Types of Neurogenic Bladders:

Supraspinal Lesions

Supraspinal lesions refer to those lesions of the central nervous system involving the area above the pons. They include cerebrovascular accident, brain tumor, Parkinson disease, and Shy-Drager syndrome.

Cerebrovascular accident

After a stroke, the brain may enter into a temporary acute cerebral shock phase. During this time, the urinary bladder will be in retention—detrusor areflexia. Almost 25% of affected individuals develop acute urinary retention after a stroke.

After the cerebral shock phase wears off, the bladder demonstrates detrusor hyperreflexia with coordinated urethral sphincter activity. This occurs because the PMC is released from the cerebral inhibitory center. When the patient manifests symptoms of detrusor hyperreflexia, the individual will complain of urinary frequency, urgency, and urge incontinence.

The treatment for the cerebral shock phase is indwelling Foley catheter or clean intermittent catheterization (CIC). When the bladder becomes hyperreflexic, institute therapies to facilitate bladder filling and storage with anticholinergic medications.

Brain tumor

Detrusor hyperreflexia with coordinated urethral sphincter is the most common observed urodynamic pattern associated with a brain tumor.

When the patient manifests symptoms of detrusor hyperreflexia, the individual complains of urinary frequency, urgency, and urge incontinence. First-line treatment for detrusor hyperreflexia includes anticholinergic medication.

Parkinson disease

This is a degenerative disorder of pigmented neurons of substantia nigra. It results in dopamine deficiency and increased cholinergic activity in the corpus striatum.

Patients with Parkinson disease manifest symptoms of bradykinesia, skeletal muscle tremor, cogwheel rigidity, and masked facies. Symptoms specific to the urinary bladder include urinary frequency, urgency, nocturia, and urge incontinence.

Typical urodynamic findings for Parkinson disease are most consistent with detrusor hyperreflexia and urethral sphincter bradykinesia. The striated urethral sphincter often demonstrates poorly sustained contraction.

Similar to other supraspinal lesions, the treatment for Parkinson disease is to facilitate bladder filling and promote urinary storage with anticholinergic agents.

If patients with Parkinson disease exhibit symptoms of bladder outlet obstruction (BOO) due to benign prostatic enlargement (BPE), the diagnosis of BOO should be confirmed by multichannel urodynamic studies. The most common cause of postprostatectomy incontinence in the patient with Parkinson disease is detrusor hyperreflexia.

If transurethral resection of the prostate (TURP) is performed without urodynamic confirmation of obstruction, the patient may become totally incontinent after the TURP procedure.

Shy-Drager syndrome

Shy-Drager syndrome is a rare, progressive, and degenerative disease affecting the ANS with multisystem organ atrophy. In addition to Parkinson-like symptoms, cerebellar ataxia and autonomic dysfunction are common. Affected individuals demonstrate orthostatic hypotension, anhidrosis, and urinary incontinence.

Degeneration of the nucleus of Onuf results in denervation of the external striated sphincter. Sympathetic nerve atrophy causes nonfunctional bladder and an open bladder neck.

Urodynamic evaluation often reveals detrusor hyperreflexia, although a few individuals may have detrusor areflexia or poorly sustained bladder contractions. Often, the bladder neck (internal sphincter) will be open at rest, with striated sphincter denervation.

The treatment for Shy-Drager syndrome is to facilitate urinary storage with anticholinergic agents coupled with CIC or indwelling catheter. Patients with Shy-Drager syndrome should avoid undergoing TURP because the risk of total incontinence is high.

Spinal Cord Lesions

Spinal cord injury

When an individual sustains a spinal cord injury from a diving accident or motor vehicle injury, the initial response from the nervous system is spinal shock. During this spinal shock phase, the affected individual experiences flaccid paralysis below the level of injury, and the somatic reflex activity is either depressed or absent.

The anal and bulbocavernosus reflex typically is absent. The autonomic activity is depressed, and the individual experiences urinary retention and constipation. Urodynamic findings are consistent with areflexic detrusor and rectum. The internal and external urethral sphincter activities, however, are normal.

The spinal shock phase typically lasts 6-12 weeks; it may be prolonged in some cases. During this time, the urinary bladder must be drained with CIC or indwelling urethral catheter.

When the spinal shock phase wears off, bladder function returns but the detrusor activity increases in reflex excitability to an overactive state—detrusor hyperreflexia. Depending on the level of the lesion, the individual may develop DSD-DH. Thus, the individual must be monitored for leaking between CIC, and periodic urodynamic testing must be performed for this alteration in detrusor behavior. During urodynamics, intravesical instillation of cold saline may indicate return of reflex activity or help better characterize the lesion.

Realizing that suprasacral lesions exhibit detrusor areflexia at initial insult but progress to hyperreflexic state over time is important. Conversely, sacral cord lesions are associated with areflexic bladders that may become hypertonic overtime.

Spinal cord lesions (above the sixth thoracic vertebrae)

Individuals who sustain a complete cord transection above the sixth thoracic vertebrae (T6) most often will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia. A unique complication of T6 injury is autonomic dysreflexia.

Autonomic dysreflexia is an exaggerated sympathetic response to any stimuli below the level of the lesion. This occurs most commonly with lesions of the cervical cord. Often, the inciting event is instrumentation of the urinary bladder or the rectum, causing visceral distention.

Symptoms of autonomic dysreflexia include sweating, headache, hypertension, and reflex bradycardia. Acute management of autonomic dysreflexia is to decompress the rectum or bladder. Decompression usually will reverse the effects of unopposed sympathetic outflow. If additional measures are required, parenteral ganglionic or adrenergic blocking agents, such as chlorpromazine, may be used.

Oral blocking agents, including terazosin, may be used for prophylactically treating patients with autonomic dysreflexia. Alternatively, spinal anesthetic may be used as a prophylactic measure whenever bladder instrumentation is considered.

Spinal cord lesions (below T6)

Individuals who sustain spinal cord lesions below T6 level will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia but no autonomic dysreflexia.

Neurologic evaluation will reveal skeletal muscle spasticity with hyperreflexic deep tendon reflexes. Affected patients will demonstrate extensor plantar response and positive Babinski sign.

These individuals will experience incomplete bladder emptying secondary to detrusor sphincter dyssynergia, or loss of facilitatory input from higher centers. Cornerstone of treatment involves CIC and anticholinergic medications.

Multiple sclerosis

MS is caused by focal demyelinating lesions of the central nervous system. It most commonly involves the posterior and lateral columns of the cervical spinal cord. Usually, poor correlation exists between the clinical symptoms and urodynamic findings. Thus, using urodynamic studies to evaluate patients with MS is critical.

The most common urodynamic finding is detrusor hyperreflexia, occurring in as many as 50-90% of patients with MS. As many as 50% of patients will demonstrate DSD-DH. Detrusor areflexia occurs in 20-30% of cases. The optimum therapy for a patient with MS and incontinence must be individualized and based on the urodynamic findings.

Peripheral Nerve Lesions

Peripheral nerve lesions due to diabetes mellitus, tabes dorsalis, herpes zoster, herniated lumbar disk disease, and radical pelvic surgery result in detrusor areflexia.

Diabetic cystopathy

Usually, neurogenic bladder dysfunction occurs 10 or more years after the onset of diabetes mellitus. Neurogenic bladder occurs because of autonomic and peripheral neuropathy. A metabolic derangement of the Schwann cell results in segmental demyelination and impaired nerve conduction.

The first symptoms of diabetic cystopathy are loss of sensation of bladder filling followed by loss of motor function. Classic urodynamic findings associated with this condition are elevated residual urine, decreased bladder sensation, impaired detrusor contractility, and, eventually, detrusor areflexia. Paradoxically, DHIC also has been observed. Treatment of diabetic cystopathy is CIC, long-term indwelling catheterization, or urinary diversion.

Tabes dorsalis (neurosyphilis)

In tabes dorsalis, central and peripheral nerve conduction is impaired. Affected patients experience decreased bladder sensation and increased voiding intervals.

The most common urodynamic finding associated with neurosyphilis is detrusor areflexia with normal sphincteric function.

Herpes zoster

Herpes zoster is a neuropathy associated with painful vesicular eruptions in the distribution of the affected nerve. The herpes virus lies dormant in the dorsal root ganglia or the sacral nerves.

Sacral nerve involvement leads to impairment of detrusor function. The early stages of herpes infection are associated with lower urinary tract symptoms of urinary frequency, urgency, and urge incontinence. Later stages include decreased bladder sensation, increased residual urine, and urinary retention. Urinary retention is self-limited and will resolve spontaneously with clearing of the herpes infection.

Herniated disc

Slow and progressive herniation of the lumbar disc may cause irritation of the sacral nerves and cause detrusor hyperreflexia. Conversely, acute compression of the sacral roots associated with deceleration trauma will prevent nerve conduction and result in detrusor areflexia.

A typical urodynamic finding of sacral nerve injury is detrusor areflexia with intact bladder sensation. Associated internal sphincter denervation may occur. If the peripheral sympathetic nerves are damaged, the internal sphincter will be open and nonfunctional. Peripheral sympathetic nerve damage often occurs in association with detrusor denervation. The striated sphincter, however, is preserved.

Pelvic surgery

Patients undergoing major pelvic surgery, such as radical hysterectomy, abdominoperineal resection, proctocolectomy, or total exenteration will experience bladder dysfunction postoperatively.

Most commonly, postsurgical patients will manifest symptoms of detrusor areflexia. However, as many as 80% of affected patients will experience spontaneous recovery of function within 6 months after surgery.

Treatment & Management: