6 Management of overactive

bladder syndrome

We gain bladder control as young children and from this time onwards a
healthy bladder is controlled by the central nervous system. The detrusor
will not normally contract until it is convenient to initiate a void. This
contraction is initiated at the level of the cerebral cortex. When detrusor
overactivity is present, however, the detrusor contracts spontaneously
during the filling phase of the micturition cycle, when micturition would
normally be inhibited. The true incidence of this condition is unknown; it
is possible that we all exhibit detrusor overactivity on occasions. For
example, many ‘healthy’ people will have symptoms of urinary urgency
when the weather is cold, when they have drunk strong coffee or when
they put their key in the front door with a full bladder. In some people, this
condition causes great distress and can manifest as severe urinary frequency
with urgency. There may be associated urge urinary incontinence; this can
be particularly distressing as the bladder may empty completely off an
unstable detrusor contraction.

Definition and aetiology

Detrusor overactivity is defined as a urodynamic observation characterised
by involuntary detrusor contractions during the filling phase that may be
spontaneous or provoked.1 It is apparent from this definition that, as there
has to be objective evidence of a detrusor contraction, detrusor overactivity
can be diagnosed only after a urodynamic study. It is neither necessary nor
desirable to investigate all women presenting with symptoms of frequency,
urgency and urge incontinence with a urodynamic study. When the history
is typical, one can usually presume that there is underlying detrusor overac-
tivity and treat empirically for 1–2 months. Urodynamics can be reserved
for those in whom empirical treatment fails.
Urgency, with or without urge incontinence, usually with frequency
and nocturia, can be described as overactive bladder syndrome (OAB).1
This symptom combination suggests detrusor overactivity but can be
caused by other forms of urethrovesical dysfunction. The term can be used
after urinary infection and other obvious pathology has been excluded.

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 Therefore, before empirical treatment, the woman should complete a
urinary diary and have urine tested for blood and infection to exclude
factors such as malignancy, untreated diabetes and polydipsia.
It is no surprise, given the wide range of people who are thought to display
detrusor overactivity, that this is not a homogeneous disease with a single
cause. In a minority of patients, there is a disturbance of the nervous control
mechanisms and, when there is objective evidence of a relevant neurological
disorder in association with detrusor overactivity diagnosed on urodynamic
testing, the term neuropathic detrusor overactivity is used.1 However, the vast
majority of patients have no associated neurological disease and this condition
is commonly termed idiopathic detrusor overactivity.
In clinical practice, the extent of neurological examination and investi-
gation varies. If there are no overt neurological symptoms, most clinicians
would not investigate further, for example with magnetic resonance
imaging (MRI). It is likely that a complete neurological assessment would
result in some idiopathic cases being reclassified as neurogenic. As the name
implies, the underlying aetiology of idiopathic detrusor overactivity is
unknown. Sometimes obstruction is implicated: men may see a resolution
of both bladder-filling symptoms (such as frequency and urgency) and
urodynamically proven detrusor overactivity after relieving prostatic
obstruction. In women, potentially obstructive continence surgery can
result in de novo detrusor overactivity. The risk of this appears to vary
according to the continence procedure chosen, with newer less obstructive
low-tension slings having less risk than older obstructive operations such as
colposuspension. The majority of women with detrusor overactivity do not,
however, have any bladder outlet obstruction and other factors must be
implicated that are currently imperfectly understood.

Conservative measures
As the pathophysiology of the disease is poorly understood, the cause
cannot yet be treated and management aims to suppress the symptoms
rather than alter the disease process itself. The natural history of idiopathic
detrusor overactivity is completely unknown. In many people, this will be
a remitting disease and symptom suppression may result in longer term
resolution. Treatment may therefore be either short or long term,
depending on the individual.

LIFESTYLE CHANGES AND BEHAVIOURAL THERAPY

Behaviour modification, such as reducing fluid intake if the urinary diary
suggests this is excessive and cutting caffeinated products out of the diet,
will often have a dramatic effect. Simple advice such as this may be all that
is required to cure frequency and urgency.

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 Bladder training may be of benefit. This entails patient education and
timed voiding with systematic delay of voiding and positive reinforcement.
The woman is asked to resist the sensation of urgency and void according
to a timetable. She is told that she is not allowed to use the toilet until the
next scheduled time of void. It requires highly motivated patients and most
clinicians would suggest that it be done in conjunction with, rather than
instead of, pharmacotherapy with anticholinergics.

PHARMACOTHERAPY
Pharmacological suppression of detrusor overactivity with anticholinergics
(antimuscarinics) is the most widely used treatment for this condition.2
Anticholinergic drugs block the muscarinic receptors that mediate detrusor
smooth muscle contruction and have a direct, relaxing effect on the
detrusor muscle. There are a number of drug treatments available
(Table 6.1). They differ in their selectivity for various muscarinic receptors
and some drugs have additional actions, such as direct smooth muscle
effects. These drugs are essentially safe and, therefore, it would seem
reasonable clinical practice to commence a short course of empirical
treatment in cases where detrusor overactivity is suspected. If symptoms
are not improved after 1 or 2 months of anticholinergics, the patient should
be referred to a specialist clinic.

Table 6.1 Currently available preparations of anticholinergic drugs

Drug Route of delivery Adult dosage

Oxybutynin Oral (a) 2.5–5 mg, 1–4 times per day

(b) 5–10 mg, once daily (SR)
Transdermal patch One patch, twice per week (3.9 mg/24 hours)
Propiverine Oral only 15 mg, 2–4 times per day
Solifenacin Oral only 5 or 10 mg, once daily
Tolterodine Oral only (a) 1–2 mg, twice daily
(b) 4 mg, once daily (SR)
Trospium Oral only 20 mg, twice daily
Darifenacin Oral only 7.5 or 15 mg, once daily (SR)
Fesoterodine Oral only 4 or 8 mg, once daily (SR)

SR = sustained release

NICE recommends that immediate-release nonproprietary oxybutynin

should be offered to women with OAB or mixed urinary incontinence as
first-line antimuscarinic drug treatment, if bladder training has been
ineffective.3 If immediate-release oxybutynin is not well tolerated,

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 darifenacin, solifenacin, tolterodine, trospium or an extended release or
transdermal formulation of oxybutynin should be considered as
alternatives.2
Oxybutynin, propiverine, tolterodine and trospium4 have been used for
many years to treat OAB symptoms. Sustained-release oxybutynin trans-
dermal patches, which release 3.9 mg every 24 hours, have recently been
launched in the UK.5
Solifenacin and darifenacin are newer bladder-selective anticholinergic
preparations. They are more recent useful additions to the list of available
drugs and may possibly have a lower incidence of adverse effects.6
Fesoterodine is the latest addition to the available list of drugs. It is a
nonselective oral antimuscarinic agent that exerts its pharmacological
effects as a competitive muscarinic receptor antagonist.7–10
Patients should be advised on the possibility of adverse effects before
starting treatment. The dosage may need to be titrated against clinical
efficacy and adverse effects profile. Some may tolerate a particular
preparation better than others and clinicians may need to try a number of
preparations before finding one that suits the individual.11–13 Adverse effects
of anticholinergics may include:
G dry mouth (in up to 30% of cases)
G constipation
G blurred vision
G nausea
G dyspepsia and flatulence
G palpitation and arrhythmia
G dizziness
G insomnia
G skin reactions.

The NICE recommendation for an initial trial of conventional-release

oxybutynin is controversial; it is the least bladder-specific anticholinergic
and therefore the one most likely to cause intolerable anticholinergic
adverse effects. The authors’ own practice is to commence patients imme-
diately on one of the second-generation, more bladder-specific products
that is likely to be better tolerated, doesn’t require dose titration and will
have higher patient compliance.
Whichever drug is chosen, an early treatment review should be
undertaken. It is unlikely, if no clinical benefit has been noted within
1 month, that further therapy will benefit the patient. If ineffective, the
drug dosage needs to be increased, if tolerated, or the anticholinergic needs
to be changed for an alternative compound. If the treatment is effective,

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 duration of therapy is controversial. It is the authors’ practice to recom-
mend therapy for 6 months in the first instance; sometimes the bladder will
retrain itself and patients may be able to continue drug-free.
If one anticholinergic drug, taken in therapeutic doses, proves ineffect-
ive, further treatment options become controversial. It is the authors’
experience that response to further anticholinergics, once one has proven
ineffective, is usually disappointing. However, if a particular drug is poorly
tolerated, switching to another compound can be beneficial; adverse effects
seem to vary considerably among patients with individual products. It is the
authors’ customary practice to try at least two anticholinergics before trying
other treatment options such as cystoscopic botulinum toxin A injections.

CONTRAINDICATIONS TO ANTICHOLINERGICS
G Acute (narrow angle) glaucoma
G Myasthenia gravis
G Urinary retention or outflow obstruction
G Severe ulcerative colitis
G Gastrointestinal obstruction

The role of estrogens

Many women develop bladder-filling symptoms after the menopause.
Estrogen treatment in postmenopausal women improves symptoms of
vaginal atrophy, such as vaginal dryness and irritation. In a review of ten
randomised placebo-controlled trials, vaginal estrogen administration was
found to be superior to a placebo when considering symptoms of urgency,
urge incontinence, frequency and nocturia.14

Use of botulinum toxin A in the management of

overactive bladder
Botulinum toxin A is an extremely potent neurotoxin derived from the
anaerobic bacterium Clostridium botulinum. Intravesical injection of botulinum
toxin A is increasingly used as an intervention for refractory overactive
bladder, with a growing body of evidence suggesting its beneficial effects.15
The toxin is injected cystoscopically under local or general anaesthesia
into the detrusor muscle in 10–30 different locations, usually sparing the
trigone (Figure 6.1). The aim is to reduce bladder detrusor activity while
preserving some muscle activity and avoiding complete paralysis and
retention. This can be a difficult compromise as urinary retention rates
are dose dependent. Recent evidence suggests that low-dose therapy

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 (50–100 units of BOTOX® (Allergan Ltd, Buckinghamshire, UK)) reduces
retention rates to less than 5% while still conveying efficacy of up to
90%.16,17

(a) (b)

Figure 6.1 Cystoscopic botulinum toxin A injections: (a) cystoscopic 4 mm needle for
cystoscopic injections; (b) injection into the bladder wall using a flexible cystoscope

If incomplete voiding or urinary retention does occur, this is best

managed with intermittent clean self-catheterisation. Patients who are
unable to self-catheterise will require an indwelling catheter. Once the
effect of the treatment wears off (usually within 3–12 months), patients
should be able to void spontaneously again. The 2006 NICE guideline3
recommends the use of botulinum toxin A for the treatment of idiopathic
detrusor overactivity in women who have not responded to conservative
treatments and who are willing and able to self-catheterise.
Overall, intravesical botulinum toxin A treatment, which is well
received by most patients, has become a very important part of the
armamentarium for the treatment of overactive bladder symptoms and
idiopathic detrusor overactivity. It must be recognised that the therapeutic
use of intravesical botulinum toxin A is relatively recent and that the long-
term effects are unknown at this stage. Furthermore, the optimal dose of
botulinum toxin A for efficacy and safety has not yet been established. Use
of intravesical botulinum toxin A treatment should still be limited to a point
in the treatment pathway where otherwise only very major surgical
interventions (such as augmentation cystoplasty or urinary diversion) with
high morbidity are available. There is a need for further data on this
treatment modality.

Neuromodulation
Control of urine storage and bladder emptying is achieved by a complex
interaction between the cerebral cortex, spinal cord and peripheral nerves.

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 Neurogenic disruption can result from proven neurological disease (such
as multiple sclerosis) or trauma (such as spinal cord injury). Detrusor
overactivity and voiding dysfunction also commonly occurs without any
overt neurological problem. Electrical nerve stimulation (neuromodulation)
has been used in both these scenarios.

PERCUTANEOUS POSTERIOR TIBIAL NERVE

STIMULATION
Percutaneous posterior tibial nerve stimulation (PTNS) is the least invasive
surgical procedure used in management of refractory symptoms of urgency
and urge incontinence. The exact mechanism of action of PTNS on the
bladder is unclear but it is thought to be mediated by retrograde stimulation
of the sacral nerve plexus. The posterior tibial nerve contains mixed sensory
motor nerve fibres that originate from the same spinal segments as the
nerves to the bladder and pelvic floor.
Current evidence on PTNS for OAB shows that it is efficacious in
reducing symptoms in the short and medium term. There are no major
safety concerns. Therefore, the procedure may be used provided that normal
arrangements are in place for clinical governance, consent and audit.3,18,19

SACRAL NERVE STIMULATION

Sacral nerve stimulation (SNS) is proven to be effective in management of
refractory symptoms of urinary incontinence and voiding dysfunction.
Electrical stimulation of the sacral reflex pathway inhibits the reflex
behaviour of the bladder. Nerve stimulation can be achieved using surface
(transcutaneous needles) or implanted electrodes.
Sacral nerve stimulation provides continuous stimulation of the S3
nerve root via an implanted electrical pulse generator and is thought to
improve the ability to suppress detrusor contractions (Figure 6.2). Overall,
neuromodulation has a 30–50% clinical success rate.20,21
Sacral nerve stimulation is recommended by NICE for the treatment of
urge incontinence due to detrusor overactivity in women who have not
responded to conservative treatments.3 Women should be offered SNS on
the basis of their response to preliminary percutaneous nerve evaluation
(PNE). It is, however, a very expensive treatment; the sacral nerve stimu-
lator alone costs approximately £10,000. Furthermore, insertion of the
implant is an invasive procedure and lifelong follow-up is required. For
these reasons, most clinicians would try botulinum toxin A therapy
initially.

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 Figure 6.2 Diagram of sacral nerve stimulation

Surgical management
Surgery is reserved for those women with debilitating symptoms who have
failed to derive benefit from medical and behavioural therapy. Procedures
such as bladder distention, detrusor myectomy and augmentation cysto-
plasty have limited efficacy and high rates of complications. Permanent
urinary diversion is occasionally indicated in women with intractable
incontinence.
Detrusor overactivity that is unresponsive to medical therapy used to
be considered for surgery. This was more commonly required in women
with neuropathic conditions, although occasionally women with severe
idiopathic detrusor overactivity would require surgical treatment. The
mainstay of surgical management is augmentation cystoplasty, although
cystodistension and bladder denervation have also been used. However,
neuromodulation and botulinum toxin A injection have transformed
practice. The Oxford Region Neuropathic Urology team used to perform six
to ten clam cystoplasties per year but, since introducing botulinum toxin A
therapy in 2003, have performed fewer than one operation per year for
neuropathic detrusor overactivity.

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 AUGMENTATION CYSTOPLASTY
Augmentation cystoplasty involves transecting the bladder and augmenting
with a compliant segment of tissue. Autologous tissue is normally used –
commonly a loop of ileum on a vascular pedicle – although other tissues
include caecum and ureter (if there is already a terminally damaged
kidney). Such surgery physically increases bladder capacity and, more
importantly, the elastic properties of the autologous segment prevent high
intravesical pressure rises when an unstable detrusor contraction occurs.
This protects the upper renal tract from reflux and cures urge incontinence.
Because bladder contractility is compromised, patients are at high risk of
subsequent retention: they should be taught preoperatively to self-cathet-
erise. When bowel has been used to augment the bladder (Figure 6.3), the
mucosa continues to secrete mucus: there is a risk of mucus retention, stone
formation and malignant change in the autologous tissue. Regular check
cystoscopies are indicated.
Figure 6.3 A bladder 10 years after
augmentation cystoplasty

DETRUSOR MYECTOMY
The complications of cystoplasty with autologous tissue are described above.
Detrosor myectomy entails removing detrusor muscle from the dome of
the bladder, leaving mucosa intact (Figure 6.4). The surgery is intuitively
attractive: the urine remains in contact with normal bladder mucosa, a
compliant ‘pouch’ is formed that theoretically confers the advantages of
the cystoplasty, while potential complications such as mucus secretion and
malignant change are circumvented. Patients are still likely to require self-
catheterisation and, as the technique is relatively new, the long-term
benefits are currently unknown.

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 Figure 6.4 Detrusor myectomy

Catheterisation and incontinence pads

Catheterisation may be required on a long-term basis in women with
intractable incontinence, usually in those who are frail and elderly with
multiple concomitant pathologies that preclude alternative management.
Many such women and their carers find permanent catheterisation a better
option than continuous severe incontinence. Catheters may be urethral or
suprapubic. Urethral catheters should be selected with the narrowest
appropriate lumen. In the long term, this may need to be slightly larger (up
to 16G) as there is a risk of encrustation of the catheter. Silicone catheters
and plastic or latex catheters coated with silicone reduce encrustation.
Female catheters are 20–25 cm long and can be used with discreet leg bags
worn under clothing. If a permanent indwelling catheter is required,
suprapubic drainage is often preferable, as this does not irritate the urethra
or trigone, and the urethra cannot be traumatised by the woman pulling on
her catheter.
Complications of catheterisation include urinary tract infection. Coloni-
sation of the foreign body may make eradication difficult and antibiotics
are only indicated if the urinary infection is symptomatic. Bypassing of
urine around the catheter is a common problem. Changing the catheter
will be helpful if there is lumen obstruction from mucus or encrustation. If,

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 however, bypassing continues then it may be due to detrusor overactivity
and can be treated with anticholinergics.
Incontinence pads may be a temporary or a permanent aid for those
with urinary or faecal incontinence. Women who use them vary from those
with extremely mild symptoms who wear a small pad for reassurance to
those with intractable severe leakage who would otherwise require a
catheter. The type of pad required thus varies enormously. Superabsorbent
hydrogels are covered by material that allows penetration of urine but
prevents backflow to the surface of the pad.

OVERACTIVE BLADDER SYNDROME: KEY POINTS

G OAB is a common condition affecting around one in six women.
Quality of life is often severely affected by OAB symptoms.
G The incidence of OAB increases with age.
G OAB is the second most common cause of urinary incontinence.
G OAB is the most common cause of incontinence in elderly women.
G Urodynamic assessment is required to make a diagnosis of detrusor
overactivity, but not of OAB.
G Conservative treatment should be tried first before urodynamic
assessment.
G Treatment with intravesical botulinum toxin A is well received by most
patients and has become a very important part of the armamentarium
for the treatment of overactive bladder symptoms.
G Surgery is reserved for those with debilitating symptoms and who have
failed to derive benefit from medical and behavioural therapy.

References
1. Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, et al. The standardisation
of terminology of lower urinary tract function: report from the Standardisation Sub-
committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.
2. Nabi G, Cody JD, Ellis G, Herbison P, Hay-Smith J. Anticholinergic drugs versus
placebo for overactive bladder syndrome in adults. Cochrane Database Syst Rev
2006;(4):CD003781.
3 National Institute for Health and Clinical Excellence. Urinary incontinence: The manage-
ment of urinary incontinence in women. NICE clinical guideline 40. London: NICE; 2006.
4. Dmochowski RR, Rosenberg MT, Zinner NR, Staskin DR, Sand PK. Extended-release
trospium chloride improves quality of life in overactive bladder. Value Health
2010;13:251–7.
5. Burgio KL, Goode PS, Richter HE, Markland AD, Johnson TM 2nd, Redden DT.
Combined behavioral and individualized drug therapy versus individualized drug
therapy alone for urge urinary incontinence in women. J Urol 2010;184:598–603.
6. Mattiasson A, Masala A, Morton R, Bolodeoku J; SOLAR Study Group. Efficacy of
simplified bladder training in patients with overactive bladder receiving a solifenacin
flexible-dose regimen: results from a randomized study. BJU Int 2010;105:1126–35.

MANAGEMENT OF OVERACTIVE BLADDER SYNDROME 57

Downloaded from https://www.cambridge.org/core. University of Warwick, on 03 Aug 2017 at 09:45:58, subject to the
Cambridge Core terms of use, available at https://www.cambridge.org/core/terms.
https://doi.org/10.1017/CBO9781139696982.007
 7. Cardozo L, Khullar V, Wang JT, Guan Z, Sand PK. Fesoterodine in patients with
overactive bladder syndrome: can the severity of baseline urgency urinary
incontinence predict dosing requirement? BJU Int 2010;106:816–21.
8. Cardozo L, Khullar V, El-Tahtawy A, Guan Z, Malhotra B, Staskin D. Modeling dose–
response relationships of the effects of fesoterodine in patients with overactive
bladder. BMC Urol 2010;10:14.
9. Dmochowski RR, Peters KM, Morrow JD, Guan Z, Gong J, Sun F, et al. Randomized,
double-blind, placebo-controlled trial of flexible-dose fesoterodine in subjects with
overactive bladder. Urology 2010;75:62–8. Errata in: Urology 2010;75:1519 and
Urology 2011;77:1513.
10. Van Kerrebroeck PE, Heesakkers J, Berriman S, Padmanabhan Aiyer L, Carlsson M,
Guan Z. Long-term safety, tolerability and efficacy of fesoterodine treatment in
subjects with overactive bladder symptoms. Int J Clin Pract 2010;64:584–93.
11. Sacco E, Pinto F, Bassi P. Emerging pharmacological targets in overactive bladder
therapy: experimental and clinical evidences. Int Urogynecol J Pelvic Floor Dysfunct
2008;19:583–98.
12. Bolduc S, Moore K, Lebel S, Lamontagne P, Hamel M. Double anticholinergic therapy
for refractory overactive bladder. J Urol 2009;182(4 Suppl):2033–8.
13. Brostrøm S, Hallas J. Persistence of antimuscarinic drug use. Eur J Clin Pharmacol
2009;65:309–14.
14. Cody JD, Richardson K, Moehrer B, Hextall A, Glazener CM. Oestrogen therapy for
urinary incontinence in post-menopausal women. Cochrane Database Syst Rev
2009;(4):CD001405.
15. Kalsi V, Apostolidis A, Gonzales G, Elneil S, Dasgupta P, Fowler CJ. Early effect on
the overactive bladder symptoms following botulinum neurotoxin type A injections
for detrusor overactivity. Eur Urol 2008;54:181–7.
16. Rovner E, Kennelly M, Schulte-Baukloh H, Zhou J, Haag-Molkenteller C, Dasgupta
P. Urodynamic results and clinical outcomes with intradetrusor injections of onabot-
ulinumtoxinA in a randomized, placebo-controlled dose-finding study in idiopathic
overactive bladder. Neurourol Urodyn 2011;30:556–62.
17. Sahai A, Dowson C, Khan MS, Dasgupta P. Improvement in quality of life after
botulinum toxin-A injections for idiopathic detrusor overactivity: results from a
randomized double-blind placebo-controlled trial. BJU Int 2009;103):1509–15.
18. National Institute for Health and Clinical Excellence. Percutaneous posterior tibial nerve
stimulation for overactive bladder syndrome. Interventional procedure guidance 362.
London: NICE; 2010.
19. MacDiarmid SA, Peters KM, Shobeiri SA, Wooldridge LS, Rovner ES, Leong FC, et al.
Long-term durability of percutaneous tibial nerve stimulation for the treatment of
overactive bladder. J Urol 2010;183:234–40.
20. Groenendijk PM, Lycklama à Nyeholt AA, Heesakkers JP, van Kerrebroeck PE,
Hassouna MM, Gajewski JB, et al.; Sacral Nerve Stimulation Study Group.
Urodynamic evaluation of sacral neuromodulation for urge urinary incontinence.
BJU Int 2008;101:325–9.
21. Kavia R, Dasgupta R, Critchley H, Fowler C, Griffiths D. A functional magnetic
resonance imaging study of the effect of sacral neuromodulation on brain responses
in women with Fowler’s syndrome. BJU Int 2010;105:366–72.

58 UROGYNAECOLOGY FOR THE MRCOG AND BEYOND

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