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Daijiro Morimoto, Toyohiko Isu, Kyongsong Kim, Tetsuaki Imai, Kazuyoshi Yamazaki, Ryoji Matsumoto and Masanori Isobe


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.


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.


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).


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.

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Juntaro Matsumoto, Toyohiko Isu, Kyongsong Kim, Naotaka Iwamoto, Daijiro Morimoto and Masanori Isobe


The etiology of low-back pain (LBP) is heterogeneous and is unknown in some patients with chronic pain. Superior cluneal nerve entrapment has been proposed as a causative factor, and some patients suffer severe symptoms. The middle cluneal nerve (MCN) is also implicated in the elicitation of LBP, and its clinical course and etiology remain unclear. The authors report the preliminary outcomes of a less invasive microsurgical release procedure to address MCN entrapment (MCN-E).


The authors enrolled 11 patients (13 sites) with intractable LBP judged to be due to MCN-E. The group included 3 men and 8 women ranging in age from 52 to 86 years. Microscopic MCN neurolysis was performed under local anesthesia with the patient in the prone position. Postoperatively, all patients were allowed to walk freely with no restrictions. The mean follow-up period was 10.5 months. LBP severity was evaluated on the numerical rating scale (NRS) and by the Japanese Orthopaedic Association (JOA) and the Roland-Morris Disability Questionnaire (RDQ) scores.


All patients suffered buttock pain, and 9 also had leg symptoms. The symptoms were aggravated by standing, lumbar flexion, rolling over, prolonged sitting, and especially by walking. The numbers of nerve branches addressed during MCN neurolysis were 1 in 9 patients, 2 in 1 patient, and 3 in 1 patient. One patient required reoperation due to insufficient decompression originally. There were no local or systemic complications during or after surgery. Postoperatively, the symptoms of all patients improved statistically significantly; the mean NRS score fell from 7.0 to 1.4, the mean RDQ from 10.8 to 1.4, and the mean JOA score rose from 13.7 to 23.6.


Less invasive MCN neurolysis performed under local anesthesia is useful for LBP caused by MCN-E. In patients with intractable LBP, MCN-E should be considered.

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Kyongsong Kim, Toyohiko Isu, Yasuhiro Chiba, Daijiro Morimoto, Seiji Ohtsubo, Mitsuo Kusano, Shiro Kobayashi and Akio Morita

Superior cluneal nerve (SCN) entrapment neuropathy is a known cause of low back pain. Although surgical release at the entrapment point of the osteofibrous orifice is effective, intraoperative identification of the thin SCN in thick fat tissue and confirmation of sufficient decompression are difficult. Intraoperative indocyanine green video angiography (ICG-VA) is simple, clearly demonstrates the vascular flow dynamics, and provides real-time information on vascular patency and flow. The peripheral nerve is supplied from epineurial vessels around the nerve (vasa nervorum), and the authors now present the first ICG-VA documentation of the technique and usefulness of peripheral nerve neurolysis surgery to treat SCN entrapment neuropathy in 16 locally anesthetized patients. Clinical outcomes were assessed with the Roland-Morris Disability Questionnaire before surgery and at the latest follow-up after surgery.

Indocyanine green video angiography was useful for identifying the SCN in fat tissue. It showed that the SCN penetrated and was entrapped by the thoracolumbar fascia through the orifice just before crossing over the iliac crest in all patients. The SCN was decompressed by dissection of the fascia from the orifice. Indocyanine green video angiography visualized the SCN and its termination at the entrapment point. After sufficient decompression, the SCN was clearly visualized on ICG-VA images. Low back pain improved significantly, from a preoperative Roland-Morris Questionnaire score of 13.8 to a postoperative score of 1.3 at the last follow-up visit (p < 0.05). The authors suggest that ICG-VA is useful for the inspection of peripheral nerves such as the SCN and helps to identify the SCN and to confirm sufficient decompression at surgery for SCN entrapment.

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Yasuhiro Chiba, Toyohiko Isu, Kyongsong Kim, Naotaka Iwamoto, Daijiro Morimoto, Kazuyoshi Yamazaki, Masaaki Hokari, Masanori Isobe and Mitsuo Kusano


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.


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.


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).


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.