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Background: A common assumption is that changes in upper limb (UL) capacity, or what an individual is capable of doing, translates to improved UL performance in daily life, or what an individual actually does. This assumption should be explicitly tested for individuals with UL paresis poststroke., Objective: To examine changes in UL performance after an intensive, individualized, progressive, task-specific UL intervention for individuals at least 6 months poststroke., Methods: Secondary analysis on 78 individuals with UL paresis who participated in a phase II, single-blind, randomized parallel dose-response trial. Participants were enrolled in a task-specific intervention for 8 weeks. Participants were randomized into 1 of 4 treatment groups with each group completing different amounts of UL movement practice. UL performance was assessed with bilateral, wrist-worn accelerometers once a week for 24 hours throughout the duration of the study. The 6 accelerometer variables were tested for change and the influence of potential modifiers using hierarchical linear modeling., Results: No changes in UL performance were found on any of the 6 accelerometer variables used to quantify UL performance. Neither changes in UL capacity nor the overall amount of movement practice influenced changes in UL performance. Stroke chronicity, baseline UL capacity, concordance, and ADL status significantly increased the baseline starting points but did not influence the rate of change (slopes) for participants., Conclusions: Improved motor capacity resulting from an intensive outpatient UL intervention does not appear to translate to increased UL performance outside the clinic.

Background: Recent studies have shown that focal injuries can have remote effects on network function that affect behavior, but these network-wide repercussions are poorly understood., Objective: This study tested the hypothesis that lesions specifically to the outflow tract of a distributed network can result in upstream dysfunction in structurally intact portions of the network. In the somatomotor system, this upstream dysfunction hypothesis predicted that lesions of the corticospinal tract might be associated with functional disruption within the system. Motor impairment might then reflect the dual contribution of corticospinal damage and altered network functional connectivity., Methods: A total of 23 subacute stroke patients and 13 healthy controls participated in the study. Corticospinal tract damage was quantified using a template of the tract generated from diffusion tensor imaging in healthy controls. Somatomotor network functional integrity was determined by resting state functional connectivity magnetic resonance imaging., Results: The extent of corticospinal damage was negatively correlated with interhemispheric resting functional connectivity, in particular with connectivity between the left and right central sulcus. Although corticospinal damage accounted for much of the variance in motor performance, the behavioral impact of resting connectivity was greater in subjects with mild or moderate corticospinal damage and less in those with severe corticospinal damage., Conclusions: Our results demonstrated that dysfunction of cortical functional connectivity can occur after interruption of corticospinal outflow tracts and can contribute to impaired motor performance. Recognition of these secondary effects from a focal lesion is essential for understanding brain-behavior relationships after injury, and they may have important implications for neurorehabilitation.