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Anterior cervical discectomy and fusion (ACDF) has long been the standard surgical treatment for cervical degenerative disc disease (DDD); however, cervical artificial total disc replacement (cTDR) has gained increasing recognition in recent years due to its ability to maintain a natural range of motion and lower the rate of adjacent segment disease. Although cTDR is only approved for one or two levels in the United States, it has been used for three or more levels in other countries. We present a case of a 59-year-old male patient who underwent three-level cTDR (C4-C7) in Germany and presented 10 years later with progressive paracervical pain and worsening dysphagia. Magnetic resonance imaging (MRI) and computed tomography (CT) scan showed hardware loosening, progressive loss of bone around the device, and a cyst ventral to C4-C5 with mass effect on the hypopharynx. The patient was successfully treated with posterior cervical fusion and showed improvement in neck pain. This case underscores the significance of long-term follow-up and thoughtful consideration when selecting an appropriate treatment modality for patients afflicted with cervical DDD.

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BACKGROUND: Surgery on patients with lesions in the dominant hemisphere for language is best done with awake language mapping. Intraoperative MRI (iMRI) has also been proposed as an ideal method for tumor resection control in patients with primary brain tumors. OBJECTIVES: This study examines the feasibility of low-field iMRI during awake craniotomy and tumor resection. METHODS: 36 patients underwent awake resection with a compact iMRI for guidance. Outcomes were grouped using an A-D classification. Outcome A was defined as gross total resection (GTR) without iMRI, B as GTR achieved secondary to iMRI findings, C as resection stopped due to mapping but prior to iMRI, and, finally, D as resection stopped after iMRI had showed residual tumor but subsequent mapping limited further resection. RESULTS: Diagnoses included primary brain tumors in all but 2 patients: 1 had mesial temporal sclerosis and 1 cysticercosis. Overall, outcomes A and D were the most common with 12 patients each, outcome C was the least common occurring in only 3 patients, and outcome B occurred in 9 patients. Hence, in 12 patients, iMRI led to increased tumor resection while in another 12 brain mapping limited the extent of resection. CONCLUSIONS: Combined awake language and motor mapping and iMRI guidance is feasible for resection of brain lesions. A compact iMRI has unique advantages for this approach.

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OBJECTIVE: To examine whether intraoperative MRI can enhance safety and extent of resection of complex intracranial meningiomas, given its positive role in the resection of malignant brain tumors and pituitary tumors. METHODS: Over a ten-year period, 70 operations were performed on 66 patients with intracranial meningiomas using the compact, mobile PoleStar N20 iMRI navigation system. A retrospective review was conducted examining patient demographics, surgical characteristics, and outcomes. RESULTS: 36 meningiomas were above the skull base and 30 were of the skull base. Four (5.7%) operations were done for recurrent meningiomas. 63 patients (95.5%) had WHO grade I and 3 patients (4.5%) had WHO grade III meningiomas. 9 (12.8%) patients required additional tumor resection based on iMRI findings, and in 4 patients (6%) iMRI imaging allowed for avoidance of additional dissection near critical neurovascular structures. CONCLUSIONS: Up to 15.7% of patients had surgery positively affected by intraoperative imaging either improving the resection or avoiding unnecessary additional dissection which could potentially harm critical neurologic structures. As iMRI becomes more widely available it may be valuable to use in an appropriate subset of patients with intracranial meningiomas.

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The aim of this study was to determine the predictability of vertebral compression fracture (VCF) development applying the spinal instability neoplastic score (SINS) prior to delivery of stereotactic spinal radiosurgery (SSRS) for spinal metastases. From two prospective cohorts of SSRS for spinal metastases, we selected patients with a low degree of cord compression or cauda equine from C3 to S1 and analyzed 79 patients enrolled according to binary SINS criteria. The primary endpoint was the development of a de novo VCF or progression of an existing fracture after SSRS. We identified 32 fractures (40.5%): 19 de novo and 13 progressive. The mean time to fracture after SSRT was 3.3 months (range, 0.4-34.1 months). In 41 patients with low SINS (0-6), 7 patients (17.1%) developed a fracture after SSRS. In 38 patients with high SINS (7-12), 25 (65.8%) developed a fracture. Among the 32 fractures, 15 were symptomatic. Patients with high SINS were more likely to experience symptomatic fractures (31.6%) than were patients with lower SINS (7.4%). On univariate and multivariate analysis, 24-month fracture-free rates were 78.7 and 33.7% in low and high SINS group, respectively and high SINS was found to be a significant risk factor for VCFs and symptomatic fractures (respectively, HR 5.6, p = 0.04; HR 5.3, p = 0.01). SINS is a useful tool for predicting the development of VCF after SSRS for spinal metastases. Prophylactic cement augmentation should not be considered for patients with lower SINS, since the risk of fracture is low.

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OBJECT: Medulloblastomas are the most common malignant brain tumors in children. These tumors are highly invasive, and patients harboring these lesions are frequently diagnosed with distant spread. In this study, the authors investigated the role of Rac1, a member of the Rho family of small guanosine triphosphatases, in medulloblastoma invasion. METHODS: Three established medulloblastoma cell lines were used: DAOY, UW-228, and ONS-76. Specific depletion of Rac1 protein was accomplished by transient transfection of small interfering RNA. Cell invasion through extracellular matrix (Matrigel) was quantified using a transwell migration assay. Mitogen activated protein kinase activation was determined using phospho-MAP kinase-specific antibodies, and inhibition of MAP kinase pathways was achieved by specific small molecule inhibitors. Localization of Rac1 and its expression levels were determined by immunohistochemical analysis using a Rac1-specific antibody, and Rac1 activation was qualitatively assessed by Rac1 plasma membrane association. RESULTS: Small interfering RNA-mediated depletion of Rac1 strongly inhibited medulloblastoma cell invasion. Although depletion of Rac1 inhibited the proliferation of UW-228 cells, and of ONS-76 cells to a lesser extent, it stimulated the proliferation of DAOY cells. Depletion of Rac1 also inhibited the activation of the ERK and JNK MAP kinase pathways, and inhibition of either pathway diminished invasion and proliferation. Immunohistochemical analysis demonstrated that the Rac1 protein was overexpressed in all medulloblastoma tumors examined, and indicated that Rac1 was hyperactive in 6 of 25 tumors. CONCLUSIONS: The authors' data show that Rac1 is necessary for the invasive behavior of medulloblastoma cells in vitro, and plays a variable role in medulloblastoma cell proliferation. In addition, these results indicate that Rac1 stimulates medulloblastoma invasion by activating the ERK and JNK pathways. The authors suggest that Rac1 and signaling elements controlled by this guanosine triphosphatase may serve as novel targets for therapeutic intervention in malignant medulloblastomas.

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Pak kinases are thought to play critical roles in cell migration and invasion. Here, we analyze the roles of Pak1 and Pak2 in breast carcinoma cell invasion using the transient transfection of small interfering RNA. We find that although both Pak1 and Pak2 contribute to breast carcinoma invasion stimulated by heregulin, these roles are mediated by distinct signaling mechanisms. Thus, whereas the depletion of Pak1 interferes with the heregulin-mediated dephosphorylation of cofilin, the depletion of Pak2 does not. The depletion of Pak1 also has a stronger inhibitory effect on lamellipodial protrusion than does the depletion of Pak2. Interestingly, Pak1 and Pak2 play opposite roles in regulating the phosphorylation of the myosin light chain (MLC). Whereas the depletion of Pak1 decreases phospho-MLC levels in heregulin-stimulated cells, the depletion of Pak2 enhances MLC phosphorylation. Consistent with their opposite effects on MLC phosphorylation, Pak1 and Pak2 differentially modulate focal adhesions. Pak2-depleted cells display an increase in focal adhesion size, whereas in Pak1-depleted cells, focal adhesions fail to mature. We also found that the depletion of Pak2, but not Pak1, enhances RhoA activity and that the inhibition of RhoA signaling in Pak2-depleted cells decreases MLC phosphorylation and restores cell invasion. In summary, this work presents the first comprehensive analysis of functional differences between the Pak1 and Pak2 isoforms.

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