No abstract

The surgical results of foramen magnum decompression in seven patients with syringomyelia associated with Chiari I malformations are reported. The patients were two men and five women, ranging in age from 23 to 54 years (mean, 30 yr). A bony foramen magnum decompression combined with the removal of the outer layer of the dura mater was performed in seven patients. In an average postoperative follow-up period of 2 years (range, 1-3 yr), neurological symptoms and signs improved in six of seven patients and were unchanged in one patient. Postoperative magnetic resonance imaging scans taken a few weeks after surgery showed a decrease in the size of the syrinx or a disappearance of the syrinx in five of seven patients; a few months were required for a similar reduction in the remaining two patients. In all seven patients, the decompression of the foramen magnum proved to be sufficient, as disclosed by postoperative magnetic resonance imaging. Foramen magnum decompression by our surgical technique is advantageous because all the procedures are extradural and there are, therefore, fewer postoperative complications than the foramen magnum decompression techniques previously reported. Foramen magnum decompression by the authors' surgical technique is effective as the initial surgical treatment for syringomyelia associated with Chiari I malformations.

Low back pain (LBP) is encountered frequently in clinical practice. The superior and the middle cluneal nerves (SCN and MCN) are cutaneous nerves that are purely sensory. They dominate sensation in the lumbar area and the buttocks, and their entrapment around the iliac crest can elicit LBP. The reported incidence of SCN entrapment (SCN-E) in patients with LBP is 1.6%–14%. SCN-E and MCN entrapment (MCN-E) produce leg symptoms in 47%–84% and 82% of LBP patients, respectively. In such patients, pain is exacerbated by lumbar movements, and the symptoms mimic radiculopathy due to lumbar disorder. As patients with failed back surgery or Parkinson disease also report LBP, the differential diagnosis must include those possibilities. The identification of the trigger point at the entrapment site and the disappearance of symptoms after nerve block are diagnostically important. LBP due to SCN-E or MCN-E can be treated less invasively by nerve block and neurolysis. Spinal surgeons treating patients with LBP should consider SCN-E or MCN-E.

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.

Two rare cases of spinal cord herniation associated with intradural spinal arachnoid cyst are reported. A preoperative magnetic resonance imaging scan demonstrated the presence of spinal cord herniation, identified as a protrusion continuous with the spinal cord. Surgery upon the intradural spinal arachnoid cyst improved progressive neurological dysfunction. The authors postulate that spinal cord herniation occurred for the following reason: The pressure of the intradural arachnoid cyst on the dorsal aspect of the spinal cord caused thinning of the dura, leading to a tear and, thus, the development of an extradural arachnoid cyst. Along with the enlargement of intradural arachnoid cyst, the spinal cord herniated through the tear in the dura into the extradural arachnoid cyst.