The mechanism of urinary incontinence after RP is complex. Most authors agree that sphincter deficiency may be the predominant factor in incontinence but the precise role of the external striated sphincter and that of the intrinsic sphincter are under debate. Many urodynamic studies, including the measurement of the maximal urethral closing pressure (MUCP) have led to conflicting results. The MUCP, measured with or without voluntary contraction of the sphincter, reflects the effectiveness of the sphincter mechanism. Based on studies of the MUCP, some authors indicated the role of extrinsic sphincter deficiency as the prime determining factor of in postoperative incontinence [5,6]. For example, Kleinhans et al. noted a significant decrease in MUCP at voluntary sphincter contraction, from 137.7 to 90.7 cmH2O in patients complaining of urinary leakage after RP, and concluded that the incontinence was a result of external striated sphincter deficiency. However, others found no correlation between postoperative stress incontinence and MUCP measured at the level of the membranous urethra, and suggested that urinary control did not depend on the extrinsic sphincter . In reality, it is probable that both extrinsic and intrinsic sphincters have an effect on postoperative continence status. The external striated sphincter (or distal sphincter) is tubular and has broad attachments over the fascia of the prostate near the apex . Its innervation arises from the pudendal nerves, the autonomic nerves in the pelvic plexus, and nerve connections with the dorsal vein complex. The striated sphincter can therefore be injured at the time of transection of the dorsal vein complex, apical dissection, and reconstruction of the urethra either by myogenic damage or by denervation . The internal sphincter (or proximal sphincter) is represented by the bladder neck and the urethral smooth muscle [8,9]. The urethral resistance, which is under sympathogenic control, may be partly responsible for urinary continence [8,9]. Myers  described five phenomena occurring after RP that may affect intrinsic sphincter function: reduction in functional urethral length, loss of vesico-urethral smooth muscle continuity, reduction of the investment of the membranous urethra by fascia and levator muscles, loss of elasticity of the vesico-urethral junction, and denervation of the urethra and bladder neck. Recently, John et al. took biopsies of the superficial trigone before and after RP, finding that protein gene-product 9.5 immunoreactive nerve fibre density in the trigone was lower after RP. Furthermore, there was a strong correlation between the expression of this protein and the continence status. The authors concluded that trigonal denervation was a significant risk factor for incontinence.
There are connections between intrinsic and extrinsic sphincters. Indeed, it has been shown that an increased tension in the bladder neck as filling progresses or urine escapes into the proximal urethra induces a stimulation of the external striated sphincter . Moreover, the role of bladder factors such as detrusor instability and reduced bladder capacity has been widely documented . Nevertheless, a distinction between early and persistent incontinence should be emphasized. Although detrusor instability is very important in early postoperative incontinence, it is the explanation in only 4% of patients who have persistent incontinence . Conversely, sphincter deficiency is present in 90–100% of patients with incontinence at any time after surgery [5,6]. Consequently, early incontinence partly depends on detrusor instability, whereas persistent stress incontinence is mainly a result of sphincter dysfunction.