Theneurogenicbladder: Anupdatewith Managementstrategies Forprimarycare Physicians
Theneurogenicbladder: Anupdatewith Managementstrategies Forprimarycare Physicians
Theneurogenicbladder: Anupdatewith Managementstrategies Forprimarycare Physicians
An Update with
Management Strategies
f o r Pr i m a r y C a re
Physicians
a, b
Adam P. Klausner, MD *, William D. Steers, MD
KEYWORDS
Neurogenic bladder Urodynamics
Bladder outlet obstruction
a
Division of Urology, Department of Surgery, Virginia Commonwealth University School of
Medicine, PO Box 980118, Richmond, VA 23298-0118, USA
b
Department of Urology, University of Virginia School of Medicine, VA, USA
* Corresponding author.
E-mail address: apklausner@vcu.edu
A patient with symptoms of or proven dysfunction of the lower urinary tract and
neurologic findings (or a known neurologic disorder) is said to have a neurogenic
bladder. Poor compliance is one consequence of neurogenic bladder dysfunction,
but compliance can only be determined during a formal urodynamic evaluation, in
which filling pressures and volumes are recorded simultaneously. Therefore, one of
the most important pieces of information that is obtained from a urodynamic evalua-
tion is a determination of the bladder compliance.
The micturition reflex is an autonomic process under voluntary control. In other
words, the reflex can be aborted midstream by inhibitory neural inputs from higher
cortical brain centers. Conversely, the reflex can be accelerated by neurologic
processes that affect or damage these areas that produce inhibitory inputs. Damage
to the cerebral cortex reduces inhibitory input to the pontine micturition center and
might cause urinary frequency, urgency, or even urge incontinence. Patients with
this type of reduced inhibitory control are those with Parkinson disease, cortical
strokes, brain tumors, normal pressure hydrocephalus, traumatic brain injury, or Alz-
heimer type dementia.5 Alternatively, patients with diseases such as multiple scle-
rosis, degenerative disk disease, or spinal cord pathology have neurologic lesions
caudal to the pontine micturition center but rostral to the sacral spinal cord. Typically,
lesions in this location result in a loss of coordination between the bladder and its
outlet, creating obstruction.5 In addition to often demonstrating detrusor overactivity,
these patients may exhibit either slowed external sphincter relaxation (eg, Parkinson
disease) or complete loss of coordination (eg, suprasacral spinal cord injury [SCI]).
Whether overactive bladder symptoms are merely caused by detrusor overactivity
or are the result of bladder outlet obstruction requires special physiologic testing of
the lower urinary tract termed urodynamics.
Urodynamic Technique
The cystometry portion of urodynamics is accomplished by infusing saline at room
temperature at the rate of 40 to 60 mL/min. Although faster than physiologic filling,
these rates have been chosen because of time constraints and to help unmask detru-
sor overactivity. During the filling phase, the urodynamicist asks the patient to identify
various sensory thresholds including the volumes at which the patient has the first
sensation of filling, the first desire to void, and a strong desire to void. The diagnosis
of increased bladder sensation is made when patients achieve sensory thresholds at
lower-than-expected volumes. Reduced or absent sensation is diagnosed when
patients achieve sensory thresholds at lower-than-expected volumes or not at all.
During the filling phase, any involuntary bladder contractions should be noted.
Although involuntary detrusor contractions (IDCs) are identified in up to 20% of
asymptomatic patients during cystometry,6,7 their presence is considered abnormal.
The Neurogenic Bladder 113
Thus, the presence of one or more IDCs during the filling phase allows the urodynam-
icist to diagnose detrusor overactivity. In the setting of known neurogenic bladder
dysfunction, the diagnosis is neurogenic detrusor overactivity as opposed to idio-
pathic detrusor overactivity. In addition, at a volume equal to about 50% of the known
or expected bladder capacity, filling is temporarily stopped and provocative maneu-
vers are sometimes performed to evaluate for the possibility of an incompetent
urethral sphincter closure mechanism, which is commonly found in patients with
stress incontinence.
Once the patient reaches cystometric capacity, the filling is discontinued and the
patient is given permission to void. Oftentimes, the patient is unable to wait and voids
involuntarily, which leads to the urodynamic diagnosis of detrusor overactivity incon-
tinence. During the voiding phase, the voiding flow rate is obtained using a flowmeter
that collects urine while calculating a urinary flow rate. Multichannel capability allows
flow and intravesical pressure to be graphed at the same time. This simultaneous
measurement of bladder pressure and urine flow is also called a pressure-flow study.
The pressure-flow study is the only test that can accurately determine whether phys-
iologic bladder outlet obstruction exists. A low peak voiding flow rate (<12 mL/s) may
suggest obstruction but cannot, in itself, exclude impaired detrusor contractility. The
diagnosis of bladder outlet obstruction is made only when elevated bladder pressures
and low urinary flow rates (ie, high pressure, low flow) are seen simultaneously. The
urodynamic criteria for obstruction in men has been clearly defined and can be
graphed on a standardized nomogram,8 whereas such a measure in women is some-
what controversial. Fluoroscopy performed simultaneously with multichannel
urodynamic evaluation (termed videourodynamics) allows the operator to note the
level of obstruction, such as the bladder neck, prostate, external sphincter, or distal
urethra.
EMG activity of the urinary sphincter is used to determine if the bladder and
sphincter are acting in a coordinated manner. In the setting of neurogenic bladder
dysfunction, obstruction often occurs because of a lack of neurally mediated coor-
dination of the sphincter and bladder, a process termed detrusor-sphincter dyssy-
nergia (DSD). It is crucial that the urodynamicist differentiate true dyssynergia
from dysfunctional voiding, a learned behavior or an artifact. The following cases
illustrate how urodynamics is used to diagnosis and treat patients with neurogenic
voiding dysfunction:
center, which clinically presents as a reduced warning time associated with urinary
urgency and urge incontinence.
This patient should first be treated with timed or prompted voiding, fluid manage-
ment, and urge suppression maneuvers. Diuretics should be avoided because
these will exacerbate his symptoms. Patients who do not fully respond to behav-
ioral modification may be managed with antimuscarinic medications. However,
many of these medications have inconvenient side effects such as dry mouth
and constipation, which limit their long-term efficacy, and some are associated
with short-term memory impairment, making them more risky for use in the elderly.9
Certainly, patients should be counseled that symptoms may improve spontaneously
in parallel with recovery of other motor and cognitive functions after an acute
stroke. Chronic symptoms that are severe, bothersome, and refractory to behav-
ioral modifications and medical therapy can be treated by sacral or tibial nerve neu-
romodulation or even with off-label usage of botulinum toxin injected into the
bladder muscle.10,11
segments of bowel or botulinum toxin injections into the detrusor. Primary care
providers should recognize that patients such as these require lifelong urologic
management and should be referred to a urologist or other providers with training in
neurourology and urodynamics.
The preceding cases illustrate many of the urodynamic risk factors for kidney damage
or upper urinary tract deterioration in patients with neurogenic bladder obstruction or
dysfunction. These risk factors include poor bladder compliance, bladder pressures
greater than 40 cm H2O, and the presence of DSD. Data supporting these risk factors
are discussed in the following sections.
DSD
DSD is defined as the involuntary contraction or lack of relaxation of the striated
sphincter during a bladder contraction.5 DSD should exist only in patients who have
a neurologic abnormality below the brain stem and above the sacral spinal cord where
motor outflow to the bladder originates. In fact, nearly 75% of patients with suprasac-
ral SCI15 will have DSD, and patients with this type of neurologic injury should be
considered to have DSD until proven otherwise.
DSD is considered a risk factor for the development of renal damage. In a study of
male patients with SCI, Linsenmeyer and colleagues16 found that patients with pro-
longed voiding had the greatest risk of developing hydronephrosis. Patients with pro-
longed voiding, like the patient in case 2, may have both DSD and poorly compliant
bladders. Untreated DSD is clearly associated with the development of renal
damage,17 and 50% of patients with untreated DSD will develop significant urologic
complications, including vesicoureteral reflux, renal damage, urolithiasis, urosepsis,
and ureterovesical obstruction.18 Pharmacologic treatment with a-blockers may be
considered because these drugs work by reducing outlet resistance at the level of
the bladder neck; however, there is limited evidence that these agents actually
improve outcomes or decrease risk of complications in patients with DSD.19–22
Because of a-blockers and other types of pharmacotherapy lack efficacy, the main-
stay of treatment of DSD is performance of intermittent catheterization. Patients
should be counseled to time the catheterizations to keep the volumes of urine below
the threshold for the development of involuntary bladder contractions and/or below
the volume at which a detrusor leak point pressure of 40 cm H2O develops. In conjunc-
tion with fluid restriction, catheterization can often be accomplished every 4 to 6 hours.
However, some patients may need to catheterize far more frequently or may not be
willing or able to catheterize at all. In these more challenging situations, patients
can be offered botulinum toxin injection to paralyze the urinary sphincter, formal
116 Klausner & Steers
associated with unchecked sympathetic outflow triggered by noxious stimuli below the
level of injury. The bladder is the most common source of AD, and primary care physi-
cians who care for patients with neurologic conditions must be aware of this condition
and be ready to treat it aggressively. The first step is to eliminate the noxious stimulus. In
patients with SCI, this elimination can often be accomplished by emptying a distended
bladder through catheterization or irrigation of an obstructed catheter. Short-term treat-
ment of hypertension using nitroglycerine paste or sublingual nifedipine is often
required, and prevention with the use of oral a-blockers can be effective. In recurrent
episodes, a search for an occult urologic cause, such as a calculus or an improper
bladder management, should be initiated.46
SUMMARY
Patients with lesions of the central nervous system often have neurogenic bladder
dysfunction. Lifelong bladder monitoring and management in these patients is neces-
sary to prevent severe complications, including renal damage. The urodynamic test,
performed by neurourologists or other specially trained providers, is the definitive
test for diagnosis and management of neurogenic bladder dysfunction. This test
can help determine if a patient has a safe or an unsafe bladder, and primary care
physicians should refer patients for urodynamic testing as soon as neurogenic bladder
dysfunction in known or suspected.
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