Joint-specific changes in locomotor complexity in the absence of muscle atrophy following incomplete spinal cord injury

Authors

Brian K. Hillen, Department of Biomedical Engineering, Florida International University, 10555 W Flagler St, EC 2602, Miami, FL; Center for Adaptive Neural Systems, Arizona State University, 1100 E. University Dr., Ste. 116, Tempe, AZFollow
Gary T. Yamaguchi, Exponent, 23445 North 19th Ave., Phoenix, AZ
James J. Abbas, Center for Adaptive Neural Systems, Arizona State University, 1100 E. University Dr., Ste. 116, Tempe, AZFollow
Ranu Jung, Department of Biomedical Engineering, Florida International University, 10555 W Flagler St, EC 2602, Miami, FL; Center for Adaptive Neural Systems, Arizona State University, 1100 E. University Dr., Ste. 116, Tempe, AZFollow

Date of this Version

8-15-2013

Document Type

Article

Abstract

ackground

Following 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.

Methods

12 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.

Results

Muscle 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.

Conclusions

Decrease 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.

Comments

This article was originally published in Biomed central Journal of NeuroEngineering and Rehabilitation 2013

Creative Commons License

This work is licensed under a Creative Commons Attribution 2.0 License.

Recommended Citation

Hillen, Brian K.; Yamaguchi, Gary T.; Abbas, James J.; and Jung, Ranu, "Joint-specific changes in locomotor complexity in the absence of muscle atrophy following incomplete spinal cord injury" (2013). Department of Biomedical Engineering Faculty Publications. 6.
https://digitalcommons.fiu.edu/biomed_eng/6