Mechanical Stress by Spasticity Accelerates Fracture Healing After Spinal Cord Injury.

Accelerated fracture healing in patients with spinal cord injuries (SCI) is often encountered in clinical practice. However, there is no distinct evidence in the accelerated fracture healing, and the mechanisms of accelerated fracture healing in SCI are poorly understood. We aimed to determine whether SCI accelerated fracture healing in morphology and strength, to characterize the healing process with SCI, and to clarify the factors responsible for accelerated fracture healing. In total, 39 male Wistar rats were randomly divided into healthy control without intervention, SCI only, fracture with SCI, botulinum toxin (BTX) A-treated fracture with SCI, and propranolol-treated fracture with SCI groups. These rats were assessed with computed microtomography, histological, histomorphological, immunohistological, and biomechanical analyses. Both computed microtomography and histological analyses revealed the acceleration of a bony union in animals with SCI. The strength of the healed fractures after SCI recovered to the same level as that of intact bones after SCI, while the healed bones were weaker than the intact bones. Immunohistology revealed that SCI fracture healing was characterized by formation of callus with predominant intramembranous ossification and promoting endochondral ossification. The accelerated fracture healing after SCI was attenuated by BTX injection, but did not change by propranolol. We demonstrated that SCI accelerate fracture healing in both morphology and strength. The accelerated fracture healing with SCI may be due to predominant intramembranous ossification and promoting endochondral ossification. In addition, our results also suggest that muscle contraction by spasticity accelerates fracture healing after SCI.

Stretching After Heat But Not After Cold Decreases Contractures After Spinal Cord Injury in Rats.

BACKGROUND: Contractures are a prevalent and potentially severe complication in patients with neurologic disorders. Although heat, cold, and stretching are commonly used for treatment of contractures and/or spasticity (the cause of many contractures), the sequential effects of these modalities remain unclear. QUESTIONS/PURPOSES: Using an established rat model with spinal cord injury with knee flexion contracture, we sought to determine what combination of heat or cold before stretching is the most effective for treatment of contractures derived from spastic paralyses and investigated which treatment leads to the best (1) improvement in the loss of ROM; (2) restoration of deterioration in the muscular and articular factors responsible for contractures; and (3) amelioration of histopathologic features such as muscular fibrosis in biceps femoris and shortening of the joint capsule. METHODS: Forty-two adolescent male Wistar rats were used. After spasticity developed at 2 weeks postinjury, each animal with spinal cord injury underwent the treatment protocol daily for 1 week. Knee extension ROM was measured with a goniometer by two examiners blinded to each other's scores. The muscular and articular factors contributing to contractures were calculated by measuring ROM before and after the myotomies. We quantitatively measured the muscular fibrosis and the synovial intima length, and observed the distribution of collagen of skeletal muscle. The results were confirmed by a blinded observer. RESULTS: The ROM of heat alone (34° ± 1°) and cold alone (34° ± 2°) rats were not different with the numbers available from that of rats with spinal cord injury (35° ± 2°) (p = 0.92 and 0.89, respectively). Stretching after heat (24° ± 1°) was more effective than stretching alone (27° ± 3°) at increasing ROM (p < 0.001). Contrastingly, there was no difference between stretching after cold (25° ± 1°) and stretching alone (p = 0.352). Stretching after heat was the most effective for percentage improvement of muscular (29%) and articular (50%) factors of contractures. Although quantification of muscular fibrosis in the rats with spinal cord injury (11% ± 1%) was higher than that of controls (9% ± 0.4%) (p = 0.01), no difference was found between spinal cord injury and each treatment protocol. The total synovial intima length of rats with spinal cord injury (5.9 ± 0.2 mm) became shorter than those of the controls (7.6 ± 0.2 mm) (p < 0.001), and those of stretching alone (6.9 ± 0.4 mm), stretching after heat (7.1 ± 0.3 mm), and stretching after cold (6.7 ± 0.4 mm) increased compared with rats with spinal cord injury (p = 0.01, p = 0.001, and p = 0.04, respectively). The staining intensity and pattern of collagen showed no difference among the treatment protocols. CONCLUSIONS: This animal study implies that heat or cold alone is ineffective, and that stretching is helpful for the correction of contractures after spinal cord injury. In addition, we provide evidence that heat is more beneficial than cold to increase the effectiveness of stretching. CLINICAL RELEVANCE: Our findings tend to support the idea that stretching after heat can improve the loss of ROM and histopathologic features of joint tissues. However, further studies are warranted to determine if our findings are clinically applicable.