After a stroke, approximately 50-75% of individuals experience significant upper extremity deficits that severely limit function. Primary impairments include weakness, spasticity, and abnormal synergies. The flexion synergy, characterized by involuntary elbow, wrist, and finger flexion when an individual attempts to lift the arm, leads to disuse of the affected arm and a flexed elbow posture, both of which may contribute to secondary changes in the musculoskeletal system. Previous studies investigating such secondary changes have reported shorter muscle fascicles and increased joint stiffness at the paretic ankle. However, quantitative data describing post-stroke adaptation in the upper extremity are lacking.

To address the current gap in knowledge, experiments were conducted to test if the paretic elbow presents with similar adaptations in fascicle length and joint stiffness as previously demonstrated at the paretic ankle. Toward this end, the first known implementation of extended field-of-view ultrasound for the measurement of both biceps (long head) and triceps (lateral head) brachii fascicle lengths was completed, and its reliability established. Fascicle lengths of these same two muscles were then measured in three elbow positions and under active and passive conditions in both limbs of 11 individuals with chronic stroke. Changes in passive elbow stiffness were also quantified in the same stroke participants. Finally, data-driven biomechanical simulations were designed to investigate how adaptations in serial sarcomere number influenced the passive joint stiffness predicted from the observed adaptations in fascicle lengths.

In these individuals with chronic stroke, fascicle lengths of both the biceps and triceps were shorter in the paretic limb;​ paretic elbow joint stiffness was increased. Results are consistent with the hypothesis that the chronically flexed posture and disuse of the affected extremity leads to secondary changes in the musculoskeletal system at the paretic elbow. Only biomechanical simulations that assumed the shorter muscle fascicles resulted from a loss of serial sarcomeres replicated the experimentally observed increases in joint stiffness. The long-term effects of current rehabilitation interventions on meaningful arm function in chronic stroke are limited. A better understanding of these secondary impairments is essential to design effective, targeted interventions to treat and possibly prevent these impairments after stroke.