Motor Evoked Potential Recordings from the Urethral Sphincter Muscles (USMEPs) during Spine Surgeries.

Bowel and bladder function are at risk during tumor resection of the conus, cauda equina, and nerve roots. This study demonstrates the ability to acquire transcranial electrical motor evoked potentials (TCeMEPs) from the urethral sphincter muscles (USMEPs) by utilizing a urethral catheter with an embedded electrode. A retrospective analysis of intraoperative neurophysiological monitoring (IONM) data from nine intradural tumors, four tethered cord releases, and two spinal stenosis procedures was performed (n = 15). The cohort included seven females and eight males (median age: 38.91 years). A catheter with embedded urethral electrodes was used for recording TCeMEPs and spontaneous electromyograph (s-EMG) from the external urethral sphincter (EUS). USMEPs were obtained in 14 patients (93%). The reliability of TCeMEP from the external anal sphincter (EAS) was variable across all patients. In patient 7, the TCeMEP recordings from the urethral sphincter were not present before incision; however, following the resection of the tumor, the USMEP recordings were obtained and remained stable for the remainder of the procedure. Patient 7 had subsequent improvement in bladder function postoperatively. Patient 4 exhibited a 50% increase in the amplitude of the USMEP following tumor resection and exhibited improved bladder function as well postoperatively. In this small series, we were able to acquire consistent and reliable MEPs when recorded from the urethral sphincters. More study is needed to establish a better understanding of the value added by this modality. USMEPs can be attempted in surgeries that put the function of the pelvic floor at risk.

Neurobiologic changes in the hypothalamus associated with weight loss after gastric bypass.

BACKGROUND: Effects of Roux-en-Y gastric bypass (RYGB) on hypothalamic food intake regulation have not been investigated. The hypothalamic arcuate nucleus (ARC) and the magnocellular (m) and parvocellular (p) parts of the paraventricular nucleus (PVN) regulate hunger and satiety, and are under control of the orexigenic neuropeptide Y (NPY), and the anorexigenic alpha-melanocyte stimulating hormone (alpha-MSH) and serotonin (5-HT). We hypothesized that after RYGB, weight loss is associated with hypothalamic down regulation of NPY and up regulation of 5-HT and alpha-MSH. STUDY DESIGN: Obesity was induced in 12 Sprague Dawley rats using a high-energy diet for 7 weeks, and then the rats were divided into three groups (n = 4/group): RYGB, sham-operated pair-fed (PF), and sham-operated ad libitum (obese control). Ten days after operation, immunohistochemical quantification of NPY, alpha-MSH, and 5-HT(1B)-receptors in ARC and PVN was performed. Data were analyzed using ANOVA and Tukey's test. RESULTS: Body weight decreased in RYGB (417 +/- 21 g; mean +/- SE) and in PF (436 +/- 14 g) rats 10 days after operation compared with obese control rats (484 +/- 15 g; p < 0.05 for each comparison). NPY in ARC, pPVN, and mPVN decreased by 43%, 43%, and 61%, respectively in RYGB and by 55%, 42%, and 71% in PF, respectively, compared with obese controls (p < 0.05 for each pairwise comparison). RYGB versus PF did not show differences. alpha-MSH in ARC, pPVN and mPVN increased by 35%, 175%, and 67%, respectively in RYGB and by 29%, 162%, and 116% in PF, respectively, compared with obese controls (each p < 0.05). In mPVN, alpha-MSH significantly decreased by 23% in RYGB versus PF (p < 0.05). 5-HT-(1B)-receptor in pPVN increased by 58% in RYGB and by 26% in PF, compared with obese controls (p < 0.05). Compared with obese controls, 5HT-(1B)-receptor in mPVN increased by 39% in RYGB (p < 0.05) and by 9% in PF (p > 0.05). An increase of 5-HT-(1B)-receptor in pPVN and mPVN occurred in RYGB versus PF (p < 0.05). CONCLUSIONS: Obese rats that undergo weight loss after RYGB demonstrate changes in hypothalamic down regulation of NPY and up regulation of alpha-MSH and serotonin.

A surgical rat model of human Roux-en-Y gastric bypass.

Obesity affects 30% of the United States population and its detrimental effects are obesity-related metabolic diseases. For patients refractory to conventional weight loss therapy, gastric bypass surgery is one of the proven methods for inducing a sustained weight loss and reversing the metabolic sequelae of obesity. To understand the mechanisms of weight loss and the amelioration of related metabolic comorbid conditions, a reproducible animal model is needed. We report our developmental experience with rat models of sequential Roux-en-Y gastric bypass after reproducing the diet-induced obesity that characterizes the hallmarks of human obesity. Four experiments were performed to induce weight reduction through successive modifications: In Experiment 1 a 20% stapled gastric pouch with a 16 cm biliary-pancreatic limb and a 10 cm alimentary limb accomplished sufficient weight loss within 10 days to ameliorate metabolic changes associated with obesity, but the occurrence of gastrogastric fistulas prevented sustained weight loss; in Experiment 2 the model was improved by dividing the stomach to avoid gastrogastric fistula, but again sustained weight loss was not achieved; in Experiment 3 the biliary-pancreatic limb was lengthened from 16 to 30 cm, reducing the common channel to approximately 18 cm. Sustained weight loss was achieved for 28 days. In Experiment 4 the model in Experiment 3 was modified by dividing the stomach between two rows of staples. Sustained weight loss was observed for 67 days. We developed a reproducible rat model of Roux-en-Y gastric bypass. The existence of this model opens a new field of research in which to study the metabolic sequelae of obesity and the mechanisms of weight loss.