To study abnormal spatial patterns of muscle activation in hemiparetic stroke, we compared EMG activity in paretic and contralateral elbow and shoulder muscles of 10 hemiparetic subjects during 1.5-s voluntary isometric contractions, against five to eight different loads. Isometric forces were generated in eight directions, referenced to a plane orthogonal to the long axis of the forearm, and were recorded by a three degrees of freedom load cell, mounted at the wrist. Surface and intramuscular EMGs of six elbow and six shoulder muscles were recorded from both impaired and contralateral upper extremities of each subject. The spatial characteristics of EMG activation of individual muscles were summarized using two measures. The first, called the 'net resultant EMG vector' is a new measure which calculated the vector sum of EMG magnitudes for each of the eight directions, and the second, index of EMG focus, is a measure of the range of EMG activation recorded for each load level. Use of these measures permitted us to describe spatial EMG characteristics quantitatively, which has not been done previously. We observed consistent and statistically significant shifts in the resultant EMG vector directions in the impaired limb, especially in shoulder and other proximal muscles. Significant increases in the angular range of EMG activity were also identified and were most evident at the elbow. Correlation analysis techniques were used to assess the degree of coactivation of different muscle pairs. There were consistent EMG coactivation patterns observed across all subjects (both normal and hemiparetic). However, in spasticparetic limbs, additional novel coactivational relationships were also recorded, especially between elbow flexors/shoulder abductors and elbow extensors/shoulder adductors. These novel coactivation patterns represent a reduction in the number of possible muscle combinations, or in the number of possible 'synergies' in the paretic limb of the stroke subject. This reduction in number of 'synergies' could result from a loss of descending command options; from an increased reliance on residual, descending brainstem pathways (such as the reticulospinal and vestibulospinal projections); from changes in spinal interneuronal excitability; or from a combination of several of these factors. The relative merits of these hypotheses are addressed.

-Ivaldi. Persistence of motor adaptation during constrained, multi-joint, arm movements. J Neurophysiol 84: [853][854][855][856][857][858][859][860][861][862] 2000. We studied the stability of changes in motor performance associated with adaptation to a novel dynamic environment during goal-directed movements of the dominant arm. Eleven normal, human subjects made targeted reaching movements in the horizontal plane while holding the handle of a two-joint robotic manipulator. This robot was programmed to generate a novel viscous force field that perturbed the limb perpendicular to the desired direction of movement. Following adaptation to this force field, we sought to determine the relative role of kinematic errors and dynamic criteria in promoting recovery from the adapted state. In particular, we compared kinematic and dynamic measures of performance when kinematic errors were allowed to occur after removal of the viscous fields, or prevented by imposing a simulated, mechanical "channel" on movements. Hand forces recorded at the handle revealed that when kinematic errors were prevented from occurring by the application of the channel, recovery from adaptation to the novel field was much slower compared with when kinematic aftereffects were allowed to take place. In particular, when kinematic errors were prevented, subjects persisted in generating large forces that were unnecessary to generate an accurate reach. The magnitude of these forces decreased slowly over time, at a much slower rate than when subjects were allowed to make kinematic errors. This finding provides strong experimental evidence that both kinematic and dynamic criteria influence motor adaptation, and that kinematic-dependent factors play a dominant role in the rapid loss of adaptation after restoring the original dynamics.

Previous studies in neurologically intact subjects have shown that motor coordination can be described by task-dependent combinations of a few muscle synergies, defined here as a fixed pattern of activation across a set of muscles. Arm function in severely impaired stroke survivors is characterized by stereotypical postural and movement patterns involving the shoulder and elbow. Accordingly, we hypothesized that muscle synergy composition is altered in severely impaired stroke survivors. Using an isometric force matching protocol, we examined the spatial activation patterns of elbow and shoulder muscles in the affected arm of 10 stroke survivors (Fugl-Meyer <25/66) and in both arms of six age-matched controls. Underlying muscle synergies were identified using non-negative matrix factorization. In both groups, muscle activation patterns could be reconstructed by combinations of a few muscle synergies (typically 4). We did not find abnormal coupling of shoulder and elbow muscles within individual muscle synergies. In stroke survivors, as in controls, two of the synergies were comprised of isolated activation of the elbow flexors and extensors. However, muscle synergies involving proximal muscles exhibited consistent alterations following stroke. Unlike controls, the anterior deltoid was coactivated with medial and posterior deltoids within the shoulder abductor/extensor synergy and the shoulder adductor/flexor synergy in stroke was dominated by activation of pectoralis major, with limited anterior deltoid activation. Recruitment of the altered shoulder muscle synergies was strongly associated with abnormal task performance. Overall, our results suggest that an impaired control of the individual deltoid heads may contribute to poststroke deficits in arm function.