The gap between clinical gaze and systematic assessment of movement disorders after stroke

Abstract Background Movement disorders after stroke are still captured by clinical gaze and translated to ordinal scores of low resolution. There is a clear need for objective quantification, with outcome measures related to pathophysiological background. Neural and non-neural contributors to joint behavior should be separated using different measurement conditions (tasks) and standardized input signals (force, position and velocity). Methods We reviewed recent literature for the application of biomechanical and/or elektromyographical (EMG) outcome measures under various measurement conditions in clinical research. Results Since 2005, 36 articles described the use of biomechanical and/or EMG outcome measures to quantify post-stroke movement disorder. Nineteen of the articles strived to separate neural and non-neural components. Only 6 of the articles measured biomechanical and EMG outcome measures simultaneously, while applying active and passive tasks and multiple velocities. Conclusion The distinction between neural and non-neural components to separately assess paresis, stiffness and muscle overactivity is not commonplace yet, while a large gap is to be bridged to attain reproducible and comparable results. Pathophysiologically clear concepts, substantiated with a comprehensive and concise measuring protocol will help professionals to identify and treat limiting factors in movement capabilities of post-stroke patients.</p

Selective activity of flexor and extensor wrist muscles is reduced in post-stroke patients

Introduction: Loss of selective muscle activation after stroke contributes to poor arm function but is difficult to quantify. The objective of this study was to quantify selective activity of flexor and extensor wrist muscles in post-stroke patients. Methods: 31 Patients in the chronic phase after stroke and 14 matched healthy controls exerted a flexion and extension torque onto a haptic wrist manipulator. EMG of the flexor and the extensor carpi radialis muscles was stratified for equal flexion and extension torques. The Activation Ratio per muscle was determined, i.e. ratio of the difference of EMG activity during flexion and extension over summed EMG activity. A ratio close to one indicates selective activation while a ratio close to zero indicates indifferent activation. Results: Control subjects could exert higher (p&lt;0.001) flexion and extension torques (25.42 Nm and 14.32 Nm) compared to post-stroke subjects (14.45Nm and 6.69Nm). The Activation Ratio’s for flexor and extensor muscle were significantly lower (p&lt;0.001) in post-stroke subjects (ARflex: 0.72 – 0.54, ARext:0.79 – 0.64). Discussion and conclusion: Activation Ratio’s allow for muscle specific determination of selective activity which is advantageous in case of diverging muscle features. In post-stroke patients the loss of selective activity has to be accounted for when explaining and intervening on loss of function. Clinical message: Quantification of muscle specific selective activation in post stroke hemiparesis allows for assessment of contribution of the muscle to co-contraction and functional loss and evaluation of therapeutic options

Estimation of tissue stiffness, reflex activity, optimal muscle length and slack length in stroke patients using an electromyography driven antagonistic wrist model

Background: About half of all chronic stroke patients experience loss of arm function coinciding with increased stiffness, reduced range of motion and a flexed wrist due to a change in neural and/or structural tissue properties. Quantitative assessment of these changes is of clinical importance, yet not trivial. The goal of this study was to quantify the neural and structural properties contributing to wrist joint stiffness and to compare these properties between healthy subjects and stroke patients. Methods: Stroke patients (n = 32) and healthy volunteers (n = 14) were measured using ramp-and-hold rotations applied to the wrist joint by a haptic manipulator. Neural (reflexive torque) and structural (connective tissue stiffness and slack lengths and (contractile) optimal muscle lengths) parameters were estimated using an electromyography driven antagonistic wrist model. Kruskal-Wallis analysis with multiple comparisons was used to compare results between healthy subjects, stroke patients with modified Ashworth score of zero and stroke patients with modified Ashworth score of one or more. Findings: Stroke patients with modified Ashworth score of one or more differed from healthy controls (P < 0.05) by increased tissue stiffness, increased reflexive torque, decreased optimal muscle length and decreased slack length of connective tissue of the flexor muscles. Interpretation: Non-invasive quantitative analysis, including estimation of optimal muscle lengths, enables to identify neural and non-neural changes in chronic stroke patients. Monitoring these changes in time is important to understand the recovery process and to optimize treatment

Loss of selective wrist muscle activation in post-stroke patients

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 &lt;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 &lt; 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.Biomechatronics & Human-Machine Contro

Early shortening of wrist flexor muscles coincides with poor recovery after stroke

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 &lt;.001) and reduced predicted slack length (P &lt;.001) indicating shortened muscles contributing to higher peripheral tissue stiffness (P &lt;.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.Biomechatronics & Human-Machine Contro