Remnant neuromuscular junctions in denervated muscles contribute to functional recovery in delayed peripheral nerve repair.

Schwann cell proliferation in peripheral nerve injury (PNI) enhances axonal regeneration compared to central nerve injury. However, even in PNI, long-term nerve damage without repair induces degeneration of neuromuscular junctions (NMJs), and muscle atrophy results in irreversible dysfunction. The peripheral regeneration of motor axons depends on the duration of skeletal muscle denervation. To overcome this difficulty in nerve regeneration, detailed mechanisms should be determined for not only Schwann cells but also NMJ degeneration after PNI and regeneration after nerve repair. Here, we examined motor axon denervation in the tibialis anterior muscle after peroneal nerve transection in thy1-YFP mice and regeneration with nerve reconstruction using allografts. The number of NMJs in the tibialis anterior muscle was maintained up to 4 weeks and then decreased at 6 weeks after injury. In contrast, the number of Schwann cells showed a stepwise decline and then reached a plateau at 6 weeks after injury. For regeneration, we reconstructed the degenerated nerve with an allograft at 4 and 6 weeks after injury, and evaluated functional and histological outcomes for 10 to 12 weeks after grafting. A higher number of pretzel-shaped NMJs in the tibialis anterior muscle and better functional recovery were observed in mice with a 4-week delay in surgery than in those with a 6-week delay. Nerve repair within 4 weeks after PNI is necessary for successful recovery in mice. Prevention of synaptic acetylcholine receptor degeneration may play a key role in peripheral nerve regeneration. All animal experiments were approved by the Institutional Animal Care and Use Committee of Tokyo Medical and Dental University on 5 July 2017, 30 March 2018, and 15 May 2019 (A2017-311C, A2018-297A, and A2019-248A), respectively.

Successful Reconstruction of a Traumatic Complete Femoral Nerve Rupture with a Sural Nerve Cable Graft: A Case Report.

CASE: We report a rare case of complete rupture of the right femoral nerve at the pelvic level, which was caused by a self-inflicted stab wound. The nerve was surgically reconstructed with use of an autologous sural nerve cable graft. Postoperatively, the patient's sensorimotor function returned to near normal. CONCLUSION: Femoral nerve rupture caused by a laceration is very unusual. A bilateral sural nerve cable graft performed in collaboration with surgeons from other specialties achieved a good outcome in this otherwise healthy young patient.

Bone Marrow Stromal Cells Combined With a Honeycomb Collagen Sponge Facilitate Neurite Elongation In Vitro and Neural Restoration in the Hemisected Rat Spinal Cord.

In the last decade, researchers and clinicians have reported that transplantation of bone marrow stromal cells (BMSCs) promotes functional recovery after brain or spinal cord injury (SCI). However, an appropriate scaffold designed for the injured spinal cord is needed to enhance the survival of transplanted BMSCs and to promote nerve regeneration. We previously tested a honeycomb collagen sponge (HC), which when applied to the transected spinal cord allowed bridging of the gap with nerve fibers. In this study, we examined whether the HC implant combined with rat BMSCs increases nerve regeneration in vitro and enhances functional recovery in vivo. We first evaluated the neurite outgrowth of rat dorsal root ganglion (DRG) explants cultured on HC with or without BMSCs in vitro. Regeneration of neurites from the DRGs was increased by BMSCs combined with HC scaffolds. In the in vivo study, 3-mm-long HC scaffolds with or without BMSCs were implanted into the hemisected rat thoracic spinal cord. Four weeks after the procedure, rats implanted with HC scaffolds containing BMSCs displayed better motor and sensory recovery than those implanted with HC scaffolds only. Histologically, more CGRP-positive sensory fibers at the implanted site and 5-HT-positive serotonergic fibers contralateral to the implanted site were observed in spinal cords receiving BMSCs. Furthermore, more rubrospinal neurons projected distally to the HC implant containing BMSCs. Our study indicates that the application of BMSCs in a HC scaffold in the injured spinal cord directly promoted sensory nerve and rubrospinal tract regeneration, thus resulting in functional recovery.

Joint capsule attachment to the extensor carpi radialis brevis origin: an anatomical study with possible implications regarding the etiology of lateral epicondylitis.

PURPOSE: To identify the unique anatomical characteristic of the extensor carpi radialis brevis (ECRB) origin and points of differentiation from other extensors and to clarify the specific relationship of the ECRB to the underlying structures. METHODS: We studied the origin of each extensor macroscopically for its muscular and tendinous parts; to identify the relationship between the ECRB origin and the deeper structures, we also examined the attachment of the joint capsule under the ECRB origin. RESULTS: The ECRB simply originated as a tendon without any muscle, whereas other extensors originated as a mixture of tendon and muscle. At the anterior part of the ECRB origin, the thin attachment of the joint capsule (average width, 3.3 mm) lay deep to the ECRB and was distinct. However, at the posterodistal portion, the joint capsule, annular ligament, and supinator were intermingled and originated as a single wide sheet from the humerus (average width, 10.7 mm). CONCLUSIONS: The anterior part of the ECRB origin was delicate, because the ECRB origin was purely tendinous, and the attachment of the articular capsule was thin compared with that of the posterodistal attachment. This thin attachment could be an initial factor leading to the development of lateral epicondylitis. CLINICAL RELEVANCE: The results of the current study may enhance magnetic resonance imaging understanding and may help clarify the etiology of the lateral epicondylitis.

Flexor tendon rupture of the little finger caused by calcium pyrophosphate dihydrate crystal deposition disease of the pisotriquetrum joint.

We report a case of closed rupture of the flexor tendons of the little finger caused by calcium pyrophosphate dihydrate crystal deposition disease of the pisotriquetrum joint. The patient could not flex the little finger and did not have wrist pain. Plain radiographs of the affected wrist joint showed severe arthritic changes of the pisotriquetrum joint and calcification around the joint. At operation, the pisotriquetrum joint capsule was ruptured and involved the flexor tendon of the little finger. The distal stump of the flexor tendon was transferred to the flexor tendon of the ring finger, and the pisiform was resected. Histological examination with polarized light microscopy revealed crystals showing weakly positive birefringence in the calcification.

Subcutaneous injections of platelet-rich plasma into skin flaps modulate proangiogenic gene expression and improve survival rates.

BACKGROUND: Flap necrosis remains a major complication of reconstructive surgery. To improve skin flap survival, various treatments with vasodilators, antiplatelet drugs, or the local administration of growth factors have been performed. However, the sufficient prevention of skin necrosis is not well established. Platelet-rich plasma has been used as an autologous factor and includes various growth factors. The authors evaluated whether or not platelet-rich plasma can improve skin flap survival in an experimental rat model. METHODS: Cranially based dorsal cutaneous flaps were elevated in 48 rats. The animals received subcutaneous injections of either platelet-rich plasma (100 µl) or platelet-poor plasma (100 µl). The rats were divided into three groups: the platelet-rich plasma group (n = 16), the platelet-poor plasma group (n = 16), and the nontreatment group (n = 16). Flap survival was measured and histologic specimens were collected on day 7. Real-time polymerase chain reaction specimens were collected after 8 hours, 24 hours, 3 days, and 7 days. RESULTS: Platelet-rich plasma significantly improved flap survival rates (61.2 percent) compared with the platelet-poor plasma treatment (35.8 percent) and nontreatment groups (28.0 percent). A histologic analysis showed that significantly fewer inflammatory cells and an increased blood vessel density were observed in the platelet-rich plasma rats versus the platelet-poor plasma or nontreatment rats. In addition, platelet-rich plasma treatment significantly increased the mRNA levels of vascular endothelial growth factor and platelet-derived growth factor. CONCLUSION: Platelet-rich plasma modulates the genes involved in angiogenesis and improves skin flap survival.

Enhancement of sciatic nerve regeneration by adenovirus-mediated expression of dominant negative RhoA and Rac1.

It is known that Rho family small GTPases activate a number of signal transduction pathways involved in cell cycle progression, gene expression, and cell survival. These small G proteins play an important role in neuronal survival and axon regeneration in neural injury. In this study, we tested whether the activity of RhoA or Rac1 regulates neurite extension in dorsal root ganglia (DRGs) in vitro and nerve regeneration in injured sciatic nerves. Regeneration of neurites from explanted DRGs was accelerated by combined suppression of RhoA and Rac1 activity using adenoviruses expressing dominant negative (DN) forms of both RhoA and Rac1 (Ad-Rho/RacDN) in vitro. Rat sciatic nerves were cut and Ad-Rho/RacDN was injected into the proximal stumps. After bridge grafting with chitosan mesh tubes, muscle evoked potentials induced by transcranial electrical stimulation were recorded eight weeks postoperatively. The terminal latencies were shorter in the Ad-Rho/RacDN group than in the control group. Histological analysis revealed extensive regrowth of neurofilament-positive and myelinated axons within the tubes in the group that received Ad-Rho/RacDN. These findings suggest that combined regulation of RhoA and Rac1 using DN adenoviral transgenic methods has the potential to modify injured peripheral nerve tissues directly.

Repair of olecranon fractures using fiberWire without metallic implants: report of two cases.

Olecranon fractures are a common injury in fractures. The tension band technique for olecranon fractures yields good clinical outcomes; however, it is associated with significant complications. In many patients, implants irritate overlying soft tissues and cause pain. This is mostly due to protrusion of the proximal ends of the K-wires or by the twisted knots of the metal wire tension band. Below we described 2 cases of olecranon fractures treated with a unique technique using FiberWire without any metallic implants. Technically, the fragment was reduced, and two K-wires were inserted from the dorsal cortex of the distal segment to the tip of the olecranon. K-wire was exchanged for a suture retriever, and 2 strands of FiberWire were retrieved twice. Each of the two FiberWires was manually tensioned and knotted on the posterior surface of the olecranon. Bony unions could be achieved, and patients had no complaint of pain and skin irritation. There was only a small loss of flexion and extension in comparison with that of the contralateral side, and the patient did not feel inconvenienced in his daily life. Using the method described, difficulty due to K-wire or other metallic implants was avoided.

Stener-like lesions of collateral ligament ruptures of the metacarpophalangeal joint of the finger.

BACKGROUND: The Stener lesion of the ulnar collateral ligament of the metacarpophalangeal (MP) joint of the thumb is characterized by an interposition of the adductor aponeurosis between a distally avulsed ligament and its insertion into the base of the proximal phalanx. Stener-like lesions of the MP joint of the finger have been previously reported in only a few cases. METHODS: The authors experienced 38 cases of collateral ligament injuries of the MP joint of the finger. The two most frequently affected sites were the radial side of the little finger (21 cases) and the radial side of the ring finger (8 cases). We have previously reported some of these cases (22 cases), as well as clinical features and arthrographic findings. One Stener-like lesion in a collateral ligament injury of the MP joint of the ring finger was also reported earlier (Ishizuki, 1988). Additionally, Stener-like lesions were found postoperatively in six of eight cases surgically treated for collateral ligament injuries of the MP joint of the finger (little finger involvement in 5 cases and long finger involvement in 1 case). RESULTS: We experienced six cases of a Stener-like lesion of the MP joint of the finger. In five of these cases the distally avulsed collateral ligament was trapped by the opened window of the injured sagittal band. In the other case the ligament was avulsed at a proximal site, and the ruptured end was trapped by the sagittal band. All of the little fingers involving Stener-like lesions were abducted and unable to adduct. Therefore, an abducted little finger is an important sign of this lesion and is considered to warrant surgical treatment. Arthrograms provided information useful for identifying the lesions. In the radial three fingers, palpation of the tumor at the level of the collateral ligament may also be an important examining tool for identifying a displaced ruptured collateral ligament of the MP joint of the finger. CONCLUSION: We experienced six cases of Stener-like lesions of the MP joint of the finger. In all cases, the avulsed collateral ligament was trapped by the ruptured sagittal band. Surgical treatment was thought to be indicated in these cases. Therefore, it is important to avoid overlooking Stener-like lesions of the MP joint of the finger.