Abstract
Normal bladder physiology is a complex system of receptor types and nervous system innervation. Regardless of the specific neurologic condition or injury, disruptions along many portions of the central or peripheral nervous systems will result in altered bladder functioning, known as a neurogenic bladder. This chapter describes that interplay between neurologic processes and bladder pathophysiology. The results of inadequately managed neurogenic bladder can have significant morbidity and even mortality. The neurogenic bladder must be adequately evaluated and managed to ensure a low bladder pressure environment that allows for controlled and complete bladder emptying. This chapter discusses that evaluation and management as well as the currently available medications, procedures, and technology to optimize short- and long-term outcomes for individuals with neurogenic bladder.
Keywords
Anticholinergic medications, autonomic dysreflexia, botulinum toxin, detrusor-sphincter dyssynergia, urodynamics, vesicoureteral reflux
| Synonyms | |
| |
| ICD-10 Codes | |
| G83.4 | Cauda equina syndrome with neurogenic bladder |
| N31.2 | Flaccid neuropathic bladder, atonic neuropathic bladder |
| N31.8 | Other neuromuscular dysfunction of bladder |
| N31.9 | Neuromuscular dysfunction of bladder, unspecified |
| N36.44 | Muscular disorders of urethra, bladder sphincter dyssynergy |
| N32.9 | Bladder disorder, unspecified |
| N32.89 | Other specified disorders of bladder |
Definition
The term neurogenic bladder describes a process of dysfunctional voiding as the result of neurologic impairment. In addition to possibly causing high bladder pressures with increased risk of vesicoureteral reflux, leading to adverse renal sequelae, this can interfere with urine storage at low bladder pressures, disrupt voluntary coordinated voiding, and lead to varying degrees of incontinence. Neurologic control of bladder function occurs at multiple levels throughout the central nervous system and is subject to multiple pathophysiologic processes. Consequently, voiding dysfunction is likely to occur in most patients with a neurologic impairment from a central nervous system disorder.
The micturition reflex center has been localized to the pontine mesencephalic reticular formation in the brainstem. Efferent axons from the pontine micturition center travel down the spinal cord in the reticulospinal tract to the detrusor motor nuclei located in the S2, S3, and S4 segments in the sacral gray matter (vertebral levels T12 to L2). Parasympathetic nerves take their origin from nuclei at the intermediolateral gray column of the spinal cord at S2, S3, and S4 and travel by the pelvic nerve and pelvic plexus to ganglia in the bladder wall. The predominant parasympathetic nerve root supplying the bladder is usually S3. Acetylcholine is released from the postganglionic nerves, which in turn excites muscarinic receptors.
Preganglionic sympathetic neurons originate in the intermediolateral gray column of the spinal cord from spinal segments T10 to L2. These nerves course to the sympathetic chain ganglion and through the pelvic plexus to the bladder neck and fundus of the bladder. Receptors at the bladder neck are primarily α-adrenergic, stimulation of which results in closure of the internal sphincter during urinary storage and, in men, during ejaculation as well. In contrast to the bladder neck, the fundus of the bladder is populated with β-adrenergic receptors, which contribute to bladder relaxation (and therefore urinary storage) during sympathetic activation.
The external urethral sphincter (voluntary striated muscle) surrounds the membranous urethra and extends up and around the distal part of the prostatic urethra. The pudendal nerves, which innervate the external sphincter, take their origin from the somatic motor nuclei in the anterior gray matter of the sacral cord (conus, S2-S4); however, it is the S2 spinal segment that provides the principal motor contribution. Toe plantar flexors also have S1 and S2 innervations. Thus, the preservation of toe plantar flexors after spinal cord injury (SCI) suggests that the external urethral sphincter is intact.
The central control of the bladder is a complex multilevel process. Advances in functional brain imaging have allowed research into this control in humans. The regions of the brain that have been implicated in the central control of continence include the pontine micturition center, periaqueductal gray, thalamus, insula, anterior cingulate gyrus, and prefrontal cortices. The pontine micturition center and the periaqueductal gray are thought to be crucial in the supraspinal control of continence and micturition. Higher centers, such as the insula, anterior cingulate gyrus, and prefrontal regions, are probably involved in the modulation of this control and cognition of bladder sensation. Further work should aim to examine how the regions interact to achieve urinary continence.
Symptoms
The symptoms of neurogenic bladder include urinary incontinence, urinary retention, suprapubic or pelvic pain, incomplete voiding, autonomic dysreflexia (paroxysmal hypertension with diaphoresis), recurrent urinary tract infections, and occult deterioration in renal function. The symptoms vary according to the level of SCI and pathophysiologic basis of the neurologic disorder.
Abnormalities in the midbrain (e.g., Parkinson disease) lead to detrusor hyperreflexia with frequent small volume voids and likely incontinence due to loss of dopamine. Lesions in segmental areas of the spinal cord lead to detrusor-sphincter dyssynergia (DSD), resulting in incomplete voiding, high bladder pressures, and vesicoureteral reflux. The elevated bladder pressures and vesicoureteral reflux may be clinically asymptomatic in its early stages, necessitating a high index of suspicion and urodynamic screening. Cortical lesions (lesions above the pontine micturition center) usually result in loss of voluntary inhibition of the micturition reflex. Lesions in the forebrain, such as cerebrovascular accidents with change in blood flow to the cingulate gyrus, can lead to hyperreflexic bladder, resulting in frequent small-volume voids and possible incontinence because of reduced dopamine D 1 with increased glutamate activity. Thus, the cingulate gyrus plays an important role in urine storage. Patients with Parkinson disease have less severe urinary dysfunction with little evidence of internal or external sphincter denervation. By contrast, in multiple system atrophy, patients have a wide-open bladder neck. The result is a hyperreflexic bladder with coordinated (synergic) sphincter function, typically resulting in complete bladder evacuation with some incontinence.
All lesions from the pons to spinal cord level S2 result in a loss of cortical inhibition and loss of coordinated sphincter activity during reflex voiding. The micturition reflex is without an inhibitory or coordinated control from higher centers. This results in a hyperreflexic bladder with dyssynergic sphincter function, which often results in incomplete voiding and high bladder pressures; it can lead to vesicoureteral reflux. Urinary retention from functional obstruction occurs, and overflow incontinence may occur with an overdistended bladder.
Spinal cord lesions in the conus at S2 or below result in lower motor neuron injury to the bladder and external sphincter. The predictable effect on the bladder is areflexia. Because the parasympathetic ganglia reside in or near the bladder wall, bladder tone is generally maintained. Bladder compliance therefore tends to decrease with time as a result of neural decentralization (or infection-related fibrosis). The result on the bladder neck and external sphincter is not as intuitive. An atonic synergic sphincter system might be expected; the external sphincter usually retains some fixed tone, although not under voluntary control; the bladder neck is often competent because of the intact sympathetic innervations (α-adrenergic activity), but is non-relaxing. Even though bladder pressures are generally low during filling and storage, obstructive physiology is often the case during voiding. Overflow incontinence is possible. A small, titrated dose of alpha blockers can maintain some continence and improve voiding.
In the acute phase of injury, most central nervous system lesions result in a temporarily areflexic bladder. This phase, termed central nervous system shock, is variable and can last several weeks. Reappearance of knee jerks heralds recovery from the shock phase. The specific patterns of voiding dysfunction with the most common neurologic abnormalities in the chronic phase are detailed in Table 138.1 and Fig. 138.1 .
| Neurologic Disorder | Detrusor Activity | Striated Sphincter | Comments |
|---|---|---|---|
| Suprapontine | Hyperreflexic | Synergic | |
| Brain tumor, cerebral palsy | Detrusor-sphincter dyssynergia may occur in those with spinal cord damage; voluntary control may be impaired | ||
| Cerebrovascular accident | Voluntary control may be impaired | ||
| Delayed central nervous system maturation | Persistence of uninhibited bladder beyond age 2–3 years; enuresis later | ||
| Dementia | Voluntary control is impaired | ||
| Parkinson disease | Detrusor contractility and voluntary control may be impaired | ||
| Pernicious anemia | Bladder compliance may be decreased | ||
| Shy-Drager syndrome | Bladder neck remains open; bladder compliance may be decreased; autonomic instability (low blood pressure) | ||
| Pons-S1 | Hyperreflexic | Dyssynergic | |
| Anterior spinal cord ischemia | Bladder compliance may be decreased | ||
| Multiple sclerosis | Varies with lesions | ||
| Myelodysplasia, trauma | Variable | ||
| Below S1 | Areflexic | Fixed tone | |
| Acute transverse myelitis | Bladder neck may be closed but nonrelaxing | ||
| Diabetes, Guillain-Barré syndrome, herniated intervertebral disc | Usually overdistended bladder | ||
| Myelodysplasia, poliomyelitis | Decreased bladder compliance may develop; bladder neck may be open (sympathetic denervation) | ||
| Radical pelvic surgery | Bladder neck is open | ||
| Tabes dorsalis, trauma | Bladder neck may be closed but nonrelaxing |
Confounding medical problems (e.g., diabetes) and many cardiovascular drugs ( Table 138.2 ) will profoundly affect bladder function. Patients who catheterize themselves intermittently should be asked about the size of catheter used and whether there is any resistance or trauma during catheterization that could indicate the presence of a urethral stricture. Patterns of voiding should be elicited, and changes in voiding habits should be scrutinized. Patients with suprasacral SCI, for example, often give a history of intermittent stream coinciding with spasticity of their lower extremities, a strong clue to DSD. Spinal cord-injured patients with incomplete lesions can void with excessive Valsalva maneuver and can produce very high intra-abdominal pressures. This can lead to vesicoureteral reflux, upper tract changes, repeated pyelonephritis, and even bladder and kidney stone disease. They need to be monitored frequently with urodynamics and managed appropriately to achieve low-pressure voiding. Approximately 50% of men ultimately have benign prostatic hyperplasia. Thus, even in the case of stable neurologic disease, these men may develop difficulty in voiding from progressive outflow obstruction. Typical symptoms include nocturia, decreased force of stream, hesitancy, and postvoid dribbling. However, patients with outflow obstruction frequently have irritative voiding symptoms as well. It is important to make sure that these symptoms (back pain, suprapubic pain, fever, dysuria, urgency, frequency, or hematuria) are not due to symptomatic infection. These symptoms are not specific and can reflect many of the processes discussed. Their presence must therefore be interpreted according to context.
| Drug | Indication | Mechanism | Side Effects and Cautions |
|---|---|---|---|
| Cholinergics Bethanechol | Areflexic bladder | Muscarinic receptor agonists Bladder has M 2 and M 3 receptors; M 3 receptors are responsible for normal detrusor contraction | Bronchospasm, miosis |
Anticholinergics
| Hyperreflexic bladder | Muscarinic receptor antagonists | Constipation, dry mouth, tachycardia |
| Adrenergic Mirabegron | Hyperreflexic bladder | β 3 adrenergic receptor agonist | Hypertension, urinary retention, dizziness |
Sympathomimetics
| Open bladder neck | α-Receptor antagonists | Arrhythmia, hypertension, coronary vasospasm, excitability, tremors |
Antiadrenergics (alpha blockers)
| Smooth sphincter dyssynergia (competent, nonrelaxing bladder neck) | α-Receptor agonists | Orthostatic hypotension, dizziness, rhinitis, retrograde ejaculation |
Tricyclic antidepressants
| Hyperreflexic bladder with stress incontinence | Anticholinergic and sympathomimetic properties | Myocardial infarction, tachycardia, stroke, seizures, blood dyscrasias, dry mouth, drowsiness, constipation, blurred vision |
Benzodiazepines
| Extremity spasticity with detrusor-sphincter dyssynergia | γ-Aminobutyric acid (GABA) channel activator, centrally acting muscle relaxant | Dizziness, drowsiness, extrapyramidal effects, ataxia, agranulocytosis |
| Baclofen | Extremity spasticity with detrusor-sphincter dyssynergia | GABA B channel activator (?); exact mechanism unknown; centrally acting muscle relaxant | Central nervous system depression, cardiovascular collapse, respiratory failure, seizures, dizziness, weakness, hypotonia, constipation, blurred vision a |
| Dantrolene | Extremity spasticity with detrusor-sphincter dyssynergia | Direct muscle relaxant by calcium sequestration in the sarcoplasmic reticulum | Hepatic dysfunction, seizures, pleural effusion, incoordination, dizziness, nausea, vomiting, abdominal pain |
| Botulinum toxin | Detrusor-sphincter dyssynergia | Inhibits release of acetylcholine | Repeated injections necessary |
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