Abstract
BackgroundWhile 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.MethodsWe 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.ResultsMost 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.ConclusionThe 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.
Highlights
The movement impairments following neurological illness such as stroke and spinal cord injury are caused by disturbances in descending commands, the precise mechanisms by which disrupted commands affect voluntary function are uncertain
In spinal cord injury (SCI) subjects, active range of motion (AROM) was ~42% smaller, movement time (MT) was approximately 7 times longer and Vp and Ap were over 70% smaller
In an attempt to possibly detect the reduced smoothness, we computed the AROM generated during the first movement unit (AROM_1MU), and the percentage of AROM covered by the first movement unit (%AROM_1MU) in paretic and spastic SCI arms
Summary
The movement impairments following neurological illness such as stroke and spinal cord injury are caused by disturbances in descending commands, the precise mechanisms by which disrupted commands affect voluntary function are uncertain. Spasticity is a motor disorder associated with lesions at different levels of the nervous system. It can directly or indirectly change mechanical properties of the neuromuscular system, in chronic patients, and has been linked to impaired voluntary movement through different mechanisms [3,4,5,6,7]. Comparison of impaired voluntary movement between stroke and SCI groups is warranted to understand possible effects of the etiology of spasticity on the nature of these impairments and their underlying mechanisms. 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. 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
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