Re: Bladder dysfunction in M.S. -- LONG!
- From: "kamel" <kamel@xxxxxxx>
- Date: Wed, 9 Nov 2005 15:48:16 -0600
Excellent article, Rose! I printed out all 14 pages of it, and will bring
it to my next neuro appt. I have persistent problems is this area that make
excursions difficult and underwear changes necessary. It gets worse when
there are big changes in temperature, like getting out of the car into 20
degrees F and a 20 MPH wind, and trying to unload groceries, etc. I'm
taking oxybutinin 2x/day, but if I increase the dose I have trouble
releasing at all. Plus, being 70 yo, I also have BPH as a complicating
factor.
My doctors, neuro and PCP,
"rose" <rosedawn_scott@xxxxxxxxx> wrote in message
news:1131549050.388803.28390@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
this is very long, but i found it very intereting as well!
lots of explanations for things i didn't understand as well previously
(why M.S. weirds out things this way or that way), also interesting and
new to me that cannabis -- THC and CBDs both -- seems to have a
beneficial effect on M.S.-related urinary troubles. almost makes me
think it's THE perfect herb for anyone with Multiple Sclerosis! they
also talk about Botox, catheterization, and drug treatments for various
types of bladder/urinary symptoms.
it really is LONG, but i thought it had enough good info to be worth a
post for those who are interested!
RD
-------------------
NOTE: To view the article with Web enhancements, go to:
http://www.medscape.com/viewarticle/515091
Therapy Insight: Bladder Dysfunction Associated With Multiple Sclerosis
Vinay Kalsi; Clare J Fowler
Nat Clin Pract Urol. 2005;2(10):492-501. ©2005 Nature Publishing
Group
Posted 11/03/2005
Summary and Introduction
Summary
Bladder dysfunction is a common problem for patients with multiple
sclerosis. The severity of symptoms often correlate with the degree of
spinal cord involvement and, hence, the patient's general level of
disability. The emphasis of management is now mainly medical and is
increasingly offered by nonurologists. Treatments can be highly
effective, relieving patients of what are otherwise very troublesome
symptoms that would compound their neurological disability. This
article gives an overview of the neural control of the bladder,
followed by an explanation of the pathophysiology of detrusor
overactivity secondary to neurological disease. A review of methods
available for treating bladder dysfunction in multiple sclerosis then
follows. The treatment options for this disorder are largely medical
and include established first-line measures such as anticholinergics,
clean intermittent self-catheterization and the use of desmopressin, as
well as potential second-line agents, such as cannabinoids,
intravesical vanilloids and intradetrusor botulinum neurotoxin type A.
The diminishing role of surgical intervention is also discussed.
Introduction
The estimated prevalence of urogenital symptoms in multiple sclerosis
(MS) has varied, depending on the populations studied. Estimates of
between 52% and 97% have been cited,[1] but, since these problems
result mainly from spinal cord involvement,[2,3] figures that show an
occurrence similar to that of lower limb dysfunction (75%)[4] or to the
MRI estimate of incidence of spinal cord lesions (74%)[5] seem more
realistic. There is a clear gender difference in the prevalence of MS,
with females being more commonly affected than males, on average by a
ratio of 2:1.[6] The nature of micturition complaints and lower urinary
tract symptoms also differ between sexes. Obstruction complaints, such
as hesitation, interrupted or weak urine flow and incomplete emptying,
are found more frequently in men, whereas incontinence complaints
(involuntary loss of urine) are more frequent in women. Irritative
complaints of urgency, frequency, nocturia and pain are found equally
between sexes.[7] Urogenital symptoms in patients with MS are therefore
common, and are clearly recognized to have significant adverse effects
on the quality of life of this group of patients.[8,9] Fortunately,
this is an area where therapeutic intervention can be highly effective,
as will be described in this review.
Neurological Control of the Bladder
Functional brain imaging studies are adding to our understanding of the
contribution of higher centers and signal processing involved in
bladder control, so that voiding can be achieved in a socially
appropriate time and place. Such studies have shown that a complex of
brain networks is involved in the two processes of bladder
storage[10,11] and voiding,[12,13] but that the final result of these
processes is either activation or inhibition of the pontine micturition
center (PMC). Direct pathways from the PMC project to the sacral
segments of the spinal cord (S2-S4) (Figure 1), and determine
parasympathetic outflow to the detrusor and reciprocal activity of the
motor neurons innervating the striated urethral sphincter.[14]
Whilst in the storage phase, detrusor pressure does not rise. This is
because the bladder fills as a result of inhibition of parasympathetic
innervation of the detrusor, and pressure within the urethra is
maintained at a higher level than within the bladder by tonic firing of
the motor units of the striated urethral sphincter and pelvic floor. At
the initiation of micturition there is relaxation of the striated
urethral sphincter and pelvic floor, followed by a coordinated
contraction of the detrusor muscle. This synergistic activity between
the sphincter and the detrusor is dependent on connections with the
pontine region. A condition known as 'detrusor sphincter dyssynergia'
(DSD) might arise if these connections are damaged or interrupted,
resulting in sphincter contraction as the detrusor contracts.[15]
The most marked abnormality occurs as a consequence of disconnection of
sacral segments from the PMC. This results in the emergence of a
segmental reflex that causes detrusor contractions in response to
bladder distension. Evidence from animal experiments and human studies
show that, following any form of spinal cord lesion, unmyelinated C
fibers that were formally quiescent (and therefore known as 'silent C
fibers') become mechanosensitive and respond to bladder stretch.[16]
Detrusor contractions are caused by this afferent activity, through
synaptic activity in the sacral segment of the cord.[17] It is this
process that is responsible for detrusor overactivity, the
pathophysiology underlying the common complaints of urinary frequency,
urgency and urgency incontinence, referred to collectively as
overactive bladder syndrome.[18,19]
Abnormal urodynamic findings in patients with dysfunctional voiding
symptoms and MS are common, as shown by a meta-analysis of 1,900
patients.[1] Table 1 summarizes the incidences of the major patterns of
urodynamic dysfunction reported in patients with MS. Detrusor
hyperreflexia, the most common urodynamic abnormality in MS, is now
referred to as 'neurogenic detrusor overactivity', following recent
changes in the nomenclature.[19] Since a relapsing and remitting, or
more commonly progressive, clinical course is a characteristic of MS,
the lower urinary tract symptoms might also worsen, and regular reviews
of bladder status have been recommended.[20,21]
The worsening of bladder dysfunction with increasing spinal cord
involvement in MS has been clinically demonstrated in a number of
studies.[2,7,22] Imaging studies using MRI have reported a correlation
between urologic complaints and spinal cord cross-sectional area, which
is used as a marker for spinal cord atrophy,[23] yet there is little
evidence for the association between urinary symptoms and brain MRI
parameters.[24,25]
As the neurological condition progresses, the bladder dysfunction can
become more difficult to treat. This can be attributed to worsening of
detrusor overactivity, inefficient emptying of the bladder in the
context of worsening paraparesis, recurrent urinary tract infections,
spasticity, reduction in general mobility, and sometimes cognitive
impairment. In contrast to urinary tract dysfunction following
traumatic spinal cord injury, progressive neurological diseases rarely
cause upper urinary tract involvement.[7,26] This is true even when
longstanding MS has resulted in severe disability and spasticity.
Although the reason behind this difference in action is unknown, the
evidence implies that the focus of management should be on symptomatic
relief. The pathophysiologic changes that occur in MS and their
symptomatic consequences lead to detrusor overactivity and detrusor
sphincter dyssynergia, resulting in incomplete bladder emptying.
Management of Lower Urinary Tract Symptoms in Multiple Sclerosis
First-line Treatments
Anticholinergic Medication. Anticholinergic agents are a logical first
treatment choice for patients with MS presenting with neurological
bladder dysfunction, as the most common symptoms are caused by detrusor
overactivity.[2] The majority of muscarinic receptors expressed in the
detrusor muscle are M2;[27,28] however, the functionally important
receptors in the detrusor muscle are the M3 receptors, as these
maintain normal bladder function.[27,29] The benefit of selective
blockade of M2 or M3 muscarinic receptors, including the possible
advantage of not affecting brain M1 receptors, has yet to be translated
into clinical effect.
A number of antimuscarinic agents, some of them only recently licensed
in the UK, are available to treat symptoms of detrusor overactivity (
Table 2 ). The long-acting (extended-life ['XL']) formulation of these
medications gives a significant advantage to patients, who need only
take the tablet once a day to provide 24-hour cover for symptoms. The
chemical structure of the antimuscarinic agents tolterodine and
trospium renders them less lipophilic and, therefore, theoretically
less likely to cross the blood-brain barrier than other antimuscarinic
agents, resulting in fewer central adverse effects.[30,31] These drugs
might therefore have particular benefit for patients with cognitive
impairment.
Prior to prescribing an anticholinergic for patients complaining
predominantly of symptoms of detrusor overactivity, it is important to
measure their postvoid residual (PVR) urine volume.[32,33] This is
particularly important if the patient's symptoms indicate that there is
a component of incomplete voiding. The PVR urine volume can now be
conveniently measured using a small hand-held ultrasound device (Figure
2), to which many specialist nurse continence advisors and MS clinic
nurses now have access, allowing them to conduct these examinations.
The importance of recognizing incomplete emptying is that any residual
volume in the bladder can trigger volume-determined reflex detrusor
contractions, exacerbating the clinical situation through worsening of
the symptoms of frequency, urgency and urgency incontinence.[34]
Often patients cannot gauge the extent to which they have incomplete
bladder emptying, but it has been shown that those who suspect that
they have this problem are often correct.[2] It is therefore important
to ask patients whether they have a sensation of incomplete bladder
emptying or if they are able to pass the same amount of urine at a
second void only minutes after the first, as these points are strong
indicators that a high PVR volume could be contributing to their
bladder problems.
Complex management and investigation protocols, such as the Clinical
Practice Guidelines for the Multiple Sclerosis Council,[35] have been
proposed for bladder dysfunction and MS. Figure 3 shows a simple
algorithm based on two main interventions (medication with
anticholinergics and intermittent catheterization) for the initial
management of the most common symptoms of bladder dysfunction in MS.
Although there has yet to be a controlled study into the efficacy of
this algorithm, it has provided a convenient, low-cost management
scheme, and has been used daily in the authors' department for 15
years. The role of cystometry and video cystometry in the investigation
of patients with MS has been promoted by some authors, because it is
only through these investigations that DSD can be diagnosed.[15,36,37]
Since there is no definitive treatment for DSD, however, other than
managing the resulting incomplete bladder emptying and raised detrusor
pressure, a pragmatic approach would recommend the use of cystometry
and video cystometry.
Desmopressin. The synthetic antidiuretic hormone desmopressin (DDAVP®,
Rhone-Poulenc Rorer Pharmaceuticals Inc., Collegeville, PA), was
originally licensed to treat the polyuria of diabetes insipidus. Having
become an established treatment for nocturnal enuresis,[44] its
efficacy for the treatment of women with MS experiencing night-time
frequency has been shown.[45] Its effectiveness, if taken during the
day, in providing patients with up to 6 hours during which they were
untroubled by urinary frequency, without any rebound night-time
frequency, has been demonstrated by a number of small studies.[46,47]
Desmopressin (10-20 µg) should only be taken once in every 24-hour
period, and should not be given to patients over 65 years of age, or
used in patients with dependant leg edema resulting from immobility who
have night-time frequency when recumbent. In spite of these
precautions, a number of patients find that this drug can provide
additional benefit to that conferred by the other first-line measures
if they are looking to be reliably free of symptoms for a long journey
or a particular social event.[47]
Indications for Additional Investigations
The first-line treatments for lower urinary tract symptoms consist of
oral anticholinergics with or without CISC, and many neurologists and
neurorehabilitation physicians, with the help of continence advisors,
can advise patients accordingly. Patients experiencing recurrent
urinary tract infections, hematuria, or pain that is thought to
originate from the upper or lower urinary tract, and those with
evidence of impaired renal function, should be referred to a urologist.
In aging men with MS, an element of lower urinary tract symptoms might
be attributable to benign prostatic hyperplasia (BPH).[48] The
challenge in these patients, therefore, is to establish to what extent
the symptoms are due to BPH, and how they much they bother the patient.
The degree to which the symptoms of BPH are bothersome will help to
determine further management, which could include watchful waiting,
medical, minimally invasive or surgical therapies. Initial evaluation
of these patients should include a detailed medical history to identify
the causes of voiding dysfunction, a physical examination, and both a
digital rectal examination and a focused neurological examination.
Following the evaluation, a urinary-flow-rate recording and measurement
of the PVR might be helpful. Surgery is only recommended in patients
who have renal insufficiency that is clearly due to BPH, and in those
patients with recurrent urinary tract infections, recurrent gross
hematuria, or bladder stones that are clearly due to BPH and refractory
to other therapies.[49] These patients should be referred to a
urologist.
Second-line Treatments for Overactive Bladder Syndrome
Undoubtedly there is a point in the progression of MS where first-line
treatment might be insufficient to control urinary symptoms, and yet
the patient does not want to have a long-term indwelling catheter
(Figure 4). This point is often reached as patients' neurological
disability, especially their mobility, is deteriorating such that they
are not in a sufficiently robust state to undergo major surgery (such
as an augmentation cystoplasty). Various new nonsurgical and, at the
time of writing, unlicensed treatment options are emerging for these
patients.
Cannabinoids. The illegal use of cannabis by patients with MS has
become common in the UK, to such an extent that a diagnosis of MS was
sometimes debated as an extenuating argument by people found growing
Cannabis sativa. In 1998, further exploration into the medicinal
properties of cannabis was proposed by a high-level UK government
report,[50] resulting in a number of small-scale, open-label studies
that examined the effect of medicinal cannabinoid extracts on patients
with chronic pain or MS. Included in these trials was a small
open-label study in patients with advanced MS, refractory to
conventional treatments, and in whom having a long-term indwelling
catheter was a looming prospect. The results of this pilot study
demonstrated a significant decrease in urinary urgency and a reduction
in the number and volume of incontinence episodes, as well as a
reduction in frequency and nocturia. Daily total voided and
catheterized volume, and urinary incontinence pad weights, were also
significantly decreased, whilst patients reported significant
improvements in spasticity, quality of sleep and level of pain
(measured by patient self-assessment).[51] Large, multicenter,
randomized placebo-controlled trials are underway, although no results
are available.
The Cannabis in Multiple Sclerosis (CAMS) study, a large, multicenter,
placebo-controlled trial funded by the UK Medical Research Council, was
established to look at the effect of oral nabilone and
tetrahydrocannabinol (THC) on patients with MS. Although the study is
ongoing, results so far have shown no change in the ashworth scale
scores ( Table 3 ); however, the patients did report subjective
improvements in spasticity.[52] A subsidiary study looked at the effect
of oral nabilone and THC on bladder symptoms and, although the data are
only reported in an abstract, the results suggest that there is a
lessening of urinary urgency and a reduced number of episodes of urge
incontinence on active treatment.[53] Whether or not this medication
becomes a licensed therapy in the UK, or other countries, for the
treatment of specific symptoms in MS such as spasticity and urinary
urgency and frequency, is yet to be decided.
Intravesical Vanilloids. The use of intravesical vanilloids to reduce
the number of afferent nerve endings of the bladder was rationalized by
the knowledge of the importance of the emergence of C-fiber reflex
causing detrusor overactivity following a spinal cord lesion.[16]
Intravesical capsaicin was the first vanilloid to be used in patients
with neurogenic detrusor overactivity.[54] Although there is good
evidence that intravesical capsaicin has a therapeutic effect,[55] its
use has been largely abandoned because it is not licensed and could
cause considerable discomfort to patients when instilled. The prospect,
therefore, of using intravesical resiniferatoxin (RTX®, Afferon
Corporation, Scottsdale, AZ), an ultra-potent capsaicinoid[56] that is
thought to have the same neurotoxic effect on bladder afferents[57] but
is less pungent,[58] was greeted with enthusiasm. Clinical trials have
been hampered by the compound's tendency to adhere to plastic, however.
In the studies published, the number of patients in whom this treatment
was effective was small.[59] It now seems unlikely that a
pharmaceutical company will market this medication in the future.
Further work with capsaicin has shown that its irritant effects can be
reduced if glucidic acid, rather than 30% alcohol, is used as the
diluting solution. A randomized controlled trial compared the efficacy
and tolerability of capsaicin in glucidic acid and resiniferatoxin in
10% alcohol in patients with neurogenic bladder overactivity. The
results revealed that the formulations were highly comparable in
relieving symptoms of detrusor overactivity.[60] Intravesical capsaicin
is still offered as a treatment option in a neurorehabilitation and
research center in Bordeaux, France.
Detrusor Injections of Botulinum Neurotoxin Type A. First described by
Schürch et al. in 2000 for patients with spinal cord injuries,
botulinum neurotoxin type A (BoNT/A) injected directly into the smooth
muscle of the detrusor is having a major impact on the treatment of
neurogenic detrusor overactivity.[61,62] Originally proposed on the
basis that BoNT/A would merely paralyze the detrusor by blocking the
presynaptic release of parasympathetic acetylcholine-mediating detrusor
contraction, the benefits of this treatment appear to exceed those
expected. It seems likely that BoNT/A also affects the vesicular
release of neurotransmitters involved in the afferent arm of reflex
bladder contractions; work on this is ongoing.[63]
In our own studies, a series of 31 patients with MS have received
injections of 300 units of BoNT/A (Botox®, Allergan, Irvine, CA)[64]
using a minimally invasive local anesthetic outpatient technique,
pioneered in our department.[65] Sparing the trigone, for reasons of
tolerability and potential ureteric reflux, this technique involves
injecting 30 equally spaced points in the bladder, using a flexible
cystoscope and a superfine 27-gauge disposable needle that locks into a
reusable sheath (Figure 5). Each injection is comprised of 10 units of
Botox® (1 ml).
Voiding-diary data are showing exceptional clinical efficacy for
BoNT/A, with significant improvements compared to baseline of urinary
urgency, frequency and incontinence episodes at 4 and 16 weeks
postinjection. Urodynamic parameters, namely maximum cystometric
capacity and detrusor pressures during filling, have also shown
significant and sustained improvement.[64] Because there is an
increased incidence in incomplete bladder emptying following treatment
in patients with neurogenic bladder dysfunction, patients must be
willing and able to perform CISC, if they are not already doing so.
Initial results of trials investigating repeated injections show
similar beneficial effects and duration of treatment action for these
and primary injections. Projected cost consequences are modest (UK£780
per annum per patient) compared with surgery or long-term
anticholiergics or neuromodulation, with a median time of 13 months
between injections.[66] Cost-effectiveness studies comparing
intradetrusor BoNT/A with anticholinergics, neuromodulation and
surgery, are currently being set up. Although not yet licensed for this
use, BoNT/A is emerging as an effective and popular second-line
treatment for symptoms of neurogenic detrusor overactivity, which is
increasingly being adopted by many urology, neurology and
rehabilitation centers worldwide.
Surgical Management. The advent of effective noninvasive treatments for
patients with bladder dysfunction secondary to MS has caused surgical
management techniques to take a lesser role. Denervation procedures,
including selective posterior rhizotomy, subtrigonal injection of
phenol or alcohol, bladder myotomy and transection, might have shown
good short-term results, but long-term results have been much less
satisfactory.[67] Augmentation procedures of the bladder, such as
augmentation cystoplasty (with or without a catheterizable limb), might
allow large volumes of urine to be contained within the bladder at low
pressures, but most patients need to perform CISC.[68,69] The ability
to do so is often lost as the neurological condition of the patient
deteriorates.
Sacral-nerve neuromodulation is being investigated in patients with MS,
and a small study of nine patients with neurogenic detrusor
overactivity, five of whom had MS, reported clinical and urodynamic
improvement at 46 months follow-up.[70] Longer follow-up and larger
cohorts of patients with MS are needed to assess carefully the
cost-effectiveness of this intervention.
Long-term Indwelling Catheter. There is a stage in the patient's
progression at which a long-term indwelling catheter becomes necessary.
This is usually when the patient has become severely disabled, being
unable to stand, or being chair-bound or even bed-bound. Cognitive
impairment, lower-limb spasticity, and loss of manual dexterity,
together with increasing detrusor overactivity, mean that CISC, even
with the aid of a caregiver, is no longer feasible. In these cases an
indwelling catheter is appropriate, and initially a urethral catheter
connected to a leg bag will familiarize the patient and their carer
with what is involved in indwelling catheterization. The urethral
catheter should then ideally be promptly replaced by a suprapubic
catheter.[71] Long-term urethral catheters are not advisable because of
the urethral trauma they commonly inflict.
Suprapubic catheters should ideally be sited by a urological surgeon,
who might want to give the patient a general anesthetic so that the
bladder can be distended to facilitate the suprapubic puncture into the
otherwise shrunken bladder. Once the suprapubic tract has been
epithelialized, usually 6-8 weeks post-puncture, the catheter can be
changed for the first time. The first catheter change should ideally be
performed under the care of a urology team; subsequent changes at
intervals of 3 months can be carried out by district or practice
nurses.
Conclusion
MS and its associated bladder symptoms have a considerable negative
impact on patients' quality of life and, although progression of the
neurological disease is proving difficult to halt, much can now be done
to improve bladder control. Intermittent self-catheterization can make
a crucial difference to management of patients in whom incomplete
voiding is contributing to bladder dysfunction. The development of more
selective oral agents is to be welcomed, as is the exciting discovery
of intradetrusor botulinum neurotoxin injections to treat severely
affected patients. Surgery has comparatively less to offer, and
effective management is becoming possible largely as an outpatient
procedure. Many patients' bladder problems are now being managed in the
same clinic as cares for their underlying neurological disease,
although urologic invention might still be necessary to deal with stone
formation, recurrent infections and placement of a suprapubic catheter.
Overall, the options for bladder management in MS have improved
greatly, and more patients are able to receive effective treatment for
very distressing symptoms that would otherwise compound their
neurological disability.
Review Criteria
PubMed was searched for articles published from January 1965 to March
2005 using the terms "multiple sclerosis", "bladder", and
"incontinence". Additional papers were also obtained from the
bibliographies of selected articles. The selection of papers was based
on relevance on subject matter, clinical importance and scientific
value.
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Sidebar: Glossary
Central adverse effects: Adverse events that are caused by central
nervous system stimulation
Reflex detrusor overactivity: Involuntary afferentmediated detrusor
contraction
Diabetes insipidus: Rare form of diabetes in which the kidney tubules
do not reabsorb sufficient water, possibly because there is inadequate
antidiuretic hormone production by the pituitary gland, leading to
excessive production of dilute urine
Ashworth scale scores:A five-point scale used as a primary clinical
measure of spasticity; It is an assessment of biological impairment,
rather than disability or handicap, and is dependent on the estimation
of the doctor or physiotherapist
Reprint Address
Correspondence: Clare J Fowler, Department of Uro-Neurology, Internal
mailbox 71, National Hospital for Neurology and Neurosurgery, Queen
Square, London WC1N 3BG, UK. Email: c.fowler@xxxxxxxxxxxxx
V Kalsi is a Registrar in Uro-Neurology and CJ Fowler is a Consultant
at the National Hospital for Neurology and Neurosurgery, Queen Square,
London, UK. CJ Fowler is also a Professor of Uro-Neurology at the
Institute of Neurology, London, UK.
Competing interests: The authors declared no competing interests.
-------------------
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