PubMed Health⌕ Search

Biomedical subjects

Timothy B Boone

Publications and source records attributed to Timothy B Boone.

At least 19 recordsLinked to original sources
PubMed2006

Receptor activated bladder and spinal ATP release in neurally intact and chronic spinal cord injured rats.

Neurally intact (NI) rats and chronic spinal cord injured (SCI) rats were studied to determine how activation of mechanosensory or cholinergic receptors in the bladder urothelium evokes ATP release from afferent terminals in the bladder as well as in the spinal cord. Spinal cord transection was performed at the T(9)-T(10) level 2-3 weeks prior to the experiment and a microdialysis fiber was inserted in the L(6)-S(1) lumbosacral spinal cord one day before the experiments. Mechanically evoked (i.e. 10 cm/W bladder pressure) ATP release into the bladder lumen was approximately 6.5-fold higher in SCI compared to NI rats (p<0.05). Intravesical carbachol (CCh) induced a significantly greater release of ATP in the bladder from SCI as compared to NI rats (3424.32+/-1255.57 pmol/ml versus 613.74+/-470.44 pmol/ml, respectively, p<0.05). However, ATP release in NI or SCI rats to intravesical CCh was not affected by the muscarinic antagonist atropine (Atr). Spinal release of ATP to bladder stimulation with 10 cm/W pressure was five-fold higher in SCI compared to NI rats (p<0.05). CCh also induced a significantly greater release of spinal ATP in SCI rats compared to controls (4.3+/-0.9 pmol versus 0.90+/-0.15 pmol, p<0.05). Surprisingly, the percent inhibitory effect of Atr on CCh-induced ATP release was less pronounced in SCI as compared to NI rats (49% versus 89%, respectively). SCI induces a dramatic increase in intravesical pressure and cholinergic receptor evoked bladder and spinal ATP release. Muscarinic receptors do not mediate intravesical CCh-induced ATP release into the bladder lumen in NI or SCI rats. In NI rats sensory muscarinic receptors are the predominant mechanism by which CCh induces ATP release from primary afferents within the lumbosacral spinal cord. Following SCI, however, nicotinic or purinergic receptor mechanisms become active, as evidenced by the fact that Atr was only partially effective in inhibiting CCh-induced spinal ATP release.

Adenosine Triphosphate↗
PubMed2006

The impact of detrusor overactivity on the management of stress urinary incontinence in women.

The presence of overactive bladder symptoms, urodynamic detrusor overactivity, and urge incontinence can complicate the diagnosis and management of stress urinary incontinence in women. The exact pathophysiology of mixed incontinence is not well characterized; in some patients, the stress and urge etiology may be pathologically linked. The role of urodynamics in evaluating patients with mixed incontinence remains controversial. Conservative therapies, such as bladder training, pelvic floor exercise, biofeedback, and electrical stimulation, offer moderate success in women with mixed incontinence. Surgery (colposuspension, bladder neck pubovaginal slings, and midurethral slings) offers excellent subjective and objective cure rates in patients with mixed incontinence. Preoperative detrusor overactivity is cured consistently 50%of the time with colposuspension and slings. Overall, the presence of preoperative detrusor overactivity does not appear to significantly worsen the outcome of conservative and surgical treatments for stress urinary incontinence in women.

Female↗
PubMed2006

Pharmacotherapy for neurogenic detrusor overactivity.

Chancellor MB, Anderson RU, Boone TB: Pharmacotherapy for neurogenic detrusor overactivity. Am J Phys Med Rehabil 2006;85:536-545. Patients with neurogenic detrusor overactivity are a heterogeneous group with voiding dysfunction secondary to neurologic injury or disease. The neurogenic detrusor overactivity syndrome, which may include urinary frequency, urgency, and incontinence, frequently contributes to a loss of independence, or even institutionalization. Urodynamic assessment provides the best method of quantifying and classifying neurogenic detrusor overactivity dysfunction in patients with primary diagnoses as diverse as Parkinson's disease, cerebral palsy, multiple sclerosis, spinal cord injury, and spina bifida. For many patients, management of urinary symptoms includes pharmacotherapy with an anticholinergic agent. Several novel approaches to managing neurogenic detrusor overactivity, including intravesical instillation of anticholinergic agents, vanilloids, and neurotoxins, are being investigated. For most patients, however, flexible dosing with an anticholinergic agent, with clean intermittent catheterization when indicated, has been shown to reduce the risks of urologic complications, improve levels of continence, and enhance patient quality of life in both children and adults.

Administration, Intravesical↗
PubMed2005

Enhanced ATP release from rat bladder urothelium during chronic bladder inflammation: effect of botulinum toxin A.

The effects of mechanoreceptor stimulation and subsequent ATP release in cyclophosphamide evoked chronic bladder inflammation was examined to demonstrate: (1) whether inflammation modulates ATP release from bladder urothelium and (2) whether intravesical botulinum toxin A administration inhibits urothelial ATP release, a measure of sensory nerve activation. ATP release was measured from rat bladders in a Ussing chamber, an apparatus that allows one to separately measure resting and mechanoreceptor evoked (e.g. hypoosmotic stimulation) ATP release from urothelial and serosal sides of the bladder. Cystometry was utilized to correlate changes in ATP release with alterations in the frequency of voiding and non-voiding bladder contractions, in vivo measures of bladder afferent activity. The resting urothelial release of ATP was not significantly affected by either cyclophosphamide or botulinum toxin A treatment. However, evoked ATP release following hypoosmotic stimulation was significantly increased (i.e. 94%) in chronic cyclophosphamide treated bladder urothelium compared to control bladders. In addition, botulinum toxin A treatment significantly reduced hypoosmotic shock induced ATP release in cyclophosphamide treated animals by 69%. Cystometry revealed that cyclophosphamide and botulinum toxin A treatments altered non-voiding (i.e. cyclophosphamide increased, botulinum toxin A decreased) but not voiding contraction frequency suggesting that alterations in urothelial ATP release selectively diminished underlying bladder C-fiber nerve activity. Finally, intravesical instillation of botulinum toxin A did not affect ATP release from the serosal side implying that its effects were confined to the urothelial side of the bladder preparation.

Adenosine Triphosphate↗
PubMed2005

In vivo effects of botulinum toxin A on visceral sensory function in chronic spinal cord-injured rats.

OBJECTIVES: To analyze the in vivo effects of botulinum toxin type A (BTX-A) on visceral sensory function in chronic spinal cord-injured (SCI) rats. METHODS: One group of rats underwent spinal cord transection at the T8-T9 level (SCI) and the other group was left untreated. In 21 days, baseline open cystometrography (CMG) was performed. The rats were then treated intravesically with either 1 mL of 1% protamine sulfate (PS) to increase urothelial permeability or saline, followed by either 1 mL of BTX-A (20 U) or saline. CMG was repeated 48 hours after instillation, and any changes in the bladder contraction frequency and amplitude were evaluated. RESULTS: After the instillation of PS and BTX-A or BTX-A alone, the bladder contraction frequency was significantly decreased in the SCI rats compared with the control rats (P < 0.05); no change was seen in the contraction amplitude. When normal rats were given intravesical PS and/or BTX-A, or SCI animals were treated with PS alone, neither the frequency nor the amplitude of the contractions was affected. Also, no significant differences were found in the bladder contraction frequency or amplitude of contractions in any animal treated with instillation of saline alone. CONCLUSIONS: Intravesical BTX-A inhibits bladder sensory mechanisms by reducing the frequency of bladder contractions in an SCI rat model. Furthermore, our results suggest that intravesically applied BTX-A does not penetrate to the smooth muscle layer even after PS disruption of the bladder urothelium. These findings may have important clinical applications in treating overactive bladders after SCI.

Animals↗
PubMed2005

Inhibitory effect of intravesically applied botulinum toxin A in chronic bladder inflammation.

PURPOSE: We evaluated a putative inhibitory effect of intravesical botulinum toxin A (BTX-A) on afferent pathways in conditions of chronic bladder inflammation. MATERIALS AND METHODS: Female Sprague-Dawley rats were divided into 4 groups, namely group 1-saline treated, group 2-BTX-A treated, group 3-cyclophosphamide (CYP) treated and group 4-BTX-A and CYP treated. At the beginning of the treatment period all animals received intravesical protamine sulfate (1%), followed by intravesical BTX-A or saline. Subsequently CYP or saline was injected intraperitoneally every 3 days for 10 days. The rats then underwent cystometrogram evaluation prior to spinal cord harvest. Sections from the L6 and S1 spinal cord segments were examined for the total number of Fos immunoreactive cells. RESULTS: Comparisons of the L6 and S1 sections showed a significant difference among groups (p <0.05). CYP treated animals had a significant increase in L6 and S1 (78% and 107%, respectively) c-fos expression compared with saline controls (p <0.001). Comparison of the CYP and BTX-A/CYP groups showed a significant decrease in L6 and S1 in c-fos expression (50% and 52%, respectively) in the BTX-A/CYP treated group (p <0.001). No significant difference was present between the saline and BTX-A alone groups. Cystometrogram studies revealed that the nonvoiding intercontractile interval increased by more than 10-fold in BTX-A/CYP treated animals compared with CYP treated rats (p <0.01). CONCLUSIONS: In a CYP model of chronic bladder inflammation intravesical BTX-A significantly inhibits the afferent neural response without impairing efferent bladder function.

Administration, Intravesical↗
PubMed2004

Botulinum toxin A inhibits ATP release from bladder urothelium after chronic spinal cord injury.

The effects of mechanoreceptor stimulation and subsequent ATP release in spinal cord injured and normal bladders was examined to demonstrate if spinal cord injury (SCI) modulates the basal or evoked release of ATP from bladder urothelium and whether intravesical botulinum toxin A (BTX-A) administration inhibits urothelial ATP release, a measure of sensory nerve activation. A Ussing chamber was used to isolate and separately measure resting and mechanoreceptor evoked (e.g. hypoosmotic stimulation) ATP release from urothelial and serosal sides of the bladder. Following spinal cord injury, resting urothelial release of ATP was ninefold higher than that of normal rats. Botulinum toxin A instillation did not significantly affect the resting release of ATP after spinal cord injury. Evoked ATP release following hypoosmotic stimulation was significantly higher in chronic spinal cord injured compared to normal rat bladders. However, botulinum toxin A treatment markedly reduced ATP release in spinal cord injured bladders by 53% suggesting that ATP release by mechanoreceptor stimulation, as opposed to basal release, occurs by exocytotic mechanisms. In contrast, there was no significant difference in basal or evoked ATP release from bladder serosa following spinal cord injury. Moreover, intravesical instillation of botulinum toxin A did not affect ATP release from the serosal side after spinal cord injury, suggesting that its effects were confined to the urothelial side of the bladder preparation. In summary: (1) increased release of ATP from the urothelium of spinal cord injured bladders may contribute to the development of bladder hyperactivity and, (2) mechanoreceptor stimulated vesicular ATP release, as opposed to basal non-vesicular release of ATP, is significantly inhibited in spinal cord injured bladders by intravesical instillation of botulinum toxin A. These results may have important relevance in our understanding of the mechanisms underlying plasticity of bladder afferent pathways following SCI.

Adenosine Triphosphate↗
PubMed2004

Loss of caveolin-1 expression is associated with disruption of muscarinic cholinergic activities in the urinary bladder.

Caveolin-1 (Cav1), a structural protein of caveolae, plays cell- and context-dependent roles in signal transduction pathway regulation. We have generated a knockout mouse homozygous for a null mutation of the Cav1 gene. Cav1 knockout mice exhibited impaired urinary bladder contractions in vivo during cystometry. Contractions of male bladder strips were evoked with electric and pharmacologic stimulation (5-40 Hz, 1-10 microM carbachol, 10 mM alpha,beta-methylene ATP, 100 mM KCl). Acetylcholine (ACh) and norepinephrine (NE) release from bladder strips were measured with a radiochemical method by incubating the strips with 14C-choline and 3H-NE prior to electric stimulation, whereas ATP release was measured using the luciferin-luciferase assay with a luminometer. A 60-75% decline in contractility was observed when Cav1 knockout muscle strips were stimulated with electric current or carbachol, compared to wildtype muscle strips. No difference in contractility was noted when contractions were evoked either by the purinergic agonist alpha,beta-methylene ATP, or by extracellular potassium. To investigate the relative contribution of non-cholinergic activity to bladder contractility, the amplitude of the electric stimulation-evoked contractions was compared in the presence of the muscarinic antagonist atropine (1 microM). While the non-muscarinic (purinergic) response was unaltered, muscarinic cholinergic response was principally disrupted in Cav1 knockout mice. The loss of Cav1 gene expression was also associated with a 70% reduction in ACh release. NE and ATP release was not altered. It is concluded that the loss of caveolin-1 is associated with disruption of M3 muscarinic cholinergic activity in the bladder. Both pre-junctional (acetylcholine neurotransmitter release from neuromuscular junctions) and post-junctional (M3 receptor-mediated signal transduction in bladder smooth muscles) mechanisms are disrupted, resulting in impaired bladder contraction.

Acetylcholine↗
PubMed2004

Botulinum toxin a has antinociceptive effects in treating interstitial cystitis.

OBJECTIVES: To present clinical evidence with botulinum toxin A (BTX-A) suggesting an antinociceptive role in patients with interstitial cystitis (IC). Intriguing evidence in a somatic pain model has suggested that BTX-A injection may have an antinociceptive effect on both acute and chronic (inflammatory) pain. METHODS: Thirteen female patients (6 in the United States and 7 in Poland) with IC according to the criteria of the National Institute of Diabetes, Digestive and Kidney Disease were included. Under short general anesthesia or sedation, 100 to 200 U of Dysport (Polish patients) or Botox (U.S. patients) was injected through a cystoscope into 20 to 30 sites submucosally in the trigone and floor of the bladder. Patients were evaluated with the O'Leary-Sant validated IC questionnaire or with voiding charts and a visual analog pain scale 1 month postoperatively and at subsequent 3-month intervals. The Polish patients also underwent pretreatment and post-treatment urodynamic evaluations. RESULTS: Overall, 9 (69%) of 13 patients noted subjective improvement after BTX-A treatment. The Interstitial Cystitis Symptom Index and Interstitial Cystitis Problem Index mean scores improved by 71% and 69%, respectively (P <0.05). Daytime frequency, nocturia, and pain by visual analog scale decreased by 44%, 45%, and 79%, respectively (P <0.01). The first desire to void and maximal cystometric capacity increased by 58% and 57%, respectively (P <0.01). CONCLUSIONS: Our results suggest that BTX-A has an antinociceptive effect on bladder afferent pathways in patients with IC, producing both symptomatic and functional (ie, urodynamic) improvements.

Administration, Intravesical↗
PubMed2004

Botulinum toxin in urology: evaluation using an evidence-based medicine approach.

Clinical reports documenting the beneficial effects of botulinum toxin (BTX) to treat various lower urinary tract disorders of muscle spasticity (e.g. detrusor hyperreflexia, detrusor sphincter dyssynergia) have led to its expanded application in non-neurogenic conditions such as idiopathic detrusor overactivity, detrusor underactivity and benign prostatic hyperplasia (BPH). As greater numbers of investigators report their results utilizing this agent, it becomes more important that clinicians are able to synthesize and describe the findings of current clinical studies in a meaningful way. Evidence-based medicine is a platform on which investigations concerning a particular topic can be evaluated for their levels of scientific evidence, so that rational clinical recommendations can be formulated. This review article applies evidence-based practices to the use of BTX in common urologic conditions. Appreciating the benefits as well as limitations of currently available studies will hopefully drive the development of well-controlled, randomized studies of BTX, particularly in highly prevalent conditions such as idiopathic detrusor overactivity and BPH.

Botulinum Toxins↗
PubMed2003

Effect of stimulation intensity and botulinum toxin isoform on rat bladder strip contractions.

The present experiments compared the inhibitory effects of botulinum toxin A (BoNT-A) and botulinum toxin D (BoNT-D) on neurally evoked contractions of rat bladder strips. We examined the effect of fatigue (trains of 100 shocks at 20Hz every 20s for 10min) followed by non-fatigue stimulation (trains of 100 shocks at 20Hz every 100s for 20min) on the onset of effect and potency of the two toxins. For non-fatigue experiments, strips were untreated (n=4); or incubated with 1.36nM BoNT-A (n=4). During fatigue experiments, strips were untreated (n=5); or treated with either 1.36nM BoNT-A (n=6) or 0.8nM BoNT-D (n=6). In non-fatigue experiments, BoNT-A produced significant decreases in contractile area after 1h of stimulation compared to untreated strips (P<0.05). After three series of fatigue stimulation, differences in recovery amplitude and area between untreated versus BoNT-A, and untreated versus BoNT-D bladder strips, were statistically significant (P<0.05). The onset of inhibitory effect was quicker in BoNT-D-treated strips, as a significant reduction (P<0.05) in recovery of contractile area was observed after 1h of stimulation compared to both untreated and BoNT-A-treated preparations. In addition, treated (BoNT-A and BoNT-D) and untreated bladder strips responded similarly to atropine, suggesting that the effects of BoNT result from inhibition of both acetylcholine and ATP release. Our results demonstrate that BoNT-D may be a more effective agent to inhibit transmitter release from autonomic nerves of the rat lower urinary tract. Moreover, in our hands, non-fatigue stimulation is as effective as fatigue stimulation in inhibiting bladder strip contractions.

Animals↗
PubMed2003

Disruption of the caveolin-1 gene impairs renal calcium reabsorption and leads to hypercalciuria and urolithiasis.

Using LoxP/Cre technology, we generated a knockout mouse homozygous for a null mutation in exon 2 of Cav1. In male Cav1-/- animals, we observed a dramatic increase in the incidence of urinary calcium stone formation. In 5-month-old male mice, the incidence of early urinary calculi was 67% in Cav1-/- mice compared to 19% in Cav1+/+ animals. Frank stone formation was observed in 13% of Cav1-/- males but was not seen in Cav1+/+ mice. Urine calcium concentration was significantly higher in Cav1-/- male mice compared to Cav1+/+ mice. In Cav1-/- mice, distal convoluted tubule cells were completely devoid of Cav1 and the localization of plasma membrane calcium ATPase was disrupted. Functional studies confirmed that active calcium absorption was significantly reduced in Cav1-/- compared to Cav1+/+ male mice. These results demonstrate that disruption of the Cav1 gene promotes the progressive steps required for urinary calcium stone formation and establish a new mouse model for urinary stone disease.

Animals↗
PubMed2003

Voiding patterns in patients with post-prostatectomy incontinence: urodynamic and demographic analysis.

PURPOSE: A significant percentage of patients with post-prostatectomy incontinence have been reported to void by Valsalva's maneuver, which is our observation as well. We determine the mechanism of voiding in patients with post-prostatectomy incontinence and correlate this to demographic data, urodynamic parameters and outcome after artificial urinary sphincter implantation, and identify possible risk factors. MATERIALS AND METHODS: Videourodynamic data from 61 consecutive patients with post-prostatectomy incontinence were reviewed to determine voiding patterns. The causes of incontinence were radical prostatectomy in 58 patients and transurethral resection of the prostate followed by radiation therapy in 3. The relationship between voiding patterns and demographic data (age, diabetes mellitus, degree and duration of incontinence, history of radiation therapy or treated bladder neck contracture) as well as urodynamic parameters (bladder capacity, compliance, instability, sensation, leak point pressure and residual urine) were studied. After artificial urinary sphincter implantation outcome was assessed in relation to the voiding patterns. RESULTS: Stress incontinence was present in all patients while concomitant urgency/urge incontinence was present in 48%. Of the patients 43 (70.5%) voided by detrusor contraction (group 1) while the remaining 18 (29.5%) voided by straining (group 2). Mean patient age +/- SD was 70.8 +/- 6.9 and 69.2 +/- 7.2 years, and duration of incontinence was 48 +/- 33 and 46 +/- 30 months in groups 1 and 2, respectively (p >0.05). Also, no significant differences were found between the groups with regard to other demographic data. Delayed first sensation (at volume greater than 140 ml.) was seen in 42.5% and 29.4%, capacity less than 300 ml. in 41.9% and 39%, impaired/poor compliance in 25.6% and 22.2%, bladder instability in 16.3% and 5.6%, abdominal leak point pressure 60 cm. H(2)O or less in 59.4% and 60% and residual urine greater than 50 ml. in 11.6% and 17.6% in groups 1 and 2, respectively (p >0.05). After artificial urinary sphincter implantation 35% and 22.2% of patients used greater than 1 pad a day in groups 1 and 2, respectively. One patient in each group reported difficulty during urination and both patients had no residual urine. CONCLUSIONS: No identifiable demographic or urodynamic risk factors could be detected in association with the strain pattern of voiding in patients with post-prostatectomy incontinence. The absence of a difference in bladder compliance, residual urine volume and outcome after artificial urinary sphincter implantation between detrusor and strain voiders would suggest no increased risk for complications in the strain voiding group.

Aged↗
PubMed2002

Pharmacologic treatment for detrusor overactivity.

Recent pharmacologic treatment for detrusor overactivity has resulted in more favorable side effect profiles, not only because of the use of different drug delivery systems for older drugs but perhaps also due to the improved bladder selectivity of newer antimuscarinic agents. These developments translate into higher patient compliance and better long-term results with the newer agents over generic immediate-release oxybutynin for the treatment of the overactive bladder.

Benzhydryl Compounds↗
PubMed2002

Surgical management of overactive bladder.

The majority of patients with overactive bladder (OAB) can be managed with office-based techniques. When medical therapy fails as treatment for OAB, surgical intervention ranging from electric stimulation administered in the office to extensive procedures, such as augmentation or urinary diversion, may be needed. Any surgical intervention should be tailored to the patient with consideration of the degree of his or her discomfort, underlying pathology, general health, and obviously, the patient's own motivation.

Electric Stimulation Therapy↗
PubMed2002

Artificial urinary sphincter for post-prostatectomy incontinence in men who had prior radiotherapy: a risk and outcome analysis.

PURPOSE: We retrospectively reviewed our experience with the artificial urinary sphincter for post-prostatectomy incontinence, comparing the outcome of those patients who did and did not receive previous radiation therapy. MATERIALS AND METHODS: A total of 86 patients with post-prostatectomy incontinence treated with implantation of artificial urinary sphincter includes 58 who did not (group 1) and 28 who did (group 2) receive prior radiation therapy during treatment of prostate carcinoma. In group 2 radiation was the primary treatment followed by salvage prostatectomy in 5 patients, adjuvant after radical retropubic prostatectomy 20 and after transurethral prostatic resection 3. Mean patient age plus or minus standard deviation was 68.3 +/- 6.6, and 69.7 +/- 6.6 years in groups 1 and 2, respectively. Activation of the sphincter was 4 weeks from the date of surgery, and deactivation at night was not adopted in either group. Patients were followed for a mean period of 31 +/- 23, and 36 +/- 21 months in groups 1 and 2, respectively. Comparison of continence, urodynamic testing, complication rate, overall satisfaction and quality of life was done between both groups. RESULTS: Reoperation was required in 13 (22.4%) patients in group 1 and 7 (25%) group 2 (p >0.05). Urethral atrophy and/or inadequate compression was seen in 8 (14%) and 4 (14%) patients, and urethral erosion was observed in 1 (2%) and 2 (7%) in groups 1 and 2, respectively (p >0.5). Infection of the device was observed in 4 (7%) patients in group 1 but none group 2 (p >0.05). Continence status was similar in both groups, with 60% and 64% of patients who wore 0 to 1 pad daily in groups 1 and 2, respectively (p >0.05). Urgency with or without urge incontinence was reported after implantation of artificial urinary sphincter in 47%, and 44% of patients in groups 1 and 2, respectively (p >0.05). On a visual analog scale (range 0 to 5, 0-not satisfied at all, 5-extremely satisfied) for satisfaction with the results of the artificial urinary sphincter 86% and 91% of patients reported 4 or greater in groups 1 and 2, respectively (p >0.05). CONCLUSIONS: The artificial urinary sphincter has a similar outcome in patients with post-prostatectomy incontinence whether or not they have received previous radiation therapy. No special precaution needs to be adopted for the men in group 2 with post-prostatectomy incontinence considering implantation of artificial urinary sphincter.

Aged↗
PubMed2002

Treatment patterns and associated symptom improvement during six months of care for overactive bladder: a prospective, observational study.

BACKGROUND: Several pharmacologic and nonpharmacologic interventions are available for the treatment of symptoms of overactive bladder (OAB). The relationship between type of initial intervention and subsequent symptom improvement and resource utilization has not been explored in detail. OBJECTIVE: The purpose of this study was to assess (1) the proportion of patients continuing with their initially prescribed treatment for OAB 3 and 6 months after the initial evaluation and (2) the relationship between actual treatment patterns, symptom improvement. and number of physician office visits. METHODS: A total of 31 physicians enrolled patients with OAB for this 6-month prospective, observational study. Baseline data on OAB symptom severity and OAB management strategies were obtained and initial treatment(s) were prescribed by physicians during a routine office visit. Follow-up data on symptom changes, treatment changes, number of physician office visits, and the frequency of absorbent pad use were collected via telephone interviews with patients 3 and 6 months after the initial visit. Stepwise logistic regression was used to assess the relationship between patient characteristics, prescription of medication, and symptom improvement. RESULTS: A total of 213 patients were enrolled; 122 (57.3%) and 100 (46.9%) patients provided follow-up data at the 3-month and 6-month assessments, respectively. The mean age was 61.2 years; 85.2% of patients were female, and 77.7% were white. OAB symptom improvement was significantly related to being prescribed medication (odds ratio [OR], 4.3; 95% CI, 1.8-9.9) and the mean number of daily leakage incidents at baseline (OR, 3.2; 95% CI, 1.2-8.4). Although patients who were prescribed drugs at baseline tended to have fewer physician office visits and were less likely to be prescribed nondrug interventions than patients who were not treated initially with drugs, these differences were not statistically significant. CONCLUSIONS: Pharmacologic treatment for symptoms of OAB appears to be associated with greater symptom improvement than nonpharmacologic treatment. Larger studies of experimental design are needed to determine whether patients treated with medication use fewer nondrug interventions and require fewer physician office visits than patients treated without medication.

Aged↗