A parallel-cascade system identification method was used to identify intrinsic and reflex contributions to dynamic ankle stiffness over a wide range of tonic voluntary contraction levels and ankle positions in healthy human subjects. Intrinsic stiffness dynamics were described well by a linear pathway having elastic, viscous, and inertial properties. A velocity-sensitive pathway comprising a delay, a static non-linearity, resembling a half-wave rectifier, followed by a low-pass filter, described reflex stiffness dynamics. The absolute magnitude of intrinsic and reflex stiffness parameters varied from subject to subject but the relative changes with contraction level and position were consistent. Intrinsic stiffness increased monotonically with contraction level while reflex stiffness was maximal at low contraction levels and then decreased. Intrinsic and reflex stiffness both increased as the ankle was dorsiflexed. As a result, reflex mechanics made their largest relative contributions near the neutral position at low levels of activity. The size of the maximum reflex contribution varied widely among subjects, in some it was so small (ca 1%) that it would be unlikely to have any functional importance; however, in other subjects, reflex contributions were large enough (as high as 55% in one case) to play a significant role in the control of posture and movement. This variability may have arisen because stretch reflexes were not useful for the torque-matching task in these experiments. It will be of interest to examine other tasks where stretch reflexes would have a direct impact on performance.
Background: Spasticity is a common impairment that follows stroke, and it results typically in functional loss. For this reason, accurate quantification of spasticity has both diagnostic and therapeutic significance. The most widely used clinical assessment of spasticity is the modified Ashworth scale (MAS), an ordinal scale, but its validity, reliability and sensitivity have often been challenged. The present study addresses this deficit by examining whether quantitative measures of neural and muscular components of spasticity are valid, and whether they are strongly correlated with the MAS.
Mirbagheri MM, Settle K, Harvey R, Rymer WZ. Neuromuscular abnormalities associated with spasticity of upper extremity muscles in hemiparetic stroke. J Neurophysiol 98: 629 -637, 2007. First published June 20, 2007 doi:10.1152/jn.00049.2007. Our objective was to assess the mechanical changes associated with spasticity in elbow muscles of chronic hemiparetic stroke survivors and to compare these changes with those recorded in the ankle muscles of a similar cohort. We first characterized elbow dynamic stiffness by applying pseudorandom binary positional perturbations to the joints at different initial angles, over the entire range of motion, with subjects relaxed. We separated this stiffness into intrinsic and reflex components using a novel parallel cascade system identification technique. In addition, for controls, we studied the nonparetic limbs of stroke survivors and limbs of age-matched healthy subjects as primary and secondary controls. We found that both reflex and intrinsic stiffnesses were significantly larger in the stroke than in the nonparetic elbow muscles, and the differences increased as the elbow was extended. Reflex stiffness increased monotonically with the elbow angle in both paretic and nonparetic sides. In contrast, the modulation of intrinsic stiffness with elbow position was different in nonparetic limbs; intrinsic stiffness decreased sharply from full-to mid-flexion in both sides, then it increased continuously with the elbow extension in the paretic side. It remained invariant in the nonparetic side. Surprisingly, reflex stiffness was larger in the nonparetic than in the normal control arm, yet intrinsic stiffness was smaller in the nonparetic arm. Finally, we compare the angular dependence of paretic elbow and ankle muscles and show that the modulation of reflex stiffness with position was strikingly different.
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