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Robot-assisted percutaneous insertion of pedicle screws is a recent technique demonstrating high accuracy. The optimal treatment for spondylodiscitis is still a matter of debate. We performed a retrospective cohort study on surgical patients treated with pedicle screw/rod placement alone without the application of intervertebral cages. In this collective, we compare conventional open to a further minimalized percutaneous robot-assisted spinal instrumentation, avoiding a direct contact of implants and infectious focus. 90 records and CT scans of patients treated by dorsal transpedicular instrumentation of the infected segments with and without decompression and antibiotic therapy were analysed for clinical and radiological outcome parameters. 24 patients were treated by free-hand fluoroscopy-guided surgery (121 screws), and 66 patients were treated by percutaneous robot-assisted spinal instrumentation (341 screws). Accurate screw placement was confirmed in 90 % of robot-assisted and 73.5 % of free-hand placed screws. Implant revision due to misplacement was necessary in 4.95 % of the free-hand group compared to 0.58 % in the robot-assisted group. The average intraoperative X-ray exposure per case was 0.94 ± 1.04 min in the free-hand group vs. 0.4 ± 0.16 min in the percutaneous group ( p  = 0.000). Intraoperative adverse events were observed in 12.5 % of free-hand placed pedicle screws and 6.1 % of robot robot-assisted screws. The mean postoperative hospital stay in the free-hand group was 18.1 ± 12.9 days, and in percutaneous group, 13.8 ± 5.6 days ( p  = 0.012). This study demonstrates that the robot-guided insertion of pedicle screws is a safe and effective procedure in lumbar and thoracic spondylodiscitis with higher accuracy of implant placement, lower radiation dose, and decreased complication rates. Percutaneous spinal dorsal instrumentation seems to be sufficient to treat lumbar and thoracic spondylodiscitis.

Background Subarachnoid hemorrhage (SAH) is a devastating disease with high morbidity and mortality. Neuroprotective effects of the noble gas argon have been shown in animal models of ischemia. The aim of this study was to investigate the effects of argon in the immediate early phase of SAH in a rat model. Methods A total of 19 male Wistar rats were randomly assigned to three treatment groups. SAH was induced using a endovascular filament perforation model. Cerebral blood flow, mean arterial blood pressure (MAP), and body temperature were measured continuously. Group A received 2 h of ventilation by 50% argon/50% O 2 ( n  = 7) immediately following SAH. Group B underwent a sham operation and was also ventilated by 50% argon/50% O 2 ( n  = 6). Group C underwent SAH and 50% O 2 /50% N 2 ventilation ( n  = 6). Preoperative and postoperative neurological and behavioral testing were performed. Histology and immunohistochemistry were used to evaluate the extent of brain injury and vasospasm. Results The cerebral blood flow dropped in both treatment groups after SAH induction (SAH, 63.0 ± 11.6% of baseline; SAH + argon, 80.2 ± 8.2% of baseline). During SAH, MAP increased (135.2 ± 10.5%) compared with baseline values (85.8 ± 26.0 mm Hg) and normalized thereafter. MAP in both groups showed no significant differences ( p  = 0.3123). Immunohistochemical staining for neuronal nuclear antigen demonstrated a decrease of hippocampal immunoreactivity after SAH in the cornu ammonis region (CA) 1–3 compared with baseline hippocampal immunoreactivity ( p  = 0.0127). Animals in the argon-ventilated group showed less neuronal loss compared with untreated SAH animals ( p  < 0.0001). Ionized calcium-binding adaptor molecule 1 staining showed a decreased accumulation after SAH + argon (CA1, 2.57 ± 2.35%; CA2, 1.89 ± 1.89%; CA3, 2.19 ± 1.99%; DG, 2.6 ± 2.24%) compared with untreated SAH animals (CA1, 5.48 ± 2.39%; CA2, 4.85 ± 4.06%; CA3, 4.22 ± 3.01%; dentate gyrus (DG), 3.82 ± 3.23%; p  = 0.0007). The neuroscore assessment revealed no treatment benefit after SAH compared with baseline ( p  = 0.385). Conclusion In the present study, neuroprotective effects of argon occurred early after SAH. Because neurological deterioration was similar in the preadministration and absence of argon, it remains uncertain if neuroprotective effects translate in improved outcome over time.

Spontaneous intracerebral hemorrhage (ICH) causes, besides the primary brain injury, a secondary brain injury (SBI), which is induced, amongst other things, by oxidative stress (OS) and inflammation, determining the patient’s outcome. This study aims to assess the impact of OS in plasma and cerebrospinal fluid (CSF) on clinical outcomes in patients with ICH. A total of 19 ICH (volume > 30 cc) patients and 29 control patients were included. From day one until seven, blood and CSF samples were obtained, and ICH volume was calculated. OS markers, like malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-sulfhydryl (GSH), and the total antioxidant status (TAS) were measured. Clinical data on treatment and outcome were determined. Patients with mRS ≤ 4 showed significantly elevated SOD and GSH-Px levels in plasma compared to patients with poor CO (p = 0.004; p = 0.002). Initial increased TAS in plasma and increased MDA in CSF were linked to an unfavorable outcome after six months (p = 0.06, r = 0.45; p = 0.05, r = 0.44). A higher ICH volume was associated with a worse outcome at week six (p = 0.04, r = 0.47). OS plays a significant role in SBI. Larger ICHs, elevated MDA in CSF, and TAS in plasma were associated with a detrimental outcome, whereas higher plasma-SOD and -GSH-Px were associated with a favorable outcome.

The cerebral thrombin system is activated in the early stage after intracerebral hemorrhage (ICH). Expression of thrombin leads to concentration dependent secondary neuronal damage and detrimental neurological outcome. In this study we aimed to investigate the impact of thrombin concentration and activity in the cerebrospinal fluid (CSF) of patients with ICH on clinical outcome. Patients presenting with space-occupying lobar supratentorial hemorrhage requiring extra-ventricular drainage (EVD) were included in our study. The CSF levels of thrombin, its precursor prothrombin and the Thrombin-Antithrombin complex (TAT) were measured using enzyme linked immune sorbent assays (ELISA). The oxidative stress marker Superoxide dismutase (SOD) was assessed in CSF. Initial clot size and intraventricular hemorrhage (IVH) volume was calculated based on by computerized tomography (CT) upon admission to our hospital. Demographic data, clinical status at admission and neurological outcome were assessed using the modified Rankin Scale (mRS) at 6-weeks and 6-month after ICH. Twenty-two consecutive patients (9 females, 11 males) with supratentorial hemorrhage were included in this study. CSF concentrations of prothrombin (p < 0.005), thrombin (p = 0.005) and TAT (p = 0.046) were statistical significantly different in patients with ICH compared to non-hemorrhagic CSF samples. CSF concentrations of thrombin 24h after ICH correlated with the mRS index after 6 weeks (r2 = 0.73; < 0.005) and 6 months (r2 = 0.63; < 0.005) after discharge from hospital. Thrombin activity, measured via TAT as surrogate parameter of coagulation, likewise correlated with the mRS at 6 weeks (r2 = 0.54; < 0.01) and 6 months (r2 = 0.66; < 0.04). High thrombin concentrations coincide with higher SOD levels 24h after ICH (p = 0.01). In this study we found that initial thrombin concentration and activity in CSF of ICH patients did not correlate with ICH and IVH volume but are associated with a poorer functional neurological outcome. These findings support mounting evidence of the role of thrombin as a contributor to secondary injury formation after ICH.

Background Thrombolysis after acute ischemic stroke has only proven to be beneficial in a subset of patients. The soluble recombinant analogue of human thrombomodulin, Solulin, was studied in an in vivo rat model of acute ischemic stroke. Methods Male SD rats were subjected to 2 hrs of transient middle cerebral artery occlusion (tMCAO). Rats treated with Solulin intravenously shortly before reperfusion were compared to rats receiving normal saline i.v. with respect to infarct volumes, neurological deficits and mortality. Gene expression of IL-6, IL-1β, TNF-α, MMP-9, CD11B and GFAP were semiquantitatively analyzed by rtPCR of the penumbra. Results 24 hrs after reperfusion, rats were neurologically tested, euthanized and infarct volumes determined. Solulin significantly reduced mean total (p = 0.001), cortical (p = 0.002), and basal ganglia (p = 0.036) infarct volumes. Hippocampal infarct volumes (p = 0.191) were not significantly affected. Solulin significantly downregulated the expression of IL-1β (79%; p < 0.001), TNF-α (59%; p = 0.001), IL-6 (47%; p = 0.04), and CD11B (49%; p = 0.001) in the infarcted cortex compared to controls. Conclusions Solulin reduced mean total, cortical and basal ganglia infarct volumes and regulated a subset of cytokines and proteases after tMCAO suggesting the potency of this compound for therapeutic interventions.

Numerous materials of implants used for cranioplasty after decompressive craniectomy (DC) have been investigated to meet certain demanded key features, such as stability, applicability, and biocompatibility. We aimed to evaluate the feasibility and safety of biocompatible calcium-phosphate (CaP) implants for cranioplasty compared to polymethylmethacrylate (PMMA) implants. In this retrospective observational cohort study, the medical records of all patients who underwent cranioplasty between January 1st, 2015, and January 1st, 2022, were reviewed. Demographic, clinical, and diagnostic data were collected. Eighty-two consecutive patients with a mean age of 52 years (range 22–72 years) who received either a PMMA (43/82; 52.4%) or CaP (39/82; 47.6%) cranial implant after DC were included in the study. Indications for DC were equally distributed in both groups. Time from DC to cranioplasty was 143.8 ± 17.5 days (PMMA) versus 98.5 ± 10.4 days (CaP). The mean follow-up period was 34.9 ± 27.1 months. Postoperative complications occurred in 13 patients with PMMA and 6 in those with CaP implants (13/43 [30.2%] vs. 6/39 [15.4%]; p  = 0.115). Revision surgery with implant removal was necessary for 9 PMMA patients and in 1 with a CaP implant (9/43 [20.9%] vs. 1/39 [2.6%]; p  = 0.0336); 6 PMMA implants were removed due to surgical site infection (SSI) (PMMA 6/43 [14%] vs. CaP 0/39 [0%]; p  = 0.012). In this study, a biocompatible CaP implant seems to be superior to a PMMA implant in terms of SSI and postoperative complications. The absence of SSI supports the idea of the biocompatible implant material with its ability for osseointegration.

Background: Subarachnoid hemorrhage (SAH) is a devastating disease with high morbidity and mortality. Hypoxia-induced changes and hemoglobin accumulation within the subarachnoid space are thought to lead to oxidative stress, early brain injury, and delayed vasospasm. This study aimed to evaluate the antioxidant status and its impact on neurological outcome in patients with aneurysmal SAH. Methods: In this prospective observational study, 29 patients with aneurysmal SAH were included (mean age 54.7 ± 12.4). Blood and cerebrospinal fluid (CSF) samples were collected on days (d) 1, 3, and 7. In addition, 29 patients without intracranial hemorrhage served as controls. The antioxidant system was analyzed by glutathione peroxidase (GSH-Px; U/L) and total and free glutathione-sulfhydryl (GSH; mg/L) in the plasma. Superoxide dismutase (SOD, U/mL) and total antioxidant capacity (TAC, µmol/L) were measured in the serum and CSF. Clinical data were compiled on admission (Hunt and Hess grade, Fisher grade, and GCS). Neurological and cognitive outcome (modified Rankin scale (mRS), Glasgow Outcome Scale Extended (GOSE) and Montreal Cognitive Assessment (MoCA)) was assessed after 6 weeks (6 w) and 6 months (6 m). Results: Plasma levels of SOD increased from day 1 to 7 after SAH (d1: 1.22 ± 0.36 U/L; d3: 1.25 ± 0.33 U/L, p = 0.99; d7: 1.52 ± 0.4 U/L, p = 0.019) and were significantly higher compared to controls (1.11 ± 0.27 U/L) at day 7 (p < 0.001). Concordantly, CSF levels of SOD increased from day 1 to 7 after SAH (d1: 1.22 ± 0.41 U/L; d3: 1.77 ± 0.73 U/L, p = 0.10; d7: 2.37 ± 1.29 U/L, p < 0.0001) without becoming significantly different compared to controls (1.74 ± 0.8 U/L, p = 0.09). Mean plasma TAC at day 1 (d1: 77.87 ± 49.72 µmol/L) was not statistically different compared to controls (46.74 ± 32.42 µmol/L, p = 0.25). TAC remained unchanged from day 1 to 7 (d3: 92.64 ± 68.58 µmol/L, p = 0.86; d7: 74.07 ± 54.95 µmol/L, p = 0.8) in plasma. TAC in CSF steeply declined from day 1 to 7 in patients with SAH becoming significantly different from controls at days 3 and 7 (d3: 177.3 ± 108.7 µmol/L, p = 0.0046; d7: 85.35 ± 103.9 µmol/L, p < 0.0001). Decreased SOD levels in plasma and CSF are associated with a worse neurological outcome 6 weeks (mRS: CSF p = 0.0001; plasma p = 0.027/GOSE: CSF p = 0.001; plasma p = 0.001) and 6 months (mRS: CSF p = 0.001; plasma p = 0.09/GOSE: CSF p = 0.001; plasma p = 0.001) after SAH. Increased plasma TAC correlated with a worse neurological outcome 6 weeks (mRS: p = 0.001/GOSE p = 0.001) and 6 months (mRS p = 0.001/GOSE p = 0.001) after SAH. Conclusion: In our study, a reduction in the antioxidative enzyme SOD and elevated TAC were associated with a poorer neurological outcome reflected by mRS and GOSE at 6 weeks and 6 months after SAH. A lower initial SOD CSF concentration was associated with the late deterioration of cognitive ability. These findings support the mounting evidence of the role of oxidative stress in early brain injury formation and unfavorable outcome after SAH.