The workup of UI begins with a detailed history as well as a complete physical examination. Urodynamics (UDS) is an adjunctive tool designed to dynamically evaluate bladder and/or urethral function. Using objective parameters, the test attempts to reproduce the patient’s bothersome voiding or incontinence symptoms. UDS is most commonly indicated for evaluation of various types of lower urinary tract symptoms (frequency, urgency, incontinence, etc.) collectively known as voiding dysfunction.3 The test should document: first sensation, first urgency, strong desire to void, bladder capacity, uninhibited detrusor contractions, bladder compliance, detrusor pressure, and valsalva leak point pressure measurements (vLPP). UDS ought to be performed on patients who do not respond to initial therapy and potential future candidates for a surgical incontinence procedure. Other indications are patients with neurological disease, prior failed incontinence surgery, prior radical pelvic surgery or radiation, and refractory urge incontinence.

• Behavioral modification (timed voiding to prevent urinary leakage with progressive lengthening of intervals between voiding)
• Dietary modification (avoidance of caffeine, spicy foods, highly acidic fruit juices, vegetables, carbonated beverages, and alcohol)
• Biofeedback
• Medication (antimuscarinics)
• Neuromodulation (Interstim® Uroplasty®)

• Non-surgical treatments (kegels, biofeedback, pelvic floor rehabilitation)
• Injectable medications (i.e. collagen, Durasphere,® Coaptite®)
• Oral medications (Imipramine)
• Minimally Invasive procedures (i.e. bladder neck slings, TVT,® Transobturator tape procedures, TVT Secure,® or other midurethral slings)
• Colposuspensions /Urethropexy

the three symptoms of Overactive bladder (OAB) usually, but not always results in UI. It is estimated that between 17–33 million Americans suffer from this condition (Figure 1). associated with OAB include: frequency (more than 8 times/24 hrs.), urgency (uncontrollable need to urinate), and urge incontinence (strong need to urinate followed by leaking or involuntary and complete voiding). Both men and women with OAB often experience urgency at inconvenient and unpredictable times. It interferes with daily routines, intimacy, and sexual function. Also it may cause embarrassment and diminish self-esteem.

In a 2004 survey by the Simon Foundation For Continence, 60% percent of women stated that OAB affects their quality of life. Additionally, 30% of women waited two years to speak with a physician about their bladder problem and 42 stated medication didn’t help their symptoms.1 Therein lies the dilemma with a reported 80%medication drop-out rate after 12 months. To improve patient compliance, the goal of therapy ought to include efficacy, tolerability, low adverse event profile, and ease of therapy. Most commonly the cause of OAB is detrusor overactivity; identified on UDS as uninhibited detrusor contractions (UDC) and sometimes a small capacity bladder. UDCs are graphically represented by a spike in the PVES lead, but not in the PABD lead. A basic understanding of micturition is necessary prior to instituting treatment, especially when dealing with rare, and/or more serious conditions (Figure 2). These may include: nerve damage caused by abdominal/pelvic trauma, prior surgery, bladder calculi, drug side effects, and neurological disease (e.g., Multiple Sclerosis, Parkinson’s disease, stroke, spinal cord lesions). When a centrally acting etiology of OAB is suspected, the condition is termed "Neurogenic Detruso Overactivity." In an otherwise healthy individual without neurological disease, the terminology is "Idiopathic Detrusor Overactivity."

Conservative measures can significantly improve the symptoms of an overactive bladder. Behavioral therapies in conjunction with dietary modification are used as first line treatment. Second line therapy involves blocking Acetylcholine (Ach), the primary neurotransmitter of bladder contraction (Figure 3).  Via the oral or transdermal route, the antimuscarinic medication class is the mainstay of pharmacological therapy for OAB in the United States. Commonly prescribed oral therapies are: darafenacin (Enablex®), oxybutynin chloride (Ditropan XL®), tolterodine (Detrol LA®), trospium chloride (Sanctura®), and solifenacin (Vesicare®). They relax the smooth muscle of the bladder via M2/M3 receptor inhibition; thereby reducing bladder contractility (Figure 4).

Other modalities that can be used in the treatment of OAB are: biofeedback, pelvic floor rehabilitation, tibial nerve stimulation (Uroplasty®), and neuromodulation (Inter-Stim® therapy). The latter is a minimally invasive procedure delivering minute electrical stimulation to the S3 pelvic nerve. After a successful two-week test phase, a small generator (43mm x 51mm x 7.5mm) is placed subdermally in the supra-luteal region. Many patients with OAB, UI, and interstitial cystitis/bladder pain syndrome have been successfully relieved of their symptoms with neuromodulation. Other considerations for UDS testing is treatment of complex neurologic cases. One such example is Multiple Sclerosis (MS). Up to 90% of people with MS during their lifetime will be affected somehow by bladder dysfunction.2 There is disruption of normal processes, and interference with the transmission of signals between the brain and urinary system.4 Urination becomes less controlled and the urge to urinate becomes a reflex response to the frequent, repeated spinal cord signals. Alternatively, emptying dysfunction results as the bladder fills with urine and the spinal cord is unable to send the appropriate message to the brain (to signal the need to void) or to the external sphincter (to signal the need to relax).4

Not uncommonly, MS patients suffer from a severe form of OAB: Neurogenic Detrusor Overactivity. Conversely, Detrusor Hyperreflexia, sphincter dyssynergia (DSD) is a potentially serious situation where the bladder contracts against a closed sphincter; occurring in approximately 25% of patients. If formal video urodynamics are not available to visualize DSD, than multichannel office urodynamics may demonstrate persistent high amplitude EMG signal during the voiding phase. As represented by the EMG lead, the pelvic floor doesn’t "relax" and patients complain of symptoms of urgency with voiding difficulties and sometimes require "straining" to void. High detrusor pressures are transmitted retrograde to the collecting system risking upper tract damage. During an autopsy review in 1964, 55%of MS deaths were due to complications of hydronephrosis or pyelonephritis.5 However, in a study approximately 30 years later, only of 5% deaths were associated with urinary tract pathology.6 Some of the reasons for this change in urinary tract morbidity may be fromimproved diagnosticmethodology, clean intermittent catheterization (CIC), and the use of anti-cholinergic medication to reduce upper tract deleterious pressures.7 Upper urinary tract complications such as hydronephrosis, renal insufficiency, or renal failure have been reported in 15 to 20 percent of MS patients with bladder dysfunction.8 (Table 1)

8. Staskin DR, Hydroureteronephrosis after spinal cord injury. Urol Clin North Am 1991: 18(2):309–325.

Jeffrey Schock, DO, FACOS, is Vice Chairman, Dept. of Urology, Botsford General Hospital and Clinical Assistant Professor, Dept. of Surgical Specialties, Mich. State University