Previous studies have shown that deficits in agonist-antagonist muscle activation in the single-joint elbow system in patients with spastic hemiparesis are directly related to limitations in the range of regulation of the thresholds of muscle activation. We extended these findings to the double-joint, shoulder-elbow system in these patients. Ten non-disabled individuals and 11 stroke survivors with spasticity in upper limb muscles participated. Stroke survivors had sustained a single unilateral stroke 6-36 months previously, had full pain-free passive range of motion of the affected shoulder and elbow and had some voluntary control of the arm. EMG activity from four elbow and two shoulder muscles was recorded during quasi-static (<5 degrees /s) stretching of elbow flexors/extensors and during slow voluntary elbow flexion/extension movement through full range. Stretches and active movements were initiated from full elbow flexion or extension with the shoulder in three different initial positions (60 degrees , 90 degrees , 145 degrees horizontal abduction). SRTs were defined as the elbow angle at which EMG signals began to exceed 2SD of background noise. SRT angles obtained by passive muscle stretch were compared with the angles at which the respective muscles became activated during voluntary elbow movements. SRTs in elbow flexors were correlated with clinical spasticity scores. SRTs of elbow flexors and extensors were within the biomechanical range of the joint and varied with changes in the shoulder angle in all subjects with hemiparesis but could not be reached in this range in all healthy subjects when muscles were initially relaxed. In patients, limitations in the regulation of SRTs resulted in a subdivision of all-possible shoulder-elbow arm configurations into two areas, one in which spasticity was present ("spatial spasticity zone") and another in which it was absent. Spatial spasticity zones were different for different muscles in different patients but, taken together, for all elbow muscles, the zones occupied a large part of elbow-shoulder joint space in each patient. The shape of the boundary between the spasticity and no-spasticity zones depended on the state of reflex inter-joint interaction. SRTs in single- and double-joint flexor muscles correlated with the positions at which muscles were activated during voluntary movements, for all shoulder angles, and this effect was greater in elbow flexor muscles (brachioradialis, biceps brachii). Flexor SRTs correlated with clinical spasticity in elbow flexors only when elbow muscles were at mid-length (90 degrees ). These findings support the notion that motor impairments after CNS damage are related to deficits in the specification and regulation of SRTs, resulting in the occurrence of spasticity zones in the space of elbow-shoulder configurations. It is suggested that the presence of spatial spasticity zones might be a major cause of motor impairments in general and deficits in inter-joint coordination in particular in patients with spasticity.