M.M. Mirbagheri

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.

The effect of locomotor training combined with functional electrical stimulation in chronic spinal cord injured subjects: walking and reflex studies

With the new developments in traumatology medicine, the majority of spinal cord injuries sustained are clinically incomplete and the proportion is likely to continue to rise. Thus, it is necessary to continue to develop new treatment and rehabilitation strategies and understand the factors that can enhance recovery of walking following spinal cord injury (SCI). One new development is the use of functional electrical stimulation (FES) device to assist locomotion. The objective of this review is to present findings from some recent studies on the effect of long-term locomotor training with FES in subjects with SCI. Promising results are shown in all outcome measures of walking, such as functional mobility, speed, spatio-temporal parameters, and the physiological cost of walking. Furthermore, the change in the walking behavior could be associated with plasticity in the CNS organization, as seen by the modification of the stretch reflex and changes in the corticospinal projection to muscles of the lower leg. In conclusion, recovery of walking is an increasing possibility for a large number of people with SCI. New modalities of treatment have become available for this population but most still need to be evaluated for their efficacy. This review has focused on FES assisted walking as a therapeutic modality in subjects with chronic SCI, but it is envisaged that the care and recovery of SCI in the early phase of recovery could also be improved.

The effects of long-term FES-assisted walking on intrinsic and reflex dynamic stiffness in spastic spinal-cord-injured subjects

The effects of long-term functional electrical stimulation (FES)-assisted walking on ankle dynamic stiffness were examined in spinal cord-injured (SCI) subjects with incomplete motor function loss. A parallel-cascade system identification method was used to identify intrinsic and reflex contributions to dynamic ankle stiffness at different ankle positions while subjects remained relaxed. Intrinsic stiffness dynamics were well modeled by a linear second-order model relating intrinsic torque to joint position. Reflex stiffness dynamics were accurately described by a linear third-order model relating halfwave rectified velocity to reflex torque. We examined four SCI subjects before and after long-term FES-assisted walking (>16 mo). Another SCI subject, who used FES for only five months was examined 12 mo latter to serve as a non-FES, SCI control. Reflex stiffness decreased in FES subjects by an average of 53% following FES-assisted walking, intrinsic stiffness also dropped by 45%. In contrast, both reflex and intrinsic stiffness increased in the non-FES, SCI control. These findings suggest that FES-assisted walking may have therapeutic effects, helping to reduce abnormal joint stiffness.

Quantitative, objective measurement of ankle dynamic stiffness: intrasubject reliability and intersubject variability

The objective of this study was to assess intrasubject reliability and intersubject variability of a parallel-cascade system identification method for quantitative, objective measurement of ankle dynamic stiffness, and separation of intrinsic and reflex components. The test-retest experiments were carried out at different operating points. Very good intrasubject reliability (r>0.8) was found, but a high intersubject variability. These findings suggest that this method can be applied for precise diagnosis and tracking the development of changes in joint stiffness.

Stretch reflex behavior of spastic ankle under passive and active conditions

A parallel-cascade system identification method was used to measure dynamic ankle stiffness in normal and spastic spinal cord injured (SCI) subjects. Modulation of reflex stiffness gain of the ankle extensor muscles (GS) was studied by applying perturbations to the ankle at different positions under passive (relaxed) and active (10% extensor maximum voluntary contraction) conditions. In SCI subjects: (1) modulation of reflex gain with ankle position was abnormal in both passive and active conditions; (2) reflex stiffness gain was always significantly higher than in normal subjects; (3) reflex gain was similar under active and passive conditions except at plantarflexion where reflex gain was slightly higher under active conditions; (4) the reflex latency was shorter. The findings demonstrate that the reflex mechanics are abnormal in SCI spastic patients. The abnormalities are likely due not only to a decrease in presynaptic inhibitory mechanisms but also to a disruption in the motoneuron recruitment order.

Abnormal stretch reflex mechanics in spastic spinal cord injured subjects

A parallel-cascade system identification method was used to identify the modulation of reflex contributions to dynamic ankle stiffness with position stimuli amplitude and frequency in both normal and spastic spinal cord injured (SCI) subjects. As amplitude increased, reflex stiffness first increased and then decreased in both normal and SCI subjects. Reflex gain was significantly higher in patients than in normal subjects at all conditions. The reflex threshold, the minimum amplitude required to elicit a stretch reflex response, was smaller in SCI than in normal subjects. As frequency increased, reflex stiffness decreased in both normal and SCI subjects; however, it was significantly higher in SCI than in normal subjects at all frequencies. These results demonstrate that the reflex mechanics are abnormal in SCI spastic patients due to both an increase in reflex gain and a decrease in reflex threshold.

Parametric modeling of the reflex contribution to dynamic ankle stiffness in normal and spinal cord injured spastic subjects

Dynamic ankle stiffness was estimated at different levels of tonic voluntary contraction in normal and spastic, spinal cord injured (SCI) subjects. A new parallel-cascade identification method was used to identify the reflex contribution to overall stiffness in terms of a static nonlinearity in series with a linear system. Linear dynamics were estimated nonparametrically as impulse response functions (IRFs). Parametric models were fit to these IRFs using non-linear, least-squares methods. A simple, second-order, low-pass model was adequate for some cases, but did not work well with data from normal subjects at high levels of activation or with from spastic subjects. Much better fits were obtained using a third order model.

Abnormal passive and intrinsic stiffness in the spastic ankle

A parallel-cascade system identification method was used to measure dynamic ankle stiffness in normal and spastic spinal cord injured (SCI) subjects. Modulation of passive and intrinsic stiffness gain of ankle extensor muscles (GS) was studied by applying perturbations to the ankle at different positions under passive (relaxed) and active (10% extensor maximum voluntary contraction) conditions. Both passive and intrinsic stiffness were described well by a linear second-order model having elastic, viscous and inertia parameters. For passive stiffness the elastic and viscous parameters increased with ankle dorsiflexion in both groups; in addition, both parameters were larger in SCI than in control subjects as ankle dorsiflexed. For intrinsic stiffness (1) the elastic parameter increased with ankle position until neutral position (90/spl deg/) in both groups, it then saturated in control subjects, but decreased as ankle moved to dorsiflexion in SCI subjects; (2) it was always smaller in SCI subjects; (3) the intrinsic viscous parameter increased at the beginning of plantarflexion then decreased slightly until maximum dorsiflexion in both groups. However, it was lower than in control subjects as the ankle moved from neutral position to maximum dorsiflexion. The results indicate that abnormal non-reflex mechanics are due to enhanced passive stiffness and reduced intrinsic stiffness.

Modulation of intrinsic and reflex contributions to dynamic ankle stiffness with the level of voluntary contraction

A parallel-cascade system identification method was used to identify intrinsic and reflex contributions to dynamic ankle stiffness at different levels of tonic voluntary contractions. Intrinsic stiffness dynamics were well modeled by a linear second-order system relating intrinsic torque to joint position. Reflex stiffness dynamics were accurately described by a linear, third-order system between half-wave rectified velocity and reflex torque. Intrinsic stiffness gain increased with the level of tonic contraction in the ankle extensors (gastrocnemius-soleus). Reflex gain decreased with the level of contraction while reflex-EMG gain increased. This suggests reflex contributions are more significant at low levels of activity.

Identification and simulation as tools for measurement of neuromuscular properties

Quantitative, objective methods for the evaluation of neuromuscular properties are required for the diagnosis of neuromuscular disorders and the evaluation of the effectiveness of treatment and rehabilitation. This paper describes how nonlinear identification and simulation methods may be used to evaluate joint properties quantitatively and distinguish the relative contributions of reflex and intrinsic mechanisms. Results from studies in normal and spinal cord injured subjects are presented to demonstrate the properties of the approach, its viability as a clinical research tool, and some of the issues that arise when comparing correlating its results with clinical evaluations.