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Correspondence

Treatment of Neurogenic Incontinence with Botulinum Toxin A

N Engl J Med 2000; 342:665March 2, 2000

Article

To the Editor:

Neurogenic urinary incontinence is most often due to detrusor hyperreflexia, and it is usually treated by partially blocking the efferent parasympathetic innervation to the detrusor muscle of the bladder with anticholinergic drugs. These drugs have troublesome side effects, however, and may not restore continence. Botulinum toxin A selectively blocks the release of acetylcholine from nerve endings and accordingly blocks neural transmission. We hypothesized that injections of botulinum toxin A into the detrusor muscle of the bladder might ameliorate detrusor hyperreflexia in patients with neurogenic incontinence by impairing parasympathetic nervous transmission.

During the past year, we treated 21 patients with neurogenic incontinence due to traumatic injury of the spinal cord with botulinum toxin A. All these patients had severe detrusor hyperreflexia and incontinence despite the use of high doses of anticholinergic drugs, and all emptied their bladder by intermittent self-catheterization. The study was approved by the local ethics committee, and all the patients gave informed consent. A total dose of 200 to 300 units of botulinum toxin A (Botox, Allergan, Irvine, Calif.) was injected at 20 to 30 different sites in the detrusor muscle, sparing the trigone, under cystoscopic and ultrasonographic guidance. The patients were asked to decrease gradually the dose of anticholinergic drugs they were taking during the first week after injection and thereafter, and, if possible, to discontinue use of the drug entirely. All 21 patients were fully examined 6 weeks after treatment, and 11 were examined 16 and 36 weeks after the injections.

At six weeks, all but 2 patients were fully continent: 6 patients were able to stop anticholinergic-drug therapy, and the remaining 13 were able to reduce the dose by at least 50 percent. Urodynamic studies found a significant increase in reflex volume and maximal bladder capacity and a significant decrease in maximal detrusor pressure during uninhibited bladder contractions. The patients were highly satisfied with the treatment, and none had any adverse effects as a result of the injections. The improvements in continence and urodynamic measurements were maintained in those who were reexamined 16 and 36 weeks after treatment (Table 1Table 1Results of Urodynamic Studies in 11 Patients with Neurogenic Urinary Incontinence before and 36 Weeks after Injections of Botulinum Toxin A into the Detrusor Muscle of the Bladder.). None of the patients examined at 36 weeks needed additional injections because of a recurrence of incontinence.

We previously described the efficacy of injections of botulinum toxin A into the external urethral sphincter to treat neurogenic detrusor–sphincter dyssynergia and improve voiding.1 However, this study deals with a different indication, incontinence due to the inability to suppress the voiding reflex. The long-lasting effect of botulinum toxin A when injected into the detrusor muscle of the bladder and the lack of side effects make this treatment a new therapeutic option for patients with severe neurogenic urinary incontinence.

Brigitte Schurch, M.D.
University Hospital Balgrist, 8008 Zurich, Switzerland

Daniel M. Schmid, M.D.
University Hospital, 8091 Zurich, Switzerland

Manfred Stöhrer, M.D.
Berufsgenossenschaftliche Unfallklinik, D8110 Murnau, Germany

1 References
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    CrossRef | Web of Science | Medline

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