In layperson terms does anything here get survivors recovered?
Spatial mapping of posture-dependent resistance to passive displacement of the hypertonic arm post-stroke
Journal of NeuroEngineering and Rehabilitation volume 20, Article number: 163 (2023)
Abstract
Background
Muscles in the post-stroke arm commonly demonstrate abnormal reflexes that result in increased position- and velocity-dependent resistance to movement. We sought to develop a reliable way to quantify mechanical consequences of abnormal neuromuscular mechanisms throughout the reachable workspace in the hemiparetic arm post-stroke.
Methods
Survivors of hemiparetic stroke (HS) and neurologically intact (NI) control subjects were instructed to relax as a robotic device repositioned the hand of their hemiparetic arm between several testing locations that sampled the arm's passive range of motion. During transitions, the robot induced motions at either the shoulder or elbow joint at three speeds: very slow (6°/s), medium (30°/s), and fast (90°/s). The robot held the hand at the testing location for at least 20 s after each transition. We recorded and analyzed hand force and electromyographic activations from selected muscles spanning the shoulder and elbow joints during and after transitions.
Results
Hand forces and electromyographic activations were invariantly small at all speeds and all sample times in NI control subjects but varied systematically by transport speed during and shortly after movement in the HS subjects. Velocity-dependent resistance to stretch diminished within 2 s after movement ceased in the hemiparetic arms. Hand forces and EMGs changed very little from 2 s after the movement ended onward, exhibiting dependence on limb posture but no systematic dependence on movement speed or direction. Although each HS subject displayed a unique field of hand forces and EMG responses across the workspace after movement ceased, the magnitude of steady-state hand forces was generally greater near the outer boundaries of the workspace than in the center of the workspace for the HS group but not the NI group.
Conclusions
In the HS group, electromyographic activations exhibited abnormalities consistent with stroke-related decreases in the stretch reflex thresholds. These observations were consistent across repeated testing days. We expect that the approach described here will enable future studies to elucidate stroke's impact on the interaction between the neural mechanisms mediating control of upper extremity posture and movement during goal-directed actions such as reaching and pointing with the arm and hand.
Introduction
Muscles in the post-stroke arm commonly demonstrate abnormal reflexes that result in increased position- and velocity-dependent resistance to movement (i.e. spastic hypertonus: [21, 25]. Spastic hypertonia is understood to reflect systematic reductions in stretch reflex thresholds [16, 24], decreased range of regulation of these stretch reflex thresholds [23, 47], as well as altered non-reflex phenomena such as abnormalities in the intrinsic mechanical properties of spastic muscles and altered viscoelastic properties of passive tissues [28, 43, 49]. Importantly, systematic reduction in stretch reflex threshold could lead to significant increase in stretch reflex excitability [17] and agonist/antagonist coactivation in some regions of the workspace [22, 30], which could lead to complex, posture-dependent and potentially time-varying joint impedances in the hemiparetic arm. Because the feedforward control of goal-directed movements relies on accurate predictions of limb impedance [38], spatial and temporal complexity of joint impedance may be a significant contributor to impairment of movement coordination post-stroke [20, 40, 48]. Although a velocity-dependent increase in muscle tone (spasticity is frequently assessed clinically and has been quantified in single joints such as the elbow and wrist [15, 23, 26, 44], quantitative assessments of multi-joint control deficits have been rare (see [30, 36]) and sometimes rely on techniques such as kinematic and/or inverse dynamics analyses, which can be insensitive to the presence and effects of abnormal muscle coactivations (e.g., [18, 33]).
The goal of this study was to develop a reliable approach for measuring the mechanical consequences of abnormal neuromuscular mechanisms as a function of hand location in the reachable workspace in the hemiparetic arm post-stroke. We are motivated in this work by a growing body of experimental evidence supporting the idea that the neural mechanisms contributing to the control of limb posture and movement can be differentially compromised by stroke [19, 27, 40], see also [8, 37, 48] and by other neuromotor disorders (cf. [10, 11]), and by the belief that greater understanding of the mechanisms contributing to sensorimotor deficits will eventually lead to improved efficacy of therapeutic interventions [13]. Our work builds on prior studies that examined transient mechanical and electromyographic responses to passive displacements of the wrist or elbow to quantitatively assess post-stroke spasticity (cf. [15, 23, 26, 44, 47]) and spastic dystonia [46]. In one example, Schmit and colleagues used a motorized device to passively flex and extend the elbow of hemiparetic stroke survivors over a range of speeds ranging from slow (6º/s) to fast (90º/s) [44]. Their goal was to assess the reliability of three different biomechanical correlates of spasticity, which they isolated from other aspects of spastic hypertonia associated with dystonia, contracture, and increased joint stiffness. They did so by subtracting the torque response to the slowest displacement from responses to faster displacements, leaving only reflex torque. This approach is effective because the stiffness of the passive tissues about the elbow joint are largely velocity insensitive [9]. Of the three biomechanical measures considered—peak torque, peak joint stiffness, and onset angle of reflex torque responses—peak torque values measured during displacements at 90°/s were most reliable on repeated measures in a single testing session (> 80% reliability), and most highly correlated with clinical assessments of spasticity (Ashworth Scale). In another example, Mirbhageri and colleagues [29] used system identification techniques to quantify the contributions of reflex and intrinsic (i.e., non-reflex) stiffness to total elbow stiffness at several different elbow angles in the paretic and nonparetic arm of chronic hemiparetic stroke survivors. Each position was examined under passive conditions in the range of full elbow flexion to full elbow extension. They reported that intrinsic and reflex stiffness both contributed strongly to net joint torque, that the effects were significantly larger in the paretic than in the non-paretic elbow muscles, and that these differences increased with the increasing joint angle indicating position dependence. Although these prior studies suggest that manifestations of spasticity and hypertonia may vary in complex ways across the reachable workspace after stroke, a more comprehensive approach to quantifying mechanical expressions of spasticity and hypertonia across the workspace has yet to be described.
We designed a set of experiments using a two-joint, planar robot to measure the dynamic and quasistatic mechanical and electromyographic responses to controlled displacements of the upper extremity at several locations in the arm’s workspace. Subjects were instructed to relax as the robot moved their hand sequentially between target locations spanning the reachable workspace at speeds ranging from very slow to fast. Trajectories were selected such that movements were largely limited to either the shoulder or elbow joint, but not both. The robot stabilized the hand at the target for at least 20 s following the end of each movement. We analyzed the time series of horizontal planar hand forces and electromyographic (EMG) activations for selected arm muscles to determine the duration of phasic, velocity-dependent resistance to stretch, to characterize the spatial topography of tonic, position-dependent hand forces throughout the workspace, and to characterize the muscle activations that give rise to these postural bias forces. The resulting data demonstrate that the robotic assessment of posture-dependent bias forces was repeatable across days, that the phasic component of these stroke-related forces lasted no more than 2 s after the end of limb re-positioning, and that these bias forces were partly neuromuscular in origin (not merely due to passive tissue resistance to stretch) such that elevated “resting” EMG activations exhibited posture-dependence in some muscles, but posture-invariance in others. We expect that quantitative evaluation of posture-dependent bias forces may facilitate future assessments of stroke's impact on the interaction between the control of upper extremity posture and movement.
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