Abstract

To evaluate the efficacy of botulinum toxin type A injections in the detrusor muscle in patients with spinal cord injury and urinary incontinence due to detrusor overactivity and refractory to anticholinergic agents. We prospectively evaluated 22 patients with spinal cord injuries, whose bladders were emptied by intermittent catheterization. All patients had detrusor overactivity and urinary incontinence that proved difficult to treat, despite using high doses of two different anticholinergics. The pre-treatment assessment included a complete urodynamic study and ultrasonography of the kidneys and urinary tract. A one-month follow-up was completed with urodynamic evaluation and the clinical response was evaluated through outpatient consultations and telephone contact. After the procedure, the maximum cystometric capacity and the bladder reflex volume increased, whereas the maximum detrusor pressure and compliance decreased. The mean duration of continence was 7±7 months. In 18 patients (81.8%), it was necessary to administer anticholinergics to achieve continence. Five patients (22.7%) had indication of reinjection, and augmentation cystoplasty was indicated in 9 patients (40.9%). The use of botulinum toxin in the treatment of neurogenic detrusor overactivity refractory to anticholinergics is an option before more invasive treatments, such as augmentation cystoplasty, are attempted. In our study as well as in the literature, there was improvement in most urodynamic parameters. Overall, 40.9% of patients underwent augmentation cystoplasty and 81.8% of patients needed anticholinergic agents to reach urinary continence. Further studies are necessary to improve the procedure and to achieve better clinical results.

Highlights

  • Suprasacral spinal cord lesions induce neurogenic detrusor overactivity and concurrent detrusor sphincter dyssynergia that impairs the storage and emptying functions of the urinary bladder

  • We evaluated the effect of botulinum-A toxin injection in the detrusor overactivity in spinal cord injury patients, clinical response correlation and implications for other treatments

  • A total of 22 patients with spinal cord injuries (16 traumatic patients and 6 non-traumatic patients), whose bladders were emptied by intermittent catheterization, had detrusor overactivity and urinary incontinence that proved difficult to treat, despite using high doses of two different anticholinergics

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Summary

Introduction

Suprasacral spinal cord lesions induce neurogenic detrusor overactivity and concurrent detrusor sphincter dyssynergia that impairs the storage and emptying functions of the urinary bladder. The subsequent high intravesical pressure leads to reduced bladder capacity and incontinence and induces potential structural damage to the bladder wall and upper urinary tract. Current treatment options rely first on emptying the bladder by clean intermittent catheterization and on oral anticholinergic medication to reduce the bladder pressure and increase bladder capacity [1]. Serotypes A and B are available for clinical use. Botulinum toxin causes flaccid paralysis by inhibiting the release of acetylcholine at the presynaptic cholinergic junction. The clinical effect of botulinum toxin is transient and dose related. Smith et al [5] have demonstrated the effect of botulinum toxin type A on acetylcholine and norepinephrine release from the bladder and urethra, respectively

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