The present communication describes new reflexes that I call "dilatation and closing urethral reflexes" and discusses their clinical significance. The study was performed on 23 healthy volunteers and 11 women with stress urinary incontinence. The technique comprised the introduction into the urethra of a balloon-tipped catheter such that the balloon lay opposite the external urethral sphincter. The balloon was inflated with air, and the response of the external urethral and anal sphincters to rapid balloon inflation and deflation was recorded on an electromyogram (EMG). Rapid urethral inflation and deflation evoked external urethral and anal sphincter contraction. Slow and gradual inflation or deflation did not induce this response. The anesthetized external urethral spincter did not respond to the stimulus, whereas the saline-infiltrated sphincter did. The latency of the reflexes was recorded. In stress urinary incontinent patients, on rapid urethral inflation the external urethral sphincter showed lower EMG activity and more prolonged latency than in normal volunteers. The sphincter did not respond to urethral deflation. The response of the external anal sphincter to rapid urethral inflation or deflation was normal. The dilatation and closing urethral reflexes seem to play an important role in the mechanisms of micturition and continence. They are believed to guard against involuntary urinary leakage. Detectable changes in the latency, amplitude or duration of the evoked response indicate a defect in the reflex pathway. The reflexes could thus be included as an investigative tool in the study of micturition disorders.
The mechanisms of urinary continence and micturition are intricate and comprise voluntary and reflex actions. However, despite many theories that have been proposed to explain these mechanisms [3][4][5]11], none has proved to be entirely satisfactory. During our study of the physiologic aspects of micturition, sudden inflation or deflation of the membranous urethra in men or women was