Abstract

BackgroundFollowing incomplete spinal cord injury (iSCI), descending drive is impaired, possibly leading to a decrease in the complexity of gait. To test the hypothesis that iSCI impairs gait coordination and decreases locomotor complexity, we collected 3D joint angle kinematics and muscle parameters of rats with a sham or an incomplete spinal cord injury.Methods12 adult, female, Long-Evans rats, 6 sham and 6 mild-moderate T8 iSCI, were tested 4 weeks following injury. The Basso Beattie Bresnahan locomotor score was used to verify injury severity. Animals had reflective markers placed on the bony prominences of their limb joints and were filmed in 3D while walking on a treadmill. Joint angles and segment motion were analyzed quantitatively, and complexity of joint angle trajectory and overall gait were calculated using permutation entropy and principal component analysis, respectively. Following treadmill testing, the animals were euthanized and hindlimb muscles removed. Excised muscles were tested for mass, density, fiber length, pennation angle, and relaxed sarcomere length.ResultsMuscle parameters were similar between groups with no evidence of muscle atrophy. The animals showed overextension of the ankle, which was compensated for by a decreased range of motion at the knee. Left-right coordination was altered, leading to left and right knee movements that are entirely out of phase, with one joint moving while the other is stationary. Movement patterns remained symmetric. Permutation entropy measures indicated changes in complexity on a joint specific basis, with the largest changes at the ankle. No significant difference was seen using principal component analysis. Rats were able to achieve stable weight bearing locomotion at reasonable speeds on the treadmill despite these deficiencies.ConclusionsDecrease in supraspinal control following iSCI causes a loss of complexity of ankle kinematics. This loss can be entirely due to loss of supraspinal control in the absence of muscle atrophy and may be quantified using permutation entropy. Joint-specific differences in kinematic complexity may be attributed to different sources of motor control. This work indicates the importance of the ankle for rehabilitation interventions following spinal cord injury.

Highlights

  • Following incomplete spinal cord injury, descending drive is impaired, possibly leading to a decrease in the complexity of gait

  • Pennation angle tended to be greater in the distal muscles than in the proximal muscles, with nonpennate muscles seen in the knee flexors and hip extensor

  • We showed that changes in kinematic complexity were joint specific, indicating that different joints are under differing control in locomotion

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Summary

Introduction

Following incomplete spinal cord injury (iSCI), descending drive is impaired, possibly leading to a decrease in the complexity of gait. As a result of spinal cord injury, the connections between the brain and the spinal circuitry below the injury are disrupted This leads to adaptations in the neurons of the brain and spinal cord as well as changes to the sensory afferents and motoneurons [1,2,3]. Along with these neural changes, the muscles in the distal limb undergo changes similar to those seen in many disuse paradigms. As spinal cord injury related muscular and neural impairments affect the legs, locomotion is often used as a measure of impairment and recovery

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