Purpose: Loss of selective muscle activation after stroke contributes to impaired arm function, is difficult to quantify and is not systematically assessed yet. The aim of this study was to describe and validate a technique for quantification of selective muscle activation of wrist flexor and extensor muscles in a cohort of post-stroke patients. Patterns of selective muscle activation were compared to healthy volunteers and test-retest reliability was assessed. Materials and methods: Activation Ratios describe selective activation of a muscle during its expected optimal activation as agonist and antagonist. Activation Ratios were calculated from electromyography signals during an isometric maximal torque task in 31 post-stroke patients and 14 healthy volunteers. Participants with insufficient voluntary muscle activation (maximal electromyography signal <3SD higher than baseline) were excluded. Results: Activation Ratios at the wrist were reliably quantified (Intraclass correlation coefficients 0.77–0.78). Activation Ratios were significantly lower in post-stroke patients compared to healthy participants (p < 0.05). Conclusion: Activation Ratios allow for muscle-specific quantification of selective muscle activation at the wrist in post-stroke patients. Loss of selective muscle activation may be a relevant determinant in assigning and evaluating therapy to improve functional outcome.Implications for Rehabilitation Loss of selective muscle activation after stroke contributes to impaired arm function, is difficult to quantify and is not systematically assessed yet. The ability for selective muscle activation is a relevant determinant in assigning and evaluating therapy to improve functional outcome, e.g., botulinum toxin. Activation Ratios allow for reliable and muscle-specific quantification of selective muscle activation in post-stroke patients.

The dynamic behavior of the wrist joint is governed by nonlinear properties, yet applied mathematical models, used to describe the measured input-output (perturbation-response) relationship, are commonly linear. Consequently, the linearly estimated model parameters will depend on properties of the applied perturbation properties (such perturbation amplitude and velocity). We aimed to systematically address the effects of perturbation velocity on linearly estimated neuromechanical parameters. Using a single axis manipulator ramp and hold perturbations were applied to the wrist joint. Effects of perturbation velocity (0.5, 1 and 3 rad/s) were investigated at multiple background torque levels (0, 0.5 and 1 N·m). With increasing perturbation velocity, estimated joint stiffness remained constant, while damping and reflex gain decreased. This variation in model parameters is dependent on background torque levels, i.e. muscle contraction. These observations support the future development of nonlinear models that are capable of describing wrist joint behavior over a larger range of loading conditions, exceeding the restricted range of operation that is required for linearization.

Background. The mechanism and time course of increased wrist joint stiffness poststroke and clinically observed wrist flexion deformity is still not well understood. The components contributing to increased joint stiffness are of neural reflexive and peripheral tissue origin and quantified by reflexive torque and muscle slack length and stiffness coefficient parameters. Objective. To investigate the time course of the components contributing to wrist joint stiffness during the first 26 weeks poststroke in a group of patients, stratified by prognosis and functional recovery of the upper extremity. Methods. A total of 36 stroke patients were measured on 8 occasions within the first 26 weeks poststroke using ramp-and-hold rotations applied to the wrist joint by a robot manipulator. Neural reflexive and peripheral tissue components were estimated using an electromyography-driven antagonistic wrist model. Outcome was compared between groups cross-sectionally at 26 weeks poststroke and development over time was analyzed longitudinally. Results. At 26 weeks poststroke, patients with poor recovery (Action Research Arm Test [ARAT] ≤9 points) showed a higher predicted reflexive torque of the flexors (P <.001) and reduced predicted slack length (P <.001) indicating shortened muscles contributing to higher peripheral tissue stiffness (P <.001), compared with patients with good recovery (ARAT ≥10 points). Significant differences in peripheral tissue stiffness between groups could be identified around weeks 4 and 5; for neural reflexive stiffness, this was the case around week 12. Conclusions. We found onset of peripheral tissue stiffness to precede neural reflexive stiffness. Temporal identification of components contributing to joint stiffness after stroke may prompt longitudinal interventional studies to further evaluate and eventually prevent these phenomena.

Background and Objective. Favorable prognosis of the upper limb depends on preservation or return of voluntary finger extension (FE) early after stroke. The present study aimed to determine the effects of modified constraint-induced movement therapy (mCIMT) and electromyography-triggered neuromuscular stimulation (EMG-NMS) on upper limb capacity early poststroke. Methods. A total of 159 ischemic stroke patients were included: 58 patients with a favorable prognosis (>10° of FE) were randomly allocated to 3 weeks of mCIMT or usual care only; 101 patients with an unfavorable prognosis were allocated to 3-week EMG-NMS or usual care only. Both interventions started within 14 days poststroke, lasted up until 5 weeks, focused at preservation or return of FE. Results. Upper limb capacity was measured with the Action Research Arm Test (ARAT), assessed weekly within the first 5 weeks poststroke and at postassessments at 8, 12, and 26 weeks. Clinically relevant differences in ARAT in favor of mCIMT were found after 5, 8, and 12 weeks poststroke (respectively, 6, 7, and 7 points; P