Neurogenic bladder (NGB) affects many adults in the United States and is commonly caused by multiple sclerosis (MS), spinal cord injury (SCI), cerebral vascular accident, and Parkinson’s disease.
Many of these patients have bothersome urinary symptoms, including urinary incontinence (UI), urinary frequency, and urgency. The primary urodynamic finding for most patients with NGB is an uninhibited bladder contraction, or neurogenic detrusor overactivity (NDO).
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Bladder disorders have been reported in 40% to 90% of patients with MS and in 37% to 72% of patients with Parkinson’s disease, with a higher rate of UI in patients with cerebral vascular accident and Parkinson’s disease than in the general population.1
In addition to their physical burden, urinary symptoms such as incontinence can significantly impair quality of life.2 The occurrence of urinary tract infections (UTIs) in the NDO population is common.3 UI also increases the risk for skin irritation and breakdown as well as depression.4,5 In some cases, NGB can lead to a higher risk for renal complications.
Pathophysiology and etiology
The two main functions of the bladder are storage and voiding, and a normal cycle depends on coordination between the bladder and the urethral sphincter.6 Normal micturition involves autonomic and somatic pathways from the lumbosacral spine to the urethral outlet, bladder neck, and detrusor muscle—and a change in any of these can produce symptoms of NGB.7 Furthermore, an alteration in bladder wall innervation, or of the pelvic floor and urethra, can trigger overactivity.
Neurologic disorders often damage and disrupt the central or peripheral pathways involved in the central control of the lower urinary tract.8 Damage to areas of the nervous system may result in detrusor overactivity, with or without detrusor-sphincter dyssynergia, detrusor underactivity, detrusor areflexia, and impaired contractility.
The causes of neurologic conditions leading to NGB include supraspinal, spinal, peripheral, or mixed.8
Supraspinal disorders involve central nervous system lesions that occur above the pontine micturition center. They include conditions such as Parkinson’s disease, Shy-Drager Syndrome, cerebral palsy, frontal lobe lesions, stroke, cerebral trauma,8 and MS. Bladder dysfunction at this level usually presents as neurogenic detrusor overactivity combined with synergistic activity between the bladder and sphincter (i.e., when the bladder contracts, the sphincter appropriately relaxes).
Suprasacral spinal neurologic conditions include SCI, spinal stenosis, spinal cord infarction, MS, transverse myelitis, cervical spondylosis, and intervertebral disk disease.8
Patients with complete cord transections above the level of the sacrum generally present with NDO and striated sphincter dyssynergia (i.e., when the bladder contracts, the external sphincter inappropriately contracts at the same time).6 Detrusor external sphincter dyssynergia (DESD) is associated with a high risk for other urologic complications such as hydronephrosis, vesicourethral reflux, urosepsis, and urolithiasis.8 In addition, patients with lesions at T6 and higher are also at risk for symptoms of autonomic dysreflexia.
Lesions in the sacral spinal cord, including those in patients with spina bifida, diabetes mellitus, herpes zoster, and herniated lumbar disk disease, often lead to an acontractile detrusor.8 In addition, poor bladder compliance can be seen, which places the patients at risk for upper urinary tract damage if bladder storage pressures are too high. These patients are at risk for poor sphincteric activity as well. Among patients with peripheral nerve lesions caused by diabetes mellitus, herpes zoster, and herniated lumbar disk disease, bladder dysfunction generally manifests as detrusor areflexia.6
It is important to realize that there are a great many exceptions to these general patient categorizations. Neurologic lesions can often be incomplete or span multiple levels; thus, each patient benefits from a complete and thorough neurourologic evaluation.
