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The reflex voiding center lies in the sacral spinal cord at the S2-S4 levels. Neurons in the intermediolateral cell column supply parasympathetic excitatory input to the detrusor muscle via the pelvic nerves and plexuses. These fibers synapse in ganglia near or within the bladder wall. Afferent inputs are also transmitted via the pelvic nerves mainly through the S2-S3 roots. Sensations of proprioception (distention), pain, and temperature are conveyed by these fibers, which give rise to the sensation of the desire to void, are carried by the spinothalamic tracts as well as the posterior columns.

Sympathetic input to the bladder arises from the T11-L4 sympathetic centers of the spinal cord and travels via the hypogastric nerves. Sympathetic activation causes the detrusor muscle to relax, blocks parasympathetic transmission at the pelvic ganglia, and promotes an increase in urethral sphincter tone as the bladder fills. The sympathetic supply to the urethral sphincter also prevents retrograde ejaculation. The striated muscles of the urethra and pelvic floor (e.g. urogenital diaphragm and levator ani muscles), comprising the external urinary sphincter, receive somatic input from anterior horn cells in the S2-S4 segments via the pudendal nerves. These same nerves also contain afferent fibers that play a role in the "guarding reflex". Voiding normally can be voluntarily interrupted by the contraction of the external sphincter.

The act of voluntary voiding is initiated at higher levels through a complex interplay of influences from the inhibitory and excitatory micturition centers. Most important are the pontine micturition center in the reticular formation, which may be involved in a long-loop reflex during normal voiding, and the paracentral lobule and anterior central gyrus of the frontal lobe. Descending influences are carried mainly by the lateral reticulospinal tracts lying near the cortiospinal tracts.

The primary symptoms of a neurogenic bladder are urinary incontinence, residual urine after voiding, inability to sense the need to void, and urinary tract infection. The last is a consequence of incomplete bladder emptying. In the later stages or a neurogenic bladder, repeated infection and fibrosis of the bladder wall cause a chronically contracted bladder with a markedly decreased capacity. In addition, ureteral and kidney function may ultimately be compromised because of high bladder pressures that interfere with normal ureteral filling as well as infection.

The anatomical level of the lesion causing a neurogenic bladder can be diagnosed fairly precisely on the basis of the concomitant neurological finding, the EMG of the pelvic floor muscles or anal sphincter, and the results of cystometry. Cystometry is a method of measuring bladder pressure-volume relationships during filling and voiding after the gradual instillation of carbon dioxide or water into the bladder through a catheter. During this procedure, the volume at the first desire to void, the total bladder capacity, the presence of uninhibited contractions, the completeness of bladder emptying, the ability to voluntarily interrupt voiding, and the response to parasympathomimetic drugs such as bethanechol chloride (Urecholine) can all be determined. Cineflouroscopic studies can yield additional information concerning the status of the bladder and urethra during voiding. Once the type of neurogenic bladder is known, treatment can be planned and an ultimate prognosis made.

An uninhibited neurogenic bladder occurs in patients whose cortical control over the sacral reflex voiding centers is impaired. Cystometry reveals uninhibited detrusor contractions, and these patients are unaware of bladder filling until detrusor contraction has already begun. They exhibit urgency incontinence, and the prevention of incontinence depends on the intactness of the guarding reflex employing the external sphincter. Because of the relative outlet obstruction, urinary infection is common. The vesicourethral control in these patients is essentially the same as that in young children or infants before bladder control is established. This form of neurogenic bladder is most common in patients suffering from the dementia of Alzheimer’s disease. It may also be seen in patients with cerebral infarction, multiple sclerosis, Parkinson’s disease, falx meningioma, or normal-pressure hydrocephalus. Anticholinergic agents such as propanthelene bromide may lessen the incontinence but can also worsen the mental status in demented patients. Condom catheters are often used in men.

The reflex neurogenic bladder occurs when both sensory and motor bladder pathways in the spinal cord are interrupted above the sacral segments. Bladder sensation is absent in the presence of lesions above the lower thoracic cord. The detrusor shows uninhibited contractions and the external sphincter may relax either in a physiological fashion, leading to incontinence, or it may relax incompletely and produce bladder-external sphincter dyssynergia. This leads to increased residual urine, which then increases the risk of infection and eventually brings about upper urinary tract deterioration. Multiple sclerosis and spinal cord trauma are the most common disorders associated with this form of bladder dysfunction.

Management strategies in patients with a reflex neurogenic bladder are aimed at reducing the detrusor hyperactivity through the use of anticholinergic agents such as propantheline bromide or smooth muscle relaxants; in extreme cases, sacral rhizotomy may be called for. When necessary, the external sphincter hyperactivity can be treated either pharmacologically (less effective) or by sphincterotomy. In many cases, intermittent self-catheterization is necessary to overcome the outlet obstruction. In cases where this is impractical, a permanent indwelling catheter may need to be installed or a urinary diversionary procedure performed.

Lesions in the sacral spinal cord causing denervation of the detrusor muscle and failure of detrusor contraction are responsible for causing the autonomous neurogenic bladder. If some degree of sphincter function is retained, continence may be preserved. Overflow incontinence is common seen and bladder sensation is absent in these patients. This form of bladder may occur in the context of lower spinal cord trauma, tumor, meningomyelocele, or multiple sclerosis. To deal with the incontinence, voiding can be done according to a fixed schedule using the Crede’ maneuver (voluntary lower abdominal pressure), but intermittent self-catheterization, which also removes residual urine, is usually the best solution.

Patients with tabes dorsalis or diabeter mellitus may have problems with a "sensory paralytic bladder", consisting of a large capacity, delayed desire to void, and increased residual urine. A "motor paralytic bladder" can occur when there is selective involvement of efferents to the bladder or their motor neurons such as in poliomyelitis or Guillain-Barre’ syndrome. In these pathological states, the bladder is atonic with an enlarged capacity, and there is residual urine but bladder sensation is intact. In many cases of a neurogenic bladder, there are combined lesions that affect both the upper and lower motor neuron supply to the bladder or that involve combinations of peripheral sensorimotor supply as well as the sacral spinal cord.