Incidence of Postoperative Hematomas Requiring Surgical Treatment in Neurosurgery : A Retrospective Observational Study

OBJECTIVE: We aimed to characterize the occurrence of postoperative hematoma (POH) after neurosurgery overall and according to procedure type and describe the prevalence of possible confounders. METHODS: Patient data between 2010 and 2012 at the Department of Neurosurgery in Helsinki University Hospital were retrospectively analyzed. A data search was performed according to the type of surgery including craniotomies; shunt procedures, spine surgery, and spinal cord stimulator implantation. We analyzed basic preoperative characteristics, as well as data about the initial intervention, perioperative period, revision operation and neurologic recovery (after craniotomy only). RESULTS: The overall incidence of POH requiring reoperation was 0.6% (n = 56/8783) to 0.6% (n = 26/4726) after craniotomy, 0% (n = 0/928) after shunting procedure, 1.1% (n = 30/2870) after spine surgery, and 0% (n = 0/259) after implantation of a spinal cord stimulator. Craniotomy types with higher POH incidence were decompressive craniectomy (7.9%, n = 7/89), cranioplasty (3.6%, n = 4/112), bypass surgery (1.7%, n = 1/60), and epidural hematoma evacuation (1.6%, n = 1/64). After spinal surgery, POH was observed in 1.1% of cervical and 2.1% of thoracolumbar operations, whereas 46.7% were multilevel procedures. 64.3% of patients with POH and 84.6% of patients undergoing craniotomy had postoperative hypertension (systolic blood pressure >160 mm Hg or lower if indicated). Poor outcome (Glasgow Outcome Scale score 1-3), whereas death at 6 months after craniotomy was detected in 40.9% and 21.7%. respectively, of patients with POH who underwent craniotomy. CONCLUSIONS: POH after neurosurgery was rare in this series but was associated with poor outcome. Identification of risk factors of bleeding, and avoiding them, if possible, might decrease the incidence of POH.Peer reviewe

Cytogenetic Characterizations of Central Nervous System Tumors: The First Comprehensive Report from a Single Institution in Korea

The World Health Organization (WHO) classification of central nervous system (CNS) tumors incorporates morphology, cytogenetics, molecular genetics, and immunologic markers. Despite the relatively large number of CNS tumors with clonal chromosome abnormalities, only few studies have investigated cytogenetic abnormalities for CNS tumors in Korea. Thus, we investigated 119 CNS tumors by conventional G-banded karyotypes to characterize patterns of chromosomal abnormalities involving various CNS tumors, and 92.4% of them were cultured and karyotyped successfully. Totally, 51.8% of karyotypable CNS tumors showed abnormal cytogenetic results, including neuroepithelial tumors (75.0%), meningeal tumors (71.1%), pituitary adenomas (4.2%), schwannomas (44.4%), and metastatic tumors (100.0%). Glioblastomas had hyperdiploid, complex karyotypes, mainly involving chromosomes Y, 1, 2, 6, 7, 10, 12, 13, and 14. Monosomy 22 was observed in 56.4% of meningiomas. There was a significant increase in the frequencies of karyotypic complexity according to the increase of WHO grade between grades I and II (P=0.0422) or IV (P=0.0101). Abnormal karyotypes were more complex at high-grade tumors, suggesting that the karyotype reflects the biologic nature of the tumor. More detailed cytogenetic and molecular characterizations of CNS tumors contribute to better diagnostic criteria and deeper insights of tumorigenesis, eventually resulting in development of novel therapeutic strategies

Genetic and Epigenetic Alterations of the NF2 Gene in Sporadic Vestibular Schwannomas

BACKGROUND: Mutations in the neurofibromatosis type 2 (NF2) tumor-suppressor gene have been identified in not only NF2-related tumors but also sporadic vestibular schwannomas (VS). This study investigated the genetic and epigenetic alterations in tumors and blood from 30 Korean patients with sporadic VS and correlated these alterations with tumor behavior. METHODOLOGY/PRINCIPAL FINDINGS: NF2 gene mutations were detected using PCR and direct DNA sequencing and three highly polymorphic microsatellite DNA markers were used to assess the loss of heterozygosity (LOH) from chromosome 22. Aberrant hypermethylation of the CpG island of the NF2 gene was also analyzed. The tumor size, the clinical growth index, and the proliferative activity assessed using the Ki-67 labeling index were evaluated. We found 18 mutations in 16 cases of 30 schwannomas (53%). The mutations included eight frameshift mutations, seven nonsense mutations, one in-frame deletion, one splicing donor site, and one missense mutation. Nine patients (30%) showed allelic loss. No patient had aberrant hypermethylation of the NF2 gene and correlation between NF2 genetic alterations and tumor behavior was not observed in this study. CONCLUSIONS/SIGNIFICANCE: The molecular genetic changes in sporadic VS identified here included mutations and allelic loss, but no aberrant hypermethylation of the NF2 gene was detected. In addition, no clear genotype/phenotype correlation was identified. Therefore, it is likely that other factors contribute to tumor formation and growth

Genomic profiling distinguishes familial multiple and sporadic multiple meningiomas

<p>Abstract</p> <p>Background</p> <p>Meningiomas may occur either as familial tumors in two distinct disorders, familial multiple meningioma and neurofibromatosis 2 (NF2), or sporadically, as either single or multiple tumors in individuals with no family history. Meningiomas in NF2 and approximately 60% of sporadic meningiomas involve inactivation of the <it>NF2 </it>locus, encoding the tumor suppressor merlin on chromosome 22q. This study was undertaken to establish whether genomic profiling could distinguish familial multiple meningiomas from sporadic solitary and sporadic multiple meningiomas.</p> <p>Methods</p> <p>We compared 73 meningiomas presenting as sporadic solitary (64), sporadic multiple (5) and familial multiple (4) tumors using genomic profiling by array comparative genomic hybridization (array CGH).</p> <p>Results</p> <p>Sporadic solitary meningiomas revealed genomic rearrangements consistent with at least two mechanisms of tumor initiation, as unsupervised cluster analysis readily distinguished tumors with chromosome 22 deletion (associated with loss of the <it>NF2 </it>tumor suppressor) from those without chromosome 22 deletion. Whereas sporadic meningiomas without chromosome 22 loss exhibited fewer chromosomal imbalance events overall, tumors with chromosome 22 deletion further clustered into two major groups that largely, though not perfectly, matched with their benign (WHO Grade I) or advanced (WHO Grades II and III) histological grade, with the latter exhibiting a significantly greater degree of genomic imbalance (P < 0.001). Sporadic multiple meningiomas showed a frequency of genomic imbalance events comparable to the atypical grade solitary tumors. By contrast, familial multiple meningiomas displayed no imbalances, supporting a distinct mechanism for the origin for these tumors.</p> <p>Conclusion</p> <p>Genomic profiling can provide an unbiased adjunct to traditional meningioma classification and provides a basis for exploring the different genetic underpinnings of tumor initiation and progression. Most importantly, the striking difference observed between sporadic and familial multiple meningiomas indicates that genomic profiling can provide valuable information for differential diagnosis of subjects with multiple meningiomas and for considering the risk for tumor occurrence in their family members.</p

The importance of nerve microenvironment for schwannoma development

Schwannomas are predominantly benign nerve sheath neoplasms caused by Nf2 gene inactivation. Presently, treatment options are mainly limited to surgical tumor resection due to the lack of effective pharmacological drugs. Although the mechanistic understanding of Nf2 gene function has advanced, it has so far been primarily restricted to Schwann cell-intrinsic events. Extracellular cues determining Schwann cell behavior with regard to schwannoma development remain unknown. Here we show pro-tumourigenic microenvironmental effects on Schwann cells where an altered axonal microenvironment in cooperation with injury signals contribute to a persistent regenerative Schwann cell response promoting schwannoma development. Specifically in genetically engineered mice following crush injuries on sciatic nerves, we found macroscopic nerve swellings in mice with homozygous nf2 gene deletion in Schwann cells and in animals with heterozygous nf2 knockout in both Schwann cells and axons. However, patient-mimicking schwannomas could only be provoked in animals with combined heterozygous nf2 knockout in Schwann cells and axons. We identified a severe re-myelination defect and sustained macrophage presence in the tumor tissue as major abnormalities. Strikingly, treatment of tumor-developing mice after nerve crush injury with medium-dose aspirin significantly decreased schwannoma progression in this disease model. Our results suggest a multifactorial concept for schwannoma formation-emphasizing axonal factors and mechanical nerve irritation as predilection site for schwannoma development. Furthermore, we provide evidence supporting the potential efficacy of anti-inflammatory drugs in the treatment of schwannomas

Delayed Migration of Fractured K-wire Causing Vertebral Artery Invagination After Anterior Atlantoaxial Fixation : A Case Report

BACKGROUND: Most of the physician's attention during spinal surgery, when using wires and screws, is toward the avoidance of injuries of critical structures (nerves and vessels). When such wires are broken during surgery, the most important point is to take them out safely or, if it is impossible, to leaf them in secure place and follow the patient closely. Migrations of broken Kirschner wire (K-wire) are well known in literature; however, to the best of our knowledge, migration of a fractured K-wire during anterior atlantoaxial fixation of cervical spine has not been reported in the literature. CASE DESCRIPTION: We report a case in which a fractured K-wire was imbedded in the lateral mass of C1 for 3 years and then migrated to endanger the dominant right vertebral artery. By using posterior approach and drilling right part of posterior arch of C1, we manage to secure the vertebral artery. The broken K-wire was extracted successfully. In our case, with optimal follow-up, the burred wire inside hard bone was moved in delayed fashion to come out of the bone, grooving the dominant vertebral artery. CONCLUSIONS: Our recommendation is to inspect the K-wire before using it and to try retrieve as much as possible when removing it.Peer reviewe