Acute low back pain is a highly prevalent condition that poses significant challenges to healthcare systems worldwide. In this manuscript, we present the most current, evidence-based guidelines from the World Federation of Neurosurgical Societies (WFNS) Spine Committee on the epidemiology, etiology, and prevention of acute low back pain (LBP) lasting ≤ 4 weeks. We performed a literature review 2012–2022 using the PubMed, Medline, and CENTRAL databases with the keywords “acute low back pain”, “acute back pain”, “low back pain”, “epidemiology”, “etiology”, “costs”, “risk factor”, “cultural”, “developed”, “developing” and “prevention”. Systematic screening criteria were applied, resulting in 13 final articles on epidemiology and etiology of LBP, 2 manuscripts on costs, 5 articles on risk factors, and 23 articles on prevention strategies for acute LBP. These were presented at two separate international meetings, where members of the WFNS Spine Committee voted on five final consensus statements presented here. and Conclusions: There is a high incidence and prevalence of acute LBP, particularly in high-income countries, which is felt to be at least partially due to demographic shifts with an aging population and lifestyle changes including higher rates of obesity and physical inactivity. Acute LBP has a significant impact on quality of life and ability to work, resulting in high direct and indirect costs worldwide. Early diagnosis and appropriate management of acute LBP is recommended to prevent this pain from turning into chronic LBP. The WFNS Spine Committee's recommendations respresent the latest guidelies to help improve patient care for acute LBP worldwide.

BACKGROUND: Standard therapeutic protocols for glioblastoma, the most aggressive type of brain cancer, include surgery followed by chemoradiotherapy. Additionally, carmustine-eluting wafers can be implanted locally into the resection cavity. OBJECTIVE: To evaluate microRNA (miRNA)-181d as a prognostic marker of responses to carmustine wafer implantation. METHODS: A total of 80 glioblastoma patients (40/group) were included in a matched pair analysis. One group (carmustine wafer group) received concomitant chemoradiotherapy with carmustine wafer implantation (Stupp protocol). The second group (control group) received only concomitant chemoradiotherapy. All tumor specimens were subjected to evaluations of miRNA-181d expression, results were correlated with further individual clinical data. The Cancer Genome Atlas (TCGA) dataset of 149 patients was used as an independent cohort to validate the results. RESULTS: Patients in the carmustine wafer group with low miRNA-181d expression had significantly longer overall (hazard ratio [HR], 35.03, [95% confidence interval (CI): 3.50-350.23], P = .002) and progression-free survival (HR, 20.23, [95% CI: 2.19-186.86], P = .008) than patients of the same group with a high miRNA-181d expression. These correlations were not observed in the control group. The nonsignificance in the control group was confirmed in the independent TCGA dataset. The carmustine wafer group patients with low miRNA-181d expression also had a significantly longer progression-free (P = .049) and overall survival (OS) (P = .034), compared with control group patients. Gross total resection correlated significantly with longer OS (P = .023). CONCLUSION: MiRNA-181d expression significantly affects treatment responses to carmustine wafer implantation.

To assess the influence of molecular markers with potential prognostic value to groups of patients with newly diagnosed glioblastoma patients were examined: group A with 36 patients (surgical resection plus standard combined chemoradiotherapy) and group B with 36 patients (surgical resection, standard combined chemoradiotherapy plus carmustine wafer implantation). Our aim was to determine chromosomal alterations, methylation status of MGMT, p15, and p16 (CDKN2A) in order to analyse the influence on patient survival time as well as radio- and chemotherapy responses. Promoter hypermethylation of MGMT, p16, and p15 genes were determined by MS-PCR. Comparative genomic hybridisation (CGH) analyses were performed with isolated, labelled DNA of each tumor to detect genetic alterations. Age of onset of the disease showed a significant effect on overall survival (OS) (p < 0.0001). Additional treatment with carmustine wafer (group B) compared to the control group (group A) did not result in improved OS (p = 0.562). Patients with a methylated MGMT promotor showed a significant longer OS compared to those patients with unmethylated MGMT promotor (p = 0.041). Subgroup analyses revealed that patients with methylated p15 showed a significant shorter OS when administered to group B rather than in group A (p = 0.0332). In patients additionally treated with carmustine wafer an amplification of 4q12 showed a significant impact on a reduced OS (p = 0.00835). In group B, a loss of 13q was significantly associated with a longer OS (p = 0.0364). If a loss of chromosome 10 occurred, patients in group B showed a significantly longer OS (p = 0.0123). A clinical benefit for the widespread use of additional carmustine wafer implantation could not be found. However, carmustine wafer implantation shows a significantly improved overall survival if parts of chromosome 10 or chromosome 13 are deleted. In cases of 4q12 amplification and in cases of a methylated p15 promotor, the use of carmustine wafers is especially not recommended. The MGMT promoter methylation is a strong prognostic Biomarker for benefit from temozolomide and BCNU chemotherapy.