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Toyohiko Isu, Kyosuke Kamada, Nobuaki Kobayashi and Shoji Mabuchi

✓ The authors describe the surgical technique of anterior cervical fusion using bone grafts obtained from cervical vertebral bodies. This series consisted of 90 patients with cervical intervertebral disc disease suffering from cervical spondylotic myelopathy. Thirty-five patients were operated on at one level, 33 at two levels, and 22 at three levels. Postoperative x-ray films showed solid bone fusion in all patients at a mean follow-up time of 24 months (range 1 year to 3 years 6 months). Anterior angulation was found in four (4.4%) of the 90 patients. This surgical procedure has two major advantages: 1) there are no complications related to the iliac donor site, allowing early patient mobilization; and 2) the extensive posterior spur can be removed safely and easily under a wide operative field without damaging the spinal cord and nerve roots.

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Yoshinobu Iwasaki, Hiroshi Abe, Toyohiko Isu and Kazuo Miyasaka

✓ The authors describe seven cases of cervical spondylosis in which small high-density areas were detected in the spinal cord on delayed computerized tomographic (CT) myelography. These high-density areas are believed to represent cavities or areas of cystic necrosis. In all seven cases the cervical spinal canal was narrow, and the spondylosis was located at multiple levels, causing a so-called “pincer effect.” On the CT scans the high-density areas resembled fried eggs in the gray matter. These areas were localized near the abnormal cervical discs. In two cases in which the Brown-Séquard syndrome was noted, the symptoms could be attributed to the morphology of the high-density area on the affected side of the cord. Following decompressive surgery, most of the symptoms improved except for numbness of the upper extremities and motor weakness of hands.

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Yoku Nakagawa, Kunio Tashiro, Toyohiko Isu and Mitsuo Tsuru

✓ A case of cerebral metastasis of chorioepithelioma with an occlusion of the angular artery is presented. The occlusion was verified angiographically, surgically, and microscopically.

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Kiyohiro Houkin, Tetsuyuki Yoshimoto, Hiroshi Abe, Kazuo Nagashima, Masahumi Nagashima, Makoto Takeda and Toyohiko Isu

The pathogenesis of moyamoya disease is still under investigation. In this study, the authors focus on the role of cytokines in the pathogenesis of moyamoya disease by using immunohistochemical analyses.

The authors examined two specimens in the circle of Willis obtained at autopsy from two patients with moyamoya disease and two additional specimens obtained from control cadavers with atherosclerotic stenosis of the intracranial carotid arteries. Immunohistochemical examinations of the sections of the major intracranial arteries were performed using antismooth muscle cells (SMCs), monocytes, growth factor, cell nuclear antigen, and fragmented DNA antibodies. Basic fibroblast growth factor (bFGF) staining was present only in the endothelial cells of the moyamoya disease specimens and was not seen in control samples. In addition, the endothelial cells and SMCs in the media were positive for terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick-end labeling of fragmented DNA method but not in the SMCs in the intima in moyamoya disease specimens, which indicates that an apoptotic process is active in only SMCs in the media but not in the intima. In conclusion, it is suggseted that the presence of bFGF in the media specifically seen in moyamoya disease suppresses the apoptotic process of SMCs in the intima.

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Yoshinobu Iwasaki, Kunio Tashiro, Seiji Kikuchi, Mayumi Kitagawa, Toyohiko Isu and Hirosi Abe

✓ The authors describe a case of flexion myelopathy due to specific morphological changes of the cervical cord, termed a “tight dural canal mechanism.” The patient was an 18-year-old man with progressive weakness and muscle atrophy of the left arm. Neuroradiological examination revealed that the lower cervical cord was compressed during flexion of the cervical spine, but that there was no disc disease or cervical vertebral instability. The cord compression was attributed to a pinching mechanism by the posterior border of the vertebral body and the posterior component of the dura on flexion.

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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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Toyohiko Isu, Kazuo Miyasaka, Hiroshi Abe, Terufumi Ito, Yoshinobu Iwasaki, Mitsuo Tsuru, Kenichi Kitaoka and Minoru Tsunoda

✓ Atlantoaxial dislocation was found in three patients with neurofibromatosis. Roentgenographic findings included marked reduction of sagittal diameter at the C-1 vertebral level, and cervical spine abnormalities associated with mesodermal dysplasia, such as posterior scalloping of the cervical spinal bodies with dural ectasia and vertebral body deformity (vertebral body dysplasia). Although the relationship of the atlas and axis did not change with neck position, all three patients had progressive neurological deficits and were treated by decompressive surgery combined with fusion. The pathogenesis of atlantoaxial dislocation associated with neurofibromatosis is discussed.