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 ¼ 13). The control groups comprised sham-operated (group S, n ¼ 10) and naive (group N, n ¼ 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) sodiumchannel 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. Keywords: sodium channel; limb lengthening; peripheral nerve; nerve elongation; dorsal root ganglion Limb lengthening is a popular method of treating leg length discrepancies or congenital anomalies, but the technique could cause peripheral nerve injury. Gradual nerve elongation is believed to be the primary cause of this form of injury because studies have demonstrated a clear correlation between the extent of lengthening and the degree of conduction slowing.1,2 However, most of these basic studies have considered only the morphological and electrophysiological alterations in the elongated nerve; 3,4 therefore, the pathophysiological mechanisms underlying chronic nerve-stretch injury are not fully understood.Clinically, the earliest symptom of neuropathy induced by limb lengthening is pain and/or paresthesia along the leg's sensory nerve distribution, 5 similar to neuropathy induced by other types of injuries. Several experimental models have been proposed for various types of nerve injuries, such as the axotomy model 6 and the sciatic nerve or spinal nerve ligation model. 7-9 These studies have identified that the underlying pathophysiology after nerve injury is closely associated with altered expression of the voltage-gated sodium channels (VGSCs) in the dorsal root ganglion (DRG). 10-12VGSCs consist of alpha and beta subunits. The mature channels in the plasma membrane are mainly composed of alpha subunits, 13 which have been further classified into two types on the basis of the differences in their physiological and pharmacological properties: tetrodotoxin-resistant (TTX...
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.
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.
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