L. Parameswaran

Bio: L. Parameswaran is an academic researcher from McGill University. The author has contributed to research in topics: Stiffness & Stretch reflex. The author has an hindex of 1, co-authored 1 publications receiving 394 citations.

Identification of intrinsic and reflex contributions to human ankle stiffness dynamics

Abstract: The authors have examined dynamic stiffness at the human ankle using position perturbations which were designed to provide a wide-bandwidth input with low average velocity. A parallel-cascade, nonlinear system identification technique was used to separate overall stiffness into intrinsic and reflex components. Intrinsic stiffness was described by a linear, second-order system similar to that demonstrated previously. Reflex stiffness dynamics were more complex, comprising a delay, a unidirectional rate-sensitive element and then lowpass dynamics. Reflex mechanisms were found to be most important at frequencies of 5-10 Hz. The gain and dynamics of reflex stiffness varied strongly with the parameters of the perturbation, the gain decreasing as the mean velocity of the perturbation increased. Under some conditions, torques generated by reflex mechanisms were of the same magnitude as those from intrinsic mechanisms. It is concluded that reflex stiffness can be large enough to be important functionally, but that its effects will depend strongly upon the particular conditions.

Structural and functional changes in spastic skeletal muscle

Abstract: This review summarizes current information regarding the changes in structure or function that occur in skeletal muscle secondary to spasticity. Most published studies have reported an increase in fiber size variability in spastic muscle. There is no general agreement regarding any shift in fiber type distribution secondary to spasticity. Mechanical studies in whole limbs as well as in isolated single cells support the notion of an intrinsic change in the passive mechanical properties of muscle after spasticity in addition to the more widely reported neural changes that occur. Evidence is presented for changes within both the muscle cell and extracellular matrix that contribute to the overall changes in the tissue. Taken together, the literature supports the notion that, although spasticity is multifactorial and neural in origin, significant structural alterations in muscle also occur. An understanding of the specific changes that occur in the muscle and extracellular matrix may facilitate the development of new conservative or surgical therapies for this problem.

Intrinsic and reflex contributions to human ankle stiffness: variation with activation level and position.

Abstract: 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.

Intrinsic and reflex stiffness in normal and spastic, spinal cord injured subjects.

Abstract: Mechanical changes underlying spastic hypertonia were explored using a parallel cascade system identification technique to evaluate the relative contributions of intrinsic and reflex mechanisms to dynamic ankle stiffness in healthy subjects (controls) and spastic, spinal cord injured (SCI) patients. We examined the modulation of the gain and dynamics of these components with ankle angle for both passive and active conditions. Four main findings emerged. First, intrinsic and reflex stiffness dynamics were qualitatively similar in SCI patients and controls. Intrinsic stiffness dynamics were well modeled by a linear second-order model relating intrinsic torque to joint position, while reflex stiffness dynamics were accurately described by a linear, third-order system relating half-wave rectified velocity to reflex torque. Differences between the two groups were evident in the values of four parameters, the elastic and viscous parameters for intrinsic stiffness and the gain and first-order cut-off frequency for reflex stiffness. Second, reflex stiffness was substantially increased in SCI patients, where it generated as much as 40% of the total torque variance, compared with controls, where reflex contributions never exceeded 7%. Third, differences between SCI patients and controls depended strongly on joint position, becoming larger as the ankle was dorsiflexed. At full plantarflexion, there was no difference between SCI and control subjects; in the mid-range, reflex stiffness was abnormally high in SCI patients; at full dorsiflexion, both reflex and intrinsic stiffness were larger than normal. Fourth, differences between SCI and control subjects were smaller during the active than the passive condition, because intrinsic stiffness increased more in controls than SCI subjects; nevertheless, reflex gain remained abnormally high in SCI patients. These results elucidate the nature and origins of the mechanical abnormalities associated with hypertonia and provide a better understanding of its functional and clinical implications.