Combining NSAIDs with a new way of administering a centuries-old "folk" remedy offers many women significant relief.
While it seems at times that dysmenorrhea made its first appearance 14 days after the first human ovulation, effective therapy had to wait until after the middle of the last century. Among those effective options, of course, were hormonal contraceptives and non-steroidal anti-inflammatory agents. But now, as the introduction of newer NSAIDs has stirred renewed interest and concerns about this family of drugs, a much older therapy has emerged as one of the best approaches to painful menstruation-heat.
Subjective pain studies and objective studies of uterine activity have established a firm connection between uterine activity and pain. These studies have also clearly shown that NSAIDs and continuous low-level topical heat therapy alter the physiology responsible for pain, making it possible to talk about true pain prevention rather than pain relief for those women who suffer from dysmenorrhea.
Attempts to understand the pathophysiology
Our understanding of the pathophysiology of primary dysmenorrhea has evolved over the course of many years. By the late 1940s, it was becoming accepted that women with primary dysmenorrhea had fundamental differences in uterine activity. One researcher, for instance, showed that these women had more electrical and mechanical activity occurring in conjunction with their menstrual pain.2 These studies suggested an electrical cause, but could provide no clue to the underlying pathophysiology.
In parallel with these studies of uterine activity were investigations that attempted to find a biochemical disturbance. One study reported that acetone and ether extracts of menstrual fluid contained a powerful "plain muscle stimulant."3 These studies were expanded and the source localized to the sloughing endometrium, and by 1963, these stimulants had been identified as prostaglandins.4
The connection between the increased uterine activity seen in dysmenorrheic women and prostaglandins came in 1965, when a researcher reported elevated levels of prostaglandin F2α in the menstrual fluid of dysmenorrheic women.5 The causative role of prostaglandin F2α in dysmenorrhea was supported when studies duplicated dysmenorrhea-like pain and uterine activity after IV injection of prostaglandins.6 (Current evidence indicates that women with primary dysmenorrhea make between two and seven times the normal amount of prostaglandin F2α.) Excess prostaglandins may also be responsible for the smooth muscle activity noted in the gastrointestinal (GI) tract of these women. Hypermobility of the gut may be responsible for the frequent coexistence of nausea, vomiting, and diarrhea in these patients. Prostaglandins appear to act as initiators and potentiators of nociceptive pain signals, further contributing to the symptoms experienced.
[Logic suggests that if prostaglandin synthesis can be reduced, menstrual pain can be prevented or lessened.] Such a direct method of altering the physiologic sequence leading to discomfort comes in the form of nonsteroidal anti–inflammatory drugs. These drugs inhibit the production and/or the action of prostaglandins. They are generally well-tolerated and need only be taken at the time of menstruation.