Impairment and restoration of the blood-nerve barrier and its correlation with pain following gradual nerve elongation of the rat sciatic nerve.

Purpose: This study aimed to evaluate the time course of impairment and restoration of the blood-nerve barrier (BNB) following gradual elongation of the sciatic nerve and to clarify its association with nociception.Materials and Methods: The right femur was lengthened at a rate of 1.5 mm/day for 10 days. Von Frey tests were performed until 50 days after lengthening. Compound muscle action potentials (CMAPs) were measured to assess gross dysfunction of the elongated nerve. Evans blue-albumin tracing and immunohistochemistry for endothelial barrier antigen (EBA), rat endothelial cell antigen-1 (RECA-1), and CD68 for qualitative and quantitative analysis of the BNB and macrophage infiltration were performed for up to 50 days after cessation of lengthening in three segments of the sciatic nerves.Results: Paw-withdrawal threshold was significantly decreased at 7 days from initiation and began to recover from day 25 after lengthening. CMAPs showed delayed latency and attenuated amplitude but recovered at day 30 after cessation. On days 10 and 30 after cessation, spotted leakage of Evans blue-albumin in the endoneurium was observed, and the ratio of EBA/RECA-1-positive microvessels was significantly decreased, which subsequently recovered simultaneously in all segments on day 50 after cessation. Macrophages did not infiltrate the BNB at any time point.Conclusion: The restoration of BNB function following gradual nerve elongation was associated with the resolution of mechanical allodynia. Our findings provide insight into the association between nerve stretch injury and chronic nociception in adult male rats, which are potentially relevant to human orthopedic procedures and chronic neuropathic pain.

Irreducible Dislocation of the Radial Head Associated With Pediatric Monteggia Lesions.

BACKGROUND: In pediatric patients with Monteggia lesions, the radial head can be reduced manually when displacement of the fractured ulna is corrected. Occasionally, however, a dislocated radial head could not be reduced manually even when the length and/or angulation of the fractured ulna had been corrected. We can find such cases in the literature, but those are single case reports. We encountered 17 cases of irreducible dislocation of the radial head in pediatric Monteggia lesions during the past 43 years. The purposes of this study were to identify the characteristics of our cases and to discuss the factors that inhibited reduction of the radial head. METHODS: Of 109 children treated for Monteggia lesions between 1972 and 2015, we encountered 17 cases of irreducible dislocation of the radial head. The patients' ages averaged 7.1 years, ranging from 2.6 to 12.1 years. Directions of the radial head dislocation were anterior in five cases, anteromedial in four, lateral in one, and anterolateral in seven. Most of the patients were referred to us from local orthopaedic clinics because of irreducibility of the radial head. We reduced the radial head surgically and confirmed the causes of irreducibility. RESULTS: In 10 of the 17 cases, the problem was identified as pseudoreduction. In those cases, the radial head was reduced in a supination position but redisplaced in a pronation position. Causes of irreducibility were traced to the annular ligament in 15 cases, biceps tendon in 1, and posterior interosseous nerve in 1. CONCLUSIONS: In cases of pediatric Monteggia lesions, we should pay attention to patients in whom the dislocated radial head is not reduced after closed reduction. The most frequent cause of hindered reduction was interposition of the annular ligament in the radiocapitellar joint. Here, the radial head seems to be reduced in the supination position but becomes redisplaced in the pronation position. After closed reduction, it is important to confirm whether the radial head is stable in both pronation and supination positions. LEVEL OF EVIDENCE: Diagnostic level IV.

Sonographic monitoring of endoscopic carpal tunnel release.

We evaluated the effectiveness of sonographic monitoring of endoscopic carpal tunnel release for the prevention of median nerve or arterial injury and incomplete release of the flexor retinaculum (FR). When the outer tube (OT) was inserted, we used sonography to confirm the relationship of the OT, median nerve, ulnar artery, and superficial palmar arch. Under real-time US monitoring, the OT was lifted up before and after FR release, the so-called lift-up test, to evaluate its mobility under sonography and confirm complete FR release. © 2016 Wiley Periodicals, Inc. J Clin Ultrasound 44:597-599, 2016.

Role of sodium channels in recovery of sciatic nerve-stretch injury in rats.

INTRODUCTION: To elucidate the mechanism of functional recovery after gradual nerve-stretch injury, we used rats in which the femur length was increased by 15 mm at 1.5 mm/day. METHODS: We performed electrophysiology, mRNA analysis of tetrodotoxin-resistant voltage-gated sodium channels (TTX-R VGSCs) in dorsal root ganglia, and histology of unmyelinated sciatic nerve fibers and examined pain thresholds at 1, 10, 20, and 30 days after cessation of lengthening. RESULTS: Electrophysiology revealed conduction block after cessation that recovered after 30 days. TTX-R VGSC levels decreased immediately after cessation but were restored after 10 (Nav1.9) or 20 (Nav1.8) days. Histology revealed that injured unmyelinated nerve fibers regenerate 30 days after cessation. Pain threshold decreased gradually during lengthening but had not recovered to the control group level after 30 days. CONCLUSIONS: Early restoration of TTX-R VGSC mRNA in dorsal root ganglia preceded functional recovery of stretched nerves before regeneration of injured unmyelinated nerve fibers.

Altered expression of sodium channel distribution in the dorsal root ganglion after gradual elongation of rat sciatic nerves.

To elucidate the pathophysiological mechanisms underlying chronic nerve-stretch injury, we gradually lengthened rat femurs by 15 mm at the rate of 0.5 mm/day (group L, n = 13). The control groups comprised sham-operated (group S, n = 10) and naive (group N, n = 8) rats. Immediately after the lengthening, we performed a conduction study on their sciatic nerves and harvested samples. Electrophysiological and histological analyses showed mild conduction slowing and axonal degeneration of unmyelinated fibers in group L rats. Altered mRNA expression of the voltage-gated sodium channels in the dorsal root ganglion was also observed. Tetrodotoxin-resistant (TTX-R) sodium-channel Nav1.8 mRNA expression was significantly decreased and TTX-R sodium-channel Nav1.9 mRNA expression showed a tendency to decrease when compared with the mRNA expressions in the control groups. However, tetrodotoxin-sensitive (TTX-S) sodium-channel Nav1.3 mRNA expression remained unaltered. The immunohistochemical alteration of Nav1.8 protein expression was parallel to the results of the mRNA expression. Previous studies involving neuropathic states have suggested that pain/paresthesia is modulated by a subset of sodium channels, including downregulation and/or upregulation of TTX-R and TTX-S sodium channels, respectively. Our findings indicate that Nav1.8 downregulation may be one of the pathophysiological mechanisms involved in limb lengthening-induced neuropathy.