Abstract
A theory is advanced, substantiated by considerable cystometric evidence, that the urinary bladder acts reflexly to stimulation of a nodal area which is located in the upper posterior urethra. Stimulation of this area may be produced via the bladder or via the meatus, producing, in order, either contraction or relaxation of the trigonal muscle. Such contraction or relaxation by its effect upon the internal sphincter area is associated with either contraction or inhibition of the bladder wall. A voluntary downward pull of the perineum in effect produces a stretch reflex contraction of the trigonal muscle, a parasympathetic type of reaction (pelvic nerve) thus stimulating a bladder contraction which is again a stretch reflex. The perineum, normally held in passive tone, maintains passive tone of the trigonal muscle. This is an inhibitory influence (or a sympathetic stimulating overbalance caused by lack of counter-parasympathetic effect). If this inhibitory stimulation is increased by an upward voluntary contraction of the perineal muscles, an active dilation of the bladder wall occurs which is associated with changes in the direction of the posterior urethra and an active internal orifice closure. In this theory the N. pudendus and the pelvic are very important as the afferent nerves of micturition. Therefore, in medical or surgical therapy directed against either of these nerves, the intermediary area or the external sphincter mechanism offers more hope for relief of neurogenic bladder than does attempting to alter innervation of the bladder wall alone. For example, in those cases showing urinary obstruction due to a spastic perineum, theoretically relief may be obtained by section of one or both pudic or pelvic nerves, or one of each as trial and error demonstrates the value. Or transurethral surgery may lower the floor of the elevated intermediary area, or possibly change the physiology of this area. Or both sphincters may be destroyed and a Cunningham incontinence clamp used. In those cases showing an atonic or paralytic perineum, again destruction of the sphincters may be preferable to a large infected residual urine. It seems unlikely that any form of perineorrhaphy could be of value without considerable innervation remaining. In such instances, however, the perineal floor or the posterior urethra muscles may be plicated with Lowsley''s ribbon catgut. In either instance correction, complete or partial, of the voluntary sphincter mechanism so that the urethra may serve as the bladder drain is far superior to any form of catheter management, systostomy or ureteral transplant.

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