Object Superior cluneal nerve (SCN) entrapment neuropathy is a poorly understood clinical entity that can produce low-back pain. The authors report a less-invasive surgical treatment for SCN entrapment neuropathy that can be performed with local anesthesia. Methods From November 2010 through November 2011, the authors performed surgery in 34 patients (age range 18–83 years; mean 64 years) with SCN entrapment neuropathy. The entrapment was unilateral in 13 patients and bilateral in 21. The mean postoperative follow-up period was 10 months (range 6–18 months). After the site was blocked with local anesthesia, the thoracolumbar fascia of the orifice was dissected with microscissors in a distal-to-rostral direction along the SCN to release the entrapped nerve. Results were evaluated according to Japanese Orthopaedic Association (JOA) and Roland-Morris Disability Questionnaire (RMDQ) scores. Results In all 34 patients, the SCN penetrated the orifice of the thoracolumbar fascia and could be released by dissection of the fascia. There were no intraoperative surgery-related complications. For all patients, surgery was effective; JOA and RMDQ scores indicated significant improvement (p < 0.05). Conclusions For patients with low-back pain, SCN entrapment neuropathy must be considered as a causative factor. Treatment by less-invasive surgery, with local anesthesia, yielded excellent clinical outcomes.

There are more than one million patients worldwide suffering paralysis caused by spinal cord injury (SCI). SCI causes severe socioeconomic problems not only to the patients and their caregivers but also to society; therefore, the development of innovative treatments is crucial. Many pharmacological therapies have been attempted in an effort to reduce SCI-related damage; however, no single therapy that could dramatically improve the serious long-term sequelae of SCI has emerged. Stem cell transplantation therapy, which can ameliorate damage or regenerate neurological networks, has been proposed as a promising candidate for SCI treatment, and many basic and clinical experiments using stem cells for SCI treatment have been launched, with promising results. However, the cell transplantation methods, including cell type, dose, transplantation route, and transplantation timing, vary widely between trials, and there is no consensus regarding the most effective treatment strategy. This study reviews the current knowledge on this issue, with a special focus on the clinical trials that have used stem cells for treating SCI, and highlights the problems that remain to be solved before the widespread clinical use of stem cells can be adopted.

Superficial peroneal nerve (S-PN) entrapment neuropathy (S-PNEN) is comparatively rare and may be an elusive clinical entity. There is yet no established surgical procedure to treat idiopathic S-PNEN. We report our surgical treatment and clinical outcomes. We surgically treated 5 patients (6 sites) with S-PNEN. The 2 men and 3 women ranged in age from 67 to 91 years; one patient presented with bilateral leg involvement. Mean post-operative follow-up was 25.3 months. We recorded their symptoms before- and at the latest follow-up visit after surgery using a Numerical Rating Scale and the Japan Orthopedic Association score to evaluate the affected area. We microsurgically decompressed the affected S-PN under local anesthesia without a proximal tourniquet. We made a linear skin incision along the S-PN and performed wide S-PN decompression from its insertion point at the peroneal tunnel to the peroneus longus muscle (PLM) to the point where the S-PN penetrated the deep fascia. One patient who had undergone decompression in the area of a Tinel-like sign at the initial surgery suffered symptom recurrence and required re-operation 4 months later. We performed additional extensive decompression to address several sites with a Tinel-like sign. All 5 operated patients reported symptom improvement. In patients with idiopathic S-PNEN, neurolysis under local anesthesia may be curative. Decompression involving only the Tinel area may not be sufficient and it may be necessary to include the area from the PLM to the peroneal nerve exit point along the S-PN.

Peroneal nerve entrapment neuropathy (PNEN) is one cause of numbness and pain in the lateral lower thigh and instep, and of motor weakness of the extensors of the toes and ankle. We report a less invasive surgical procedure performed under local anesthesia to treat PNEN and our preliminary outcomes. We treated 22 patients (33 legs), 7 men and 15 women, whose average age was 66 years. The mean postoperative follow-up period was 40 months. All patients complained of pain or paresthesia of the lateral aspect of affected lower thigh and instep; all manifested a Tinel-like sign at the entrapment point. As all had undergone unsuccessful conservative treatment, we performed microsurgical decompression under local anesthesia. Of 19 patients who had undergone lumbar spinal surgery (LSS), 9 suffered residual symptoms attributable to PNEN. While complete symptom abatement was obtained in the other 10 they later developed PNEN-induced new symptoms. Motor weakness of the extensors of the toes and ankle [manual muscle testing (MMT) 4/5] was observed preoperatively in 8 patients; it was relieved by microsurgical decompression. Based on self-assessments, all 22 patients were satisfied with the results of surgery. PNEN should be considered as a possible differential diagnosis in patients with L5 neuropathy due to lumbar degenerative disease, and as a causative factor of residual symptoms after LSS. PNEN can be successfully addressed by less-invasive surgery performed under local anesthesia.

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OBJECT Superior cluneal nerve (SCN) entrapment neuropathy (SCNEN) is a cause of low-back pain (LBP) that can be misdiagnosed as a lumbar spine disorder. The clinical features and etiology of LBP remain poorly understood. In this study, 5 patients with intermittent LBP due to SCNEN who had previously received conservative treatment underwent surgery. The findings are reported and the etiology of LBP is discussed to determine whether it is attributable to SCNEN. METHODS Intermittent LBP is defined as a clinical condition in which pain is induced by standing or walking but is absent at rest. Between April 2012 and March 2013, 5 patients in this study who had intermittent LBP due to SCNEN underwent surgery. The patients included 3 men and 2 women, with a mean age of 66 years. The affected side was unilateral in 2 patients and bilateral in 3 (total sites, 8). The interval from symptom onset to treatment averaged 51.4 months; the mean postoperative follow-up period was 17.6 months. The clinical outcomes were assessed using the numerical rating scale (NRS) for LBP, the Japanese Orthopaedic Association (JOA) scale, and the Roland-Morris Disability Questionnaire (RDQ) preoperatively and at the last follow-up; these data were analyzed statistically. RESULTS None of the 5 patients reported LBP at rest. Intermittent LBP involving the iliac crest and buttocks was induced by standing or walking an average of 136 m. In 2 patients with unilateral involvement, LBP was improved only by SCN block. Surgeries were performed on 6 sites in 5 patients because the SCN block was only transiently effective. Patients’ SCNs penetrated the orifice of the thoracolumbar fascia. SCN kinking at the orifice was exacerbated at the lumbar-extension provocation posture, and radiating pain increased upon manual intraoperative compression of the SCN in this posture. After releasing the SCN surgically, disappearance of the pain was intraoperatively confirmed by manual compression of the SCN with the patients in the lumbar-extension posture. Surgery was effective in all 5 patients, and all clinical outcome scores indicated significant improvement (p < 0.05). CONCLUSIONS To the authors’ knowledge, this is the first report of patients with intermittent LBP due to SCNEN. Clinical and surgical evidence presented suggests that their LBP was exacerbated by lumbar extension and that symptom relief was obtained by SCN block or surgical release of the SCN entrapment. These results suggest that SCNEN should be considered as a causal factor in patients for whom walking elicits LBP.

Neuropathic pain severely impairs rehabilitation and quality of life after spinal cord injury (SCI). The sphingosine-1phosphate receptor agonist, FTY720, plays an important protective role in neuronal injury. This study aims to examine the effects of FTY720 in a rat acute SCI model, focusing on neuropathic pain. Female rats with SCI induced by 1-min clip compression were administered vehicle or 1.5 mg/kg of FTY720 24 h after the injury. Using the mechanical nociceptive threshold test, we monitored neuropathic pain and performed histological analysis of the pain pathway, including the l opioid receptor (MOR), hydroxytryptamine transporter (HTT), and calcitonin gene-related peptide (CGRP). Motor score, SCI lesion volume, residual motor axons, inflammatory response, glial scar, and microvascular endothelial dysfunction were also compared between the two groups. FTY720 treatment resulted in significant attenuation of post-traumatic neuropathic pain. It also decreased systemic and local inflammation, thereby reducing the damaged areas and astrogliosis and resulting in motor functional recovery. Whereas there was no difference in the CGRP expression between the two groups, FTY720 significantly preserved the MOR in both the caudal and rostral areas of the spinal dorsal horn. Whereas HTT was preserved in the FTY720 group, it was significantly increased in the rostral side and decreased in the caudal side of the injury in the vehicle group. These results suggest that FTY720 ameliorates post-traumatic allodynia through regulation of neuroinflammation, maintenance of the blood-brain barrier, and inhibition of glial scar formation, thereby preserving the connectivity of the descending inhibitory pathway and reducing neuropathic pain.

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