Background A larger defect in the annulus fibrosus following lumbar discectomy is a well-known risk factor for reherniation. Procedures intended to prevent reherniation by sealing or occluding the annular defect warrant study in high-risk patients. This study sought to determine 3-year results of lumbar discectomy with a bone-anchored annular closure device (ACD) or lumbar discectomy only (controls) in patients at high risk for reherniation. Methods This multicenter randomized trial enrolled patients with sciatica due to lumbar intervertebral disc herniation who failed conservative treatment. Patients with large annular defects after lumbar limited microdiscectomy were intraoperatively randomly assigned to receive ACD or control. Clinical and imaging follow-up was performed at routine intervals over 3 years. Main outcomes included rate of reherniations, reoperations, and endplate changes; leg and back pain scores on a visual analogue scale; Oswestry Disability Index (ODI); Physical Component Summary (PCS) and Mental Component Summary (MCS) scores from the SF-36; and adverse events adjudicated by a data safety monitoring board. Results Among 554 randomized patients, the modified intent-to-treat population consisted of 272 patients in which ACD implantation was attempted and 278 receiving control; device implantation was not attempted in 4 patients assigned to ACD. Outcomes at 3 years favored ACD for symptomatic reherniation (14.8% vs. 29.5%; P < 0.001), reoperation (11.0% vs. 19.3%; P = 0.007), leg pain (21 vs. 30; P < 0.01), back pain (23 vs. 30; P = 0.01), ODI (18 vs. 23; P = 0.02), PCS (47 vs. 44; P < 0.01), and MCS (52 vs. 49; P < 0.01). The frequency of all-cause serious adverse events was comparable between groups (42.3% vs. 44.5%; P = 0.61). Conclusions The addition of a bone-anchored ACD in patients with large annular defects following lumbar discectomy reduces the risk of reherniation and reoperation, and has a similar safety profile over 3-year follow-up compared with lumbar limited discectomy only. Trial registration ClinicalTrials.gov NCT01283438

Radicular pain is characterized by radiating buttock and leg pain in a lumbar nerve root distribution, which may be accompanied by neurosensory and motor deficits. Radicular pain caused by lumbar disc herniation improves in most patients with conservative treatment only. Yet, 1 in 5 individuals will experience persistent symptoms and/or neurological deficit^1,2 such that lumbar discectomy may be indicated to surgically remove the herniated disc material. Recurrent herniation occurs in 7% to 18% of patients following discectomy^3-5 and a large defect in the annulus fibrosus after surgery is a major risk factor for reherniation.⁶ In a meta-analysis involving more than 1600 patients undergoing lumbar discectomy, the risk of symptom recurrence (odds ratio, 2.5; P = .004) and reoperation (odds ratio, 2.3; P < .001) was higher in patients with large vs small annular defects.⁶ Reoperations for lumbar disc herniation are more costly,⁴ less effective,^7,8 and are associated with higher risk of disability⁹ than primary procedures. Therefore, intraoperative strategies intended to close or occlude large annular defects may lower the clinical and economic burden related to surgery for recurrent herniation. This randomized clinical trial evaluated the 5-year clinical and radiographic outcomes of patients with large annular defects after lumbar microdiscectomy treated with or without a bone-anchored annular closure device.

Spinal infection (SI) is a life-threatening condition and its treatment remains challenging. Recent studies have supported early and aggressive surgery, but mortality still reaches 5% to 10% and it remains unclear, if an aggressive surgical strategy also applies for severely sick patients. The aim of this analysis was to generate an assessment score to predict mortality of SI in order to facilitate decision-making. Retrospective risk factor analysis. Two hundred fifty-two patients were retrospectively analyzed. Physiologic measures, functional measures. Diagnosis was based on clinical presentation, imaging findings and inflammatory markers. Factors associated with mortality were identified by multivariate analysis, weighted according to their relative risk ratio (RR) and included in the novel assessment score. Eight parameters were included: (1) BMI, (2) ASA score, (3) presence of sepsis, (4) age-adjusted Charlson Comorbidity Index, (5) presence and degree of renal failure, (6) presence of hepatopathy, (7) neurological deficits and (8) CRP levels at diagnosis. Each parameter was assigned a certain range of points, resulting in a maximum total score of 20. The mortality in spinal infection (MSI-20) score - indicating poorer status with higher values - was obtained for each patient and correlated with mortality. An MSI-20 score of 11 or more points seems to identify the small group of patients being "too sick to undergo surgery," while early surgery can be recommended in the remainder (MSI-20 ≤10). Our results need to be confirmed in prospective studies, but may give guidance for indicating surgery even in rather sick and comorbid patients.

Radiation necrosis represents a potentially devastating complication after radiation therapy in brain tumors. The establishment of the diagnosis and especially the differentiation from progression and pseudoprogression with its therapeutic implications requires interdisciplinary consent and monitoring. Herein, we want to provide an overview of the diagnostic modalities, therapeutic possibilities and an outlook on future developments to tackle this challenging topic. The aim of this report is to provide an overview of the current morphological, functional, metabolic and evolving imaging tools described in the literature in order to (I) identify the best criteria to distinguish radionecrosis from tumor recurrence after the radio-oncological treatment of malignant gliomas and cerebral metastases, (II) analyze the therapeutic possibilities and (III) give an outlook on future developments to tackle this challenging topic. Additionally, we provide the experience of a tertiary tumor center with this important issue in neuro-oncology and provide an institutional pathway dealing with this problem.

Vasospasm-related delayed cerebral ischemia (DCI) significantly impacts on outcome after aneurysmal subarachnoid hemorrhage (SAH). Erythropoietin (EPO) may reduce the severity of cerebral vasospasm and improve outcome, however, underlying mechanisms are incompletely understood. In this study, the authors aimed to investigate the effect of EPO on cerebral metabolism and brain tissue oxygen tension (PbtO2).

Introduction: Diclofenac, a nonsteroidal antiinflammatory drug, is commonly used as antipyretic therapy in intensive care. The purpose of this study was to investigate the effects of parenteral diclofenac infusion on brain homeostasis, including brain-tissue oxygen tension (P_btO₂) and brain metabolism after aneurysmal subarachnoid hemorrhage (aSAH). Methods: We conducted a prospective, observational study with retrospective analysis of 21 consecutive aSAH patients with multimodal neuromonitoring. Cerebral perfusion pressure (CPP), mean arterial pressure (MAP), intracranial pressure (ICP), body temperature, and P_btO₂ were analyzed after parenteral diclofenac infusion administered over a 34-minute period (20 to 45 IQR). Data are given as mean ± standard error of mean and median with interquartile range (IQR), as appropriate. Time-series data were analyzed by using a general linear model extended by generalized estimation equations (GEEs). Results: One-hundred twenty-three interventions were analyzed. Body temperature decreased from 38.3°C ± 0.05°C by 0.8°C ± 0.06°C (P < 0.001). A 10% decrease in MAP and CPP (P < 0.001) necessitated an increase of vasopressors in 26% (n = 32), colloids in 33% (n = 41), and crystalloids in 5% (n = 7) of interventions. P_btO₂ decreased by 13% from a baseline value of 28.1 ± 2.2 mm Hg, resulting in brain-tissue hypoxia (P_btO₂ <20 mm Hg) in 38% (n = 8) of patients and 35% (n = 43) of interventions. P_btO₂ <30 mm Hg before intervention was associated with brain-tissue hypoxia after parenteral diclofenac infusion (likelihood ratio, 40; AUC, 93%; 95% confidence interval (CI), 87% to 99%; P < 0.001). Cerebral metabolism showed no significant changes after parenteral diclofenac infusion. Conclusions: Parenteral diclofenac infusion after aSAH effectively reduces body temperature, but may lead to CPP decrease and brain-tissue hypoxia, which were both associated with poor outcome after aSAH.