Cervical schwannoma with acute worsening and intratumoral hemorrhage.

BACKGROUND: Primary spinal tumors are rare and include schwannomas. In the cervical region, these lesions can cause pain, radiculopathy, and/or myelopathy. CASE DESCRIPTION: A 53-year-old male presented with 9 months of chronic neck pain and left upper extremity radiculopathy/myelopathy. The MRI revealed an intradural extramedullary C6-C7 left-sided mass with foraminal extension. Following a C5-C7 laminectomy with C5-T2 instrumented fusion, the diagnosis of schwannoma with evidence of recent hemorrhage was confirmed by biopsy. Three weeks postoperatively, the patient was pain free, no longer taking opioids, and neurologically intact. Although the MRI 6 months later showed no tumor, the MRI 15 months later documented a recurrent enhancing C6-C7 lesion. The patient elected to be treated with external beam radiotherapy and remained asymptomatic. CONCLUSION: A 53-year-old underwent resection of a cervical C6-C7 schwannoma with intratumoral hemorrhage. Fifteen months following C5-C7 laminectomy with C5-T2 fusion, the tumor recurred and required external beam radiation therapy.

Images in Spine: A Rare Abnormal Bony Fusion.

Klippel-Feil syndrome (KFS) is characterized by failed segmentation of the cervical spine leading to inappropriately fused vertebral bodies. A 64-year-old male with a previous L5-S1 decompression presented with significant neck pain with radiation into the entire right upper extremity and hand. Imaging demonstrated fusion of the vertebral bodies at C2-3, C4-6, and C7-T1 with associated disc bulges at C3-4 and C6-7. Common presentation of KFS includes significant spondylosis and cervical myeloradiculopathy in addition to the classic triad of short neck, low posterior hairline, and restricted neck motion. We present exemplary images of this rare condition to aid clinicians in future diagnoses.

Extracranial metastasis of gliobastoma: Three illustrative cases and current review of the molecular pathology and management strategies.

Glioblastoma (GBM) is the most common and the most malignant primary brain tumor in adults, accounting for ~12-15% of all intracranial neoplasms. Despite advances in surgical, medical and radiation therapies, the mortality of GBM remains high, with a median survival ranging between 40 and 70 weeks. Similar to other primary brain tumors, the extracranial metastasis of GBM is extremely rare, occurring in <2% of patients. To demonstrate the clinical characteristics of this rare tumor, we herein present three cases of extracranial GBM metastasis: One to the lungs, which represents the longest reported survival of lung metastases from GBM to date; the second to the soft tissue of the posterior neck; and the third to the lumbar intradural space. Unlike tumors elsewhere, there are unique barriers in the brain that prevent the hematogenous and lymphatic spread of intracranial tumors, such as the dura mater and the thickened basement membrane of the blood vessels. In addition, central nervous system tumor cells lack extracellular matrix proteins required to invade surrounding connective tissue, a prerequisite for tumor dissemination. In this study, we aimed to investigate the different possible mechanisms underlying the extracranial metastasis of GBM and determine the biomolecular and genetic characteristics differentiating GBMs that metastasize from those that do not. We also reviewed the role of systemic chemotherapy and bevacizumab in the treatment of disseminated GBMs. Early identification and differentiation of these tumors may enable patients to benefit from surgical resection, radiation and combination chemotherapy prior to developing other comorbidities from metastatic disease, which may translate into prolonged survival with an acceptable quality of life.

Depths and grids in brain tumors: implantation strategies, techniques, and complications.

Patients with intracranial mass lesions are at increased risk of intractable epilepsy even after tumor resection due to the potential epileptogenicity of lesional and perilesional tissue. Risk factors for tumoral epilepsy include tumor location, histology, and extent of tumor resection. In epilepsy that occurs after tumor resection, the epileptogenic zone often does not correspond precisely with the area of abnormality on imaging, and seizures often arise from a relatively restricted area despite widespread changes on imaging. Invasive monitoring via subdural grids and/or depth electrodes can therefore be helpful to delineate areas of eloquence and localize the epileptogenic zone for subsequent resection. Subdural grids offer excellent contiguous coverage of superficial cortex and allow resection using the same craniotomy, facilitating understanding of anatomic relationships. Depth electrodes offer superior coverage of deep structures, are easier to use in cases where a previous craniotomy is present, are not associated with anatomic distortion due to brain shift, and may be associated with a lower complication rate. We review the biology of focal postoperative epilepsy and invasive diagnostic strategies for the surgical evaluation of medically refractory epilepsy in patients who have undergone resection of intracranial mass lesions.

Controlled release of lipopolysaccharide in the subarachnoid space of rabbits induces chronic vasospasm in the absence of blood.

OBJECTIVE: Leukocyte-endothelial cell interactions appear to play a role in the development of vasospasm after SAH. Using a purely inflammatory protein, LPS, we evaluated the effect of inflammation on the development of chronic vasospasm in the absence of blood and compared it to SAH-induced vasospasm in rabbits. METHODS: Lipopolysaccharide was incorporated into EVAc polymers to produce 20% LPS/EVAc polymers (wt/wt). Rabbits (n = 23) were randomized to 4 experimental groups: (1) empty polymer (n = 6), (2) SAH (n = 5), (3) 0.7 mg/kg polymeric LPS dose (n = 6), and (4) 1.4 mg/kg polymeric LPS dose (n = 6). Blood and polymers were inserted into the cisterna magna. The rabbits were killed 3 days postoperatively, and the basilar arteries were harvested for morphometric analysis. Clinical response and lumen patencies were analyzed using ANOVA and a post hoc Newman-Keuls Multiple Comparisons test. RESULTS: Significant narrowing of the basilar artery was observed by insertion of 20% LPS/EVAc polymers into the subarachnoid space at a polymeric dose of 1.4 mg/kg (actual dose, 66 microg kg(-1) d(-1)) (75.4% +/- 4.2%; P < .01) and by SAH (80.3% +/- 8.1%; P < .01) as compared with the empty polymer group. A trend toward narrowing was observed in the 0.7 mg/kg polymeric LPS dose group (actual dose, 33 microg kg(-1) d(-1)) (85.2% +/- 2.6%; P > .05). Symptoms associated with SAH were noted in 50% of the rabbits in the 0.7 mg/kg LPS group and in 100% of rabbits in the 1.4 mg/kg LPS group. CONCLUSION: Controlled release of LPS into the subarachnoid space of rabbits produced chronic vasospasm in a dose-dependent manner. At a polymeric dose of 1.4 mg/kg, LPS-induced vasospasm was equivalent to that induced by SAH. This suggests that LPS and SAH may induce vasospasm through similar mechanisms and provides further evidence that inflammation plays a central role in the etiology of chronic vasospasm.