Definition

The term neurogenic bladder describes a process of dysfunctional voiding as the result of neurologic impairment. 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 is at multiple levels throughout the central nervous system and subject to multiple pathophysiologic processes. Voiding dysfunction occurs in most of the neurologically impaired patients [1].

The micturition reflex center has been localized to the pontine mesencephalic reticular formation in the brainstem [2,3]. 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 [4,5].

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 [6], 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 (striated muscle, voluntary) 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 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 [7].

Symptoms

The symptoms of neurogenic bladder have a wide spectrum of presentation and include urinary incontinence, urinary retention, suprapubic or pelvic pain, incomplete voiding, paroxysmal hypertension with diaphoresis (autonomic dysreflexia), recurrent urinary tract infections, and occult deterioration in renal function. The symptoms vary according to the level of spinal cord injury and pathophysiologic basis of the neurologic disorder.

Abnormalities in the midbrain (e.g., Parkinson disease) lead to detrusor hyperreflexia due to loss of dopamine. Lesions in segmental areas of the spinal cord lead to detrusor-sphincter dyssynergia (DSD). 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 because of reduced dopamine D₁ 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 more symptoms and wide-open bladder neck. The result is a hyperreflexic bladder with coordinated (synergic) sphincter function [8,9]. In the absence of outflow obstruction (e.g., urethral stricture, benign prostatic hyperplasia, large uterine leiomyoma, fecal impaction), complete bladder evacuation with some incontinence is the outcome. The findings of postmicturition residuals of more than 100 mL, detrusor–external sphincter dyssynergia, and open bladder neck at the start of bladder filling, with significant postural hypotension and neurogenic sphincter motor unit potentials, are highly suggestive of multiple system atrophy [8,9]. It seems DSD reported in such patients may be a voluntary contraction of external sphincter to avoid leakage and is therefore not true DSD. The patient can have unstable blood pressure, which is aggravated with a postural change, indicating some degree of autonomic failure. Similarly, after a severe head injury, an autonomic failure can result in unstable postural hypotension and wide-open bladder neck. The insula and anterior cingulate seem to be responsible for the modulation of autonomic function [10].

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 above T5-T6 result in autonomic dysreflexia above the key level (T5-T8) that innervates the splanchnic bed and regulates blood supply to control blood pressure. Accentuated visceral activity (e.g., full bladder, fecal impaction), which causes sympathetically mediated vasoconstriction, is normally inhibited by secondary output (a negative feedback) from the medulla and is countered by vasodilation in the splanchnic bed through the greater splanchnic nerve. Without the proper inhibitory reflexes or control of the splanchnic bed to redistribute circulating blood volume, blood pressure rises sharply. With the carotid bodies and vagal nerves intact, bradycardia results. The full syndrome is characterized by paroxysmal and extreme elevation in blood pressure, facial flushing, perspiration, goose pimples, headache, and some degree of bradycardia. This is virtually always seen in conjunction with detrusor-sphincter dyssynergia [11].

Spinal cord lesions in the conus at S2 or below result in lower motor neuron injury to the bladder and external sphincter. The effect on the bladder is predictable: 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) [1,12]. 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; and the bladder neck is often competent because of the intact sympathetic innervations (α-adrenergic activity) but is nonrelaxing. Even though bladder pressures are generally low during filling and storage, obstructive physiology is often the case during voiding [1,13]. 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 [14,15]. 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 137.1 and Figure 137.1.

Confounding medical problems, such as diabetes and many cardiovascular drugs (Table 137.2), 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—clues to the presence of a urethral stricture. Patterns of voiding should be elicited, and changes in voiding habits should be scrutinized. Patients with suprasacral spinal cord injury, for example, often give a history of intermittent stream coinciding with spasticity of their lower extremities, a strong clue to detrusor-sphincter dyssynergia. 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 therefore 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 are not due to symptomatic infection: back pain, suprapubic pain, fever, dysuria, urgency, frequency, or hematuria. These symptoms are not specific and can reflect many of the processes discussed. Their presence must therefore be interpreted according to context.

Physical Examination

General considerations include the level of disability and the capability to use upper and lower extremities. The neurologic examination focuses on the strength and dexterity of the upper extremities and the tone and reflexes of the lower extremities. Neurourologic examination includes perianal sensation for evidence of sacral sparing, anal sphincter voluntary contraction, and bulbocavernosus reflex.