Vagus nerve stimulation.

Vagus nerve stimulation (VNS) is a key tool in the treatment of patients with medically refractory epilepsy. Although the mechanism of action of VNS remains poorly understood, this modality is now the most widely used nonpharmacological treatment for drug-resistant epilepsy. The goal of this work is to review the history of VNS and provide information on recent advances and applications of this technology.

Primary and secondary patencies of transposed femoral vein fistulas are significantly greater than with the HeRO graft.

INTRODUCTION: For access-challenged patients with bilateral upper extremity central venous stenosis, solutions include the Hemodialysis Reliable Outflow (HeRO) device or an autogenous AV fistula in the lower limb. We evaluated HeRO grafts and transpositions of the femoral vein in maintaining primary and secondary patency. METHODS: We retrospectively analyzed 40 patients with a HeRO device and 18 patients with superficial femoral artery to transposed femoral vein autogenous arteriovenous fistula (SFA-tFV). All patients had bilateral central venous obstruction. All procedures were outpatient performed by a single surgeon at one center between 2009-2015. Operative details, intraoperative flows, and flows at the first-week postoperative visit were analyzed, as were primary and secondary patency and intervention rates. Complications were compared between groups. RESULTS: The one-year cumulative primary patency was 30% for HeRO grafts and 79% for SFA-tFV fistulas (p = 0.0001); secondary patency was 71% for HeRO grafts and 93% for SFA-tFV fistulas (p = 0.03). To maintain patency, HeRO patients required a mean 2.1 interventions per year and thigh fistula patients required a mean 0.4 interventions per year. Thirty-seven percent of thigh fistula patients had a hematoma or seroma versus 5% of HeRO patients and 17% of thigh fistula patients experienced delayed wound healing versus 2.5% of HeRO patients (p<0.05). None of the thigh fistula patients had distal ischemia. CONCLUSIONS: HeRO patients had lower primary and secondary patency rates versus thigh fistula patients and HeRO grafts required five-fold more interventions to maintain secondary patency. However, patients with thigh fistulas had significantly more wound healing problems. Thus, the SFA-tFV has become our access of choice for patients with bilateral central venous stenosis.

First-week postoperative flow measurements are highly predictive of primary patency of radiocephalic arteriovenous fistulas.

PURPOSE: This study was conducted to determine whether volume flow rate at the first postoperative visit could predict early failure of radiocephalic arteriovenous fistulas (RCAVFs). METHODS: We retrospectively studied the records of 264 patients who received a RCAVF between 2007 and 2013 at our centers. Data collected included patient demographics, medical history, arterial and venous mapping, and volume flow rate intraoperatively after fistula creation but before closing the surgical incision. An intraoperative flow rate >100 mL/minute was targeted. We measured volume flow at the first postoperative visit 1 week after surgery and thereafter as needed. RESULTS: Intraoperative flow was not a significant predictor of primary patency (p = 0.44) but flow at the first postoperative visit was a statistically significant predictor of fistula primary patency (p = 0.002). No fistula with a blood flow <200 mL/minute at the 1-week postoperative visit reached maturity without receiving a maturation procedure. The hazard ratio for the first follow-up flow (mL/min) was 0.9973 (95% CI 0.9956, 0 .9989), indicating that for every 100 mL increase in blood flow the primary patency increases by 10%. CONCLUSIONS: Flow rate at the 1-week postoperative visit was the most important predictor of RCAVF patency. Thus, it should be possible to identify patients who would benefit from early intervention or closer follow-up as soon as the first postoperative visit. This should help reduce the use of bridging hemodialysis catheters and minimize the risks of catheter dependency.

Clinical experience with the surgicel family of absorbable hemostats (oxidized regenerated cellulose) in neurosurgical applications: a review.

INTRODUCTION: Oxidized regenerated cellulose has a long history of safe and effective use in the surgical setting. Surgicel Original, Fibrillar and Nu-Knit absorbable hemostats are composed of oxidized regenerated cellulose and are sterile, absorbable knitted fabrics that are flexible and adhere readily to bleeding surfaces. The purpose of this paper is to discuss neurosurgical applications for these absorbable hemostatic agents. METHODS: The authors reviewed the literature and described their clinical experience with Surgicel hemostatic products. RESULTS: Neurosurgical applications of the hemostatic products include the management of diffuse capillary oozing following bipolar cautery in brain tumor resection beds and the control of epidural oozing during spinal surgery. As an adjunct to standard hemostatic procedures, these products facilitate rapid hemostasis and have bactericidal activity that extend to antibiotic-resistant organisms such as methicillin-resistant Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus pneumonia, as well as Pseudomonas aeruginosa. Although generally safe and well-tolerated, these hemostatic agents should be removed when used around, in, or in proximity to, foramina in bone, areas of bony confine, the spinal cord, and/or the optic nerve or chiasm because it may otherwise swell and cause unwanted pressure. CONCLUSION: The physical, hemostatic, and bactericidal characteristics of this material makes it a useful adjunct for conventional hemostatic and controlling capillary, venous, and small arterial hemorrhage during neurosurgery. .

A review of laboratory and clinical data supporting the safety and efficacy of cyclosporin A in traumatic brain injury.

For decades, cyclosporin A (CsA) has proved to be safe and effective for use in transplantation. In the past 10 years, this agent has shown neuroprotective effects in animal models of traumatic brain injury (TBI). This review article provides a critical overview of the literature on CsA neuroprotective effects in animal studies and current findings of clinical trials in the treatment of TBI with an emphasis on the possible CsA molecular mechanism of action. Animal data provide compelling evidence of the therapeutic benefits of CsA in TBI, but the outcome indices are heterogeneous with respect to the animal model of TBI as well as the route, dose, and timing of CsA administration. Similarly, clinical studies (phase II trials) adapting almost identical patient inclusion criteria have demonstrated the safety of CsA use in TBI, but the clinical trials are also heterogeneous based on study design, especially with regard to the variable timing of CsA administration after TBI. In view of the translational shortcomings of the preclinical studies and the rather pilot nature of the limited clinical trials that recently reached phase III, we offer guidance on the future directions of laboratory investigations on CsA that could improve the safety and efficacy of this agent in subsequent larger clinical trials.

Cyclosporine-A as a neuroprotective agent against stroke: its translation from laboratory research to clinical application.

Stoke remains a leading cause of death and disability with limited treatment options. Extensive research has been aimed at studying cell death events that accompany stroke and how to use these same cell death pathways as potential therapeutic targets for treating the disease. The mitochondrial permeability transition pore (MPTP) has been implicated as a major factor associated with stroke-induced neuronal cell death. MPTP activation and increased permeability has been shown to contribute to the events that lead to cell death. Cyclosporine A (CsA), a widely used immunosuppressant in transplantation and rheumatic medicine, has been recently shown to possess neuroprotective properties through its ability to block the MPTP, which in turn inhibits neuronal damage. This newfound CsA-mediated neuroprotection pathway prompted research on its use to prevent cell death in stroke and other neurological conditions. Preclinical studies are being conducted in hopes of establishing the safety and efficacy guidelines for CsA use in human trials as a potential neuroprotective agent against stroke. In this review, we provide an overview of the current laboratory and clinical status of CsA neuroprotection.