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Determining the stability of the cervical spine is paramount to the successful management of patients with cervical spine trauma or neoplastic disease. While this article will discuss both traumatic instability and neoplastic instability, the underlying pathology of each requires a different approach. Traumatic cervical spine injuries must be broken down into upper and lower cervical spine injuries, and the stability is predicated on both the boney and ligamentous injury. This article will go through the different fracture patterns and discuss the stability of each one. Additionally, it will discuss the important biomechanical and clinical issues that lead to the diagnosis of metastatic instability in the cervical spine.

Spinal stenosis occurs most commonly in the elderly population and patients typically present with symptoms of neurogenic claudication. Complex stenosis is that which occurs in conjunction with spondylolisthesis or scoliosis. In addition to typical complaints, patients commonly develop radicular pain and back pain. In most cases initial treatment is nonoperative. Patients who fail to respond symptomatically are treated surgically. Surgical intervention in cases of complex stenosis necessitates decompression of the neural elements, and recent literature supports the addition of instrumented fusion to the decompression. More minimally invasive strategies are beginning to surface to treat complex stenosis as well.

Background context The reported incidence of vertebral hemangioma within the spinal column is common. Most often these benign vascular tumors are incidental radiographic findings and do not cause neurological sequelae. Rarely, vertebral hemangiomas will cause compressive neurological symptoms, such as radiculopathy, myelopathy and paralysis. In these cases the clinical presentation is usually the subacute or delayed onset of progressive neurological symptoms. This report demonstrates a symptomatic vertebral hemangioma presenting with rapid onset neurologic sequelae. Purpose To discuss diagnostic and management issues presented by symptomatic vertebral hemangioma. Study design Case report and review of literature. Patient sample Sixty-one-year-old white woman with low back pain and rapidly progressive myelopathic symptoms. Methods A case of vertebral hemangioma with neurological sequelae is presented followed by a discussion of the literature concerning diagnostic and therapeutic options in the management of this pathologic entity. Results The results of our review reveal that the incidence of vertebral hemangioma causing compressive neurological symptoms is rare despite the overall prevalence of vertebral hemangioma. Vertebral hemangioma may present with rapid onset myelopathic symptoms and may mimic those symptoms caused by a malignancy. Radiographic imaging modalities are extremely useful and display characteristic findings in the diagnostic evaluation of these tumors. Angiographic embolization of feeding vessels has been effective in minimizing operative blood loss, and surgical decompression and stabilization is frequently indicated. Postsurgical radiotherapy has also been demonstrated to serve as a limited adjunct to surgery by reducing tumor recurrence in the event of less than complete tumor resection. Conclusions Because of the rapid presentation of myelopathic symptoms in this case, preoperative angiographic embolization was not performed, and the patient underwent emergent decompressive surgery. In this case emergent operative decompression and stabilization was effective in reversing the patient's myelopathic symptoms, while maintaining long-term stability of the spinal column. Postoperative radiation was not administered because of the extent of tumor resection. Surgical intervention has produced long-term cure of this patient's myelopathy and T10 vertebral hemangioma.

Vascular rejection after renal transplantation is connected with a higher frequency of allograft dysfunction or graft loss. Plasmapheresis as an adjunctive therapy in the treatment of humoral mediated acute graft rejection was compared with protein A immunoadsorption. Eleven patients with acute graft rejection and high titers of cytotoxic HLA- Ab and/or signs of vascular rejection at graft biopsy (performed in 9 patients) have been treated. Six of them have a stable graft function, the longest graft survival until now is 41 months, four are back on haemodialysis and one patient died from CMV-pneumonia with a stable graft function 9 months after transplantation. We conclude that IA is a useful adjunctive therapy in the treatment of vascular rejection after renal transplantation. Further investigations are necessary to optimize criteria for inclusion.