Table of Contents
Dataset Papers in Medicine
Volume 2013 (2013), Article ID 580927, 5 pages
Dataset Paper

Efficacy and Safety of Botulinum Toxin A for Treating Bladder Hyperactivity in Children and Adolescents with Neuropathic Bladder Secondary to Myelomeningocele

Division of Pediatric Surgery, Second University of Naples, Via S. Pansini 5, 80131 Naples, Italy

Received 4 October 2012; Accepted 6 November 2012

Academic Editors: P. Crispen, T. Efferth, P. Ferrante, and B. Weinstock-Guttman

Copyright © 2013 Antonio Marte et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We verified the efficacy and safety of botulinum toxin A (BTX-A) in treating bladder overactivity in children with neurogenic bladder (NB) secondary to myelomeningocele (MMC). Forty-seven patients (22, females; 25, males; age range, 5–17 years; mean age, 10.7 years) with poorly compliant/overactive neurogenic bladder on clean intermittent catheterization (CIC) and resistance or noncompliant to anticholinergics were injected with 200 IU of BTX-A intradetrusor. All patients experienced a significant 66.45% average increase of leak point volume (Wilcoxon paired rank test = 7.169 e-10) and a significant 118.57% average increase of specific bladder capacity at 20 cm H2O (Wilcoxon paired rank test = 2.466 e-12). Ten patients who presented with concomitant uni/bilateral grade II–IV vesicoureteral reflux were treated at the same time with Deflux. No patient presented with major perioperative or postoperative problems. Twenty-two patients needed a second and 18 a third injection of BTX-A after 6–9 months for the reappearance of symptoms. After a mean follow-up of 5.7 years, 38 out of 47 patients achieved dryness between CICs, and 9 patients improved their incontinence but still need pads. Our conclusion is that BTX-A represents a viable alternative to more invasive procedure in treatment of overactive NB secondary to MMC.