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Multi-center randomized controlled trial of cognitive treatment, placebo, oxybutynin, bladder training, and pelvic
Jan D van Gool1, Tom P V M de Jong, Pauline Winkler-Seinstra
1Institute for Medical Informatics, Biometry and Epidemiology, Essen-Duisburg University, Essen, Germany; Pediatric Renal Center, WKZ/UMC, Utrecht, The Netherlands.
Insights
Cognitive treatment, not added interventions, successfully treated childhood incontinence by addressing symptom-urodynamic mismatches. Social stress may underlie symptoms, potentially mediated by specific signaling pathways.
Area of Science:
- Pediatric Urology
- Behavioral Medicine
- Clinical Trials
Background:
- Functional urinary incontinence affects 8.4% of school-aged children, predominantly girls, causing significant morbidity.
- Overactive bladder (OAB) and dysfunctional voiding (DV) are common diagnoses associated with childhood incontinence.
Purpose of the Study:
- To compare the efficacy of oxybutynin, placebo, and bladder training for OAB.
- To evaluate cognitive treatment versus pelvic floor training for DV in children.
- To investigate the role of urodynamic studies in diagnosing and managing childhood incontinence.
Main Methods:
- A multi-center controlled trial randomized children with OAB or DV to different treatment arms.
- Interventions included oxybutynin, bladder training, cognitive treatment, and pelvic floor training, with all children receiving standardized cognitive treatment.
- Urodynamic studies were conducted pre- and post-treatment to assess bladder and pelvic floor activity.
Main Results:
- For OAB, cure rates were similar across placebo (39%), oxybutynin (43%), and bladder training (44%).
- For DV, cure rates were 52% for controls and 49% for pelvic floor training.
- Pre-treatment urodynamic patterns did not correlate with clinical diagnoses, and new patterns emerged post-treatment in at least 20% of cases.
Conclusions:
- Cognitive treatment emerged as the primary driver of success, highlighting a mismatch between clinical symptoms and urodynamic findings.
- The unpredictable nature of urodynamic changes and treatment response suggests underlying factors beyond simple bladder or pelvic floor dysfunction.
- Gender-specific prevalence and the impact of cognitive treatment point towards social stress, potentially mediated by corticotropin-releasing factor pathways, as a significant contributing factor to childhood incontinence.
Objective:
Functional urinary incontinence causes considerable morbidity in 8.4% of school-age children, mainly girls. To compare oxybutynin, placebo, and bladder training in overactive bladder (OAB), and cognitive treatment and pelvic floor training in dysfunctional voiding (DV), a multi-center controlled trial was designed, the European Bladder Dysfunction Study.
Methods:
Seventy girls and 27 boys with clinically diagnosed OAB and urge incontinence were randomly allocated to placebo, oxybutynin, or bladder training (branch I), and 89 girls and 16 boys with clinically diagnosed DV to either cognitive treatment or pelvic floor training (branch II). All children received standardized cognitive treatment, to which these interventions were added. The main outcome variable was daytime incontinence with/without urinary tract infections. Urodynamic studies were performed before and after treatment.
Results:
In branch I, the 15% full response evolved to cure rates of 39% for placebo, 43% for oxybutynin, and 44% for bladder training. In branch II, the 25% full response evolved to cure rates of 52% for controls and 49% for pelvic floor training. Before treatment, detrusor overactivity (OAB) or pelvic floor overactivity (DV) did not correlate with the clinical diagnosis. After treatment these urodynamic patterns occurred de novo in at least 20%.
Conclusion:
The mismatch between urodynamic patterns and clinical symptoms explains why cognitive treatment was the key to success, not the added interventions. Unpredictable changes in urodynamic patterns over time, the response to cognitive treatment, and the gender-specific prevalence suggest social stress might be a cause for the symptoms, mediated by corticotropin-releasing factor signaling pathways.
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