The neuroanatomy and neurophysiology of the external urethral closure mechanisms still are under debate because the motor fibers that emanate from the sacral plexus and pudendal nerve to supply this segment have not been traced, nor has their functional interrelationship been established. Therefore, we dissected 3 male human cadavers (aged 31 to 69 years) by tracing the entire sacral plexus, particularly the pudendal nerve, from the cauda equina throughout the branching of the nerves to their final destination. The dissection demonstrated that the extrinsic urethral sphincter, formed by the rhabdosphincter around the membranous urethra as well as the levator ani muscle and pelvic floor (especially the transversus perinei muscle), is innervated by somatic nerve fibers that emanate primarily from sacral roots S2 and S3. In 5 patients with neurogenic lower urinary tract dysfunction electrostimulation of the sacral root and pudendal nerve markedly increased intraurethral closure pressures. Stimulation of the pudendal nerve or its transversus perinei branch alone resulted in an increase in intraurethral closure pressure to 60 to 70 cm. water--an increase similar to that produced by stimulation of the sacral root without neurotomy. By means of neurotomy and/or neural blockade with lidocaine we were able to differentiate between the contributions of each muscular element to the external sphincteric mechanism. Almost 70 per cent of the closure pressure of the external urethral sphincter is induced by stimulation of the S3 ventral root, while the other 30 per cent derives from S2 and S4 neuronal impulses.