The intent of this chapter is to review the current guidelines for the management of neurogenic bladder dysfunction. For an in-depth review of the anatomy and pathophysiology of the genitourinary system, please see Chapter 5. For a review of common medications used in the treatment of neurogenic bladder and bowel, please see Chapter 55.
The lower urinary tract has two main functions, storage and periodic elimination of urine, which are mediated by a central nervous system (CNS) and the spinal cord. Intracerebral and intrathecal injections of the drugs indicate that the micturition reflex pathways may pass through multiple relay stations in the brainstem and be modulated by inputs from various centers in the brain.1 The cholinergic agonists are known to act on centers in pons and medulla to facilitate micturition. Cortical and pontine regions that modulate voiding include the pontine micturition center (PMC), periaqueductal gray (PAG), thalamus, insula, anterior cingulate gyrus, and prefrontal cortices. The PMC and the PAG are thought to play a key role in the supraspinal control of continence and voiding.2 The anterior cingulate gyrus and insula possibly process autonomic arousal, visceral storage, and sensation.3 Several neurotransmitters including gamma-aminobutyric acid (GABA), opioids, peptides, and glutamic acid appear to have a role in the central pathways controlling micturition. The frontal cortex is crucial for decision making for micturition in an emotional and social context. The influence of these centers on the PMC is mediated primarily via the PAG, which also integrates bladder sensory information, thereby moderating coordinated voiding and storage of urine. CNS lesions below the PMC are associated with detrusor sphincter dyssenergia (Fig. 51–1). Intracranial lesions (e.g., head injuries, dementia, and tumors) and other conditions such as parkinsonism are usually associated with detrusor hyperreflexia. Possible causes of urge incontinence include dysfunction of the prefrontal cortex or limbic system.2
Neural control of the pelvic organ is through somatic and autonomic nervous systems and is well integrated via lumber sacral reflexes (see Fig. 51–1). Central representation of bladder and colon has been demonstrated by dual transsynaptic tracing in the rat.3 These analyses have demonstrated that Barrington’s nucleus (three neuronal populations) is synaptically linked to both the bladder and the bowel.
These anatomic substrates underlie the central coordination of bladder and colon function and play a role in disorders characterized by a coexistence of bladder and colonic symptoms. Dysfunctions in this circuit may underlie the coexistence of colon and bladder symptoms observed in functional bowel disorders.
Parasympathetic motor innervations to the bladder wall and rectosigmoid are through the sacral 2, 3, and 4 (S2, S3, and S4) nerve roots. The third sacral nerve root is the predominant one for bladder motor innervation, and the cell bodies are located in the bladder wall. This is the reason that the bladder does not become atonic due to spinal cord injury unless there is serious damage to the conus and/or overdistension of the bladder wall. Possible etiologies of bladder overdistension include repeated infections resulting in fibrosis of the bladder wall. The detrusor musculature is also innervated with beta-adrenergic agonists for compliance (similar innervations are seen to the rectal and bronchial musculatures). The bladder neck has sympathetic alpha-adrenergic innervation (T12–L1). In males, there is heavier innervation than in females and higher receptor density (Fig. 51–2) to prevent retrograde ejaculation; the bladder neck behaves like an arteriole, responding to all the drugs that affect arterioles.
Neurogenic bladder dysfunction has a wide spectrum of presentations that includes urinary incontinence, urinary retention, suprapubic or pelvic pain, incomplete voiding, paroxysmal hypertension with diaphoresis (autonomic dysreflexia), recurrent urinary tract infections, and occult deterioration of renal function. The symptoms vary according to the level of injury and pathophysiologic basis of the neurologic disorder. Poor bladder drainage, high intravesicular pressures, and repeated urinary tract infections lead to upper tract damage.
It is important to evaluate level of physical disability and the capability to use the upper and lower extremities. Assessments of the strength and dexterity of the upper extremities and tone and reflexes of the lower extremities are helpful in strategizing rehabilitation goals. Neurourologic examination in incomplete tetraplegics with intact perianal sensation, positive anal sphincter voluntary contraction, and intact perianal sensation indicates an incomplete central spinal cord lesion.4 The genitalia are examined for the condition of the penis: whether it is circumcised, its size, and the condition of the skin. Critical to the examination is to discriminate between a lower motor neuron and upper motor neuron bladder (Table 51–1).
| LMN Bladder | UMN Bladder | |
| Urinary problem | Failure to empty | Failure to store |
| Causesa |
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| Lesion location |
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| Clinical presentation |
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| Treatment |
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Patients (particularly females) with long-term indwelling catheters that hang freely may have urethral sphincter and meatal damage with leakage of urine around the catheter. It is therefore important to tape the catheter in the suprapubic region to prevent this complication. Pelvic examination in females will identify other factors leading to voiding dysfunction, such as uterine prolapsed, uterine masses, or tumors.
In men, anorectal examination is also important to document the size of the prostate and the presence of fecal impaction. A loaded rectum does impair bladder evacuation.
After general neurologic assessment, voluntary contraction of the anal sphincter indicates control over the perineal muscles. In quadriplegics, this indicates an incomplete central spinal cord type of lesion.4 The bulbocavernosus reflex should be tested, and its presence indicates an intact sacral reflex arc (S2, S3, and S4). The presence of a knee jerk reflects the status of the spinal cord at L2, L3, and L4, and hyperreflexia at the knee indicates increased tone at the pelvic diaphragm as well as detrusor sphincter dyssynergia. Absence of the toe plantar flexors reflects either damage to S2 or a supraconal lesion and therefore predicts damage to the external urinary sphincter and possible involvement of the bladder (see Fig. 51–2). The return of deep reflexes below the level of injury heralds the recovery from spinal shock.
Documentation of abdominal musculature tone, palpation of the colon for fecal masses, and palpation of the bladder indicate incomplete bladder and bowel evacuations. Postvoid residual urine in the bladder can be either estimated with ultrasound and/or confirmed with catheterization.
It is important to carefully evaluate bladder dysfunction. Supraconal lesions in the spinal cord lead to an upper motor neuron bladder (UPMN), resulting in a reflex bladder. UPMN bladder is suspected with increased knee jerks, positive ankle jerks, absent perianal sensation, and a positive bulbocavernous reflex. Cauda equina and conal lesions are usually associated with lower motor neuron bladder, which is accompanied by absent ankle jerks and absent bulbocavernous reflex. The bladder is areflexic and rarely atonic following severe conal lesions.
The acute phase usually lasts a few days to 3 to 4 weeks. The bladder is areflexic during this period, and adequate bladder drainage is necessary to prevent the areflexic bladder from getting overdistended. Bladder overdistension may lead to detrusor muscle damage and detrusor atonicity. Indwelling continuous Foley catheterization is helpful to ensure bladder drainage. After the initial phase of metabolic response and diuresis, intermittent catheterization may be performed to reduce urinary tract infections and stone disease. Depending on their general condition, whenever feasible, patients are trained to carry out self-catheterization every 4 to 6 hours. Frequency of catheterization is restricted to a maximum of five times in 24 hours and residual urine not greater than 500 mL each catherization.5
