not permitted.

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© 2017 EDIZIONI MINERVA MEDICA European Journal of Physical and Rehabilitation Medicine 2017 December;53(6):975-80
Online version at http://www.minervamedica.it DOI: 10.23736/S1973-9087.17.04992-9

SPECIAL ARTICLE
MANAGEMENT OF NEUROGENIC LOWER URINARY TRACT DYSFUNCTION

Diagnosis and clinical evaluation of neurogenic bladder

Gerard AMARENCO *, Samer SHEIKH ISMAËL, Camille CHESNEL,
Audrey CHARLANES, Frederique LE BRETON

Sorbonne Universities,
UTenon Hospital, Paris, France
*Corresponding author: Gerard Amarenco, Department of Neurourology, Tenon Hospital, Paris, France. E-mail: gerard.amarenco@aphp.fr

ABSTRACT
Neurologic diseases lead to urinary dysfunctions. The aim of this article was to present an overview of diagnosis and evaluation of neurogenic
bladder with a special focus on urodynamic tests. Overactive bladder, with high detrusor pressure associated with detrusor sphincter dyssynergia,
can lead to severe complications with renal failure, upper urinary tract dilatation and infectious complications. Underactive bladder with voiding
dysfunction and urinary retention, is also a risk factor of urological alterations. Full clinical examinations, including urodynamics and selective
radiographic imaging studies, are essential to best manage these patients.
(Cite this article as: Amarenco G, Sheikh Ismaël S, Chesnel C, Charlanes A, Le Breton F. Diagnosis and clinical evaluation of neurogenic bladder.
Eur J Phys Rehabil Med 2017;53:975-80. DOI: 10.23736/S1973-9087.17.04992-9)
Key words: Urinary bladder, neurogenic - Urinary bladder, overactive - Urodynamics.

M ost of neurologic diseases can be revealed or ac-

companied by urinary symptoms.
Indeed, bladder coordination centers and conduction
pathways are widely scattered in the whole central and
peripheral somatic nervous system.1-5 Autonomic ner-
vous systems is also involved in the bladder control.
Thus, a lesion of those systems can lead to bladder
dysfunction: focal lesions (stroke, tumor, traumatic spi-
nal cord injury, myelopathies due to cervico-arthrosis,
spina bifida), disseminated lesions (Parkinson disease,
brain trauma, multiple sclerosis, meningo-encephalitis)
and peripheral neuropathies (diabetes mellitus), lead to
various and numerous urinary symptoms. These symp-
toms range from overactive bladder with urgency and
urge incontinence to underactive bladder with urinary
or other proprietary information of the Publisher.
postvoid residual, can lead to severe complications with
renal failure, upper urinary tract dilatation and infec-
tious complications.
Full clinical examinations, including urodynam-
ics and selective radiographic imaging studies, are
essential in every case of neurogenic bladder to best
manage these patients since these investigations allow
to choose the right treatments and control their effi-
cacy.6-9
Diagnosis and evaluation
Neurogenic bladder can lead to permanent urologi-
cal alterations, such as hydronephrosis, reflux, recur-
rent urinary tract infections, stones, renal alteration,

retention or difficulties to empty the bladder. These and it always inevitably leads to diminished patient
symptoms, and particularly symptoms secondary to quality of life. Overactive bladder (OAB), combined
overactive detrusor with high bladder pressure and with urgency, frequency, nocturia and urge inconti-
detrusor external sphincter dyssynergia (DESD) with nence, is the most common syndrome, which is some-

Vol. 53 - No. 6 European Journal of Physical and Rehabilitation Medicine 975

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AMARENCO DIAGNOSIS AND CLINICAL EVALUATION OF NEUROGENIC BLADDER
times also associated with voiding dysfunction and uri-
nary retention. Clinical evaluation is always necessary.
Urodynamic investigations may contribute to a better
understanding of the pathophysiology of these symp-
toms that are generally related to overactive detrusor
and DESD.10, 11
The different patterns of neurogenic lower urinary tract
dysfunction
Overactive bladder and voiding dysfunction with a
risk of urinary retention are the most common symptom
patterns in neurogenic lower urinary tract dysfunction
(NLTUD).
Urge incontinence is one of the main symptoms of
overactive bladder. Some cases of overactive bladder
can be attributed to specific conditions, such as acute
or chronic urinary tract infection, and bladder stones,
but most cases result from neurologic dysfunction
with inability to suppress detrusor contractions. This
neurogenic detrusor overactivity (NDO) can be due
to suprapontine lesions or spinal cord lesions (above
the lumbosacral level). NDO is likely to be mediated
by capsaicin-sensitive C-fiber afferents. In addition to
changes in reflex pathways, it has been demonstrated
that a functional outlet obstruction resulting from de-
trusor sphincter dyssynergia may alter the properties
of bladder afferent neurons. Decreased afferents due to
pelvic floor deficiency can lead to involuntary detrusor
contraction and can be observed in neurogenic patients.
Recently, a role of the urothelium in afferent activation
has been strongly suggested. It has been demonstrated
that the transduction mechanisms can be altered with
modification of the activation of sensory afferent fibers
during bladder filling.
Voiding dysfunction and particularly urinary reten-
tion can be observed in NLUTD. Underactive detrusor
can be one of the mechanisms, especially in peripheral
nervous system lesions (radiculopathies, peripheral
neuropathies) but in fact the main cause is a detrusor-
external sphincter dyssynergia (DESD). DESD is char-
acterized by involuntary contractions of the external
urethral sphincter during an involuntary detrusor con-
or other proprietary information of the Publisher.
traction. It is caused by neurological lesions between
the brainstem (pontine micturition center) and the sacral
spinal cord (sacral micturition center). This is the case
in multiple sclerosis and spinal cord injuries patients.
976 European Journal of Physical and Rehabilitation Medicine December 2017
DESD was hypothesized to be an abnormal flexor re-
sponse of the perineal musculature to bladder contrac-
tion and considered as a continence reflex exaggerated
owing to the loss of supraspinal influences.
This incoordination between detrusor smooth muscle
and external urethral sphincter and/or bladder neck,
induces an obstruction which determines excessive
bladder pressures during voiding and residual volume.
Thereby, the risk of recurrent urinary tract infections,
ureteral reflux, hydronephrosis and pyelonephritis, in-
creases.
Discoordination between bladder and urethra during
voiding, determines a weak stream and/or urinary re-
tention. Urinary flow can be low during all the voiding
(tonic dyssynergia) or can be irregularly interrupted by
perineal muscle spasms (clonic dyssynergia). Symp-
toms are often variable and can be influenced by general
fatigue, subject position, bladder repletion, concomitant
anorectal dysfunction, urinary tract infection, urinary li-
thiasis, orthopedic complications, and generally by any
factor inducing spasticity increase.
Clinical evaluation
Urinary tract dysfunction during the course of neu-
rogenic bladders requires full clinical evaluation since
these urinary disorders represent a considerable psy-
chosocial burden and a real risk of upper urinary tract
involvement and kidney disease.
A thorough history is always the first step in the eval-
uation of urinary dysfunction in neurogenic population.
Onset, duration of complaint, precipitants (position
change, urinary tract infection), frequency, severity,
quantity, number of pads, constipation, associated dis-
eases (diabetes, surgeries, obesity), medications (e.g.,
anticholinergics, calcium channel blockers, diuretics,
sedatives, alpha-agonists, alpha-antagonists) must be
précised.
Quantitative evaluation of urinary symptoms can be
done by means of specific symptoms scores.
The 24-hour bladder diary can provide an accurate
record of urinary output, average voided volume, fre-
quency of voiding, and frequency and nature of incon-
tinent episodes, as well as type and volume of fluid in-
take. Patients are asked to measure their urine output in
a measuring cup during any “normal” 24-hour period
they choose. Since urinary dysfunction can have a ma-
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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DIAGNOSIS AND CLINICAL EVALUATION OF NEUROGENIC BLADDER AMARENCO
jor impact on all aspects of well-being in neurogenic
patients with urinary disorders, this impact can be as-
sessed by using validated condition-specific quality of
life instruments (e.g. Qualiveen questionnaire).
Physical examination is necessary to detect contribu-
tory factors and any underlying serious medical condi-
tions. Evaluations should always consider associated
urogynecologic alterations (benign prostatic hypertro-
phy in male, associated stress urinary incontinence in
female patients) since these alterations may modify
pathophysiology of the different symptoms and thera-
peutic strategies. The sacral dermatomes should be
tested by assessing anal tone, perineal sensation and the
bulbocavernosus reflex.
Postvoid residual (PVR) urine volume is assessed
by catheterizing and measuring residual urine within 5
minutes after voiding (or by means of ultrasonography).
Numerous and various symptoms can be observed in
NLUTD.
Overactive bladder syndrome characterized by ur-
gency, urinary frequency and/or urge incontinence is
very frequent. Obstructive symptoms with voiding dys-
function, urinary retention are also frequently reported.
Overactive bladder and voiding dysfunction often coex-
ist in many cases.
The clinical presentation of vesicourethral dysfunc-
tion is variable over time and there is little correlation
between the clinical and urodynamic symptomatology.
Two factors are often associated with presence and se-
verity of vesicourethral dysfunction: the duration of the
neurologic disease and the severity of the neurological
deficiencies and disabilities. The prevalence of urinary
dysfunction is correlated with the severity of the overall
deficiencies especially in MS patients.
The first line evaluation is based on simple param-
eters.
A specific questionnaire about voiding must be used
in all the patients (frequency, number and easiness of
voiding, appraising voiding volume, sensation of com-
plete emptying or not), continence (number and ap-
praising volume of leakage, use of pads), symptoms of
urinary tract infection (and associated fever) and ano-
rectal symptoms (constipation, fecal incontinence).
or other proprietary information of the Publisher.
Combined rapid tests of urine, ‘‘dipstick’’ test, is
advisable for all patients presenting with new bladder
symptoms. Negative predictive value for ruling out uri-
nary tract infection is excellent (0.98%) but the posi-
Vol. 53 - No. 6 European Journal of Physical and Rehabilitation Medicine 977
tive predictive value for confirming infection is only
50%.
In all the cases, it is necessary to track down uri-
nary retention. A measure of postvoid residual urine by
supra-pubic ultrasonography or in-out catheterization
must be done.
When micturitional symptoms are discovered or
spontaneously reported during this minimal evalu-
ation, other evaluations must be performed with a
three-day voiding chart, an ultrasound scan of the uri-
nary tract, a urine bacteriology, a urodynamic study,
a urinary creatinine clearance, and finally an evalua-
tion of the impact of urinary symptoms on a quality-
of-life scale (which may be based on the specific and
validated Qualiveen Questionnaire in MS and spinal
cord injury). When risk factors are observed, e.g. high
vesical pressure during the filling phase or during mic-
turition, specific radiologic investigations must be per-
formed (CT-scan, cystourethrography and sometimes
renal scintigraphy when urinary creatinine clearance is
altered).
Urodynamic evaluation
Urodynamic explorations allow a precise evaluation
of pathophysiology of urinary dysfunction and of risk
factors for urinary tract damage in neurogenic patients
with urinary dysfunction, thus helping to plan their
optimal management. Indeed, diagnosis of urinary in-
continence and more generally of urinary dysfunction,
is complex with intricate pathophysiologic factors.
Thus, in many cases, urodynamic investigations are
necessary to better understand symptoms pathophysi-
ology and choose the best therapeutic strategies. But
in all the cases, urodynamic must be considered as a
complementary investigation and always interpreted in
conjunction with clinical data and the results of the
others morphological and/or radiological investiga-
tions.
Measurement of the urinary flow rate (uroflowmetry)
is used to confirm the presence of bladder outlet ob-
struction and more precisely the presence of a DESD.
Urinary flow rate is measured with a flowmeter that
measures a quantity of fluid passed per unit time, ex-
pressed in mL/s. Uroflow depends on detrusor contrac-
tility and urethra-sphincter resistance. Voided volume
should be greater than 150 mL. Patients are instructed
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
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(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
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COPYRIGHT 2017 EDIZIONI MINERVA MEDICA
AMARENCO DIAGNOSIS AND CLINICAL EVALUATION OF NEUROGENIC BLADDER
to void normally as in usual conditions, with a comfort-
ably full bladder, which is sometimes difficult in these
neurogenic patients with neurogenic detrusor overactiv-
ity leading to a reduced bladder capacity. Measurement
of residual urine volume (by means of ultrasounds or
catheterization) is necessary to properly interpret the
uroflowmetry results. The precise shape of the flow
curve is decided by detrusor contractility, the presence
of any abdominal straining and by the bladder outlet.
A normal flow curve is a smooth curve without any
rapid changes in amplitude. Rapid changes in flowrate
may evoke detrusor sphincter dyssynergia with lack
of urethral sphincter relaxation during micturition and
sometimes involuntary flow interruption and abdominal
straining (Figure 1).
Cystometry is the method used to measure the pres-
sure-volume relationships of the bladder. The intravesi-
cal pressure is measured while the bladder is filled, but
this simple technique is not accurate because intravesi-
cal pressure does not represent in all the cases the true
detrusor pressure: as the bladder is an intra-abdominal
organ, the intravesical pressure is subjected to changes
(during cough, patient movements, …) and not rep-
resent the real detrusor pressure. Thus, it is more ap-
propriate to use subtracted cystometry which involves
Upper motor
neuron
lesions
Sacral
parasym-
pathetic
center
Lower motor
neuron
lesions
Figure 1.—Upper motor neuron lesions (lesions of neural pathway
above the anterior horn cell of the spinal cord): lead to overactive de-
or other proprietary information of the Publisher.
trusor with uninhibited detrusor contraction associated with detrusor
sphincter dyssynergia and high detrusor pressure during micturition (top
curve); lower motor neuron lesions (lesions are either in the anterior
horn cell or distal to the anterior horn cell): lead to underactive detrusor
with high compliance, decreased filling sensation and absence of detru-
sor contraction (lower curve).
978 European Journal of Physical and Rehabilitation Medicine December 2017
measurement of both the intravesical and intra-abdom-
inal pressure simultaneously. Electronic subtraction
of the intra-abdominal pressure from the intravesical
pressure enables detrusor pressure measurements. In
current practice intra-abdominal pressure is estimated
from rectal pressure (or vaginal pressure in female).
Urinary tract infection should always be checked be-
fore urodynamic investigation. Artificial bladder fill-
ing is used, via a catheter, with sterile water or normal
saline. In current practice the filling rate is usually 50
mL/min. Different events must be analyzed during fill-
ing and voiding phases: first sensation of bladder fill-
ing (feeling of the bladder filling), first desire to void,
strong desire to void. Increased bladder sensation is
defined as an early first sensation of bladder filling (or
an early desire to void) and/or an early strong desire to
void, which occurs at low bladder volume and which
persists. Reduced bladder sensation is defined as dimin-
ished sensation throughout bladder filling. This fact is
always observed in peripheral lesions (lesions of sacral
roots or plexus injury, peripheral neuropathy). Absent
bladder sensation means that, during filling cystometry,
the individual has no bladder sensation. Urgency, dur-
ing filling cystometry, is a sudden compelling desire to
void.
Assessment of the detrusor function during filling
cystometry is one of the major goals of the urodynamic
investigation in neurogenic patients with urinary dys-
function. All detrusor activity before the “permission
to void” is defined as “involuntary detrusor activity”.
Normal detrusor function is defined as bladder filling
with little or no change in pressure. No involuntary pha-
sic contractions occur despite provocation (rapid filling,
ice water, postural changes, hand washing). Detrusor
overactivity is a urodynamic observation characterized
by involuntary detrusor contractions during the fill-
ing phase which may be spontaneous or provoked. In
central disease (upper motor neuron lesions), there are
certain patterns of detrusor overactivity: phasic detru-
sor overactivity, defined by a characteristic wave form
and may or may not lead to urinary and often observed
in spinal cord lesions; terminal detrusor overactivity,
defined as a single, involuntary detrusor contraction,
occurring at cystometric capacity, which cannot be sup-
pressed and results in incontinence usually resulting in
bladder emptying (voiding) and often observed in corti-
cal lesions (stroke, tumor).
not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, log
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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DIAGNOSIS AND CLINICAL EVALUATION OF NEUROGENIC BLADDER AMARENCO
Bladder compliance describes the relationship be-
tween change in bladder volume and change in detrusor
pressure. Compliance (C) is calculated by dividing the
volume change (∆V) by the change in detrusor pres-
sure (∆pdet) during any change in bladder volume (C=
∆V/∆pdet). Cystometric capacity is the bladder volume
at the end of the filling cystometry, when “permission to
void” is usually given. Alteration of bladder compliance
can be observed in congenital lesions (spina bifida) or in
spinal cord lesions.
Urodynamic investigations allow the diagnosis of
DESD in neurogenic patients with voiding dysfunc-
tion. The classic test to recognize DESD is combined
cystometry and external sphincter electromyography.
Meanwhile, DESD can be suggested if a uroflowmetry
examination is possible to perform, when an interrupt-
ed urine flow with residual volume observed.
Cystometry may be recorded with a rectal pres-
sure measurement to analyze abdominal pressure si-
multaneously with bladder pressure to eliminate ar-
tifacts due to abdominal muscle contraction. Indeed,
the diagnosis of DESD requires a detrusor contrac-
tion. However, many patients are unable to initi-
ate such a contraction, particularly in severe DESD.
Furthermore, in moderate DESD, some patients will
strain to try to urinate, which causes a simultaneous
increase in sphincter activity, bladder and rectal pres-
sure. Sphincter dyssynergia is diagnosed by increased
EMG activity during an involuntary detrusor contrac-
tion. DESD is further suggested by a high voiding
pressure, persistent elevated MUP (maximal urethral
pressure). Smooth sphincter dyssynergia is more dif-
ficult to confirm. Video imaging techniques allow the
diagnosis of bladder neck dyssynergia. Fluoroscopic
imaging during an involuntary contraction objectifies
persistent narrowing of the internal sphincter and /or
of the bladder neck.
When the micturition is possible, combined uroflow
and sphincter EMG (possibly with a single rectal pres-
sure record) allow DESD screening.
In fact, a very common and important question, is
whether dyssynergia can be diagnosed in the absence of
a bladder contraction. Even if the DESD rigorous defi-
or other proprietary information of the Publisher.
nition is not applicable, we can consider that DESD is
the only mechanism of urinary retention in a neurogenic
patient who complains of overactive bladder without
bladder neck or urethral organic obstruction (urethral
Vol. 53 - No. 6 European Journal of Physical and Rehabilitation Medicine 979
stenosis, prostatic hypertrophy). However, recognizing
DESD is not the main problem in the management of
neurogenic bladder. The real challenge is not to prove
absolutely DESD with urodynamic tests, but to evalu-
ate its consequences, especially high detrusor pressure
during storage and/or micturition, which can determine
bladder or renal complications.
Conclusions
Urinary incontinence, overactive bladder and more
generally urinary dysfunction is a major clinical prob-
lem and a significant cause of disability in neurogenic
patients. Indeed, the bothersome symptom of urinary
dysfunction may adversely affect social relationships
and activities in these patients. Since many causes of
urinary dysfunction are described, a thorough evalua-
tion including history, clinical examination and evalua-
tion of quality of life is necessary.
Clinical evaluation is still the main step in the man-
agement of urinary disorders in neurogenic patients.
Questionnaires are highly recommended and signifi-
cantly improve symptoms comprehension and thera-
peutic decision. Investigations, biological, radiological
or urodynamic are indicated in all symptomatic patients.
Specific algorithms can be used in order to track down
any complications and help to a better follow-up of the
patients.12, 13
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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use i
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other
©
COPYRIGHT 2017 EDIZIONI MINERVA MEDICA
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Conflicts of interest.—The authors certify that there is no conflict of interest with any financial organization regarding the material discussed in the manuscript.
Article first published online: October 25, 2017. - Manuscript accepted: October 25, 2017. - Manuscript received: September 17, 2017.
or other proprietary information of the Publisher.

980 European Journal of Physical and Rehabilitation Medicine December 2017