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.

Torque-angle relations at the elbow and ankle joints of relaxed normal controls and patients with hemiparetic stroke were compared. Low velocity flexion/ hold/extension angular perturbations were applied to the joint under examination. The resulting torque-angle profiles described a hysteresis loop with similar slopes during the extension and flexion stages but separated by a vertical torque offset. Torque-angle responses obtained in the absence of significant muscle activation, as recorded by surface electromyographic activity, were designated as passive.Elbow passive stiffness estimates were calculated from the slope of the torqueangle response during the flexion stage of the perturbation. The elbow torque-angle plots exhibited linear passive stiffness with magnitude significantly lower than the passive stiffness of the ankle in both normal subjects and spastic patients. Changing ramp velocity had no significant effect on the passive torque-angle hysteresis loop at the elbow.A comparison of the torque-angle relations between hemiparetic spastic and normal control arms showed no significant differences in passive stiffness. Furthermore, no significant differences were found between paretic and contralateral upper limbs of a given hemiparetic subject. By contrast, significant differences in the torque-angle hysteresis loop were present between the paretic and contralateral ankles in all hemiparetic patients tested. These differences were more significant during dorsiflexion, and therefore seem to be related to preferential changes in mechanical properties of plantar flexor muscles.It is hypothesised that the differences in the torque-angle hysteresis loop between elbow and ankle joints are related primarily to the larger amount of connective tissue in the calf muscles, as well as to a larger total physiological cross sectional area of calf muscles compared with elbow muscles.It is fiurther hypothesised that the preferential increases in passive stiffness at the ankle in spastic legs result from immobilisation induced changes in muscle connective tissue, which are most prominent in muscles with predominantly slow-twitch fibres (such as soleus).Connective tissue surrounding such slow twitch muscle fibres have been shown to be more sensitive to immobilisation than those in fast twitch muscle. The functional, pathophysiological, and clinical implications of our findings are reviewed.(J Neurol Neurosurg Psychiatry 1995;59:271-279) Keywords: Stroke; passive stiffness; spasticity Increases in stiffness of the spastic limb are generally attributed to spasticity, which is, in turn, related to abnormal stretch reflex behaviour.' The increased resistance perceived by the clinician could, however, also be produced by changes in the underlying mechanical properties of muscle and tendon.23 The total mechanical resistance to an externally imposed change in joint angle is the result of the combined contributions of passive tissues and active contractile properties of the muscle-tendon complex, so that the presence of in...

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