Muscle and reflex changes with varying joint angle in hemiparetic stroke

Abstract

Background: Despite intensive investigation, the origins of the neuromuscular abnormalities associated with spasticity are not well understood. In particular, the mechanical properties induced by stretch reflex activity have been especially difficult to study because of a lack of accurate tools separating reflex torque from torque generated by musculo-tendinous structures. The present study addresses this deficit by characterizing the contribution of neural and muscular components to the abnormally high stiffness of the spastic joint.

Methods: Using system identification techniques, we characterized the neuromuscular abnormalities associated with spasticity of ankle muscles in chronic hemiparetic stroke survivors. In particular, we systematically tracked changes in muscle mechanical properties and in stretch reflex activity during changes in ankle joint angle. Modulation of mechanical properties was assessed by applying perturbations at different initial angles, over the entire range of motion (ROM). Experiments were performed on both paretic and non-paretic sides of stroke survivors, and in healthy controls.

Results: Both reflex and intrinsic muscle stiffnesses were significantly greater in the spastic/paretic ankle than on the non-paretic side, and these changes were strongly position dependent. The major reflex contributions were observed over the central portion of the angular range, while the intrinsic contributions were most pronounced with the ankle in the dorsiflexed position.

Conclusion: In spastic ankle muscles, the abnormalities in intrinsic and reflex components of joint torque varied systematically with changing position over the full angular range of motion, indicating that clinical perceptions of increased tone may have quite different origins depending upon the angle where the tests are initiated.Furthermore, reflex stiffness was considerably larger in the non-paretic limb of stroke patients than in healthy control subjects, suggesting that the non-paretic limb may not be a suitable control for studying neuromuscular properties of the ankle joint. Our findings will help elucidate the origins of the neuromuscular abnormalities associated with stroke-induced spasticity.

Figure 1

The apparatus including the joint stretching motor device, the height adjustable chair, and force and position sensors.

Figure 2

The parallel cascade structure used to identify intrinsic and reflex stiffness. Intrinsic dynamic stiffness is represented in the upper pathway by the intrinsic stiffness impulse response function. Reflex dynamic stiffness is represented by the lower pathway as a differentiator, followed by a static nonlinear element and then a linear impulse response function. The nonlinear element is a half wave rectifier which shows the direction of stretch.

Figure 3

A segment from a typical sequence trial for a spastic under relaxed conditions. A Position, B Half-wave rectified gastrocnemius electromyogram (GS), C Predicted intrinsic torque, D Predicted reflex torque and E Predicted overall torque (thick curve) superimposed on the actual torque (thin curve). Displacements in the PF direction were taken as negative and those in the DF direction as positive. Torque was assigned a polarity consistent with the direction of the movement that it would generate (e.g. PF torque was taken as negative).

Figure 4

Typical intrinsic and reflex dynamics and their predicted torques estimated for the Paretic (left column) and Non-paretic (right column). A, B Intrinsic compliances; C, D Predicted intrinsic torques; E, F Reflex stifnness; and G, H Predicted reflex torques. The dashed curves are the nonparametric IRF, the solid curve are the parametric fits.

Figure 5

Paretic stiffness parameters plotted against non-paretic values for all stroke subjects. A Reflex stiffness gain (G_R), B Intrinsic stiffness elasticity or gain (K), and C Intrinsic stiffness viscosity (B).

Figure 6

Position dependence of Reflex stiffness gain (G_R) for paretic, non-paretic and normal groups as functions of position (Group averages). Error bars indicate ± 1 standard error. NP: Neutral Position (90°).

Figure 7

Position dependence of intrinsic stiffness for paretic, non-paretic and normal groups as functions of position (Group averages). A Intrinsic stiffness gain (K); asterisks represent points where differences between paretic group and both non-paretic and normal control groups are statistically significant. B Intrinsic stiffness viscous parameter (B); asterisks represent points where differences between paretic group and normal control group was significant. Error bars indicate ± 1 standard error. NP: Neutral Position (90°).

Figure 8

Percentage change of stroke effects as functions of position (Group averages). A Reflex stiffness gain (G_R), B Intrinsic stiffness gain (K), C Intrinsic viscous parameter (B). Error bars indicate ± 1 standard error. NP: Neutral Position (90°). The dotted lines reflect the mean percentage change over the range of motion.