The interrelation between uterine activity and pain from primary dysmenorrhea has been of interest for many years. Objective studies of uterine activity during non-steroidal antiinflammatory drug therapy have supported the assertion that uterine activity causes pain and that reducing that activity leads to pain reduction. Unfortunately, those studies could not refute the counter-assertion that reductions in uterine activity come about because of reduced pain through central analgesia and not by direct pharmacologic action. In an effort to clarify this question, a small number of women were studied using intrauterine pressure recording and analysis to evaluate objective changes in uterine physiology during transcutaneous electrical nerve stimulation (TENS) therapy for dysmenorrhea. The preliminary studies indicated that despite successful subjective therapy with TENS, intrauterine pressure parameters remained steady or showed signs of worsening. These findings indicate that TENS provides pure analgesia by an alteration of the body's ability to receive or perceive the pain signal rather than by a direct uterine effect. It appears that the reduction in uterine activity seen in objective drug studies represents direct drug action rather than a change from reduced pain through central analgesic effects.