor integration is impaired in focal dystonia. Although elemental sensation is normal in patients with tics, tics can be associated with sensory phenomena. Some neurophysiological studies suggest that an altered "gating" mechanism also underlies the development of tics. This review underlines the importance of abnormal sensorimotor integration in the pathophysiology of movement disorders. Although the physiological mechanism remains unclear, the defect is of special clinical relevance in determining the development of focal dystonia.

Abstract: The following sequences of two single movements were examined in 10 patients with Parkinson's disease and compared with the performance of 9 normal subjects of similar age. Isometric opposition of thumb and fingers to a force of 30 N ('squeeze'), followed by isotonic elbow flexion ('flex') through 15 degrees with the same arm. 'Squeeze' with the left hand followed by 'flex' with the right elbow. Isotonic opposition of thumb and fingers ('cut') through 90 degrees followed by isotonic 'flex' with the same arm. Isotonic elbow 'flex' followed by isometric 'squeeze' with the same arm. All movements were self-paced. Subjects were given instructions to move as rapidly as possible and to start the second movement immediately after the end of the first. Patients were slower than normal when each single movement was performed separately. There was a further decrease in speed when two movements were executed sequentially. This was due to an increase in movement duration of each of the component movements, especially the second, and to an increase in the pause between the first and second movements. In both normals and patients, there was no correlation between the times taken to perform the first and second movements of any of the four sequences that were studied. Because of this we suggest that the two components of the sequence remained under the control of two separate motor programs. When performing the sequential tasks, normal subjects automatically chose an interval between the onsets of the two separate movements of about 230 ms, even in tasks in which the duration of the first movement was less than 200 ms. If normal subjects were instructed to begin the second movement with an interonset interval of less than 200 ms, the speed of the second movement was much slower. Patients with Parkinson's disease automatically chose a much longer interonset interval of 400-500 ms. In addition, they exhibited difficulty in switching from the first to the second movement in the sequence. We suggest that the problems exhibited by patients with Parkinson's disease when they try to perform two rapid sequential movements can be seen as a deficit in the capacity to switch from one motor program to another within an overall motor plan.