Bladder Managment for Adults with Spinal Cord Injury - 14

BLADDER MANAGEMENT FOR ADULTS WITH SPINAL CORD INJURY

the bulk of the fibers found at the membranous urethra, but fibers also run up to the bladder neck. In females, striated skeletal muscle fibers circle the upper two-thirds of the urethra. In non-SCI individuals, it is under voluntary control. Changes frequently occur after SCI. In those with SCI, the distinction between the internal and external sphincter becomes less clear. There may be substantial invasion of the alpha-adrenergic nerve fibers in the smooth and striated muscle in the urethra of individuals with SCI with lower motor neuron lesions. Moreover, those with SCI frequently do not have control of their external sphincter. If the sphincter does not relax when the bladder is relaxing (detrusor sphincter dyssynergia), high pressures often build in the bladder, which can affect kidney drainage. In those with sacral injuries, there may be less ability of the sphincter to contract, allowing urinary incontinence to occur. This will be discussed further when discussing the various types of SCI.

N e u ro a n a t o m y o f t h e L o w e r U r i n a r y Tr a c t
Bladder storage and emptying is a function of interactions among the peripheral parasympathetic, sympathetic, and somatic innervation of the lower urinary tract. Additionally, there is modulation from the central nervous system. The parasympathetic efferent (motor) supply originates from the sacral cord at S2–S4. Sacral efferents travel via the pelvic nerves to provide excitatory input to the bladder. Parasympathetic bladder receptors are called cholinergic because the primary postganglionic neurotransmitter is acetylcholine. These receptors are distributed throughout the bladder. Stimulation causes a bladder contraction. The sympathetic efferent nerve supply to the bladder and urethra begins in the intermediolateral gray column from T11 through L2 and provides inhibitory input to the bladder. Sympathetic impulses travel a relatively short distance to the lumbar sympathetic paravertebral (sympathetic) ganglia. From here the sympathetic impulses travel over long postganglionic fibers in the hypogastric nerves to synapse at alpha- and beta-adrenergic receptors within the bladder and urethra. The primary postganglionic neurotransmitter for the sympathetic system is norepinephrine. Sympathetic efferent stimulation facilitates bladder storage. This is because of the strategic location of the adrenergic receptors. Beta-adrenergic receptors predominate in the superior portion (i.e., body) of the bladder. Stimulation of betareceptors causes smooth muscle relaxation so the bladder wall relaxes. Alpha-receptors have a higher

density near the base of the bladder and prostatic urethra; stimulation of these receptors causes smooth muscle contractions of the sphincter and prostate, which increases the outlet resistance of the bladder and prostatic urethra. After SCI, changes in receptor location, density, and sensitivity may occur. Evidence exists that there is invasion of alpha-receptors into the external striated sphincter so that it responds to alpha stimulation. Moreover, when smooth muscle is denervated, its sensitivity to a given amount of neurotransmitter increases (i.e., denervation supersensitivity). As a result, smaller doses of various pharmacologic agents would be expected to have a much more pronounced effect in those with SCI as compared to those with nonneurogenic bladders. Recently scientists have been gaining a better understanding of the afferent (sensory) system of the bladder. The most important afferents pass to the sacral cord via the pelvic nerves. These afferents are of two types: small myelinated A-delta and unmyelinated (C) fibers. The small myelinated Adelta fibers respond in a graded fashion to bladder distention and are essential for normal voiding. The unmyelinated (C) fibers have been termed “silent C-fibers” because they do not respond to bladder distention and therefore are not essential for normal voiding. These “silent C-fibers” exhibit spontaneous firing when they are activated by chemical or cold temperature irritation at the bladder wall. These unmyelinated (C) fibers have been found to “wake up” and respond to distention and to stimulate uninhibited (involuntary) bladder contractions in animals with suprasacral SCI. This has been further confirmed in studies with two C-fiber neurotoxins, capsaicin and resiniferous (RTX) toxin. Both of these experimental agents dramatically block uninhibited bladder contractions. Further work is being done on their potential for clinical use.

Vo i d i n g C e n t e r s
Facilitation and inhibition of voiding is under three main centers, the sacral micturition center, the pontine micturition center, and the higher centers (cerebral cortex). The sacral micturition center (S2–S4) is primarily a reflex center in which efferent parasympathetic impulses to the bladder cause a bladder contraction, and afferent impulses to the sacral micturition center provide feedback regarding bladder fullness. The pontine micturition center is primarily responsible for coordinating relaxation of the urinary sphincter when the bladder contracts. Suprasacral SCI disrupts the signals from the pontine micturition center, which is why detrusor

Bladder Managment for Adults with Spinal Cord Injury

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