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Chapter 12 Pharmacological Treatment of Urinary Incontinence
atrophy at the site of injection. Because of reversibility of the effect, there is an interval
of 3–6 months with improvement of OAB symptoms. Several recent studies show a
good benefit in treatment, for example in spinal cord-injured patients with detrusor
external sphincter dyssynergia or detrusor hyperreflexia. It is also an alternative in patients with anticholinergic drug-refractory symptoms.
12.9 Drugs Used for Treatment of Stress Incontinence
Goals of treatment in stress urinary incontinence (SUI) are increasing intraurethral
pressure by influencing the intrinsic or extrinsic factors. Different types of medications can increase the intraurethral tonus, but only α-AR agonists and estrogens have
been used in the past for off-label indications (Table 12.2).
12.9.1 α-Adrenoceptor Antagonists
Stimulation of the α1-adrenergic receptors,located on the bladder neck and proximal
urethra, results in contraction of the smooth muscle and an increase in outlet resistance. Pseudoephedrine, midodrine hydrochloride and phenylpropanolamine could
improve symptoms of mild stress urinary incontinence in off-label usage.
In 2000, phenylpropanolamine was found to have a 16-fold increase in hemorrhag-
ic stroke in women under 50 years of age. Therefore the US FDA recommended no future using of phenylpropanolamine and other α-agonists in this group.
177
12.9.2 β-Adrenoceptor Antagonists
β-Adrenergic blocking agents potentiate an α-adrenergic effect with an increase in
urethral resistance.There are no randomized controlled trials in the literature,only a
bit of information on using propanolol for treatment of SUI. The efficacy is not clearly described.
Table 12.2. Drugs used in the treatment of stress incontinence.Assessment according to the Oxford system (Andersson et al. 2002)
Drug Level Grade
Alpha-adrenoceptor agonists
Ephedrine 3 C
Norephedrine (phenylpropanolamine) 2 Not recommended
Other drugs
Imipramine 4 C
Clenbuterol 4 C
(Duloxetine) Under investigation
Hormones
Estrogens 2 D
of evidence of recommendation
178
Gert Naumann, Heinz Koelbl
12.9.3 Imipramine
Tricyclic antidepressants such as imipramine show effects on bladder contractility and
urethral resistance.Decreasing the contractility of the detrusor muscle and increasing
the outlet resistance,symptoms of stress urinary incontinence can be treated. Because
of various side effects, this type of drugs is not primary used.
12.9.4 Duloxetine
Duloxetine, a selective noradrenaline and 5-HT re-uptake inhibitor, increases rhabdosphincter contractility via stimulation of pudendal motor neuron a-1 adrenergic
and 5-HT-2 serotonergic receptors.It should be the first effective and practicable drug
in treatment of stress urinary incontinence, since September 2004 available in Germany as Yentreve. In one of four double-blind, placebo-controlled studies (Dmochowski
et al. 2003) with the same results in women with stress incontinence (n=2,188), dulox-
etine (40 mg twice daily) was shown to cause significant improvements in several efficacy measures (ICS 1-h stress pad test, 24-h pad weight, number of incontinence episodes, quality of life assessment). The drug was well tolerated and there were only a
few discontinuations due to side effects (24% for duloxetine, 4% for placebo).Duloxetine is a drug with demonstrated efficacy and safety. The metaanalysis showed only
mild side effects, the most common being nausea in up to 23% of patients.The drug is
still undergoing clinical trials.
11
12.10 Hormonal Treatment of Urinary Incontinence
Estrogens have no direct effect on the urethral continence mechanism,but the positive
trophic effect on the connective tissue,muscle and vessels are responsible for the improvement of urinary leakage.
Estrogen stimulates connective metabolism and collagen production; in the meno-
pause hormone levels are low, leading to atrophy of the supportive tissues of the bladder and urethra, which unmasks or eventually leads to stress incontinence.
The estrogen-sensitive tissues of the bladder, urethra and pelvic floor all play an
important role in the continence mechanism. For a woman to remain continent, the
urethral pressure must exceed the intravesical pressure at all times except during micturition. The functional layers of the urethra,which all play a part in the maintenance
of a positive urethral pressure, are the epithelium, vasculature, connective tissue and
muscle.
While menopause has been recognized by many as a risk factor for incontinence,
the precise mechanism is unknown.
Estrogens increase urethral closure pressure and improve abdominal pressure
transmission to the proximal urethra.
12.10.1 Estrogens for Stress Incontinence
Several subtypes of estrogens are used in treatment of urogenital atrophy and urinary
incontinence in different doses and application forms. This acts on the controversial
discussion about the role of estrogen in the treatment of stress incontinence.
Chapter 12 Pharmacological Treatment of Urinary Incontinence
With a lack of randomized studies,only two meta-analyses can clarify the situation
further.Fantl et al. (1994) reviewed all available literature for estrogen treatment of all
causes of incontinence in postmenopausal women between 1969 and 1992.There were
only six controlled trials and 17 uncontrolled series in 166 articles published in English. The investigators found a significant subjective improvement for all patients but
no significant differences for objective parameters. Loss of urine was not changed and
also maximum urethral closure pressure did not increase significantly.
In 1990 Sultana and Walters reviewed eight controlled and 14 uncontrolled prospec-
tive trials in women in menopause with all types of estrogen treatment. The results
showed good effects on symptoms of urgency and frequency but no significant difference in stress incontinence.
12.10.2 Estrogens for Urge Incontinence
There is clinical evidence that estrogens have a positive influence on postmenopausal
urgency and urge incontinence, although this has not been studied in randomized
trials.
In a double-blind multicenter study of 64 postmenopausal women with the urge
syndrome, Cardozo et al. (1993) showed no differences between oral estriol 3 mg daily
and placebo in subjective and objective improvement on bladder disorders.
In the Heart and Estrogen/Progestin Replacement Study 2001, Grady et al. reported
a comparison of hormone replacement therapy with 0.625 mg of conjugated estrogens
plus 2.5 mg of medroxyprogesterone acetate in one tablet daily (n=768) or placebo
(n=757) with follow-up of 4.1 years. Incontinence improved in 26% of the women assigned to placebo compared with 21% assigned to hormones, while 27% of the placebo group worsened compared with 39% of the hormone group (p=0.001).
The results showed a worsening of urinary incontinence symptoms in case of in-
take of daily oral estrogen plus progestin.A discussion is currently taking place in the
literature on the influence of progestin on the negative results on incontinence and
cardiovascular events.
179
12.11 Conclusion
The recent innovative trends in pharmacological treatment of urinary incontinence
(Huggins et al. 2003) emphasize that medical therapy is a cornerstone for helping incontinent patients. A modern drug therapy should be effective, improving patient
compliance and cost-effective use of resources.
The development of new pharmacological drugs with selective efficacy and only
minimal side effects with improvement of quality of life will be the future in the treatment of bladder and urethral disorders.
References
Andersson KE, Appell R, Awad S, Chapple C, Drutz H, Finkbeiner A, Fourcroy J,Haab F, Wein A
(2002) Pharmacological treatment of urinary incontinence. In:Abrams P, Cardozo L,Khoury
S, Wein A (eds) Incontinence, 2nd International Consultation on Incontinence. Plymbridge
Distributors, Plymouth, UK, pp 481–511
11
180
Gert Naumann, Heinz Koelbl
Cardozo L,Rekers H,Tapp A et al (1993) Oestriol in the treatment of postmenopausal urgency: a
multicentre study. Maturitas 18: 47–53
Chancellor M, Freedman S, Mitcheson HD et al (2000) Tolterodine, an effective and well-tolerat-
ed treatment for urge incontinence and other overactive bladder symptoms.Drug Invest 19:
83–88
Chapple CR, Rechberger T, Al-Shukri S, Meffan P, Everaert K, Huang M, Ridder A (2004) Ran-
domized, double-blind placebo and tolterodine-controlled trial of the once-daily antimuscarinic agent solifenacin in patients with symptomatic overactive bladder. BJU Int 93: 303–310
Dmochowski R, Miklos J,Norton PA,Zinner N, Yalcin I, Bump C (2003) Duloxetine vs placebo for
the treatment of north American women with stress urinary incontinence. J Urol 170:
1259–1263
Fantl JA,Cardozo LD, McClish DK et al (1994) Estrogen therapy in the management of urinary
incontinence in postmenopausal women: a meta-analysis. First report of the Hormones and
Urogenital Therapy Committee. Obstet Gynecol 83: 12–18
Grady D, Brown JS, Vittinghoff E et al (2001) Postmenopausal hormones and incontinence: the
Heart and Estrogen/Progestin Replacement Study.Obstet Gynecol 97: 116–120
Haab F, Stewart L, Dwyer P (2004) Darifenacin, an M3 selective receptor antagonist is an effective
and well-tolerated once-daily treatment for overactive bladder. Eur Urol 45: 420–429
Hofner K, Halaska M, Primus G et al (2000) Tolerability and efficacy of Trospium chloride in a
long-term treatment (52 weeks) in patients with urge-syndrome: a double-blind,controlled,
multicentre clinical trial. Neurourol Urodyn 19: 487–488
Huggins ME, Bathia N, Ostergard DR (2003) Urinary incontinence: newer pharmacotherapeutic
trends. Curr Opin Obstet Gynecol 15 :419–427
Madersbacher H, Halaska M,Voigt R et al (1999) A placebo-controlled, multicentre study com-
paring the tolerability and efficacy of propiverine and oxybutynin in patients with urgency
and urge incontinence.BJU Int 84: 646–651
Sultana CJ, Walters MD (1990) Estrogen and urinary incontinence in women. Maturitas 20 :
129–138
Thuroff JW, Bunke B, Ebner A et al (1991) Randomized, double-blind, multicenter trial on treat-
ment of frequency,urgency and incontinence related to detrusor hyperactivity: oxybutynin
versus propantheline versus placebo.J Urol 145: 813–816
Thuroff JW, Chartier-Kastler E, Corcus J et al (1998) Medical treatment and medical side effects
in urinary incontinence in the elderly.World J Urol 16 [Suppl 1] : S48–S61
Van Kerrebroeck P, Kreder K, Jonas U et al (2001) Tolterodine once-daily: superior efficacy and
tolerability in the treatment of the overactive bladder. Urology 57: 414–421
Versi E, Appell R, Mobley D et al (2000) Dry mouth with conventional and controlled-release
oxybutynin in urinary incontinence. The Ditropan XL Study Group. Obstet Gynecol 95 :
718–721
Chapter 13
Chapter 13 Medical, Behavioural and Minimally Invasive
Medical, Behavioural and Minimally
Invasive Therapy – A Urologist’s View
Christopher R. Chapple, Sawrabh Bhargava, Karl-Erik Andersson
181
13
Contents
13.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 182
13.2 Nervous Control of Micturition . . . . . . . . . . . . . . 182
13.3 Treatment of Incontinence . . . . . . . . . . . . . . . . . 183
13.3.1 Life Style Changes . . . . . . . . . . . . . . . . . . . . . . 183
13.3.1.1 Body Weight . . . . . . . . . . . . . . . . . . . . . . . . . 183
13.3.1.2 Caffeine . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
13.3.1.3 Fluid Intake . . . . . . . . . . . . . . . . . . . . . . . . . 184
13.3.1.4 Constipation . . . . . . . . . . . . . . . . . . . . . . . . 184
13.3.2 Behavioural Therapy . . . . . . . . . . . . . . . . . . . . 184
13.3.2.1 Pelvic Floor Muscle Training . . . . . . . . . . . . . . . . 184
13.3.2.2 Bladder Retraining . . . . . . . . . . . . . . . . . . . . . 186
13.3.2.2 Timed Voiding . . . . . . . . . . . . . . . . . . . . . . . 187
13.3.2.4 Prompted Voiding . . . . . . . . . . . . . . . . . . . . . . 188
13.3.3 Medical Treatment . . . . . . . . . . . . . . . . . . . . . 188
13.3.3.1 Drugs used for Treatment of Bladder Overactivity . . . 188
13.3.4 Minimally Invasive Therapy in Urinary Incontinence . . 194
13.4 Economics of Conservative Therapy . . . . . . . . . . . 194
References . . . . . . . . . . . . . . . . . . . . . . . . . . 196
182
Christopher R. Chapple, Sawrabh Bhargava, Karl-Erik Andersson
13.1 Introduction
It is estimated that whilst more than 200 million people worldwide are affected by incontinence, only a small proportion of these people have received appropriate advice
and therapy for their condition. It is equally clearly established that urinary incontinence has a significant impact on the physical, social and mental well-being of individuals, and escalates in prevalence with advancing age.With this in mind a number of
initiatives have been instituted by various continence organisations to promote continence awareness and develop appropriate care pathways.A combination of an increasingly elderly population in the Western world and greater health awareness in the
community, combined with the development of new pharmacotherapeutic agents,has
focused attention in recent years on this disease area. The likely economic consequences of these developments have emphasised the importance of critically evaluating the robustness, cost-effectiveness and cost-benefit of available treatment options
for urinary incontinence in both male and female patients.
A major recent development has been the initiation of a worldwide consensus
group under the auspices of the WHO and major scientific associations to critically
evaluate and develop standardized methodology for research into lower urinary tract
function and dysfunction, with particular reference to the classification of incontinence, the standardisation of techniques and the documentation of urodynamic procedures.This has provided a sound platform for the future assessment of the outcomes
of both surgical and pharmacological treatment options, which will hopefully facilitate the development of newer and more effective forms of treatment.Certainly review
of the existing literature base clearly underlines the limitations of existing knowledge
and in particular the paucity of adequately powered studies comprising adequate follow-up data and with sufficiently robust methodology.With these limitations in mind,
it is the purpose of this chapter is to discuss the role of medical, behavioural and minimally invasive therapy in the treatment of urinary incontinence in both male and female patients.
13
13.2 Nervous Control of Micturition
The bladder and urethra comprise a functional unit that is controlled by a complex
interplay between the central and peripheral nervous systems and local regulatory factors. Malfunction at various levels may result in micturition disorders, which roughly
can be classified as disturbances of storage or of emptying. Failure to store urine may
lead to various forms of incontinence (mainly urge and stress incontinence), and failure to empty can lead to urinary retention,which may result in overflow incontinence.
The peripheral nervous mechanisms for urine storage and bladder emptying com-
prise a complex pattern of efferent and afferent signalling in parasympathetic,sympa-
thetic and somatic nerves (de Groat et al.1999). During storage (at low levels of vesical
afferent activity) spinal reflexes are active,mediating contraction of urethral sphincter
mechanisms through somatic (striated muscle) and sympathetic (smooth muscle)
nerves. Sympathetic nerves may also mediate detrusor and ganglionic inhibition. During storage, there is no activity in the sacral parasympathetic outflow. Micturition is
initiated by distension of the bladder, activating mechanoreceptors in the bladder wall.
This triggers a high level of activity in small myelinated afferent nerves (A), and this
activity reaches the lumbosacral spinal cord via the dorsal root ganglia. The A affer-
Chapter 13 Medical, Behavioural and Minimally Invasive Therapy
ents connect to a spinobulbospinal reflex consisting of an ascending limb from the
lumbosacral spinal cord,integration centres in the rostral brain stem, and a descending limb back to the parasympathetic nucleus in the lumbosacral spinal cord.Afferent
information may also be conveyed by small unmyelinated (C-fibre) vesical afferents,
which have a high mechanical threshold, but which may be activated by irritation of
the bladder mucosa. They may also be active in spinal cord injuries. Efferent micturition reflex pathways reach the bladder through the pelvic nerves.
Normal bladder contraction in humans is mediated mainly through stimulation of
muscarinic receptors in the detrusor muscle. Atropine resistance, i.e. contraction of
isolated bladder muscle in response to electrical nerve stimulation after pretreatment
with atropine, has been demonstrated in most animal species,but seems to be of little
importance in normal human bladder muscle.A significant degree of atropine resistance may exist in morphologically and/or functionally changed bladders, and has
been reported to occur in hypertrophic bladders, interstitial cystitis, neurogenic bladders, and in the ageing bladder.
Molecular cloning studies have revealed five distinct genes for muscarinic acetyl-
choline receptors in rats and humans, and it is now generally accepted that five receptor subtypes correspond to these gene products. Detrusor smooth muscle from various species contains muscarinic receptors of the M
There is general agreement that M
receptors are mainly responsible for the normal
3
micturition contraction, whereas the role of the M
(≈ 2/3) and M3(≈ 1/3) subtype.
2
receptors has not been clarified.
2
Muscarinic receptor function in the bladder may be altered in certain disease states,
such as outflow obstruction, neurogenic damage, and diabetes and in such circumstances, M2receptors may contribute to contraction of the bladder. It is also very clear
from the above discussion that higher centres have an important role in the control of
lower urinary tract function, and indeed this is the basis for the use of behavioural
therapy in the management disorders of bladder storage function.
183
13.3 Treatment of Incontinence
13.3.1 Life Style Changes
Most of the current literature suggests an association between life style factors and
urinary incontinence; however, the small numbers of randomised trials evaluating the
role of life style alterations are largely confined to the study of patients with female incontinence; information on male incontinence is mostly derived from generic epidemiological studies.
13.3.1.1 Body Weight
While in men there is no clear association between body weight and lower urinary
tract symptoms (LUTS); conversely weight loss is an acceptable form of treatment option for morbidly obese women.Brown et al. (1996) reported an increase in the prevalence of daily incontinence by an odds ratio of 1.6 per 5 body mass index (BMI) units.
This compares favourably with the results reported by Subak et al. (2002),where with
at least a 5% reduction in body weight they achieved a 50% reduction in the frequency of incontinence episodes in their group of patients.
184
Christopher R. Chapple, Sawrabh Bhargava, Karl-Erik Andersson
13.3.1.2 Caffeine
The clinical significance of caffeine intake in urinary incontinence has attracted differing opinions. In patients with detrusor overactivity, caffeine administration has
been shown to increase the detrusor pressure measured during bladder filling; whereas in patients with normal bladder function no such increase in detrusor pressure has
been observed. Evidence from small clinical trials does suggest that reducing caffeine
intake improves incontinence.
13.3.1.3 Fluid Intake
Despite the fact that urine production is significantly related to fluid intake, especially
in geriatric patients, there is little evidence to suggest that it influences the outcome of
treatment in patients with urinary incontinence, who have a normal fluid intake of
1.5–2 l a day. Thus it is recommended that reduction in fluid intake should be reserved
for patients with a particularly high intake of fluid.
13.3.1.4 Constipation
Chronic straining at stool may ultimately lead to a reduction in pelvic floor neural
function and this is considered to be a risk factor for both urinary incontinence and
pelvic organ prolapse. There are no studies that have longitudinally assessed the consequences of a programme of active management of constipation on the prevalence of
urinary incontinence.
13
13.3.2 Behavioural Therapy
Behavioural interventions include a spectrum of techniques that modify patients’
voiding patterns to achieve urinary continence and these include: bladder training/
drill, timed voiding,prompted voiding and pelvic floor muscle training (PFMT).Bladder drill was perhaps the earliest intervention used to treat the storage symptoms
associated with the symptomatic diagnosis of overactive bladder, namely frequency,
urgency with or without urge incontinence.
13.3.2.1 Pelvic Floor Muscle Training
It is believed that a strong contraction of the pelvic floor musculature works in a variety of potential ways: (a) it occludes the urethra, thereby increasing the intraurethral
pressure and helping preventing leakage,(b) it compresses the urethra against the pubic symphysis, (c) it acts to prevent urethral descent during any sudden rise in the
intra-abdominal pressure,and also (d) it may act via a neural reflex feedback loop (the
voluntary urinary inhibition reflex) to inhibit detrusor contraction, which may further
contribute to its potential role in treating urge incontinence. Consequently, PFMT has
been widely advocated for the treatment of both urge and stress-related incontinence.
Since its first description by Arnold Kegel in 1948,PFMT has entered routine clinical
Chapter 13 Medical, Behavioural and Minimally Invasive Therapy
practice and is now routinely used by health care professionals, in particular by physiotherapists, being taught either on an individual or group basis. Inevitably with any
such therapy that is intrinsically difficult to clearly define, there is a lack of consistency in the methodology used for PFMT programs, which has made comparison of the
results of different studies rather difficult. In this section we will discuss the role of
PFMT in treating male and female urinary incontinence.
Post-Prostatectomy Incontinence
Prostatectomy is an important cause of incontinence in men, and certainly incontinence is more common after radical prostatectomy (5%–15%) as compared to transurethral resection of prostate (1%). Non-surgical causes of male incontinence relate
principally to abnormalities of detrusor function and include detrusor overactivity,
bladder outlet obstruction leading to retention with overflow and poor bladder compliance. Despite conflicting reports in the literature; pelvic floor muscle training
(PFMT) is thought to beneficial in the treatment of post-prostatectomy incontinence
and it is believed that earlier return of continence may be achieved in patients who additionally receive electrical stimulation (ES),biofeedback or transcutaneous electrical
stimulation. In one of the largest randomized control trials conducted to date and including 120 men; van Kampen et al. (2000) studied the effect of PFMT on patients who
had undergone radical prostatectomy. They reported that continence was achieved in
88% of the treatment group and 56% of the control group by the end of 3 months and
this was sustained out to the end of 1 year in 95% of the treatment group and 81% of
the control group. Porru et al. (2001) suggested that patients receiving PFMT continence improved significantly up to 3 weeks after surgery as compared to the control
group,but beyond this period the continence rates were similar in both groups.Whilst
the initiation of PFMT after prostatectomy remains controversial, as the exercises are
easy and simple to perform and teach,it seems likely that initiating PFMT early in the
post-operative period is to be recommended.
185
PFMT in Female Incontinence
The role of PFMT in the management of stress incontinence has been studied in both
short- and medium-term studies and has been reported to produce a 65%–75% shortterm improvement, but as it is patient led, its long-term efficacy is poorly documented; on the other hand its role in treating urge incontinence remains unclear. Shafik and
Shafik (2003) in a recent study reported that PFM contractions may produce their effect by preventing the internal sphincter relaxation produced by the micturition reflex. Failure of the internal sphincter to relax produces a reflex detrusor relaxation, an
action possibly mediated through a voluntary urinary inhibition reflex.
It is clear that a therapist skilled in teaching and assessing the pelvic floor muscles
is likely to achieve the optimal benefits from PFMT in patients under their care.Whilst
it is difficult to define an ideal PFMT program; the two important components of
PFMT include effective strength training and effective load training.For effective
strength training it is recommended that co-contraction of other muscle groups
should be avoided in order to specifically target the PFM (Bo 1995). Effective load
training comprises methods aimed at recruiting the maximum number of motor units
to provide bulk to the PFM by hypertrophy. It has been recommended by the WHO
13
186
Christopher R. Chapple, Sawrabh Bhargava, Karl-Erik Andersson
consensus meeting that PFMT protocols should include three sets of 8–12 slow velocity
maximal contractions sustained for 6–8 s each,three or four per week for 15–20 weeks.
Both subjective (self-reported cure/improvement) and objective parameters (pad test)
improve after institution of PFMT irrespective of the type of incontinence (Hay-Smith
et al. 2001).Recent randomized control trials comparing PFMT to no treatment or placebo indicate PFMT provides higher cure/improvement rates as compared to no treatment or placebo. The meta-analysis by Hay-Smith showed women getting PFMT were
far more likely to show cure/improvement as compared to those receiving no treatment.
Comparisons between home-based self-administered programmes and intensive individualized PFMT programmes provide conflicting evidence.Whilst Bo (1995) favoured
an intensive approach, others (Wilson and Herbison 1998) reported no significant differences between the two training methods. Biofeedback (BF) techniques have been
employed in conjunction with PFMT to improve the outcome of treatment.BF relies on
the use of monitoring devices to monitor physiological changes induced by a certain
intervention in order to bring this to the patient’s consciousness and hence assist PFMT.
This is based on the postulate that presenting the physiological response of the treatment to the patient helps motivate them,thereby achieving improved cure rates.Berghmans et al. (1996) reported an advantage during the initial 6 weeks for those patients receiving BF, although in the longer term they did not observe any difference between
those receiving BF and those treated with PFMT alone.
Other adjuvant techniques utilized in conjunction with PFMT include electrical
stimulation (ES) and weighted vaginal cones.Weighted vaginal cones (VC) are thought
to prompt the patient to contract the PFM when there is a sensation of losing the cone,
whilst undoubtedly this is a useful adjunct to PFMT; there is at present little objective
evidence to support an increased benefit accruing from using a VC in conjunction
with PFMT.
The rationale behind using ES is both to improve the efficacy of PFM in preventing
stress incontinence and additionally to potentially contribute to inhibition of the detrusor in urge incontinence. It has been widely advocated for use in the treatment of
the overactive bladder and stress incontinence and potentially may act by kick starting the pelvic floor and educating the patient on the correct muscles to contract. ES
may also improve urinary incontinence by reflexly inhibiting parasympathetic excitatory neurones at the level of the pelvic nerve and by activating sympathetic inhibitory
neurones in the hypogastric nerve. There is, however, at present little supportive evidence to show any beneficial effects of combining PFMT with ES and indeed there is
insufficient evidence that ES is better than no treatment at all.
Certainly one of the problems are the highly variable treatment protocols which are
available. Brubaker (2000) has suggested that given at 10 Hz continually over 20 min
daily or twice daily for 20 weeks for overactive bladder,there is good evidence to indicate that it is effective,with an overall 50% improvement/cure rate. Currently there is
great interest in utilising patient-specified outcomes,which should make it possible to
gauge the level of treatment that may be required and if behavioural treatments fail,
involve patients in making the decision as to whether they wish to try medication, or
proceed on to surgery.
13.3.2.2 Bladder Retraining
The first report of disciplining the bladder was from Jeffcoate and Francis in 1966;
since then it has become a widely used treatment for urge, stress and mixed inconti-
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