Interventions to Reduce Spasticity and Improve Function in People With Chronic Incomplete Spinal Cord Injury: Distinctions Revealed by Different Analytical Methods.

Background. Spinal cord injury (SCI) results in impaired function, and ankle joint spasticity is a common secondary complication. Different interventions have been trialed with variable results. Objective. We investigated the effects of pharmacological and physical (locomotor training) interventions on function in people living with incomplete motor function loss caused by SCI and used different analytical techniques to understand whether functional levels affect recovery with different interventions. Methods. Participants with an incomplete SCI were assigned to 3 groups: no intervention, Lokomat, or tizanidine. Outcome measures were the 10-m walk test, 6-minute walk test, and the Timed Up and Go. Participants were classified in 2 ways: (1) based on achieving an improvement above the minimally important difference (MID) and (2) using growth mixture modeling (GMM). Functional levels of participants who achieved the MID were compared and random coefficient regression (RCR) was used to assess recovery in GMM classes. Results. Overall, walking speed and endurance improved, with no difference between interventions. Only a small number of participants achieved the MID. Both MID and GMM-RCR analyses revealed that tizanidine improved endurance in high-functioning participants. GMM-RCR classification also showed that speed and mobility improved after locomotor training. Conclusions. Improvements in function were achieved in a limited number of people with SCI. Using the MID and GMM techniques, differences in responses to interventions between high-and low-functioning participants could be identified. These techniques may, therefore, have potential to be used for characterizing therapeutic effects resulting from different interventions

Facilitatory effects of anti-spastic medication on robotic locomotor training in people with chronic incomplete spinal cord injury

Background: The objective of this study was to investigate whether an anti-spasticity medication can facilitate the effects of robotic locomotor treadmill training (LTT) to improve gait function in people with incomplete spinal cord injury (SCI). / Methods: Individuals with chronic incomplete SCI were recruited and carried out a 4 week intervention of either locomotor treadmill training (LTT) alone (n = 26) or LTT combined with Tizanidine (TizLTT), an anti-spasticity medication (n = 22). Gait function was evaluated using clinical outcome measures of gait, speed and endurance. To better understand the underlying mechanisms of the therapeutic effects, maximal strength, active range of motion (AROM) and peak velocity (Vp) of ankle dorsi- and planter-flexor muscles were also measured. Differences were assessed using two-way mixed design analysis of variance. The number of subjects that achieved the minimal important difference (MID) for clinical scores was also measured for each group, and the results of those that did attain the MID were compared with those that did not. / Results: Both LTT and TizLTT resulted in significant improvements in walking speed and dorsiflexion maximum strength, with no significant differences between them, using group-averaging analysis. However, using the MID analysis, a higher proportion of subjects in the TizLTT group achieved the MID for walking speed (40%) compared with LTT alone (13%). Those that achieved the MID for walking speed were significantly higher functioning at baseline than those that did not in the TizLTT group, and the change in walking speed was associated with the change in dorsiflexion peak velocity (R2 = 0.40; P < 0.05). / Conclusion: Tizanidine appears to facilitate the effects of LTT on gait function in individuals with chronic SCI that are higher functioning at baseline. We speculate that this may be due to restoration of inhibitory mechanisms by Tizanidine, resulting in greater stretch in the planterflexor muscles during the LTT

Quantification of the effects of an alpha-2 adrenergic agonist on reflex properties in spinal cord injury using a system identification technique

<p>Abstract</p> <p>Background</p> <p>Despite numerous investigations, the impact of tizanidine, an anti-spastic medication, on changes in reflex and muscle mechanical properties in spasticity remains unclear. This study was designed to help us understand the mechanisms of action of tizanidine on spasticity in spinal cord injured subjects with incomplete injury, by quantifying the effects of a single dose of tizanidine on ankle muscle intrinsic and reflex components.</p> <p>Methods</p> <p>A series of perturbations was applied to the spastic ankle joint of twenty-one spinal cord injured subjects, and the resulting torques were recorded. A parallel-cascade system identification method was used to separate intrinsic and reflex torques, and to identify the contribution of these components to dynamic ankle stiffness at different ankle positions, while subjects remained relaxed.</p> <p>Results</p> <p>Following administration of a single oral dose of Tizanidine, stretch evoked joint torque at the ankle decreased significantly (p < 0.001) The peak-torque was reduced between 15% and 60% among the spinal cord injured subjects, and the average reduction was 25%. Using systems identification techniques, we found that this reduced torque could be attributed largely to a reduced reflex response, without measurable change in the muscle contribution. Reflex stiffness decreased significantly across a range of joint angles (p < 0.001) after using tizanidine. In contrast, there were no significant changes in intrinsic muscle stiffness after the administration of tizanidine.</p> <p>Conclusions</p> <p>Our findings demonstrate that tizanidine acts to reduce reflex mechanical responses substantially, without inducing comparable changes in intrinsic muscle properties in individuals with spinal cord injury. Thus, the pre-post difference in joint mechanical properties can be attributed to reflex changes alone. From a practical standpoint, use of a single "test" dose of Tizanidine may help clinicians decide whether the drug can helpful in controlling symptoms in particular subjects.</p

Upper limb impairments associated with spasticity in neurological disorders

<p>Abstract</p> <p>Background</p> <p>While upper-extremity movement in individuals with neurological disorders such as stroke and spinal cord injury (SCI) has been studied for many years, the effects of spasticity on arm movement have been poorly quantified. The present study is designed to characterize the nature of impaired arm movements associated with spasticity in these two clinical populations. By comparing impaired voluntary movements between these two groups, we will gain a greater understanding of the effects of the type of spasticity on these movements and, potentially a better understanding of the underlying impairment mechanisms.</p> <p>Methods</p> <p>We characterized the kinematics and kinetics of rapid arm movement in SCI and neurologically intact subjects and in both the paretic and non-paretic limbs in stroke subjects. The kinematics of rapid elbow extension over the entire range of motion were quantified by measuring movement trajectory and its derivatives; i.e. movement velocity and acceleration. The kinetics were quantified by measuring maximum isometric voluntary contractions of elbow flexors and extensors. The movement smoothness was estimated using two different computational techniques.</p> <p>Results</p> <p>Most kinematic and kinetic and movement smoothness parameters changed significantly in paretic as compared to normal arms in stroke subjects (p < 0.003). Surprisingly, there were no significant differences in these parameters between SCI and stroke subjects, except for the movement smoothness (p ≤ 0.02). Extension was significantly less smooth in the paretic compared to the non-paretic arm in the stroke group (p < 0.003), whereas it was within the normal range in the SCI group. There was also no significant difference in these parameters between the non-paretic arm in stroke subjects and the normal arm in healthy subjects.</p> <p>Conclusion</p> <p>The findings suggest that although the cause and location of injury are different in spastic stroke and SCI subjects, the impairments in arm voluntary movement were similar in the two spastic groups. Our results also suggest that the non-paretic arm in stroke subjects was not distinguishable from the normal, and might therefore be used as an appropriate control for studying movement of the paretic arm.</p

Muscle and reflex changes with varying joint angle in hemiparetic stroke

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p> <p>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.</p> <p>Our findings will help elucidate the origins of the neuromuscular abnormalities associated with stroke-induced spasticity.</p

Muscle weakness and lack of reflex gain adaptation predominate during post-stroke posture control of the wrist

Instead of hyper-reflexia as sole paradigm, post-stroke movement disorders are currently considered the result of a complex interplay between neuronal and muscular properties, modified by level of activity. We used a closed loop system identification technique to quantify individual contributors to wrist joint stiffness during an active posture task. Continuous random torque perturbations applied to the wrist joint by a haptic manipulator had to be resisted maximally. Reflex provoking conditions were applied i.e. additional viscous loads and reduced perturbation signal bandwidth. Linear system identification and neuromuscular modeling were used to separate joint stiffness into the intrinsic resistance of the muscles including co-contraction and the reflex mediated contribution. Compared to an age and sex matched control group, patients showed an overall 50% drop in intrinsic elasticity while their reflexive contribution did not respond to provoking conditions. Patients showed an increased mechanical stability compared to control subjects. Post stroke, we found active posture tasking to be dominated by: 1) muscle weakness and 2) lack of reflex adaptation. This adds to existing doubts on reflex blocking therapy as the sole paradigm to improve active task performance and draws attention to muscle strength and power recovery and the role of the inability to modulate reflexes in post stroke movement disorders.Mechanical, Maritime and Materials Engineerin

The relation between neuromechanical parameters and Ashworth score in stroke patients

Quantifying increased joint resistance into its contributing factors i.e. stiffness and viscosity ("hypertonia") and stretch reflexes ("hyperreflexia") is important in stroke rehabilitation. Existing clinical tests, such as the Ashworth Score, do not permit discrimination between underlying tissue and reflexive (neural) properties. We propose an instrumented identification paradigm for early and tailor made interventions.BioMechanical EngineeringMechanical, Maritime and Materials Engineerin

Abnormal joint torque patterns exhibited by chronic stroke subjects while walking with a prescribed physiological gait pattern

<p>Abstract</p> <p>Background</p> <p>It is well documented that individuals with chronic stroke often exhibit considerable gait impairments that significantly impact their quality of life. While stroke subjects often walk asymmetrically, we sought to investigate whether prescribing near normal physiological gait patterns with the use of the Lokomat robotic gait-orthosis could help ameliorate asymmetries in gait, specifically, promote similar ankle, knee, and hip joint torques in both lower extremities. We hypothesized that hemiparetic stroke subjects would demonstrate significant differences in total joint torques in both the frontal and sagittal planes compared to non-disabled subjects despite walking under normal gait kinematic trajectories.</p> <p>Methods</p> <p>A motion analysis system was used to track the kinematic patterns of the pelvis and legs of 10 chronic hemiparetic stroke subjects and 5 age matched controls as they walked in the Lokomat. The subject's legs were attached to the Lokomat using instrumented shank and thigh cuffs while instrumented footlifters were applied to the impaired foot of stroke subjects to aid with foot clearance during swing. With minimal body-weight support, subjects walked at 2.5 km/hr on an instrumented treadmill capable of measuring ground reaction forces. Through a custom inverse dynamics model, the ankle, knee, and hip joint torques were calculated in both the frontal and sagittal planes. A single factor ANOVA was used to investigate differences in joint torques between control, unimpaired, and impaired legs at various points in the gait cycle.</p> <p>Results</p> <p>While the kinematic patterns of the stroke subjects were quite similar to those of the control subjects, the kinetic patterns were very different. During stance phase, the unimpaired limb of stroke subjects produced greater hip extension and knee flexion torques than the control group. At pre-swing, stroke subjects inappropriately extended their impaired knee, while during swing they tended to abduct their impaired leg, both being typical abnormal torque synergy patterns common to stroke gait.</p> <p>Conclusion</p> <p>Despite the Lokomat guiding stroke subjects through physiologically symmetric kinematic gait patterns, abnormal asymmetric joint torque patterns are still generated. These differences from the control group are characteristic of the hip hike and circumduction strategy employed by stroke subjects.</p

Review of natural fibre-reinforced hybrid composites

Natural fibre-reinforced hybrid composites which contain one or more types of natural reinforcement are gaining increasing research interest. This paper presents a review of natural fibre-reinforced hybrid composites. Both thermoplastic and thermoset composites reinforced by hybrid/synthetic fibres or hybrid/hybrid fibres are reviewed. The properties of natural fibres, the properties and processing of composites are summarised