Abstract

Neuromodulation is a therapeutic technique that is well-established in the treatment of idiopathic Lower urinary tract (LUT) dysfunction such as overactive bladder (OAB). We have recently developed a novel neuromodulation approach, Transcutaneous Electrical Spinal Cord Neuromodulation (TESCoN) and demonstrated its acute effects on LUT dysfunction after spinal cord injury (SCI) during urodynamic studies. We found that TESCoN can promote urinary storage and induce urinary voiding when delivered during urodynamic studies. The objective of this study was to determine whether TESCoN can retrain the spinal neural networks to induce chronic improvement in the LUT, such that positive changes can persist even in the absence of stimulation. In addition, we wished to examine the effect of TESCoN on LUT dysfunction due to multiple pathologies. To achieve this objective, 14 patients [SCI = 5, stroke = 5, multiple sclerosis (MS) = 3, and idiopathic OAB (iOAB) = 1] completed 24 sessions of TESCoN over the course of 8 weeks. Patients completed urodynamic studies before and after undergoing TESCoN therapy. Additionally, each subject completed a voiding diary and the Neurogenic Bladder Symptom Score questionnaire before and after receiving TESCoN therapy. We found that TESCoN led to decreased detrusor overactivity, improved continence, and enhanced LUT sensation across the different pathologies underlying LUT dysfunction. This study serves as a pilot in preparation for a rigorous randomized placebo-controlled trial designed to demonstrate the effect of TESCoN on LUT function in neurogenic and non-neurogenic conditions.New And NoteworthyNon-Surgical modality to reduce incidence of urinary incontinence and improve neurogenic bladder symptom scores (NBSS) in individuals with neurogenic bladder due to spinal cord injury or stroke.

Highlights

  • The lower urinary tract (LUT, consisting of the bladder and bladder outlet) serves two main roles: to store and empty urine

  • Stroke patients did not demonstrate a change in bladder capacity or voiding efficiency

  • After completing the 8-week therapeutic intervention, both sets of patients (n = 5 Stroke and n = 5 spinal cord injury (SCI)) demonstrated an increased bladder capacity (P < 0.05, Figures 5A,F); no change in voiding efficiency was observed in either group (Figures 5B,G)

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Summary

Introduction

The lower urinary tract (LUT, consisting of the bladder and bladder outlet) serves two main roles: to store and empty urine. LUT dysfunction occurs when either storage or voiding are impaired, resulting in urinary incontinence or retention. LUT dysfunction is common in patients with neurological disease and the general population (de Groat, 1997; Jeong et al, 2010). In the case of neurological disease, LUT dysfunction occurs because the normal pathways responsible for communication between the LUT and the neural micturition centers become disrupted. While the mechanism of idiopathic LUT dysfunction is not as obvious, the nervous system is thought to be at least partially implicated in the majority of cases. LUT dysfunction has profound effects which range from endangering patients’ health [as the case of poorly managed LUT dysfunction after spinal cord injury (SCI)] to significantly impacting patients’ quality of life [as in the case of idiopathic over active bladder (iOAB) and post-stroke LUT dysfunction]

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