Kinoshita S1, Ozawa J2, Yakuwa T3, Inoue S3, Nomura M3,4, Wakimoto Y3, Li C3, Hatakeyama J1, Tsubaki T1, Wakigawa T1, Kito N2, Sakai Y5, Akisue T6, Moriyama H6
1Kobe University School of Medicine Faculty of Health Sciences, Physical Therapy Major, Kobe, Japan, 2Hiroshima International University, Department of Rehabilitation, Faculty of Rehabilitation, Higashihiroshima, Japan, 3Kobe University Graduate School of Health Sciences, Department of Rehabilitation Science, Kobe, Japan, 4Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan, 5Kobe University Graduate School of Medicine, Division of Rehabilitation Medicine, Kobe, Japan, 6Kobe University, Life and Medical Sciences Area, Health Sciences Discipline, Kobe, Japan
Background: Joint contractures are major complications of spinal cord injuries (SCI), and are characterized by limitations in the passive range of motion (ROM). Spasticity is originally believed to trigger contractures from clinical observations. We have previously proposed the SCI-specific characteristics of contractures. However, what triggers them has not been investigated, and whether spasticity plays a part in contracture development after SCI remains controversial.
Purpose: Using an established rat model with SCI with knee flexion contractures, we aimed to verify whether spasticity contributes contracture development after SCI.
Methods: Total 20 male Wistar rats were randomly divided into a healthy group that had no intervention (control group), an untreated group with SCI (SCI group), and a botulinum toxin (BTX) injections group after SCI (BTX group). To evaluate the effect of spasticity on contracture development, the rats were received BTX injections into both sides of all the knee flexors at the first postoperative day of SCI. The rats at 2 and 4weeks after the injections were evaluated and compared with the age-matched animals in the control and SCI groups. Knee extension motion was measured with a goniometer, and the muscular and articular factors responsible for contractures were calculated by measuring joint motion before and after the myotomies. We quantitatively measured the muscle atrophy, muscle fibrosis, and synovial intima length.
Results: The rats with SCI demonstrated spastic paraplegia, and BTX suppressed it. All outcome displayed a similar tendency, regardless of the duration of the intervention. The limitation in ROM developed after SCI, whereas BTX injections did not completely prevent it. BTX was effective in preventing the muscular factor, but is not the articular factor. SCI induced muscle atrophy, and BTX significantly accelerated muscle atrophy and fibrosis. The synovial intima length decreased significantly after SCI, and BTX did not prevent this shortening.
Conclusion(s): This study is the first to resolve the longstanding questions of whether spasticity is a trigger of contractures. Our findings provide new evidence that spasticity is not a trigger rather is only a partial contributor of contractures after SCI. The widely held belief that spasticity triggers joint contracture may not always be true.
Implications: In the treatment aimed to prevent and/or improve contracture, more attention should be directed to treating the factors other than spasticity after SCI.
Keywords: Spasticity, joint contracture, spinal cord injury
Funding acknowledgements: This study was supported by the Japan Society for the Promotion of Science (17K19908).
Purpose: Using an established rat model with SCI with knee flexion contractures, we aimed to verify whether spasticity contributes contracture development after SCI.
Methods: Total 20 male Wistar rats were randomly divided into a healthy group that had no intervention (control group), an untreated group with SCI (SCI group), and a botulinum toxin (BTX) injections group after SCI (BTX group). To evaluate the effect of spasticity on contracture development, the rats were received BTX injections into both sides of all the knee flexors at the first postoperative day of SCI. The rats at 2 and 4weeks after the injections were evaluated and compared with the age-matched animals in the control and SCI groups. Knee extension motion was measured with a goniometer, and the muscular and articular factors responsible for contractures were calculated by measuring joint motion before and after the myotomies. We quantitatively measured the muscle atrophy, muscle fibrosis, and synovial intima length.
Results: The rats with SCI demonstrated spastic paraplegia, and BTX suppressed it. All outcome displayed a similar tendency, regardless of the duration of the intervention. The limitation in ROM developed after SCI, whereas BTX injections did not completely prevent it. BTX was effective in preventing the muscular factor, but is not the articular factor. SCI induced muscle atrophy, and BTX significantly accelerated muscle atrophy and fibrosis. The synovial intima length decreased significantly after SCI, and BTX did not prevent this shortening.
Conclusion(s): This study is the first to resolve the longstanding questions of whether spasticity is a trigger of contractures. Our findings provide new evidence that spasticity is not a trigger rather is only a partial contributor of contractures after SCI. The widely held belief that spasticity triggers joint contracture may not always be true.
Implications: In the treatment aimed to prevent and/or improve contracture, more attention should be directed to treating the factors other than spasticity after SCI.
Keywords: Spasticity, joint contracture, spinal cord injury
Funding acknowledgements: This study was supported by the Japan Society for the Promotion of Science (17K19908).
Topic: Neurology: spinal cord injury; Musculoskeletal: lower limb; Disability & rehabilitation
Ethics approval required: Yes
Institution: Kobe University
Ethics committee: Institutional Animal Care and Use Committee
Ethics number: P130408
All authors, affiliations and abstracts have been published as submitted.
