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Urology. 2007 Jan;69(1):57-61; discussion 61-2.

Recovery of detrusor function after urethral botulinum A toxin injection in patients with idiopathic low detrusor contractility and voiding dysfunction.

Author information

  • Department of Urology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan. hck@tzuchi.com.tw

Abstract

OBJECTIVES:

To investigate the effect of urethral botulinum A toxin (BoNT-A) injection on idiopathic low detrusor contractility and the correlation of this effect with baseline urodynamic parameters.

METHODS:

Twenty-seven patients with idiopathic low detrusor contractility received urethral injection of BoNT-A. Videourodynamic studies were performed at baseline and after treatment. Recovery of detrusor contractility was defined as an increase in detrusor pressure and maximal flow rate and reduced postvoid residual urine volume. The therapeutic results and changes in urodynamic parameters were compared between patients with and without recovery of detrusor contractility.

RESULTS:

The recovery of detrusor contractility after urethral BoNT-A injection occurred in 13 patients (48%). Patients with recovery of detrusor contractility had baseline data characterized by normal bladder sensation during bladder filling combined with a poor relaxation or hyperactive urethral sphincter activity. In contrast, patients without recovery of detrusor contractility had poor bladder sensation and a nonrelaxing urethral sphincter. Patients with baseline characteristics of low detrusor contractility combined with poorly relaxed or hyperactive urethral sphincter activity had better results than those with true detrusor underactivity. Of the 13 patients with recovery of detrusor contractility, 5 had a long-term therapeutic effect without the need of repeat urethral injection of BoNT-A for more than 1 year of follow-up.

CONCLUSIONS:

Patients with detrusor underactivity with normal bladder sensation combined with a poor relaxation or hyperactive urethral sphincter were significantly more likely to recover normal detrusor function. Neuromodulation of the hyperactive urethral sphincter by urethral BoNT-A is the likely mechanism for this therapeutic effect.

PMID:
17270614
[PubMed - indexed for MEDLINE]
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