No abstract

Objective Meningiomas are among the most frequent intracranial tumors. Although the majority of meningiomas can be cured by surgical resection, up to 20% of the patients develop an aggressive clinical course with tumor recurrence or progressive disease. Cytogenetically, meningiomas frequently harbour a normal karyotype or monosomy of chromosome 22 as the sole anomaly. However, progression of meningiomas is associated with a non-random pattern of secondary losses of the chromosomes and chromosomal regions 1p, 6, 10, 14, 18, and 19. There is evidence, that loss of chromosome 17 might be involved in the clonal cytogenetic evolution of recurrent meningiomas. The aim of this study was to determine the role of deletions in the 17q chromosomal region in patients with recurrent meningiomas. Results The authors retrospectively reviewed all patients that underwent repeated surgery for recurrent meningiomas between 1999 and 2015 at the Department of Neurosurgery of the Saarland University Hospital. Patients were included in this study if tumor samples from two or more different meningiomas were available. A total of 7 patients underwent repeated surgery for recurrent meningiomas (4 males, 3 females, mean age: 45.4 years at the date of surgery) between 1999 and 2015. Collectively, 22 biopsies were analyzed with FISH (fluorescence-in-situ-hybridization) for the chromosomal region 17q23.3. In 20/22 (90.1%) specimens, the tumor samples harboured a significant deletion in the chromosomal region 17q (range: 10 to 63% of the cells). In 3/3 (100%) cases, deletion in the 17q chromosomal region was detectable in the primary tumor. In the tumor evolution, there was no steady in- or decrease in the percentage of this deletion. Conclusion Deletion in the 17q chromosomal region was present in the patients’ primary tumors as well as in late recurrences. Overall, a significant deletion in the 17q chromosomal region was detected in 90.1% of the tumors. Thus, the authors assume that deletion in the 17q chromosomal region displays rather an early event in meningioma progression. Accordingly, deletion in the 17q chromosomal region might clinically serve as a potential early marker for malignancy and a higher risk for recurrence in meningiomas.

IMPORTANCE: Myeloperoxidase (MPO)-DNA complexes, biomarkers of neutrophil extracellular traps (NETs), have been associated with arterial and venous thrombosis. Their role in aneurysmal subarachnoid hemorrhage (aSAH) is unknown. OBJECTIVES: To assess whether serum MPO-DNA complexes are present in patients with aSAH and whether they are associated with delayed cerebral ischemia (DCI). DESIGN, SETTING, AND PARTICIPANTS: Post-hoc analysis of a prospective, observational single-center study, with de novo serum biomarker measurements in consecutive patients with aSAH between July 2018 and September 2020, admitted to a tertiary care neuroscience ICU. MAIN OUTCOMES AND MEASURES: We analyzed serum obtained at admission and hospital day 4 for concentrations of MPO-DNA complexes. The primary outcome was DCI, defined as new infarction on brain CT. The secondary outcome was clinical vasospasm, a composite of clinical and transcranial Doppler parameters. We used Wilcoxon signed-rank-test to assess for differences between paired measures. RESULTS: Among 100 patients with spontaneous subarachnoid hemorrhage, mean age 59 years (sd ± 13 yr), 55% women, 78 had confirmed aSAH. Among these, 29 (37%) developed DCI. MPO-DNA complexes were detected in all samples. The median MPO-DNA level was 33 ng/mL (interquartile range [IQR], 18–43 ng/mL) at admission, and 22 ng/mL (IQR, 11–31 ng/mL) on day 4 (unpaired test; p = 0.015). We found a significant reduction in MPO-DNA levels from admission to day 4 in patients with DCI (paired test; p = 0.036) but not in those without DCI (p = 0.17). There was a similar reduction in MPO-DNA levels between admission and day 4 in patients with (p = 0.006) but not in those without clinical vasospasm (p = 0.47). CONCLUSIONS AND RELEVANCE: This is the first study to detect the NET biomarkers MPO-DNA complexes in peripheral serum of patients with aSAH and to associate them with DCI. A pronounced reduction in MPO-DNA levels might serve as an early marker of DCI. This diagnostic potential of MPO-DNA complexes and their role as potential therapeutic targets in aSAH should be explored further.

Background: Posterior cervical foraminotomy is a feasible treatment option for cervical radiculopathy. In this article, we want to give a short review on the advantages, indications and limitations of this treatment procedure.

Background: Myeloperoxidase (MPO)-DNA complexes have been associated with arterial and venous thrombosis. Their role in patients with aneurysmal subarachnoid hemorrhage (aSAH) is unknown. Here, we sought to explore whether serum MPO-DNA-complexes are present in patients with aSAH, and whether levels of serum MPO-DNA complexes are associated with delayed cerebral ischemia (DCI). Methods: We performed a post-hoc analysis of a prospective, blinded, observational single-center biomarker study that enrolled consecutive patients with spontaneous SAH between July 2018 and September 2020. Serum samples obtained on admission and on hospital day 4 were analyzed for concentrations of MPO-DNA complexes. The primary outcome was the occurrence of DCI defined as new infarction on brain CT-scan. The secondary outcome was clinical vasospasm, a composite of clinical and transcranial doppler parameters. We used Wilcoxon's signed-rank-test to assess for differences between paired measures. Results: Among 100 patients with spontaneous SAH, mean age 59 (SD+13) years, 55% women, 78 patients had an aneurysmal SAH and complete DCI information. Among these, 29 (37%) developed DCI. MPO-DNA complexes were detected in all serum samples. The median MPO-DNA level was 33 ng/ml (IQR, 18-43 ng/ml) on admission, and 22 ng/ml (IQR, 11-31 ng/ml) on day 4 (Mann-Whitney test: p=0.015). In the primary outcome analysis, we found a significant reduction in MPO-DNA levels from admission to day 4 in patients with DCI (paired test, p=0.036) but not in those without DCI (p=0.171). The secondary analysis showed a similar reduction in MPO-DNA levels between admission and day 4 in patients with (p=0.006), but not in those without clinical vasospasm (p=0.473). Conclusions: MPO-DNA-complexes are detectable in peripheral serum samples of patients with aSAH. A pronounced reduction in MPO-DNA levels over the first days after aSAH might herald DCI. The potential of MPO-DNA serum levels to serve as a biomarker of DCI requires further exploration.