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) facilitate the storage of urine in the bladder. 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 their stimulation relaxes the bladder wall. Conversely, the prevalence of alpha-adrenergic receptors is greater in the lower portion of the bladder including the sphincter and their stimulation increases bladder outlet resistance. In contrast, parasympathetic nerves are responsible for bladder contractions and emptying. The parasympathetic nerves originate from S2 to S4 and provide increased excitatory input to cholinergic (e.g., acetycholine) receptors in the bladder wall in response to bladder filling. In individuals with SCI lesions, these pathways may be interrupted leading to impairments in urine storage and emptying (Hanno 2001). Enhancing bladder storage, as discussed earlier in the chapter, involves relaxing the detrusor muscle thereby allowing for increased bladder volumes. Individuals with impaired bladder emptying have either a sphincter that fails to fully relax or alternatively weak or nonexistent detrusor muscle contractions; both of which compromise emptying. These individuals can be treated pharmacologically with oral alpha-adrenergic blockers or botulinum toxin (injected into the sphincter). Both interventions are intended to improve voiding by decreasing the resistance to outflow but may also increase incontinence; a point not highlighted in the studies presented below. However, in male individuals who already have incontinence and are using condom drainage, but have persistently elevated residuals, alpha blockers or botulinum toxin (injected into the sphincter) may improve emptying.