Updated: Jan 26, 2009
In the practice of physical medicine and rehabilitation, voiding disorders are usually a result of neurologic conditions, such as spinal cord injury (SCI) or disease, cerebrovascular accident (CVA), traumatic brain injury (TBI), multiple sclerosis (MS), or dementia. Incontinence and urinary retention can cause social embarrassment and added morbidity, such as infections, stones, or renal injury.
Related eMedicine topics:
Urinary Incontinence
Voiding Dysfunction
The sympathetic nervous system regulates the process of urine storage in the bladder. In contrast, the parasympathetic nervous system controls bladder contractions and the passage of urine. Parasympathetic nerve impulses travel from S2-S4 ventral gray matter via the pelvic nerves to the ganglia near the bladder wall. Postganglionic nerve impulses then travel to the smooth muscle cholinergic receptors to produce bladder contraction.
Sympathetic efferent nerve fibers originate from the lateral gray column of the spinal cord from T11-L2. The sympathetic system has a long postganglionic chain that runs with the hypogastric nerve to synapse with alpha-receptors and beta-receptors in the bladder wall and bladder neck or internal sphincter. Beta-receptors are responsible for mediating relaxation of the bladder with filling. Alpha-receptors are responsible for tonically contracting the internal sphincter during bladder filling.
The somatic efferent nerve fibers originate from the pudendal nucleus of S2-S4 and supply the external periurethral sphincter. The external sphincter is under voluntary control and normally contracts in response to coughing or the Valsalva maneuver or when a person actively tries to prevent or halt urine flow.
Three areas of the CNS (ie, the sacral micturition center, the pontine micturition center, the cerebral cortex) control bladder function. The sacral micturition center is located at the S2-S4 levels and is responsible for bladder contraction. The pontine micturition center may play a role in coordinating relaxation of the external sphincter with bladder contractions while the cerebral cortex plays an inhibitory role in relation to the sacral micturition center.
Lesions of the peripheral nerves or the sacral micturition center cause detrusor areflexia that manifests as distended bladder with overflow incontinence. Lesions of the spinal cord or brainstem below the pontine micturition center, but above the sacral micturition center, lead to uninhibited bladder contractions with uncoordinated sphincter activity. The external sphincter may contract reflexively when the bladder contracts, a problem known as detrusor sphincter dyssynergia. Lesions above the pontine micturition center lead to lack of inhibition from the cerebral cortex and result in uninhibited bladder contractions, but voluntary relaxation of the urethral sphincter remains intact. This problem is encountered commonly in patients with CVA, TBI, or dementia.
Individuals with lesions below the pontine micturition center have both detrusor hyperreflexia and sphincter-detrusor muscle dyssynergia. These are the patients with SCIs, MS, and transverse myelitis.
Incidence of neurogenic bladder dysfunction depends on the primary cause. Etiology and level of central or peripheral nervous system injury correlate with different causes and classifications of bladder dysfunction. Bladder disorders are reported in 40-90% of patients with MS. Estimates of incidence of urologic symptoms in patients who have sustained a CVA vary, ranging from 33-60% in the acute setting and persisting in 15% at 6 months to 1 year.
The rate of urologic dysfunction in patients with Parkinson disease has been reported to be 37-72%. The rate of urinary incontinence is higher in patients with dementia and other types of cognitive impairment (eg, TBI, CVA, Parkinson disease) than in the general population. Bladder disorders are nearly universal in children with myelomeningocele and in patients with SCI.
Related eMedicine topics:
Neurogenic Bladder
Urinary Tract Infection
Urinary Tract Infection, Female
Urinary Tract Infection, Females
Urinary Tract Infection, Male
Urinary Tract Infection, Males
Urinary Tract Infections in Pregnancy
This condition has no racial predilection.
The male-to-female ratio varies greatly between disease entities causing neurogenic bladder dysfunction. One study reported the male-to-female ratio as 1.6:8.5 in patients aged 15-64 years without consideration of etiology. Incidence of urinary incontinence, regardless of etiology, has been reported in 8.5% of females aged 15-64 years. In the same age group, only 1.6% of the male population report being affected with urinary incontinence.
Age of occurrence of bladder disorders is related to age of onset of the neurologic disorder.
| Brown-Sequard Syndrome | Multiple Sclerosis |
| Central Cord Syndrome | Myelomeningocele |
| Cervical Disc Disease | Parkinson Disease |
| Lumbar Spondylolysis and
Spondylolisthesis | Spinal Cord Injury: Definition, Epidemiology,
Pathophysiology |
Urinary outflow obstruction
Prostatism
Urinary tract infection
Chronic neurogenic bladder dysfunction may lead to thickening of the bladder wall secondary to an increase in collagen and connective tissues, leading to potentially less efficient bladder contractions.
Early mobilization and transfer training is recommended to minimize urinary incontinence and other complications such as pressure sores. Pressure sores can easily become infected in patients who are incontinent.
Activities of daily living and self-care training are important to encourage maintenance of hygiene and a more efficient use of hand and upper extremity function.
A variety of techniques are used to maintain continence and/or empty the bladder.
Related eMedicine topics:
Incontinence, Urinary: Nonsurgical Therapies
Incontinence, Urinary: Comprehensive Review of Medical and Surgical Aspects
Injectable Bulking Agents for Incontinence
Related eMedicine topic:
Incontinence, Urinary: Surgical Therapies
Consult with a urologist for diagnostic and therapeutic management of new and complicated cases.
Cholinergic agonists are used in patients with detrusor areflexia; these agents include bethanechol chloride, which may mimic effects of acetylcholine and cause detrusor contractions.
Alpha-adrenergic blocking agents include phenoxybenzamine and prazosin. Phenoxybenzamine is useful in reducing bladder outlet resistance in SCI, as long as detrusor bladder contractions are present. This medication is not helpful in areflexic bladders. Phenoxybenzamine is helpful in patients with detrusor sphincter dyssynergia.
Anticholinergic agents may help to alleviate symptoms in patients with urinary incontinence due to uninhibited bladder contractions secondary to suprasacral lesions. This group of drugs includes propantheline bromide, oxybutynin, and tolterodine tartrate, which competitively block acetylcholine receptors at postganglionic autonomic receptor sites, suppressing uninhibited bladder contractions.
Tricyclic antidepressants (TCAs) may (1) have peripheral alpha-adrenergic and central anticholinergic effects, (2) suppress bladder contractions, and (3) enhance bladder neck resistance. Alpha-adrenergic agents are used to enhance bladder neck resistance in patients with stress incontinence or denervation of the bladder neck.
Intravesical agents such as oxybutynin have been used with fewer adverse systemic effects; however, they have a more time-consuming and inconvenient manner of administration. Experimental agents capsaicin and resinferatoxin are effective in early investigative studies.
Stimulate cholinergic receptors in the smooth muscle of the urinary bladder and GI tract, resulting in increased peristalsis.
Used for selective stimulation of the bladder to produce contraction to initiate micturition and empty the bladder. Found to be most useful in patients who have bladder hypocontractility, provided they have functional and coordinated sphincters. Rarely used due to difficulty in timing effect and because of GI stimulation.
10-50 mg PO tid/qid
Not established
Concurrent administration with ganglion-blocking compounds may cause drop of blood pressure to critical levels
Documented hypersensitivity; peptic ulcer disease, obstructive pulmonary disease, bradycardia, vasomotor instability, hypotension, atrioventricular conduction defects, hyperthyroidism, epilepsy, and mechanically obstructed GI or GU tract
C - Safety for use during pregnancy has not been established.
Urinary retention secondary to possible reflux of urine into kidneys may occur
Have been used to decrease bladder overactivity.
Improves urine flow rates by relaxing smooth muscle. This relaxation is produced by blocking alpha1-adrenoceptors in the bladder neck and prostate.
When increasing dosages, give first dose of each increment hs to reduce syncopal episodes.
Although doses >20 mg/d usually do not increase efficacy, some patients may benefit from up to 40 mg/d.
Initial dose: 10 mg PO qd; can be increased by 10 mg PO q5d, given at intervals of 8-12h
Not established
Acute postural hypotensive reaction from beta-blockers may worsen; indomethacin may decrease antihypertensive activity; verapamil may increase serum levels and may increase patient's sensitivity to prazosin-induced postural hypotension; may decrease antihypertensive effects of clonidine
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
Drowsiness and dizziness may occur after first dose of this drug; caution in renal insufficiency and when driving or handling machinery
Decreases bladder contractions through long-lasting noncompetitive alpha-adrenergic blockade of the postganglionic synapses at the smooth muscle and exocrine glands.
Initial dose: 10 mg PO qd; can be increased by 10 mg PO q5d q8-12h
Not established
May interact with compounds that stimulate both alpha-adrenergic and beta-adrenergic blocking agents to produce exaggerated hypotensive effect
Documented hypersensitivity; those in whom a fall in blood pressure would be undesirable; orthostatic hypotension
C - Safety for use during pregnancy has not been established.
Caution in cerebral or coronary arteriosclerosis and renal impairment; can worsen symptoms of respiratory tract infections
These drugs inhibit the binding of acetylcholine to the cholinergic receptor, thereby suppressing involuntary bladder contraction of any etiology. In addition, they increase the volume of the first involuntary bladder contraction, decrease the amplitude of the involuntary bladder contraction, and may increase bladder capacity.
Used for anticholinergic effect to control symptoms of urinary incontinence secondary to uninhibited bladder contractions related to upper motor neuron lesions.
7.5-15 mg PO q6h
Not established
Effects decrease when administered concurrently with antacids; toxicity increases when administered concurrently with disopyramide, TCAs, phenothiazines, corticosteroids, and bretylium
Documented hypersensitivity; bowel obstruction, myasthenia gravis, intestinal atony, obstructive uropathy, severe ulcerative colitis, and narrow-angle glaucoma
C - Safety for use during pregnancy has not been established.
Caution in elderly patients with autonomic neuropathy, congestive heart failure (CHF), and renal or hepatic disease
Commonly used drug in bladder disorder and is known for anticholinergic-antispasmodic effects. Has a smooth muscle relaxing effect distal to the cholinergic receptor site. Also available in long-acting form for qd dosing.
5 mg PO tid
2.5 mg PO tid
Coadministration with other anticholinergic agents may exacerbate anticholinergic adverse effects, including dry mouth, drowsiness, and constipation; CNS effects increase when administered concurrently with other CNS depressants
Documented hypersensitivity; patients diagnosed with glaucoma, partial or complete GI obstruction, myasthenia gravis, ulcerative colitis, and toxic megacolon
B - Usually safe but benefits must outweigh the risks.
Caution in urinary tract obstruction, reflux esophagitis, and heart disease
Competitive muscarinic receptor antagonist for overactive bladder; however, it differs from other anticholinergic types in that it has selectivity for urinary bladder over salivary glands. Exhibits a high specificity for muscarinic receptors, has minimal activity or affinity for other neurotransmitter receptors and other potential targets, such as calcium channels.
2 mg PO bid; can be adjusted to 1 mg PO bid
Not established
Patients being treated with macrolide antibiotics or antifungal agents should not receive doses of tolterodine higher than 1.0 mg PO bid
Documented hypersensitivity; urinary retention, gastric retention, or uncontrolled narrow-angle glaucoma
C - Safety for use during pregnancy has not been established.
Do not give doses >1.0 mg PO bid to patients with significantly reduced hepatic function; caution in renal impairment
Quaternary ammonium compound that elicits antispasmodic and antimuscarinic effects. Antagonizes acetylcholine effect on muscarinic receptors. Parasympathetic effect reduces smooth muscle tone in bladder. Indicated for overactive bladder (eg, urinary incontinence, urgency, frequency).
20 mg PO bid; on empty stomach at least 1 h before meals
CrCl <30 mL/min: 20 mg PO hs
>75 years: May titrate dose downward to 20 mg PO qd based on tolerability
Not established
High-fat meals decrease absorption; coadministration with drugs that compete for tubular secretion (eg, digoxin, procainamide, pancuronium, morphine, vancomycin, metformin, tenofovir) may decrease elimination; coadministration with other drugs that elicit anticholinergic effects (eg, antihistamines, antispasmodics) may increase adverse effects
Documented hypersensitivity; urinary retention; gastric retention; uncontrolled narrow-angle glaucoma
C - Safety for use during pregnancy has not been established.
Anticholinergic effects may occur (eg, dry mouth, constipation, dry eyes, blurred vision); increased anticholinergic effects may occur in individuals >75 y; decrease dose with severe renal impairment (ie, CrCl <30 mL/min)
Elicits competitive muscarinic receptor antagonist, which results in anticholinergic effect and inhibition of bladder smooth muscle contraction. Indicated for overactive bladder with symptoms of urgency, frequency, and urge incontinence.
5 mg PO qd; if tolerated, may be increased to 10 mg PO qd prn
Not established
CYP-3A4 substrate; because of decreased clearance, do not exceed 5 mg/dose when coadministered with CYP-3A4 inhibitors (eg, ketoconazole, erythromycin); CYP-3A4 inducers (eg, rifampin, carbamazepine) may increase clearance; may increase risk of QT prolongation when coadministered with drugs known to prolong QT interval (eg, sotalol, thioridazine, moxifloxacin)
Documented hypersensitivity, severe hepatic impairment (Child-Pugh class C), uncontrolled narrow-angle glaucoma, urinary retention, gastric retention
C - Safety for use during pregnancy has not been established.
Caution with renal or hepatic impairment (do not exceed 5 mg with CrCl <30 mL/min or moderate hepatic impairment [Child-Pugh class B]); caution with controlled narrow-angle glaucoma, history of prolonged QT interval, bladder outflow obstruction, or decreased GI motility; tab must be swallowed whole (not crushed) with liquid
Extended-release product eliciting competitive muscarinic receptor antagonistic activity. Reduces bladder smooth muscle contractions. Has high affinity for M3 receptors involved in bladder and GI smooth muscle contraction, saliva production, and iris sphincter function. Indicated for overactive bladder with symptoms of urge incontinence, urgency, and frequency. Swallow whole; do not chew, divide, or crush.
7.5 mg PO qd initially; after 2 wk may increase to 15 mg PO qd based on response
Moderate hepatic impairment (Child-Pugh class B) or potent CYP-450 3A4 inhibitors: Do not exceed 7.5 mg PO qd
Not established
CYP-450 2D6 and 3A4 substrate; potent CYP-450 3A4 inhibitors (eg, ketoconazole, itraconazole, ritonavir, nelfinavir, clarithromycin, nefazodone) decrease clearance (do not exceed 7.5 mg/d); may cause additive toxicity with other anticholinergics (eg, antihistamines); coadministration with CYP-2D6 substrates that have a narrow therapeutic index (eg, flecainide, thioridazine, TCA [imipramine]) may cause toxicity of these other substrates; may increase midazolam or digoxin levels
Documented hypersensitivity; urinary retention; gastric retention; severe hepatic impairment; uncontrolled narrow-angle glaucoma
C - Safety for use during pregnancy has not been established.
Common adverse effects include xerostomia, constipation, and blurred vision; caution with significant bladder outflow obstruction, decreased GI motility, controlled narrow-angle glaucoma, or moderate hepatic impairment; may cause heat prostration due to decreased ability to sweat
Competitive muscarinic receptor antagonist. Antagonistic effect results in decreased bladder smooth muscle contractions. Indicated for symptoms of overactive bladder (eg, urinary urge incontinence, urgency, and frequency). Available as 4- or 8-mg extended-release tab.
4 mg PO qd; may increase to 8 mg/d; not to exceed 4 mg PO qd in severe renal dysfunction (ie, CrCl <30 mL/min) or with coadministration of drugs that decrease fesoterodine's metabolism (eg, ketoconazole, itraconazole, clarithromycin)
Not established
Coadministration with other drugs that cause antimuscarinic or anticholinergic effects may exacerbate adverse effects (eg, xerostomia, constipation); coadministration with strong CYP3A4 inhibitors (eg, ketoconazole, itraconazole, clarithromycin) increases maximum concentration and AUC of fesoterodine
Documented hypersensitivity; urinary or gastric retention; uncontrolled narrow-angle glaucoma; severe liver impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Common adverse effects include xerostomia and constipation; caution in myasthenia gravis, hepatic or renal impairment, controlled narrow-angle glaucoma, and decreased gastrointestinal motility; may cause anticholinergic effects (eg, dry eyes, dry throat, urinary retention); may increase heart rate
Have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The exact mechanisms by which these drugs act in the treatment of incontinence, however, are not understood fully. The Agency for Health Care Policy and Research (AHCPR) guidelines caution that TCAs should be reserved for use in carefully evaluated patients.
Facilitates urine storage by decreasing bladder contractility and increasing outlet resistance.
Inhibits reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) at presynaptic neuron.
10-25 mg PO bid/qid
<6 years: Not established
>6 years: 25 mg PO hs; may be increased to 50 mg PO hs after 1 wk if results are unsatisfactory with initial dosage
Increases toxicity of sympathomimetic agents such as isoproterenol and epinephrine by potentiating effects and inhibiting antihypertensive effects of clonidine
Documented hypersensitivity; narrow-angle glaucoma; in acute recovery phase following myocardial infarction; avoid in patients taking MAOIs or fluoxetine or who took them in previous 2 wks
D - Unsafe in pregnancy
May impair mental or physical abilities required for performance of potentially hazardous tasks; caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism, or receiving thyroid replacement
Increase urethral pressure.
Use in neurogenic bladder based on increasing urethral pressure that would help patients with mild-to-moderate stress incontinence by directly stimulating alpha- and beta-adrenergic receptors.
25 mg PO qid
Not established
Theophylline, atropine, or MAOIs may increase toxicity; alpha- and beta-blockers decrease vasopressor effects; cardiac glycosides and general anesthetics increase cardiac stimulation
Documented hypersensitivity; angle-closure glaucoma; cardiac arrhythmias; hyperthyroidism
C - Safety for use during pregnancy has not been established.
Caution in elderly patients or those with diabetes mellitus, hyperthyroidism, hypertension, cardiovascular disease, prostatic hypertrophy, or cerebrovascular insufficiency
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bladder management, urine, bladder, urination, urinary tract, urinary tract infection, incontinence, bladder problems, urinary tract infections, urinary incontinence, urinary problems, bladder control, urinary retention, neurogenic bladder dysfunction, voiding disorders, neurologic conditions, spinal cord injury, SCI, spinal cord disease, cerebrovascular accident, CVA, stroke, traumatic brain injury, TBI, multiple sclerosis, MS, dementia, social embarrassment
Ramon S Lansang Jr, MD, Consulting Staff, Department of Orthopedics, Charleston Area Medical Center
Ramon S Lansang Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and American Medical Association
Disclosure: Nothing to disclose.
Teresa L Massagli, MD, Residency Director, Professor, Department of Rehabilitation Medicine and Pediatrics, University of Washington School of Medicine
Teresa L Massagli, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Physical Medicine and Rehabilitation, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Richard Salcido, MD, Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society
Disclosure: Nothing to disclose.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
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