Abstract
ObjectiveTo examine the urodynamic effects of fesoterodine on neurogenic detrusor overactivity and/or low compliance bladder.MethodsA total of 77 patients (52 men, 25 women; aged 61.6 ± 20.3 years) were given fesoterodine 4–8 mg/day and prospectively followed for 12 weeks. The primary end‐point variable was change in the maximum cystometric capacity on urodynamic study. The secondary end‐point was to assess the number of patients whose neurogenic detrusor overactivity disappeared, and the changes in the urodynamic parameters, lower urinary tract symptoms questionnaires and the 3‐day frequency volume chart parameters after the treatment.ResultsA total of 13 patients (16.9%) withdrew because of adverse events (dry mouth or blurred vision), and four patients dropped out for unknown reasons. Finally, 60 patients completed the study. Bladder capacity at first desire to void, maximum cystometric capacity and bladder compliance increased by 29.2 mL, 79.9 mL and 22.2 mL/cm H2O, respectively, showed statistical significance (P = 0.026, P < 0.001 and P < 0.001). Neurogenic detrusor overactivity disappeared in 12 of 51 patients (23.5%), and a significant increase was observed in bladder capacity at first involuntary contraction (P < 0.001), and a significant decrease was observed in maximum detrusor contraction (P < 0.001). In patients with low compliance bladder (with detrusor underactivity without neurogenic detrusor overactivity; n = 9), maximum cystometric capacity and bladder compliance increased significantly (P = 0.003 and P = 0.006, respectively). Overactive bladder symptom score, International Consultation on Incontinence Questionnaire–Short Form, most items of King’s Health Questionnaire, and the number of urgency episodes and leaks in a day decreased significantly after treatment.ConclusionsFesoterodine seems to be a valid treatment option for neurogenic detrusor overactivity and/or low compliance bladder in neurogenic bladder patients.
Highlights
The main concern regarding patients with neurogenic bladder is renal damage attributable to high detrusor storage and/or voiding pressures. These high detrusor pressures can be caused by DO or LCB
LCB, which reported an increase in bladder capacity and reduction in detrusor pressure, and an improvement in urinary incontinence.[2–4]
The dose of fesoterodine was increased in 20 patients, and decreased in no patients
Summary
The main concern regarding patients with neurogenic bladder is renal damage attributable to high detrusor storage and/or voiding pressures. These high detrusor pressures can be caused by DO or LCB. NDO might cause urinary incontinence and deteriorate quality of life. The main therapeutic goal for NDO and LCB might be achieving a low-pressure reservoir and improvement in the patient’s quality of life.[2–5]. Anticholinergics alone or in combination with CIC is the mainstay therapy for NDO or LCB,[5–7] and assessment with UDS is useful both for the diagnosis and treatment evaluation of NDO.[7,8]. There have been some reports on antimuscarinic drugs for the treatment of NDO or LCB, which reported an increase in bladder capacity and reduction in detrusor pressure, and an improvement in urinary incontinence.[2–4] Anticholinergics alone or in combination with CIC is the mainstay therapy for NDO or LCB,[5–7] and assessment with UDS is useful both for the diagnosis and treatment evaluation of NDO.[7,8] There have been some reports on antimuscarinic drugs for the treatment of NDO or LCB, which reported an increase in bladder capacity and reduction in detrusor pressure, and an improvement in urinary incontinence.[2–4]
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