Pharmacological management of dysfunctional bladder emptying is based on understanding the neuroanatomy of the lower urinary tract. The normal coordinated effort of the lower urinary tract includes bladder storage and emptying. During the filling process, sympathetic adrenergic receptors (e.g., norepinephrine) are responsible for allowing the bladder to store urine. These efferent nerves originate from T11 to L2 and offer inhibitory input to the bladder. Beta-adrenergic receptors populate the smooth muscle of the bladder and stimulation causes bladder wall relaxation. Conversely, alpha-adrenergic receptors are denser in the lower portion of the bladder including the sphincter and stimulation results in increased bladder outlet resistance. The parasympathetic nerves originating from S2 to S4 supply the cholinergic (e.g., acetycholine) receptors that are responsible for bladder contraction as a result of increased excitatory feedback from filling. In individuals with SCI lesions, these pathways may be interrupted and this causes impairment in storing or impairment in emptying (Hanno, 2001).
Enhancing bladder storage, as discussed earlier in the chapter, involves relaxing the detrusor muscle and allowing for increased bladder volumes. Individuals with impairment of bladder emptying are those whose sphincter is unable to relax or who have weak or nonexistent detrusor muscle contractions, both causing failure to empty. These individuals can be treated pharmacologically with oral alpha adrenergic blockers and botulinum toxin (injected into the sphincter). Both interventions are intended to improve voiding but also may increase the tendency towards incontinence, a point not highlighted in the studies presented below. However, in those male patients who already have incontinence, and are using condom drainage, but have persistently elevated residuals, alpha blockers or botulinum toxin (injected into the sphincter) may result in more complete emptying.