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INTRODUCTION AND OBJECTIVE:We have previously shown that detrusor sphincter dyssynergia (DSD) in spinal cord injured (SCI) cats can be blocked with high frequency, biphasic, bilateral stimulation o...

We determined the role of opioid and metabotropic glutamate 5 receptors in the pudendal inhibition of bladder overactivity.Cystometrograms were performed in 11 cats under α-chloralose anesthesia by slowly infusing the bladder with saline or 0.25% acetic acid. Pudendal nerve stimulation at intensities of multiple times the threshold to induce observable anal twitching was applied during cystometrogram to inhibit the bladder overactivity induced by acetic acid irritation. Naloxone (0.1, 0.3 and 1 mg/kg intravenously) was administered to block opioid receptors, followed by MTEP (3 and 10 mg/kg intravenously) to block metabotropic glutamate 5 receptors. After each drug dose, pudendal inhibition of bladder overactivity was examined during cystometrogram.Acetic acid irritated the bladder, induced bladder overactivity and significantly decreased mean ± SE bladder capacity to 23.6% ± 2.7% of saline control capacity. Pudendal nerve stimulation at 1 to 1.5 and 4 × threshold suppressed bladder overactivity and significantly increased mean capacity to 57.5% ± 8.1% (p = 0.0005) and 106% ± 15% (p = 0.0002), respectively, of saline control capacity. Naloxone had no effect on pudendal inhibition but MTEP eliminated the inhibition induced by low intensity stimulation and significantly decreased the inhibition induced by high intensity stimulation (p0.05). Neither naloxone nor MTEP altered baseline bladder overactivity.Opioid receptors are not involved in pudendal inhibition of bladder overactivity but metabotropic glutamate 5 receptors are partially involved. Understanding neurotransmitter mechanisms could improve the efficacy of neuromodulation therapy for overactive bladder and identify molecular targets for developing new drugs for overactive bladder.

We determined whether transcutaneous electrical foot stimulation combined with a low dose of tramadol (Sigma-Aldrich®) could completely suppress bladder overactivity.Repeat cystometrograms were performed in 18 α-chloralose anesthetized cats by infusing the bladder with saline or 0.25% acetic acid. Transcutaneous electrical stimulation (5 Hz) of the cat hind foot at 2 to 4 times the threshold intensity needed to induce observable toe movement was applied to suppress acetic acid induced bladder overactivity. Tramadol (1 to 3 mg/kg intravenously) was administered to enhance foot inhibition.Acetic acid irritated the bladder, induced bladder overactivity and significantly decreased bladder capacity to a mean ± SE of 26% ± 5% of saline control capacity (p0.01). Without tramadol, foot stimulation at 2 and 4 threshold intensity applied during acetic acid cystometrograms significantly increased bladder capacity to a mean of 47% ± 5% and 62% ± 6% of saline control capacity, respectively (p0.05). Without foot stimulation, tramadol (1 mg/kg) only slightly changed bladder capacity to a mean of 39% ± 2% of saline control capacity (p0.05), while 3 mg/kg significantly increased capacity to 85% ± 14% that of control (p0.05). However, 1 mg/kg tramadol combined with foot stimulation increased bladder capacity to a mean of 71% ± 18% (2 threshold intensity) and 84% ± 14% (4 threshold intensity), respectively, which did not significantly differ from saline control capacity. In addition, long lasting (greater than 1.5 to 2 hours) post-stimulation inhibition was induced by foot stimulation combined with 3 mg/kg tramadol treatment.This study suggests a new treatment strategy for overactive bladder by combining foot stimulation with a low dose of tramadol, which is noninvasive and has potentially high efficacy and fewer adverse effects.

We examined the role of opioid receptors in the inhibition of bladder overactivity induced by electrical stimulation of the foot.Experiments were done in 6 cats under α-chloralose anesthesia when the bladder was infused with saline or 0.25% acetic acid. Naloxone (1 mg/kg intravenously) was administered to block opioid receptors. To modulate reflex bladder activity electrical stimulation (5 Hz, 0.2 millisecond pulse width) was applied to the foot via skin surface electrodes at intensities of multiple times the threshold needed to induce observable toe movement.Acetic acid irritated the bladder, induced bladder overactivity and significantly decreased bladder capacity to a mean ± SE 25.3% ± 5.9% that of saline control capacity (p = 0.0001). Foot stimulation at 4T suppressed acetic acid induced bladder overactivity and significantly increased bladder capacity to 47.1% ± 5.9% of control (p = 0.0007). Naloxone did not significantly change bladder capacity during acetic acid irritation but it completely eliminated the inhibition of bladder overactivity induced by foot stimulation.Results indicate that opioid receptors have an important role in foot afferent inhibition of bladder overactivity. This raises the possibility that opioid receptors might be used as a pharmacological target to enhance the efficacy of foot stimulation for inhibiting bladder overactivity.

INTRODUCTION AND OBJECTIVES: Recent fMRI studies revealed supraspinal networks in response to bladder filling involved in perception and processing of bladder distension. However significance of supraspinal network activity and network localizations varied largely due to the different filling protocols. Therefore, our aim was to standardize filling paradigms using a MR-synchronized pump system for accurate timing and filling volume. METHODS: 31 right-handed healthy subjects, 16 women and 15 men, mean age 34 years (range 19e54) with no history of urinary urgency and/or urinary incontinence were included, were prospectively investigated using a 3 Tesla Phillips scanner. After catheterization, bladder was pre-filled until a persistent desire to void was perceived by each subject. The scan paradigm comprised automated, repetitive bladder filling of 100 mL body warm saline over 15sec by using a MRcompatible pump system, i.e. block design study. Neuroimaging data was analyzed with SPM8. Blood-oxygenation-level dependent signal analysis during bladder filling was compared to rest, i.e. pre-filled bladder. Second-level random effects group analysis was corrected for gender, age and total intracranial volume and was performed to account for between-subject variability, i.e. within-group results at P1⁄40.05 familywise error rate (FWE). RESULTS: 3 subjects, 2 women and 1 man, were excluded from further analysis due to excessive head motions. Within-group results from the remaining 28 subjects revealed activation in the following brain regions: bilateral insula, left inferior parietal lobe (BA40) and right frontal inferior operculum (BA44). CONCLUSIONS: Automated, repetitive bladder filling of body warm saline elicited robust brain activity on a high significance level in specific areas known to be involved in supraspinal lower urinary tract control.

INTRODUCTION AND OBJECTIVES: Spinal cord transection (SCT) results in disruption of the Ad-fiber mediated supraspinal voiding reflex with emergence of a C-fiber mediated spinal reflex. Pudendal nerve stimulation (PNS) can increase bladder capacity and reduce storage pressures in both acute and chronic spinal cord injury models. Metabotropic glutamate receptor 5 (mGluR5) is widely expressed in the CNS and has been shown to suppress excitatory transmission of the micturition reflex. This study investigates the role and location of mGluR5 in pudendal nerve inhibition of C-fiber mediated spinal bladder reflex using an acute SCT model. METHODS: Cystometrograms (CMGs) were performed on 12 cats under a-chloralose anesthesia. Saline control capacity was establish followed by acute SCT at T9/T10. CMGs were performed using 0.25% acetic acid (AA) to activate nociceptive C-fiber bladder afferents and induce spinal bladder reflexes. PNS was applied at 5 Hz at 2 and 4 times the threshold (T) for inducing anal twitch. Under isovolumetric conditions, MTEP (a selective mGluR5 antagonist) was given (3 mg/kg, i.v.) to determine its effect on PNS. Six of the cats were treated with propranolol (3 mg/kg, i.v.) prior to MTEP administration. Hexamethonium (10 mg/kg, i.v.) was given at the end of each experiment to block the spinal bladder reflex. RESULTS: Following T9/T10 SCT and AA irritation, CMGs showed a spinal bladder reflex resulting in low amplitude (

INTRODUCTION AND OBJECTIVES: The goal of this video is to present a streamlined approach to laparoscopic abdominal sacralcolpopexy. In light of the FDA warnings regarding transvaginal mesh placement and the withdrawal of transvaginal mesh kits from the marketplace, patients are seeking alternative minimally invasive options to address vaginal prolapse. The open abdominal sacralcolpopexy technique has stood the test of time and consistently delivers 95% success rates with tolerable complication rates and specifically, very low mesh complication rates. Translating the open approach to the laparoscopic approach has been made possible with modern technology. METHODS: A compendium of cases by one surgeon is presented in video format to illustrate the main technical points of the procedure. These include: port placement, dissection planes, mesh attachment to vaginal vault and to sacral promontory, and mesh coverage. A novel new vaginal manipulator specifically designed for this procedure will also be shown. RESULTS: Use of a novel new vaginal manipulator facilitates dissection of the vaginal vault and makes it easier to perform intracorporal laprascopic suturing without the need for expensive robotic technology. CONCLUSIONS: Laparoscopic abdominal sacral colpopexy is feasible and safe and can be performed within a reasonable time frame with few complications, by surgeons who are comfortable with other laparoscopic procedures.