What is biofeedback therapy for urinary incontinence
What is biofeedback?
Biofeedback takes information about something happening in the body and presents it in a way that you can see or hear and understand. Getting on a scale to check your weight or having your blood pressure taken are very simple examples of biofeedback, which can be used to measure any body response such as heart rate or muscle contraction and relaxation.
In biofeedback, the measurement can be displayed on a computer screen or heard as a tone and used to learn about a subtle body function.
How is biofeedback used to treat incontinence and bladder problems?
Biofeedback has been proven effective in the treatment of urinary incontinence in numerous research studies. It can be used to help women learn to control and strengthen the pelvic floor muscles. The pelvic floor muscles (PFM) are a group of muscles that play an important role in bladder control. Weakness or dysfunction of the pelvic floor muscles can lead to problems with both bladder and rectal support and control.
Because you cannot see the pelvic floor muscles, you may have found it difficult to locate them. Perhaps you are uncertain if you are doing the pelvic muscle exercises correctly. This is where biofeedback can help.
Biofeedback therapy uses computer graphs and audible tones to show you the muscles you are exercising. It also allows the therapist to measure your muscle strength and individualize your exercise program. It does not do anything to your muscles. It is a teaching tool to help you learn to control and strengthen the pelvic floor area.
How is biofeedback done?
Two small sensors are placed with a sticky pad on either side of your anus, where the pelvic floor muscles are close to the skin. These can be placed under your loose clothing. Another set of sensors is placed across the abdomen. The sensors around the anus are connected to a computer screen and display a graph of your muscles as they are being exercised.
Since many women incorrectly use their stomach muscles when doing pelvic floor exercises, the sensors on the abdomen display a computerized graph to show you when you are using these muscles instead of those on the pelvic floor. The graphs also are helpful in measuring your growth in strength between biofeedback visits.
How long is each visit and how many will I need?
Biofeedback sessions are generally 30 minutes. The average number of sessions is four, but a few more or less may be needed to get the best results. Visits are scheduled every two to three weeks. Since biofeedback is a learning tool, it is important to practice pelvic floor exercises every day at home as well.
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Medication may have some benefit in stress and urge urinary incontinence. These agents are not uniformly effective, and adverse effects may limit their long-term use. Medications used for treatment of urinary incontinence include the following:
Tricyclic antidepressants (TCAs)
TCAs have historically been used to treat major depression, but their pharmacologic effects also make these drugs good choices for mixed incontinence, nocturia, and nocturnal enuresis. TCAs have also been used in the treatment of stress incontinence.
TCAs have complicated direct and indirect effects on the lower genitourinary tract. They possess both a central and peripheral anticholinergic effect, as well as being alpha-adrenergic agonists and central sedatives. The resultant clinical effect is bladder muscle relaxation and increased urethral sphincter tone. High pretreatment urethral closure pressure has served as a predictor of success.
Imipramine (Tofranil) is the most widely used TCA for urologic indications. It facilitates urine storage by decreasing bladder contractility and increasing outlet resistance. It has an alpha-adrenergic effect on the bladder neck, an antispasmodic effect on the detrusor muscle, and a local anesthetic effect on the bladder mucosa. (Note the black box warning: In short-term studies, antidepressants increased the risk of suicidal thinking and behavior in children, adolescents, and young adults (< 24 y) taking antidepressants for major depressive disorders and other psychiatric illnesses.)
Adult dosing is 10-50 mg 1 to 3 times daily, with a range of 25-100 mg qd. Pediatric dosing is not established. Imipramine is a pregnancy category D drug.
The combination of imipramine and oxybutynin (Ditropan) produces a synergistic effect to relax the unstable bladder, allowing it to better hold urine and preventing urge incontinence.
Amitriptyline (Elavil) is a TCA with sedative properties that increases circulating levels of norepinephrine and serotonin by blocking their reuptake at nerve endings. It is ineffective for use in urge incontinence but extremely effective in decreasing symptoms of urinary frequency in women with pelvic floor muscle dysfunction. It restores serotonin levels and helps break the cycle of pelvic floor muscle spasms.
Amitriptyline is well tolerated and effective in most women with urinary frequency. Adult dosing is 10 mg qd; titrate if necessary by 10 mg/wk until a maximum dose of 150 mg is reached, urinary symptoms disappear, or adverse effects become intolerable. Pediatric dosing is not established. Amitriptyline is also a pregnancy category D drug.
In addition to anticholinergic adverse effects, serious allergic reactions have been reported with TCAs, although rarely. Cardiotoxicity rarely is problematic at the low doses used for treatment of urinary incontinence. Central effects, such as sedation and tremor, may be troublesome to some patients. On occasion, prescribing imipramine at bedtime and a musculotropic agent in the daytime may be helpful.
These products are no longer commonly used in the treatment of incontinence.
The serotonin/norepinephrine reuptake inhibitor duloxetine is the first drug developed and marketed specifically for stress urinary incontinence. Duloxetine has been approved for the treatment of stress incontinence in Europe, but is not approved for this indication by the US Food and Drug Administration (FDA).
In animal models, duloxetine seems to increase pudendal motor nerve output via increased levels of serotonin and norepinephrine in the pudendal motor nucleus of the sacral spinal segments. As a result, urethral muscular tone and closure pressure is augmented. Similarly, studies in humans suggest that duloxetine enhances urethral closure through neuromodulation of the external urethral sphincter. 
A number of clinical trials have demonstrated the efficacy of duloxetine compared with placebo in the treatment of mild and moderate stress incontinence. A small, prospective, double-blind, randomized, placebo-controlled trial demonstrated modest efficacy in patients with severe stress urinary incontinence. 
In this study, patients with pure, urodynamically confirmed stress incontinence who were awaiting surgery were treated with duloxetine for 8 weeks. All participants had, on average, 14 or more episodes of stress incontinence per week. Significant improvement was observed in the quality of life indices and in frequency of incontinence episodes and use of protective pads in the patients treated with duloxetine compared with placebo. All positive clinical responses were observed within 2 weeks after initiation of therapy–some as early as 5 days.
The most common side effect was nausea, which tended to decrease with continued use. Discontinuation of therapy was significantly more common in the treatment group, with equal numbers of patients withdrawing because of nausea, vomiting, worsening of hypertension, and headache. Other common side effects included constipation and dry mouth. At the end of the 8-week trial, 20% of the treatment group patients were no longer interested in surgical therapy, versus 0% in the placebo arm.
Another small study demonstrated similar results, with 24% of the patients who received duloxetine declining their planned surgical therapy. Of note, 48% of the patients stopped the medication due to side effects at the 40 mg twice-daily dose schedule used in this study. 
A multicenter, double-blind, randomized, placebo-controlled study in 2,758 women with predominant stress incontinence found that after 6 weeks, the decrease in weekly incontinence episode frequency was significantly greater with duloxetine compared with placebo (-50 vs -29.9%). In an uncontrolled, open-label, 72-week extension of the study in 2,290 patients, 21.5% of patients discontinued the drug because of adverse effects. However, the efficacy of duloxetine was maintained in those women who remained on therapy. 
The clinical and urodynamic effects of blocking cholinergic receptors in the bladder are as follows:
Increased bladder capacity
Increased volume threshold for initiation of an involuntary contraction
Decreased strength of involuntary contractions
Propantheline bromide is an anticholinergic agent that has been used to treat detrusor overactivity. Propantheline commonly is prescribed in dosages of 15-30 mg every 4-6 hours. In one study, propantheline bromide decreased the rate of urge incontinence by 13-17% when 30 mg were used qid. When higher doses were used, 60 mg qid, the cure rate was reported to be over 90%. Because gastrointestinal (GI) absorption is poor, it is often recommended that propantheline be taken on an empty stomach.
Typical anticholinergic adverse effects can be expected, including dry mouth, constipation, dry eyes, blurred vision, orthostatic hypotension, and increased heart rate. This agent probably should be avoided by patients with heart disease and closed-angle glaucoma. Improvement rates in various studies generally have been approximately 50%. Propantheline is no longer considered a first-line drug for detrusor instability due to relatively poor efficacy and a high incidence of adverse effects.
Oxybutynin (Ditropan XL), which has both antimuscarinic and antispasmodic effects, reduces incontinence episodes by 83-90%. The total continence rate has been reported to be 41-50%. Mean reduction in urinary frequency was 23%. In clinical trials, only 1% stopped taking the drug because of dry mouth and less than 1% stopped taking it due to central nervous system adverse effects.
Tolterodine (Detrol) is a potent antimuscarinic agent for treating detrusor overactivity. In animal models, the drug has shown selectivity for the urinary tract over the salivary glands. Tolterodine has performed well in clinical trials, showing comparable efficacy to oxybutynin with lower discontinuance rates. The dosage range is 1-2 mg twice daily.
In clinical studies, the mean decrease in urge incontinence episodes was 50% and the mean decrease in urinary frequency was 17%. The mean decrease in urge incontinence episodes per week was 53% for long-acting tolterodine (Detrol LA) 4 mg qd.
In the Overactive Bladder: Judging Effective Control and Treatment (OBJECT) trial, extended-release oxybutynin 10 mg was statistically superior to tolterodine 2 mg bid in controlling urge incontinence, total incontinence, and micturition frequency. Both drugs had similar adverse-effect profiles.  OBJECT was a large double-blind, multicenter, prospective, randomized controlled study in 276 women and 56 men with symptoms of overactive bladder.
Two small studies examining the use of transdermal scopolamine in the treatment of detrusor overactivity have been reported. The results of these studies are conflicting in terms of both efficacy and tolerability of adverse effects.
Trospium (Sanctura) elicits antispasmodic and antimuscarinic effects. It acts by antagonizing acetylcholine effect on muscarinic receptors. Parasympathetic effect reduces smooth muscle tone in the bladder.
Trospium is indicated to treat urinary incontinence, urgency, and frequency. The typical dosage is 20 mg bid taken on an empty stomach at least 1 h before meals. The dose is reduced to 20 mg hs in patients with kidney insufficiency (ie, creatinine clearance [CrCl] < 30 mL/min). Elderly individuals (ie, > 75 y) may require a similar dose reduction to avoid adverse effects. Mild anticholinergic effects (eg, dry mouth, constipation, dry eyes, blurred vision) may occur.
Solifenacin (VESIcare) is a competitive muscarinic receptor antagonist that causes anticholinergic effects and inhibits bladder smooth muscle contraction. The initial dosage is 5 mg qd, which may be increased to 10 mg/d if tolerated and warranted.  The tablet must be swallowed whole (not crushed) with liquid.
Precautions include the following:
Kidney or liver impairment (do not exceed 5 mg in patients with creatinine clearance < 30 mL/min or moderate liver impairment [Child-Pugh class B])
Controlled narrow-angle glaucoma
History of prolonged QT interval
Bladder outflow obstruction
Decreased GI motility
Another anticholinergic agent is the extended-release product darifenacin (Enablex). It has high affinity for M3 receptors involved in bladder and GI smooth muscle contraction, saliva production, and iris sphincter function. A prospective, randomized, placebo-controlled, double-blind study demonstrated the efficacy of extended-release darifenacin with regard to reductions in incontinence episodes, decreases in frequency and urgency, and improved bladder capacity. 
The initial dose is 7.5 mg PO qd. After 2 weeks, the dose may be increased to 15 mg/d based on response.  Do not exceed 7.5 mg/d if moderate hepatic impairment (Child-Pugh class B) is present or the patient is also taking potent CYP-450 3A4 inhibitors.
Additive toxicity may occur if administered with other anticholinergics (eg, antihistamines). Coadministration with CYP-2D6 substrates that have a narrow therapeutic index (eg, flecainide, thioridazine, TCAs) may cause toxicity of these other 2D6 substrates. Coadministration may also increase midazolam or digoxin levels.
Increasingly, prolongation of the QT interval has been recognized as a potential problem in antimuscarinic drugs as well as medications of many different classes. Individuals with pharmacologic prolongation of the QT interval may be at increased risk for potentially fatal polymorphic ventricular tachyarrhythmia. Additional risk factors for this problem include female sex, advanced age, hypokalemia, and polypharmacy.
No direct studies compare the incidence of prolonged QT intervals or clinically concerning tachyarrhythmias among commonly prescribed antimuscarinic agents. However, in a study of 188 healthy volunteers receiving therapeutic (15 mg) and supratherapeutic doses of darifenacin, no prolongation of the corrected QT interval could be documented. 
More commonly observed adverse effects include dry mouth, constipation, and blurred vision. Darifenacin must be swallowed whole; do not chew, divide, or crush.
Fesoterodine (Toviaz) has been FDA approved for symptoms of overactive bladder (eg, urinary urge incontinence, urgency, frequency). It is a competitive muscarinic receptor antagonist and administered once daily.
Rule out narrow-angle glaucoma prior to prescribing an anticholinergic agent. Experienced ophthalmologists can convert narrow-angle glaucoma to open-angle glaucoma. Patients who are taking an anticholinergic agent should be monitored to prevent pharmacologically induced urinary retention.
Calcium channel blockers
In a small study, verapamil was no more effective than placebo and less effective than oxybutynin. However, verapamil combined with oxybutynin was more effective than oxybutynin alone. Terodiline was once a very popular drug for the treatment of detrusor overactivity in Europe but has since been withdrawn from the market due to a potential for serious adverse cardiac effects.
A small study showed magnesium hydroxide to be beneficial for some patients with sensory urgency and detrusor overactivity.  The presumed mechanism of action is through calcium antagonism. More work is needed before this treatment is recommended.
These agents relax beta-adrenergic receptors that are contained in smooth muscle, such as the bladder. Studies of terbutaline and clenbuterol have yielded mixed results. The role of these drugs as adjuncts to other pharmacologic therapies has not been explored.
Mirabegron (Myrbetriq), a beta-3 adrenergic receptor agonist, causes relaxation of the detrusor muscle and increases bladder capacity. It is indicated for overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency. A guideline from the American Urological Association recommends beta-3-adrenergic receptor agonists as second-line therapy in patients with an inadequate response to behavioral therapy. 
The agent 1-desamino-8-D-arginine vasopressin (DDAVP) has been used in children with nocturnal enuresis, with good results. The hormone causes water to be reabsorbed from the renal collecting system. Reduction in nighttime urine production may be beneficial in patients with detrusor overactivity and a significant degree of nocturia. Caution is needed when using this drug in elderly patients. Do not use in patients with significant heart failure or in children younger than 5 years (eg, water intoxication).
Vibegron (Gemtesa) is another beta-3 adrenergic agonist that is indicated for adults with overactive bladder who have symptoms of urge urinary incontinence, urgency, and urinary frequency. Approval was based on the EMPOWUR phase 3 clinical trial, which compared vibegron with tolterodine and placebo. Of 1518 randomized patients, 90.4% completed the trial. At 12 weeks, micturition episodes decreased by an adjusted mean of 1.8 episodes per day for vibegron compared with 1.3 for placebo (P < 0.001) and 1.6 for tolterodine. Among incontinent patients, urge incontinence episodes decreased by an adjusted mean 2 episodes per day for vibegron compared with 1.4 for placebo (P < 0.0001) and 1.8 for tolterodine. 
In a 52-week continuation study of EMPOWUR, vibegron demonstrated favorable long-term safety, tolerability, and efficacy. For this study, patients who had completed 12 weeks of once-daily vibegron 75 mg or tolterodine 4 mg extended release continued double-blind treatment, while patients who had completed 12 weeks of placebo were randomly assigned to receive double-blind vibegron or tolterodine. Of the 506 participants, 430 (85%) completed the study; only 12 (2.4%) discontinued owing to adverse events. Patients receiving vibegron maintained improvements in efficacy endpoints. 
Estrogen therapy may have several positive effects in women with stress incontinence who are estrogen deficient. Estrogen may increase the density of alpha-receptors in the urethra. In addition, it increases the vascularity of the urethral mucosa and may augment the coaptive abilities of the urethral mucosa. In theory, those effects should translate into improved continence; however, several studies stand in opposition of those assumptions.
A number of small studies show oral estrogen therapy to be of no clinical benefit to women with stress incontinence or detrusor overactivity. In a subgroup analysis of postmenopausal women enrolled in the Heart and Estrogen/Progestin Replacement Study (HERS), worsening of incontinence occurred in 39% of patients in the hormone treatment group, compared with 27% of patients in the placebo group. 
In the Women’s Health Initiative Study, women with baseline incontinence being treated with combined or unopposed estrogen oral therapy also showed exacerbation of symptoms significantly more often than women in the placebo group. In addition, women in the hormone-exposed groups with no baseline incontinence developed symptoms more often than those in the placebo group. 
Both of these trials present level 1 evidence against oral hormone therapy to treat incontinence. No adequate studies of local estrogen therapy exist. A meta-analysis found some evidence that local estrogen may improve incontinence, but there was little evidence on post-treatment results and none on long-term effects.  Local urogenital treatment provides more rapid and reliable effects in treating genitourinary atrophy and deserves study as a preoperative adjunct.
Pharmacologic therapy using estrogen derivatives results in few cures (0-14%) but may cause subjective improvement in 29-66% of women. It may be useful in postmenopausal women with atrophic vaginitis or intrinsic sphincter deficiency.
A neurotoxin produced by Clostridium botulinum, onabotulinumtoxinA (Botox) prevents acetylcholine release from presynaptic membrane. Therapy for urinary incontinence consists of 30 intradetrusor injections via cystoscopy.
In 2011, onabotulinumtoxinA was approved by the FDA for urinary incontinence in patients with neurologic conditions (eg, spinal cord injury, multiple sclerosis) who have overactive bladder. Placebo-controlled trials have shown significant reduction in urinary incontinence episodes and improved urodynamics at 12 weeks in patients who received onabotulinumtoxinA. [80, 81, 82]
In 2013, the FDA expanded the approved use of onabotulinumtoxinA to treatment of adults with overactive bladder who cannot use or do not adequately respond to anticholinergic drugs. The new indication was based on results of two placebo-controlled clinical trials in 1105 patients with symptoms of overactive bladder. After 12 weeks, patients who received injections of 100 units of onabotulinumtoxinA (20 injections of 5 units each) experienced urinary incontinence an average of 1.6 to 1.9 times less per day than patients treated with placebo. Treatment with onabotulinumtoxinA can be repeated if necessary, but at least 12 weeks should elapse between treatments. 
The ABC trial (Anticholinergic therapy vs onabotulinum toxinA for urgency incontinence) shed some light on the utility of 100 units of onabotulinumtoxinA in the setting of overactive bladder. The data have shown comparable efficacy of 100 units of onabotulinumtoxinA to anticholinergic medications with reduced systemic side effects in the onabotulinumtoxinA-injected group, yet higher rates of retention and urinary tract infections. Patients receiving onabotulinumtoxinA were more likely to be dry, however. Patients who received anticholinergic drugs were more likely to suffer from dry mouth and other systemic side effects. 
In a study that compared sacral neuromodulation and onabotulinumtoxinA in 364 women with refractory urge urinary incontinence, treatment with onabotulinumtoxinA resulted in a greater reduction in the 6-month mean number of daily episodes of urge incontinence. However, the authors note that although the difference was statistically significant, it is of uncertain clinical importance. In addition, treatment with onabotulinumtoxinA resulted in a higher risk of urinary tract infection (UTI) and need for transient self-catheterizations. 
A comparative study shows neuromodulation and botulinum toxin to have fairly equivalent success rates at 200 units. 
Other intravesical pharmacotherapy
Intravesical instillation of oxybutynin chloride has been used in patients who are nonresponsive to oral oxybutynin or have severe adverse effects from it. Intravesical oxybutynin has proved effective for treatment of neurogenic bladder dysfunction, although the effects are often transient.. Honda et al reported that intravesical oxybutynin chloride solution supplemented with hydroxypropylcellulose (HPC), a mucosal adhesive substance, provided long-term improvement in bladder compliance in three of four children (ages 1 to 3 years) with neurogenic bladder. 
In older patients, intravesical oxybutynin can be self-administered following clean catheterization and has been shown to be safe and efficacious. Studies have shown that tissue and plasma concentration of the drug are higher after intravesical administration than after oral administration.  Despite higher plasma levels, adverse effects appear to be minimal. This finding suggests that a hepatic metabolite may be responsible for many of the adverse effects observed after oral administration.
Intravesical capsaicin, the main pungent ingredient of hot peppers, has shown benefit for the treatment of detrusor overactivity and neurogenic detrusor overactivity. [89, 90] Similarly, resiniferatoxin, a naturally occurring pungent substance from the Euphorbia resinifera plant that has very potent capsaicinlike activity, has been used successfully to treat detrusor overactivity and neurogenic detrusor overactivity. However, intravesical capsaicin has not been approved for use in neurogenic detrusor overactivity, and resiniferatoxin was found to adhere to the plastic bags it was dispensed in; both agents have largely been superseded by onabotulinumtoxinA. 
Potassium channel openers relax smooth muscle by increasing potassium efflux, with resultant membrane depolarization. Supersensitivity of the detrusor muscle to depolarizing stimuli, such as potassium, in individuals with urge incontinence is the theoretical basis for the use of these agents in patients with detrusor overactivity. One problem in the development of potassium channel openers for use in bladder disorders has been the lack of organ specificity. Overall progress toward the development of a viable clinical formulation has been disappointing.
Prostaglandin may have an excitatory role in bladder contractility, and prostaglandin inhibitors, in theory, may block bladder contractility. Clinical trials (eg, with indomethacin) have shown mixed and generally not impressive results. One research group reported evidence of the role of a relative prostacyclin deficiency in the promotion of bladder contractions. Pharmacotherapy to increase the ratio of prostacyclin to other prostaglandins has not been investigated to date.
A pilot study by Kuismanen et al suggested that urethral injection of a combination of patient-derived adipose stem cells (ASCs) and collagen can improve the symptoms of stress urinary incontinence in women, possibly providing a nonsurgical alternative to sling procedures for this condition. All five women in the study, each of whom received ASCs and collagen for stress urinary incontinence, demonstrated subjective improvement. In addition, three women passed the cough stress test at 1-year follow-up, and two women considered themselves cured. [92, 93]