Object The COVID-19 pandemic has disrupted all aspects of society globally. As healthcare resources had to be preserved for infected patients, and the risk of in-hospital procedures escalated for uninfected patients and staff, neurosurgeons around the world have had to postpone non-emergent procedures. Under these unprecedented conditions, the decision to defer cases became increasingly difficult as COVID-19 cases skyrocketed. Methods Data was collected by self-reporting surveys during two discrete periods: the principal survey accrued responses during 2 weeks at the peak of the global pandemic, and the supplemental survey accrued responses after that to detect changes in opinions and circumstances. Nine hypothetical surgical scenarios were used to query neurosurgeons' opinion on the risk of postponement and the urgency to re-schedule the procedures. An acuity index was generated for each scenario, and this was used to rank the nine cases. Results There were 494 respondents to the principal survey from 60 countries. 258 (52.5%) reported that all elective cases and clinics have been shut down by their main hospital. A total of 226 respondents (46.1%) reported that their operative volume had dropped more than 50%. For the countries most affected by COVID-19, this proportion was 54.7%. There was a high degree of agreement among our respondents that fast-evolving neuro-oncological cases are non-emergent cases that nonetheless have the highest risk in postponement, and selected vascular cases may have high acuity as well. Conclusion We report on the impact of COVID-19 on neurosurgeons around the world. From their ranking of the nine case scenarios, we deduced a strategic scheme that can serve as a guideline to triage non-emergent neurosurgical procedures during the pandemic. With it, hopefully, neurosurgeons can continue to serve their patients without endangering them either neurologically or risking their exposure to the deadly virus.

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An additional tumor suppressor gene on chromosome 9p telomeric to the CDKN2A/B locus has long been postulated to exist. Using Affymetrix 250K single nucleotide polymorphism arrays to screen for copy number changes in glioblastoma multiforme (GBM), we detected a high frequency of deletions of the PTPRD gene, which encodes a receptor protein tyrosine phosphatase at chromosome 9p23-24.1. Missense and nonsense mutations of PTPRD were identified in a subset of the samples lacking deletions, including an inherited mutation with somatic loss of the wild-type allele. We then sequenced the gene in melanoma and identified 10 somatic mutations in 7 of 57 tumors (12%). Reconstitution of PTPRD expression in GBM and melanoma cells harboring deletions or mutations led to growth suppression and apoptosis that was alleviated by both the somatic and constitutional mutations. These data implicate PTPRD in the pathogenesis of tumors of neuroectodermal origin and, when taken together with other recent reports of PTPRD mutations in adenocarcinoma of the colon and lung, suggest that PTPRD may be one of a select group of tumor suppressor genes that are inactivated in a wide range of common human tumor types. [Cancer Res 2008; 68(24):10300-6]

Using immunohistochemistry, we studied the IgG subclass distribution of the anti-Hu antibody in serum, nervous system, and tumor of patients with anti-Hu-associated paraneoplastic encephalomyelitis/sensory neuropathy (PEM/PSN). The nervous system was also examined for deposits of complement and the distribution and type of inflammatory cells. IgG1 and IgG3 were the predominant isotypes of the anti-Hu IgG in serum, nervous system, and tumor. A few patients also had anti-Hu IgG2, but this isotype was not consistently present in all the regions of the nervous system studied. There was no correlation between neurologic symptoms and specific anti-Hu isotype, nor was there evidence that different anti-Hu isotypes recognized specific brain regions. Although IgG1 and IgG3 can activate complement, only weak complement reactivity was found, and that only in a few areas of the nervous system. This finding, in addition to the absence of natural killer (NK) cells, suggested that complement-mediated toxicity and antibody-dependent cell cytotoxicity mediated by NK cells are not pathogenic in PEM/PSN. Inflammatory infiltrates included CD19+ (B cells) and CD4+ (helper/inducer) cells in the perivascular spaces, and lymphocytes bearing CD8+CD11b- markers (cytotoxic T cells) in the interstitial spaces. Infiltrates of EBM11+ (monocyte/macrophage) cells were identified in the perivascular spaces (macrophage phenotype) and in those interstitial regions (microglial phenotype) with severe pathologic changes. The ability of the IgG1 and IgG3 isotypes to bind Fc receptors may have played a role in the recruitment of these monocyte/macrophage cells.(ABSTRACT TRUNCATED AT 250 WORDS)