Until tolterodine “has been subject to the same detailed neuropsychiatric testing as oxybutynin,” and-most importantly-compared directly with oxybutynin in randomized studies designed and adequately powered to answer this question, the differences in CNS side effects between the drugs remain unclear. It is unclear how quantitative electroencephalograph results (cited as evidence of the greater CNS impact of oxybutynin vs tolterodine) correspond with clinical CNS adverse events and it remains uncertain whether the higher lipophilicity of oxybutynin indeed accounts for observed differences in side effect profiles observed across existing studies. 6“Adverse CNS events” in this trial were “comparable and low level among placebo- and tolterodine-treated patients,” yet the definition and prevalence of such events are not given. Finally, despite the authors' claims, this study adds little to the debate concerning tolterodine versus oxybutynin CNS side effects. ![]() ![]() Third, the trial was short (4 weeks), limiting its generalizability to clinical settings in which longer treatment duration would be expected, and-as the authors note-possibly contributing to the modest drug response. Second, no patient-based satisfaction or quality-of-life outcomes were reported, limiting our knowledge of how patients themselves rated drug efficacy. These modest responses to medication are paralleled by virtually no placebo response (highly unusual for UI drug treatment trials), perhaps reflecting that placebo subjects had significantly worse UI and for a longer duration. The number of patients who became continent was not reported. First, treatment efficacy for UI was only moderate, with the standard dose resulting in a 25% median decrease in UI episodes/24 hours (95% confidence interval (CI) maximum, 46% decrease). These outcomes are mitigated by several factors. However, subclinical retention (elevated postvoiding residual) could have been missed by the insensitive technique of abdominal palpation. Despite the relatively high prevalence of male subjects (35%), none developed symptomatic urinary retention. Nearly half of subjects on 2 mg bid complained of dry mouth, yet few found it severe and only 3% withdrew. Although both dosages significantly decreased voiding frequency, only 2 mg bid significantly decreased urge UI episodes. By targeting OAB rather than urge incontinence alone, the study included continent patients with urinary frequency and urgency alone (23% of subjects). Phase II–III trials had established 2 mg twice daily as the effective dose in predominantly younger patients with OAB, 5 leaving open whether tolterodine was equally effective in older patients and whether a lower dosage could be used. 1 report a multi-center trial of the muscarinic antagonist tolterodine, comparing both the standard dose (2 mg bid) and a lower dose (1 mg bid) with placebo in older persons with overactive bladder (OAB). ![]() All papers address long-held “truisms” of geriatric UI: drug therapy should always “start low, go slow” UI in postmenopausal women is related to estrogen deficiency and responds to hormone replacement daytime prompted voiding effects carry over to improvement in nocturnal UI for incontinent NH residents and consensus exists for UI treatment preferences in the long-term care setting. 4 Three papers focus particularly on nursing home residents, 2- 4 who, despite their extremely high prevalence of UI, remain largely undertreated. The series of papers on urinary incontinence (UI) in this issue examines whether existing behavioral and medication treatments are effective in older, frailer adults, 1- 3 and looks at patient preferences for similar treatments.
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