Sacral nerve stimulation ameliorates colonic barrier functions in a rodent model of colitis.

BACKGROUND: The mucosal barrier damage is recognized as one of the key factors in the pathogenesis of colitis. While sacral nerve stimulation (SNS) was reported to have therapeutic potential for colitis, its mechanisms of actions on colonic permeability remained largely unknown. METHODS: In this study, colitis was induced by intrarectal administration of TNBS in rats. Five days later, they were treated with SNS or sham-SNS for 10 days. The effects of SNS on colonic permeability were assessed by measuring the expression of tight-junction proteins involved in regulating permeability and the FITC-dextran test. The mechanism of actions of SNS was investigated by studying the function of the enteric nervous system (ENS) cells and analyzing the autonomic nervous system. KEY RESULTS: SNS decreased the disease activity index, microscopic and macroscopic scores, myeloperoxidase activity, and pro-inflammatory cytokines (TNF-α, IL-6). SNS increased the expression of Zonula Occludens-1, Occludin, Claudin-1, and Junctional adhesion molecule-A in the colon tissue. The FITC-dextran test showed that the colonic permeability was lower with SCS than sham-SNS. SNS increased ChAT, pancreatic polypeptide, and GDNF and reduced norepinephrine NGF, sub-P, and mast cell overactivation in the colon tissue. Concurrently, SNS increased acetylcholine in colon tissues and elevated vagal efferent activity. CONCLUSIONS & INFERENCES: SNS ameliorates colonic inflammation and enhances colonic barrier function with the proposed mechanisms involving the increase in parasympathetic activity and modulation of the activity of the ENS and immune system, including mast cells.

Refractory overactive bladder patients who chose sacral neuromodulation therapy after failed OnabotulinumtoxinA treatment: A systematic review and meta-analysis.

OBJECTIVE: To systematically review outcomes in patients with refractory overactive bladder (OAB) patients who underwent sacral neuromodulation therapy (SNM) therapy after unsuccessful onabotulinumtoxinA (BTX) therapy, and to compare outcomes with those who SNM as initial therapy. METHODS: A systematic search of Cochrane Library, Pubmed and Embase databases from July 2002 to November 2019, to analyze randomized controlled trials and retrospective studies of SNM therapy after failed initial BTX therapy. Two reviewers independently screened the studies and extracted data. A quality assessment of the included literature was conducted using Newcastle-Ottawa Scale (NOS), and Stata 12.0 software was used to conduct a meta-analysis of the collected data. RESULTS: A total of seven studies involving 319 patients were finally included. The success rate in refractory OAB patients who used SNM therapy after failed BTX therapy was 58.5%, 95% CI (0.47-0.70). There was no significant difference between refractory OAB patients who chose SNM as replacement therapy after failed BTX therapy and those who used SNM therapy as first choice [RR = 0.96, 95%CI (0.72-1.26), P = 0.735]. CONCLUSION: OAB patients for whom an initial choice of BTX therapy ends in failure or dissatisfaction may consider switching to SNM therapy. There is no difference in outcomes between these patients and those whose first choice was SNM therapy.

[Overactive bladder-which treatment when?] / Überaktive Blase ­ wann welche Therapie?

The term OAB (overactive bladder) describes a symptom complex. Therefore, initial treatment should be based on clinical symptoms and the results of basic diagnostics. Patient preference is essential for the choice of the initial treatment. Behavioural therapy, electrostimulation and medical treatment are available treatment options. If these are not effective, extended diagnostic examinations should be performed prior to minimally invasive treatments, like onabotulinumtoxin injections in the detrusor or sacral neuromodulation. Surgical interventions like augmentation cystoplasty are rarely required today.

Femoral nerve injury complicating continuous psoas compartment block.

OBJECTIVES: The objective of this case report is to describe a femoral nerve injury after a psoas compartment block (PCB) and to discuss the probable mechanisms of injury and neuron regeneration. To date, this is the first report of severe femoral nerve injury after PCB. CASE REPORT: A 60-year-old, American Society of Anesthesiologists II woman underwent right total knee replacement under general anesthesia and continuous PCB for postoperative analgesia. Postoperatively, she showed signs of severe femoral nerve injury. A physical therapy program and muscle electrical stimulation were instituted and continued for 6 months. The patient recovered completely with no residual motor or sensory deficit and had no other complication. CONCLUSIONS: Severe nerve injuries after regional anesthesia techniques remain infrequent and probably unreported. Our case report suggests that severe femoral nerve injury should be added to the list of reported complications during PCB. This case report is also encouraging because it shows the possibility of a good recovery after such injury.