Urogynecology: Evidence-Based Clinical Practice 2nd ed.

7. Step-by-Step Guide to Treatment of Overactive Bladder (OAB)/Detrusor Overactivity

Kate H. Moore1


Department Obstetrics & Gynaecology, St George Hospital, Kogarah, New South Wales, Australia


If a patient has a main complaint of frequency/urgency/nocturia/urge incontinence on history or if urodynamic testing has revealed detrusor overactivity, then bladder training is an essential part of treatment. Most continence clinicians would not prescribe anticholinergic drugs without teaching bladder training first.

If a patient has a main complaint of frequency/urgency/nocturia/urge incontinence on history or if urodynamic testing has revealed detrusor overactivity, then bladder training is an essential part of treatment. Most continence clinicians would not prescribe anticholinergic drugs without teaching bladder training first.

Explain the Condition

This is the first step. Many patients with this problem think that they are “neurotic”; often they are an embarrassment to their families as they frequently need to rush to the toilet at social occasions. In fact, during the 1970s and 1980s, several studies suggested that this condition was largely psychosomatic, but conclusive evidence of this was not found.

Since the introduction of quality of life testing in the 1990s, we have learned that patients with detrusor overactivity have a much poorer quality of life than those with stress incontinence and are more anxious and depressed because of the unpredictable nature of their condition.

Recent studies have indicated that:

·               The subepithelial nerves are overabundant in this condition (increased by about 35% compared to controls [24]; see Fig. 7.1), and neuropeptides involved in conveying “nociceptive” or painful symptoms are increased by 80–90% [32].


Figure 7.1

Increased subepithelial nerves in detrusor overactivity patient

·               The ability of the cerebral cortex to inhibit the desire to void is reduced in this condition but can be strengthened by training. Functional MRI studies performed during urodynamics show changes in cerebral blood flow in OAB [17].

·               The detrusor muscle is overly contractile, giving rise to “muscle cramps” in the bladder. Pharmacological studies show that, in the organ bath, the muscle strips from these patients do not relax entirely when atropine is administered (whereas detrusor strips from control patients do relax after atropine is applied). (For review, see Kumar et al. [22]).

Stretch of the bladder causes more rapid release of ATP (a signaling molecule that activates afferent nerves) in patients with OAB compared to controls [10].

Therefore, the patient must understand that she is not neurotic but has an abnormality of the afferent (subepithelial nerves) and efferent (detrusor contractility) limbs of the micturition reflex.

The next step in bladder training is to look at the frequency–volume chart with the patient. Because severity of frequency varies in this condition, the therapist needs to find a realistic target “voiding interval” toward which the patient can aim. For example, if the chart shows that the patient usually toilets every hour but sometimes can hold for 2 h, then the target voiding interval should be 2 h (Fig. 7.2).


Figure 7.2

A typical example of a patient with OAB, with the usual voiding frequency circled and the “target” voiding interval underlined

Once the target (e.g., 2 h) is chosen, the instructions to the patient are as follows.

Step-by-Step Guide to Bladder Training

When you get a desire to go to the toilet, look at your watch.

If it is more than 2 h since you last went to the toilet, just go ahead and pass urine.

If it is less than 2 h since you last went, then you need to do three things:

·               A. Sit down.

The reason for this is that the bladder has gravity nerves inside the wall that give you a stronger desire to toilet when you are standing than when you are sitting.

·               B. Contract your pelvic floor muscle (PFM).

The reason is that you must stop any drops of urine escaping from your bladder into your urethra. Once the fluid gets into your urethra, there is an automatic reflex that will make you start passing urine onto your pad, so you need to “nip this in the bud.”

·               C. Send a strong message from your brain, down your spinal cord to the level of the tailbone, then out to your bladder, saying, “No, I am not going to the toilet for 2 minutes.” There is a direct pathway from the front of your brain, down the spine, to the bladder, but in your condition, the message signals on this pathway seem to have become “rusty” or weak. These messages can be strengthened by focused concentration.

Sit quietly for 2 min, contracting your PFM. At the end of 2 min, stand up (contracting your PFM as you stand), and walk slowly to the toilet (do not run or you are more likely to leak).

However, if you have waited 2 min, it is likely that you will no longer want to go.

This is because the bladder spasms that cause your leakage are like a muscle cramp; they normally only last 1–2 min, and then the muscle cannot hold the spasm any more; it relaxes.

Therefore, you may be able to hold on for another half an hour or so, until another spasm occurs. If this happens after you have successfully stopped the previous spasm, then you should go ahead and walk to the toilet for this one.

Before the patient can successfully undertake step B, she must be examined to make sure that she can contract her PFM, and if not, undergo a program of pelvic floor muscle training, as described in Chap. 6. Do not disappoint the patient by expecting her to succeed with bladder training until she has learned how to contract the pelvic floor muscle.

The patient needs to understand that bladder training is an essential part of treating the overactive bladder. If drugs are prescribed for this condition, they will help to relax the bladder spasms, but the patient must try to inhibit the premature desire to void.

Also, if a patient suffers from nocturia, the bladder training works to increase her bladder capacity during the day. Gradually, her bladder capacity will also increase at night. She must attempt to inhibit the desire to void at night if she is awakened by a snoring husband or a dog that is barking. She must avoid nocturnal trips to the toilet out of habit.

Is bladder training of proven efficacy? Unfortunately, bladder training was introduced before the era of evidence based medicine. An often quoted paper from 1980 set the stage. In it, 25 women had inpatient bladder drill, and 25 women had drug therapy (with imipramine and an outdated drug flavoxate). Of the bladder drill group, 76 % “were rendered symptom free,” versus 48 % of those given drugs [21]. In the same year, outpatient bladder drill was reported to achieve subjective cure in 87% and objective cure in 53% of 90 women [15]. Since then, there has never been an adequately powered trial comparing bladder training with no therapy, but most clinicians find that bladder training is important.

How Do Anticholinergic Drugs Work?

Anticholinergic drugs work through the parasympathetic nervous system; they are antagonists that work at the muscarinic receptor to inhibit (and in some cases abolish) detrusor muscle contractions. For the patient, this can be likened to a muscle relaxant acting on the bladder. There are several types of anticholinergic drugs, with varying pharmacological properties.

Propantheline (Pro-Banthine): 15 mg TDS is a very old antimuscarinic drug. As it is a quaternary amine, it is poorly absorbed from the gut. Side effects of dry mouth and constipation are ubiquitous, but the drug is cheap.

Oxybutynin (Ditropan): Maximum 5 mg TDS has been used since the 1970s. It is an antimuscarinic drug but also has local anesthetic properties (thus, it can be given intravesically) and also a smooth muscle relaxation effect. It is very effective in reducing detrusor contractions, but about 60% of patients will get annoying dry mouth/dryness of the esophagus/difficulty swallowing and stop taking it. It is very cheap. When giving oxybutynin, titrate the dose against the symptoms. For severe nocturia but less daytime leak, give 2.5 mg mane and 5 mg nocte. Some patients are worse in the morning but have no nocturia; give 5 mg mane and 2.5 mg after lunch. The drug works within 1 h and lasts 6–8 h. A long-acting “slow-release” form of oxybutynin has been developed but is not marketed in all countries; this gives less dry mouth (about 25%). A transdermal patch Oxytrol also gives less side effects by avoiding production of a liver metabolite, but pruritus at the patch site occurs in about 7% [27].

Imipramine (Tofranil): 25–50 mg nocte, is also a very old drug. In much larger doses (75–100 mg daily), it is an antidepressant. It has a beta-mimetic action to relax the dome of the bladder but also has anticholinergic effects. Because a common side effect is drowsiness, it is very useful for nocturia. It also lowers the pain threshold by an uncertain mechanism and can be used when the bladder spasms are appreciated as painful (or in painful bladder syndrome; see Chap. 12).

Tolteridine (Detrusitol): 2 mg BD, was developed in the 1990s. It attaches to the bladder muscarinic receptors to a much greater extent than to such receptors in the salivary glands, so it gives less dry mouth than oxybutynin but is just as effective. It also has a slightly longer duration of effect, hence the BD dosage. In some patients, 4 mg BD can be given without dry mouth. A slow-release form has been made which is somewhat more effective with even less dry mouth but is not available in all countries.

Propiverine (Detrunorm): 15 mg TDS, is an antimuscarinic agent that is also a calcium channel blocker. Dry mouth occurs in about 20% of patients but is not usually distressing. It is not available in many countries.

Trospium (Regurin): 20 mg BD, is a nonselective quaternary amine but does not give as much dry mouth (4%). Its structure also limits blood–brain barrier penetration, thus reducing CNS effects in the elderly (confusion). It is widely used in the United Kingdom.

Darifenacin (Enablex, Emselex): selectively acts at the M3 receptor, which is thought to be most functionally important for mediating detrusor contractions, available in most countries.

Solifenacin (Vesicare): 5–10 mg daily, is also selective for the M3 receptor and also does not attach well to the salivary gland receptors. It was developed in early 2000s and achieved continence in 51% of one trial, with 11% suffering from dry mouth, available in most countries.

Fesoteridine (Toviaz): 4–8 mg daily, is the most recently developed anticholinergic, which was derived from tolteridine. It is available in the UK and Europe.

Duloxetine: This is a recently developed serotonin reuptake inhibitor that also affects Onuf’s nucleus in the pelvic nerve plexus. It was designed for the medical treatment of stress incontinence because it enhances the strength of the internal urethral sphincter mechanism. Because it also enhances bladder capacity, it has also been used in overactive bladder. It is licensed in Denmark for use in incontinence.

Desmopressin (Minirin): Consider treating with this if nocturia cannot be helped by other agents. This synthetic vasopressin analogue markedly reduces the production of urine for about 6 h. It is given as 1–2 nasal sprays to each nostril before bedtime; oral tablets are also available. It is useful for patients with debilitating nocturia who are practicing bladder training during the day but have not yet improved their bladder capacity, so they have not yet seen any reduction in nocturia. It is not a good long-term strategy. Particularly in the elderly, prolonged use is associated with hyponatremia that can be life threatening. Be very careful in patients with nocturnal polyuria, however (defined as passing more than 30% of total urine output at night). This drug is contraindicated in such patients so a frequency volume chart must be completed before starting this drug. In children with bedwetting, long-term usage has been shown to be safe.

Are Anticholinergic Drugs Effective?

This is controversial. Most pharmacotherapy trials only consider efficacy at 12 weeks or thereabouts. An initial Cochrane meta-analysis [20] found that, in a review of 6,713 patients in 51 studies, the placebo effect was much higher than expected (about 45 % with respect to control) but that the drugs gave an additional 15% over placebo. Overall, anticholinergic drugs achieved one less leak per 48 h and one less void per 48 h, with respect to placebo. This may seem like a small effect, but most of these trials did not include formal bladder training programs, so they do not reflect ordinary clinical practice. The most recent Cochrane review of 61 trials (11,956 adults) concluded that anticholinergic drugs produce a statistically significant improvement in symptoms of overactive bladder [27].

The natural history of detrusor overactivity has received little attention. Recently, a review of 76 patients with proven DO at a median of 6 years [26] found that symptoms had largely resolved in only about 16 %. Symptoms were no different in 59% of patients and were worse in the remaining 25% (Fig. 7.3). Thus, some form of long-term anticholinergic therapy may be needed in up to three quarters of patients.


Figure 7.3

Histogram showing course of disease in 76 patients with detrusor overactivity at a median follow-up of 6 years (Data from Morris et al. [26])

Having said that, patients may not have to take the full dose to achieve good symptom control. Many patients have “good days” and “bad days.” In a randomized controlled trial, Burton [8] showed that patients who took tablets only on their “bad days” (the “PRN regime”) obtained equally good effect as those who took the daily dose.

Role of Topical Estrogens

Theoretically, the effect of vaginal estrogen upon the bladder base/trigone should promote tissue elasticity and enhance bladder capacity. Also the effects of estrogen seen in patients with stress incontinence (thickening the urethral mucosa to prevent leakage of urine) should also help to reduce leakage in women with OAB.

Unfortunately, few studies have investigated this. Small studies from the early 1980s showed significant improvement in urge incontinence symptoms, but no objective outcome parameters were employed. A large RCT of topical estrogen versus placebo showed no significant benefit for urge symptoms, but the dose of estrogen was found to be insufficient when the effect of estrogen upon the cytopathology of urethral epithelial swabs was fully evaluated [3].

Alternative Therapies for Detrusor Overactivity

TENS (Transcutaneous Electrostimulation Therapy)

TENS has been used for many years in the labor ward, to inhibit the sensation of pain during uterine contractions. TENS (Fig. 7.4) has been applied with some success in patients who feel the urge to void as a painful spasm. It works by modifying sensory input, by interrupting the relay of afferent impulses to the cerebral cortex (called the gateway theory of pain control).


Figure 7.4

TENS machine for the treatment of detrusor overactivity

The electrodes are applied over the pubic bone or over the sacrum, and the patient self-regulates the electrical impulses coming from the stimulator (worn attached to her belt) until she feels a strong buzzing or throbbing sensation over the application site. Small clinical trials have shown promising results [518]. The device costs about 50 Euros.


Acupuncture has also been helpful for detrusor overactivity. Initially, it was thought to work via the gateway theory of pain control, but later it was found that acupuncture increases the levels of endogenous opioids (beta-endorphin and met-enkephalin) in the patient’s cerebrospinal fluid. Pharmacological experiments show that enkephalins inhibit detrusor contractions.

The traditional bladder points are documented in the literature; in one small study [28] (n  =  16), acupuncture abolished detrusor overactivity incontinence in 63%. In a larger study (n  =  26 patients on active acupuncture, 24 sham therapy), symptom improvement occurred in 85%, with 75% becoming urodynamically stable [9].

SANS Electro-Acupuncture (Stoller Afferent Nerve Stimulator)

This is a device that mimics acupuncture but adds an electrical stimulus to the needle that is inserted into a bladder point over the medial malleolus of the ankle (near the posterior tibial nerve). This device can be employed by trained nurse continence advisors, because the relevant bladder point is easily identified from surface anatomy (Fig. 7.5) Acute administration of SANS during cystometry significantly increased the volume at first detrusor contraction and the maximum cystometric capacity [1]. After 12 weeks of SANS in 53 patients, a 25% reduction in frequency, 21% reduction in nocturia, and a 35% benefit for urge incontinence were noted [16]. Maintenance therapy with repeated treatments may be necessary however [34].


Figure 7.5

SANS device, applied to the bladder acupuncture point at the medial malleolus


Hypnotherapy has also been helpful [14]. After 1 month of 12 sessions, 58% of 63 patients became symptom free; 14% were unchanged. Cystometry showed that 50% had become stable, with 36% improved. Of 30 patients reviewed at 2 years, 33% remained symptom-free. The author commented that patients required an audiocassette tape to be used in their own homes at regular intervals in order to maintain symptomatic benefit, so this therapy requires a motivated user.

The Cochrane Collaboration has not evaluated hypnotherapy or acupuncture for detrusor overactivity.


As discussed in Chap. 6, electrostimulation is a recognized technique for strengthening the pelvic floor muscle, by inducing repetitive tetanic muscle contractions. It can also be used for patients with detrusor overactivity (DO). Electro­stimulation of the nerves of the perineum or anus is known to cause reflex inhibition of detrusor contractions. In the 1970s, electrostimulation was usually delivered via an anal electrode, which was not popular among middle-aged women. In the largest sham-controlled RCT, Brubaker et al. [6] showed that intra-vaginal electrostimulation resulted in a urodynamically stable bladder in 49% of patients with DO (no significant change in the sham group).

Extracorporeal Electromagnetic Stimulation Therapy

As mentioned in Chap. 6, this is a form of electrostimulation therapy that avoids the need for a vaginal probe. “On-chair” cystometry studies show that the magnetic stimulus abolishes detrusor overactivity in the majority of cases, but a sham-controlled study (using a sham chair that delivered no current) showed no benefit for active treatment over sham [25].


Originally, Helmstein’s cystodistention was undertaken for 5–7 h (under epidural anesthesia) in order to produce necrosis of superficial bladder tumors. Later studies showed that this degree of distension produced tissue anoxia, which was thought to reduce detrusor contractility. Studies in the 1970s showed subjective response for DO in 70%, with 65–80% of bladders becoming urodynamically stable [29]. Later studies showed symptomatic response in 32%, with a stable bladder in 19% [12]. These days, it is difficult to justify epidural anesthesia and day-only admission for such a response rate.

However, in patients over age 50 with refractory detrusor overactivity (defined as failure to respond to two anticholinergic drugs with bladder training for more than 12 months [24]), it is reasonable to offer cystoscopy to exclude carcinoma in situ (which may cause chronic irritative symptoms, e.g., frequency, urgency, and nocturia) and at the same time perform a simple cystodistention. This involves distending the bladder to capacity under general anesthetic, then allowing the total fluid volume to remain in the bladder for 3–5 min (with the infusion bag at a height of 1 m above the bladder). A refill examination can then be performed in patients who also complain of suprapubic pain (see Chap. 12) to exclude interstitial cystitis.

Botox Therapy (Botulinum Toxin A Injections)

Since 2004, Botox injections to the detrusor muscle have been widely used in neuropathic DO (especially multiple sclerosis); limited trials have been performed in idiopathic DO. The neurotoxin binds to cholinergic terminals locally to inhibit acetylcholine release and to some extent ATP resulting in reduced detrusor contractions at the injected muscle site. It also blocks the release of some afferent neuropeptides involved in transmission of noxious stimuli. About 30 injections of 200–300 units are usually given, via cystoscopy. One ampoule of 100 U costs about 800 $US. Symptom benefit lasts 6–9 months. Three RCTs of Botox versus placebo injection for idiopathic detrusor overactivity have shown significant reductions in urge incontinence and a variety of other OAB symptoms. The largest RCT showed that 72% of patients had 75% or greater reduction in leakage at 1 month but benefits fall over time [7]. Up to 45% of patients needed to self-­catheterize (Cochrane review [13]).

Intravesical Resiniferatoxin (RTX) Installation

This has been used for several years for neuropathic DO, with considerable success. This agent acts to desensitize the vanilloid receptors in the bladder lining, which normally convey the sense of urgency. Small trials undertaken in idiopathic DO showed early promise, but later studies including RCT showed no benefit. For review, see Cruz [11].

Clam Cystoplasty

This was popular in the 1980s. In patients with completely refractory disease, the bladder was opened transversely (in the manner of opening a clam), and a segment of flattened bowel was inserted into the bladder opening, then the bladder was closed with its interposed bowel segment in continuity. The idea was to increase the bladder capacity and interpose an autologous tissue that would impair detrusor muscle contractility.

This procedure has a 1% mortality rate. the initial 90 % subjective response was not sustained over time. The bladder becomes stable in about 60% of cases. At a mean of 6 years [2], 53% of 51 patients were continent, but 40% needed to self-catheterize and suffered recurrent UTI. Mucous plugs from the bowel segment caused urinary retention in 20%.

Partial Detrusor Myomectomy

The concerns about risks versus benefits for the clam cystoplasty procedure led to its development [2333]. It yields better results with less morbidity but is still a major surgical undertaking.

Implantation of S3 Sacral Nerve Root Stimulator

A two-stage procedure is can be effective for refractory DO, it is expensive (approx. US$10,000) and requires careful follow-up of the patient. The first stage involves peripheral nerve evaluation (PNE). With the patient lying prone, the S3 foramen is located; a spinal needle is used to test that the nerve root has been located by electrical stimulation, and then a temporary stimulation wire is inserted and taped securely, see Fig. 7.6. This is attached to a temporary pulse generator device that the patient wears externally. The patient goes home for 5–7 days and records the impact of the S3 stimulation upon their DO symptoms. If the symptomatic benefit after PNE is greater than 50–70%, a permanent electrode is implanted into the S3 foramen. The pulse generator is then implanted below the posterior superior iliac crest. Early results [4] and long-term follow-up [3031] indicate that the frequency and severity of urge incontinence episodes are substantially reduced (see Cochrane [19] review).


Figure 7.6

Insertion of sacral nerve stimulation lead at S3

Because S3 sacral stimulation has no appreciable mortality, it has essentially replaced clam cystoplasty and detrusor myomectomy in patients with severe refractory detrusor overactivity.


Idiopathic detrusor overactivity is often very distressing for patients, because they cannot predict when they will leak. It is also rather frustrating for the clinician, because we do not yet understand the cause of the condition and we have no “cure.” Patients need to be treated as sympathetically as possible, with careful bladder training and attempts to find the best therapy for each woman. Sacral nerve stimulation has recently superseded open surgery such as clam cystoplasty for severe cases. The patient should be told that a great deal of research is ongoing, to discover the cause and find better treatments for this problem.



Amarenco G, Ismael SS, Even-Scneider A, Raibaut P, Demaille-Wlodyka S, Parratte B, Derdraon J. Urodynamic effect of acute transcutaneous posterior tibial nerve stimulation in overactive bladder. J Urol. 2003;169:2210–5.PubMedCrossRef


Awad SA, AlSahrani HM, Gajewski JB, Bourque-Kehoe AA. Long-term results and complications of augmentation ileocystoplasty for idiopathic urge incontinence in women. Br J Urol. 1998;81:569–73.PubMedCrossRef


Benness C. Vaginal oestradiol for postmenopausal urinary symptoms, a double blind placebo controlled study. In: Proceedings of FIGO. Stockholm; 1992.


Bosch J, Groen J. Sacral (S3) segmental nerve stimulation as a treatment for urge incontinence in patients with detrusor instability: results of chronic electrical stimulation using an implantable neural prosthesis. J Urol. 1995;154:504–9.PubMedCrossRef


Bower WF, Moore KH, Adams R. A urodynamic study of surface neuromodulation versus sham in detrusor instability and sensory urgency. J Urol. 1998;106:2133–6.


Brubaker L, Benson JT, Bent A, Clark A, Shott S. Transvaginal electrical stimulation for female urinary incontinence. Am J Obstet Gynecol. 1997;177:536–40.PubMedCrossRef


Brubaker L, Richter HE, Visco A, et al. Refractory idiopathic urge urinary incontinence and Botulinum A injection. J Urol. 2008;180:217–22.PubMedCentralPubMedCrossRef


Burton G. A randomised cross over trial comparing oxybutynin taken three times a day or taken “when needed”. Neurourol Urodyn. 1994;13:351–2.


Chang PL. Urodynamic studies in acupuncture for women with frequency, urgency and dysuria. J Urol. 1988;140:563–6.PubMed


Cheng Y, Mansfield KJ, Allen W, Walsh CA, Burcher E, Moore KH. Does Adenosine Triphosphate released into voided urodynamic fluid contribute to urgency signaling in women with bladder dysfunction? J Urol. 2010;183:1082–6.PubMedCrossRef


Cruz F. Vanilloid receptor and detrusor instability. Urology. 2002;59(Suppl 5A):51–60.PubMedCrossRef


Delaere KP, Debruyne FM, Michiels H, Moonen W. Prolonged bladder distension in the management of the unstable bladder. J Urol. 1980;124:334–6.PubMed


Duthie JB, Vincent M, Herbison GP, Wilson DI, Wilson D. Botulinum toxin injections for adults with overactive bladder syndrome. Cochrane Database Syst Rev. 2010;(12):CD005493. DOI: 10.1002/14651858.pub3.


Freeman RM. A psychological approach to detrusor instability incontinence in women. Stress Med. 1987;3:9–14.CrossRef


Frewen WK. The management of urgency and frequency of micturition. Br J Urol. 1980;52:367–9.PubMedCrossRef


Govier FE, Litwiller S, Nitti V, Kreder KJ, Rosenblatt P. Cutaneous afferent neuromodulation for the refractory overactive bladder: results of a multicenter study. J Urol. 2001;165:1193–8.PubMedCrossRef


Griffiths D, Tadic SD, Schaefer W, Resnick NM. Cerebral control of the bladder in normal and urge-incontinent women. Neuroimage. 2007;1:1–7. Epub 2007 May 18.CrossRef


Hasan ST, Robson WA, Pridie AK, Neal DE. Outcome of transcutaneous electrical stimulation in patients with detrusor instability. Neurourol Urodyn. 1994;13:349–50.


Herbison G, Arnold E. Sacral neuromodulation with implanted devices for urinary storage and voiding dysfunction in adults. Cochrane Database Syst Rev. 2009;(2):CD004202.


Herbison P, Hay-Smith J, Ellis G, Moore KH. Effectiveness of anticholinergic drugs compared with placebo in the treatment of overactive bladder: systematic review. Br Med J. 2003;326:841–7.CrossRef


Jarvis GJ. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. Br J Urol. 1981;53:565–6.PubMedCrossRef


Kumar V, Cross R, Chess-William R, Chapple C. Recent advances in basic science for overactive bladder. Curr Opin Urol. 2005;15:222–6.PubMedCrossRef


Leng WW, Blalock HJ, Fredriksson WH, English SF, McGuire EJ. Enterocystoplasty or detrusor myectomy? Comparison of indications and outcomes for bladder augmentation. J Urol. 1999;161:758–63.PubMedCrossRef


Moore KH, Gilpin SA, Dixon JS, Richmond DH, Sutherst JR. An increase of presumptive sensory nerves of the urinary bladder in idiopathic detrusor instability. Br J Urol. 1992;70:370–2.PubMedCrossRef


Morris A, O’Sullivan R, Donkley P, Moore KH. Extracorporeal magnetic stimulation in female detrusor overactivity simultaneous cystometry testing and a randomized sham controlled trial. Eur Urol. 2007;52:876–83.PubMedCrossRef


Morris AR, Westbrook JI, Moore KH. Idiopathic detrusor over-activity in women – a 5–10 year longitudinal study of outcomes. Neurourol Urodyn. 2003;22:460–2.


Nabi G, Cody JD, Ellis G, Hay Smith J, Herbison GP (2009) Anticholinergic drugs versus placebo for overactive bladder syndrome in adults. Cochrane Database Syst Rev. 2009. DOI: 10.1002/14651858.CD003781.pub2.


Philp T, Shah PJR, Worth PHL. Acupuncture in the treatment of bladder instability. Br J Urol. 1988;61:490–3.PubMedCrossRef


Ramsden PS, Smith M, Dunn M, Ardran GM. Distention therapy for the unstable bladder: later results including an assessment of repeat distensions. Br J Urol. 1976;48:623–9.PubMedCrossRef


Scheepens WA, Van Koeveringe GA, DeBie RA, Weil EH, Van Kerrebroeck PE. Long term efficacy and safety results of the two stage implantation techniques in sacral neuromodulation. BJU Int. 2002;90:840–5.PubMedCrossRef


Shaker HS, Hassouna MM. Sacral nerve root neuromodulation: effective treatment for refractory urge incontinence. J Urol. 1998;159:1516–9.PubMedCrossRef


Smet P, Moore KH, Jonavicius J. Distribution and colocalisation of calcitonin gene-related peptide, tachykinins, and vasoactive intestinal peptide in normal and idiopathic unstable human urinary bladder. Lab Invest. 1997;77:37–49.PubMed


Swami KS, Feneley RC, Hammonds JC, Abrams P. Detrusor myectomy for detrusor overactivity: a minimum 1 year follow-up. Br J Urol. 1998;81:68–72.PubMedCrossRef


Van der Pal F, Van Balken MR, Heesakkers JP, Debruyne FM, Bemelmans BL. Percutaneous tibial nerve stimulation in the treatment of refractory overactive bladder syndrome; is maintenance treatment necessary? BJU Int. 2006;97:547–50.PubMedCrossRef