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An 11-year-old boy was admitted to our hospital due to severe pain in his right knee when he landed after jumping over a vaulting box. A plain X-ray image and computed tomography scan showed an avulsion fracture of the lower pole of the patella and patella alta. Furthermore, magnetic resonance imaging (MRI) revealed an articular cartilage lesion and rupture between the inferior pole of the patella and the patella tendon. We diagnosed a sleeve fracture of the patella and performed surgical treatment. Open reduction and internal fixation were performed by the pull-out technique using transosseous no. 2 MaxBraid™​​​​​​ ​(Zimmer Biomet, Tokyo, Japan) sutures. While postoperative weight-bearing was permitted, the knee joint was immobilized in a brace for four weeks. Three months of postoperative assessment revealed excellent functional outcomes.

Isolated brachial muscle injuries are relatively rare injuries and reportedly occur during forced elbow extension. Though commonly conservative treatment approach is adopted, the treatment criteria remain unclear. Here, we report the case of a patient who experienced functional recovery after conservative treatment for an isolated brachial muscle injury. The patient was an 8-year-old boy whose chief complaint was left elbow pain. The injury occurred when the patient fell while playing on gymnastics bars and bruised the palmar side of his left elbow on the bar. Owing to the pain in the left elbow, the patient came to our institution. There were no clear signs of deformities or swelling in the left elbow and no obvious tenderness. X-ray and computed tomography (CT) imaging examinations revealed no signs of a fracture or dislocation, and the patient was diagnosed with left brachialis muscle rupture based on magnetic resonance imaging (MRI). Although the brachialis muscle was complete ruptured, a healing tendency was seen on body surface ultrasound examinations over time, and the patient was treated conservatively. After 3 weeks of cast immobilization, the patient underwent range of motion exercises. Two months after the injury, there were no issues with elbow joint function in daily life activities and no limitations in range of motion. Here, MRI was used to diagnose brachialis muscle rupture, and ultrasound examinations were utilized to make treatment decisions.

A number of studies have investigated electrophy-siological and morphological changes of peripheral nerves during gradual elongation. There has been, however, no report on the distribution of sodium channels at Ranvier’s nodes during peripheral nerve elongation. We investigated peripheral nerve injury after the gradual elongation of rat sciatic nerves. Indirect nerve elongation was induced by leg lengthening at a rate of 3mm/day by 15 or 30mm. At 7days after the leg lengthening, the electrophysiological properties of sciatic nerves, the ultrastructures of the Ranvier’s nodes and axons, and the distribution of voltage-dependent sodium channels were examined. In the control nerves, most sodium channels were localized at Ranvier’s nodes in myelinated axons, providing the physiological basis of saltatory conduction. In the elongated nerves, both the amplitude and conduction velocity of compound nerve action potential decreased following leg lengthening. The elongated nerves also showed paranodal demyelination in Ranvier’s nodes longer than those in the control group. In addition, the distribution of sodium channels became diffuse or disappeared at Ranvier’s nodes of elongated nerves. The diffuse distribution and/or disappearance of sodium channels may underlie the electrophysiological changes in compound nerve action potential induced by nerve elongation.

Following nerve degeneration, we investigated effects of linear elongation on subsequent nerve regeneration in a total of 92 Wistar rats (weight 380–430 g). The nerve was ligated at the midthigh and then elongated incrementally by a total of 15 mm by leg lengthening at a rate of 3 or 5 mm/day. Seven days after initiation of nerve elongation, the external fixator was removed and normal leg length was restored with internal fixation. Then a 10 mm nerve segment at the ligature site was excised, and the nerve was repaired with sutures (group D). At 2, 4, 6, and 8 weeks after nerve suturing, we examined transverse semi-thin nerve sections compared with group I (severed and repaired after leg lengthening without a nerve ligature) and control group (severed and repaired without leg lengthening). After lengthening at 3 mm/day, nerve regeneration in group D was enhanced at 4 weeks. After lengthening at 5 mm/day, nerve regeneration in group D also was enhanced at 6 and 8 weeks. Pre-degenerated nerve showed better regeneration after suturing than intact nerve. Elongation holds promise as an alternative to nerve grafting in treatment of nerve injury.

Leg lengthening procedure is used increasingly to treat leg length discrepancy and some forms of dwarfism. We investigated adaptation in rat sciatic nerve to the gradual nerve elongation that occurs with leg lengthening. Indirect nerve elongation was produced by leg lengthening by a total of 15, 30, 45, or 70 mm at a rate of 1 mm/day. One day after leg lengthening completion, transverse semithin sections of sciatic nerve were prepared and examined; a teased-fiber study also was performed. Elongation decreased axon diameter, but not significantly. In teased-fiber preparations, internodal length was increased by 93%, and the longest internode measured 3000 μm after leg lengthening by 70 mm. Slopes of fiber diameter–internodal length regression lines increased with increasing elongation. Paranodal demyelination caused by nerve elongation worsened as elongation increased, stimulating remyelination (i.e., intercalation of a segment). Only 0.8% of axons showed degeneration in the group with 70 mm of elongation. We concluded that adult rat sciatic nerve can adapt itself to leg lengthening procedure with even doubling internodal length.

Nerve elongation resulting from leg-lengthening surgery can be injurious. We investigated peripheral nerve injury and recovery after gradual elongation of the rat sciatic nerve by progressive stretching. Indirect nerve elongation was produced by leg lengthening by 15 mm, at a rate of 3 mm/day (group I) or 5 mm/day (group II). The elongated length was then maintained. At 0 weeks, representing the 7th day after starting leg lengthening, and at weeks 2, 4, and 6, transverse semithin sections of sciatic nerve were examined. At the same time a teased fiber study was performed. As a result of nerve elongation axon diameter was decreased, although it later recovered. Axon diameter recovered more slowly in group II than I. Myelin thickness did not change compared with controls. In the teased fiber study, internodal length was increased by about 10% after nerve elongation in each group. Almost all nerve fibers showed demyelination at 0 weeks; myelination recovered with time, more slowly in group II than I. More obvious demyelination, axonal degeneration, and remyelination were observed in group II. We conclude that mild demyelination was repaired by elongation of internodes, while more severe demyelination was repaired by intercalation of segments.