Abstract

ObjectivesTo assess and compare the effect of transcutaneous Dorsal Genital Nerve Stimulation (DGNS), Tibial Nerve Stimulation (TNS), Sacral Nerve Stimulation (SNS), and Spinal Stimulation (SS) on Neurogenic Detrusor Overactivity (NDO) and bladder capacity in people with Spinal Cord Injuries (SCI).Materials and MethodsSeven male participants with supra-sacral SCI were tested. Standard cystometry (CMG) was performed to assess bladder activity at baseline and with stimulation applied at each site. This was conducted over four separate sessions. All stimulation was monophasic, 15 Hz, 200 μS pulses and applied at maximum tolerable amplitude. Results were analysed against individual control results from within the same session.ResultsDorsal Genital Nerve Stimulation increased bladder capacity by 153 ± 146 ml (p = 0.016) or 117 ± 201%. DGNS, TNS and SNS all increased the volume held following the first reflex contraction, by 161 ± 175, 46 ± 62, and 34 ± 33 ml (p = 0.016, p = 0.031, p = 0.016), respectively. SS results showed small reduction of 33 ± 26 ml (p = 0.063) from baseline bladder capacity in five participants. Maximum Detrusor Pressure before leakage was increased during TNS, by 10 ± 13 cmH2O (p = 0.031) but was unchanged during stimulation of other sites. DGNS only was able to suppress at least one detrusor contraction in five participants and reduced first peak detrusor pressure below 40 cmH2O in these 5. Continuous TNS, SNS, and SS produced non-significant changes in bladder capacity from baseline, comparable to conditional stimulation. Increase in bladder capacity correlated with stimulation amplitude for DGNS but not TNS, SNS or SS.ConclusionIn this pilot study DGNS acutely suppressed detrusor contractions and increased bladder capacity whereas TNS, SNS, and SS did not. This is the first within individual comparison of surface stimulation sites for management of NDO in SCI individuals.

Highlights

  • Neural control of the bladder during storage and micturition involves complex interactions between centres in the brain, spinal cord and peripheral nerves

  • Change in End Fill Volume (EFV) between pre and post stimulation control fills for individual sites was 23 ± 97 ml in DGNS tests, 36 ± 91 ml in TNS, 36 ± 55 ml in Sacral Nerves of S2-4 (SNS) and −48 ± 49 ml in SS

  • A Wilcoxon signed rank test was used to look for significance of change from baseline in each site, with significance level set at p < 0.05

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Summary

Introduction

Neural control of the bladder during storage and micturition involves complex interactions between centres in the brain, spinal cord and peripheral nerves. The aberration of pelvic functions following Spinal Cord Injury (SCI) involves the development of uncontrolled and overactive reflex arcs, leading to Neurogenic Detrusor Overactivity (NDO) and Detrusor Sphincter Dyssynergia (DSD) (Craggs et al, 2006). Improvements have been made in treatment options available for managing NDO following SCI. The range of antimuscarinic medication (AM), introduction of β3-agonists (Wöllner and Pannek, 2016) and success of Botulinum-A toxin injections (BTX) (Reitz et al, 2004) contribute to satisfactory management of the bladder post SCI. For refractory cases the major surgical option is cystoplasty. This has very good long term results, it is a major undertaking with significant morbidity (Hoen et al, 2017)

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