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✓ Intracranial schwannomas are relatively common benign tumors arising from Schwann cells. Among the cranial nerves, the vestibular division of the vestibulocochlear nerve is the site most commonly affected by these lesions, followed by the trigeminal nerve. The authors report a case of bilateral schwannomas arising from both of the pterygoid canals. A 13-year-old girl presented with intermittent headaches and left-sided facial palsy. Preoperative computerized tomography scans and magnetic resonance images revealed nonenhancing round masses within the bilateral vidian canals, bone erosion, and sclerosis. The transnasal transseptal transsphenoidal approach was used to remove the masses. Postoperatively, the patient recovered uneventfully. On histopathological examination, the masses were confirmed as schwannomas. The clinical presentation and probable histogenesis of schwannomas arising in this location are discussed together with a review of the literature.

✓ Surgical treatment of intraforaminal disc herniations at the L5–S1 level is technically demanding. The 2 most commonly used procedures involve either a medial or lateral ipsilateral approach and often require a partial or even complete facet resection, which may in turn result in vertebral instability and/or back pain, as well as, in some cases, a fusion or stabilization procedure. In this report, the authors present a new minimally invasive technique for the treatment of L5–S1 intraforaminal disc herniations. Using this technique, which involves tubular retractors and an operative microscope to approach the neural foramen from the contralateral side, the authors could easily visualize and remove the herniated disc material and perform a thorough microdiscectomy with minimal resection of osseous and ligamentous structures. To illustrate this new minimally invasive technique for the treatment of intraforaminal disc herniations at L5–S1, they describe the cases of 2 patients who underwent the procedure and in whom successful results were achieved.

Combined anterior and posterior surgery is frequently chosen for the treatment of prior, severe C1–2 dislocations that occurred during early childhood because of the difficulty in achieving reduction and satisfactory decompression. The authors treated a prior, severe C1–2 dislocation that was causing progressive quadriparesis. The patient was a 14-year-old boy who had suffered a C1–2 fracture-dislocation at 3 years of age and had been treated with a Minerva body jacket cast. The treatment involved posterior C1–2 segmental screw fixation, without direct bone decompression or additional surgery. Satisfactory neural decompression was achieved with the techniques used, and complete bone union was confirmed. The patient showed satisfactory neurological recovery at the 5-year follow-up assessment.

Object.Granulocyte—macrophage colony—stimulating factor (GM-CSF) is a potent hemopoietic cytokine that stimulates stem cell proliferation in the bone marrow and inhibits apoptotic cell death in leukocytes. Its effects in the central nervous system, however, are still unclear. The present study was undertaken to determine if GM-CSF can rescue neuronal cells from apoptosis and improve neurological function in a spinal cord injury (SCI) model.

Methods.研究了gm - csf对凋亡的影响neuronal death, the authors used a staurosporine-induced neuronal death model in an N2A cell line (in vitro) and in a rat SCI model (in vivo). The N2A cells were preincubated with GM-CSF for 60 minutes before being exposed to staurosporine for 24 hours. To inhibit GM-CSF, N2A cells were pretreated with antibodies against the GM-CSF receptor for 60 minutes. Clip compression was used to induce SCI. Animals were treated with daily doses of GM-CSF (20 µg/day) for 5 days. The number of apoptotic cells in the spinal cord and neurological improvements were assessed.

Pretreatment with GM-CSF was found to protect N2A cells significantly from apoptosis, and neutralizing antibodies for the GM-CSF receptors inhibited the rescuing effect of GM-CSF on apoptosis. In the rat SCI model, neurological function improved significantly in the GM-CSF—treated group compared with controls treated with phosphate-buffered saline. Terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling staining showed that GM-CSF administration reduced apoptosis in the injured spinal cord.

Conclusions.Treatment of SCI with GM-CSF showed beneficial effects. Neuronal protection against apoptosis is viewed as a likely mechanism underlying the therapeutic effect of GM-CSF in SCI.