Painful menstruation or dysmenorrhea should properly be considered a symptom of an underlying abnormality and not a disease. Many older authors refer to this symptom as menorrhalgia.
When the cause is obscure or not dependent on demonstrable organic pelvic pathology, or is associated with manifestation of a disease entity or a discernible dysfunction, the symptom complex is referred to as primary dysmenorrhea. This type of dysmenorrhea is present from the onset of the menses, or occurs shortly thereafter.
Acquired or secondary dysmenorrhea refers to demonstrable organic pelvic pathology or is associated with systemic organic pathology, lesions, or disease entities. Other causative factors can be found without organic pathology. These will be discussed as separate entities with the conditions that give rise to them.
There is increasing evidence that the menarche is ovulatory with regular succeeding cycles and even dysmenorrhea in at least 15 per cent from the first cycle.1 There is additional evidence that probably another 60 per cent have ovulatory cycles with progressive maturation of the luteal phase. Therefore, there is increasing speculation that dysmenorrhea in the postpuberal and adolescent girl may not be solely dependent on ovulatory, regular, "normal" cycles and that dysmenorrhea in these girls may be of the acquired type. Management therefore may or should be different.
If one includes in the symptom complex of dysmenorrhea the entire spectrum - from irritability, emotional lability, premenstrual tension, and abdominal cramps to severe incapacitating discomfort and pains, nausea, vomiting, and loss of appetite with weight gain, constipation, and bloating - the incidence may be as high as 90 per cent of all young women. It is generally agreed that severe dysmenorrhea alone is present in 1 to 5 per cent of adolescents and young adults. Menstrual cramps appearing two or more years after the menarche strongly suggest the presence of organic disease. Normal menstrual cycles are not usually attended by or associated with pain beyond a slight sensation of heaviness, so that a symptom complex of premenstrual tension and dysmenorrhea, individually or in combination, may denote mild, moderate, or severe degrees of a disturbance of menstruation. The endometrium shed may reflect the severity of dysmenorrhea, from normal-appearing endometrium to decidual or deciduoid formation in the most severe form - the so-called membranous dysmenorrhea.
This syndrome complex has often been referred to as "disease of theories" and "disease of treatment regimens." This certainly attests to the marked confusion and contradictory observations surrounding this syndrome.
Historically, numerous theories had staunch adherents. But each was met by logical objections. Congenital stenosis has been offered as a possible explanation for some cases. However, passing a sound only occasionally relieves the pain. Acute anteflexionsare not today accepted as an adequate explanation for dysmenorrhea - especially since anteflexion, even "acute," is more often noted without pain.There is no anatomic evidence that anteflexion causes any appreciable hindrance to the escape of menstrual blood. Deficiency of trypsin and other enzymes and decreased elasticity of the uterus have long been discarded as plausible theories for painful menses. Also, the concept of hypoplasia and an infantile uterus is not compatible with the concept of maturity of the cycles. Retrodisplacements have similarly been discarded as causative factors. Nervousness and psychoneurosis have been advanced as possible explanations; however, today it is generally accepted that these are the result of the subjective symptom complex and not the cause.
Nutritional disturbance may be important when related to dysmaturity of the cycle and the effect on the histologic picture of the endometrium.
Endocrine imbalance is still accepted as a plausible theory for dysmenorrhea. It has been suggested that a decrease in estrogen levels, an increase in a progesterone level, or an altered estrogen-progesterone ratio may very well affect disturbances of the sympathetic nervous system or may affect the function or physiology of the isthmus or even the glands or stroma of the endometrium itself. But to date there is no demonstrable, measurable abnormality of estrogen or progesterone levels between those with and those without dysmenorrhea.
During the 1920s and the 1930s the toxin theory was proposed. It was suggested that this substance arose in the secretory endometrium and seemed to be more abundant during abnormal menstrual cycles and severe dysmenorrhea cycles. (They acted like smoothmuscle stimulants.) I think this "toxin theory" may very well fit the action of prostaglandins. Prostaglandins are hydroxy fatty acids that cause contraction of smooth muscle and may play a role in increasing the contractions of myometrium. Unlike other substances, such as hormones, prostaglandins might represent locally specific active agents rather than circulating agents. Studies by Pickles, Hall, and Best in 1965 suggested the possibility that excess endometrial prostaglandins represent the essential link in the complex mechanism responsible for primary dysmenorrhea.2 Furthermore, it was suggested that changes in the endometrium short of full maturity relate to changes in either production or effect of the prostaglandins. Prostaglandins are found in the decidua and are known to influence myometrial contractions; they can stimulate oxytocin release and may influence the life span of the corpus luteum.
It is thought that sites for prostaglandin production are the predeciduoid and decidual cells. Ghstavii suggests that control of prostaglandin synthesis resides in lysosomes of the endometrium. Some chemicals or heat can cause extensive lysosomal breakdown that can lead to digestion of the cell. Some agents, called lysosomal labilizers, can cause release of lysosomal enzymes without destruction of the cell. Other agents, called stabilizers (corticosteroids, aspirin, and indomethacin), increase stability of lysosomal membranes. It is thought that the primary labilizing influences may very well be estrogen and progesterone.
Dysmenorrhea is a symptom complex. The initial step in making a diagnosis is to elicit an adequate and comprehensive history and to conduct a thorough general physical examination to eliminate the presence of any constitutional disease or gross lesions. A thorough rectal or vaginal examination should be done to eliminate the presence of lesions related to acquired dysmenorrhea. There is an occasional place for endoscopy, laparoscopy, and culdoscopy in helping to establish a diagnosis. Pain is a subjective symptom and may vary in intensity, frequency, or duration according to the individual patient and even, at different times, in the same patient. Pain is generally suprapubic but may radiate to the back or down the thighs or to the vagina. Generally, the crampy and colicky pain is most severe with the onset of menstrual flow. It usually continues for 12 hours but may extend, with less severity, into the second day. Nausea, vomiting, pallor, and sweating may occur with the sensation of, or actual, syncope.
Diarrhea, constipation, and anorexia can occur. These symptoms tend to diminish with increasing age. The pain is unaffected by marriage and tends to diminish with parity. The presence of any intermenstrual pain should not be considered part of the symptom complex of primary dysmenorrhea. There is no hypermenorrhea or polymenorrhea with primary dysmenorrhea.
With dysmenorrhea, hypertonic dysrhythmic uterine contractions are usually present; these contractions are considered the result of vasoconstriction. When the contraction patterns are well organized and rhythmic, there is no distress. When the patterns are disorganized, dysrhythmic, and hypertonic, severe distress occurs.3
Hamblen once remarked: "The long list of remedies which has been hailed as successful in dysmenorrhea bears testimony to the willingness of the dysmenorrhic female to report relief when they are convinced that their physician needs encouragement."
All management, medical or surgical, is of necessity directed toward relieving the distressing symptoms. It is indeed intriguing that when each specific regimen is evaluated, about 75 per cent of the subjects in each report are relieved or cured by a specific regimen.
Regardless of the form of treatment, the problem is temporary; recurrences are usually less severe and finally disappear spontaneously within a few months or a few years. It is interesting to speculate - since all "cure regimens" are concurrent with or promote, hasten, or aid anatomic, endocrinologie, and sociopsychologic maturity - that the primary disturbance might well be related to some degree of lack of full maturity of the menstrual cycle. There is no evidence that exercise, frank discussion of biologic functions, and healthy sexual and reproductive attitudes prevent this symptom complex. Minimal restriction of activities is recommended.
Marriage, pregnancy, and delivery are not always completely curative. General measures - such as good nutrition, adequate sleep, and exercise - are of questionable help.
In general, it is desirable to prescribe the minimal effective amount of medication. Phenacetin, salicylates, and acetanilid, in appropriate doses, are desirable. Even codeine is advisable; but opiates are not encouraged. Estrogen alone and progesterone alone or in cyclic combination are helpful with or without suppression of ovulation.
Suppression of ovulation is not always helpful, since it has been demonstrated that combination birth control medication might be effective but sequential medication may be no better than placebo. Successful management may be related more to modification of the premenstrual or menstrual endometrium, in that the endometrium is changed so that there is an alteration of prostaglandin production, secretion, or absorption and, thus, relief of dysmenorrhea.2
Antispasmodics must be able to exert a demonstrable effect on the myometrium muscle fibers directly or on the vascular supply, not on the autonomic nervous system, to be logically effective.
In the presence of depression and demonstrable edema, antidepressants and diuretics might be used. Since many older remedies contained about 20 per cent alcohol, the reported effectiveness might reflect the effect of the alcohol on the vascular bed.
Testosterone, chorionic gonadotropin, and pitocin are not considered effective and are contraindicated.
Surgical management is considered in about 5 per cent of younger patients who do not respond to the medical regimens. Dilatation with or without curettage is occasionally effective in decreasing or relieving the dysmenorrhea. An inserted stem pessary (intrauterine and/or cervical pessary, first described about 900 years ago) may act as a foreign body by increasing both vascularity and contractions of the myometrium and decreasing the effect of the circular musculature around the internal os. It is usually retained for two to three cycles.
According to scattered American and British reports, the spectrum of symptoms of the menstrual molimina of premenstrual tension and dysmenorrhea can curb productivity, contributing to industrial and home accidents, and provoke or modify antisocial behavior. Dysmenorrhea can be influential in restricting daily activities in many women and is a cause of absenteeism. Household, industrial, and road accident rates increase around the menstrual period. The common denominator may be either slow reaction time or increased agitation and decreased tolerance of distress. In France, at one time, premenstrual tension and dysmenorrhea were thought, for legal purposes, to be a form of temporary insanity, since the reaction may be so acute and the behavior so irrational.
During the adolescent years, acquired dysmenorrhea is much less frequent. There is usually a systemic or local organic factor. The pain may be present before menses; it may persist after cessation of the menses. Causative factors are usually identical with those associated with the patient's mother or sister. Complications of pregnancy, endometriosis, ovarian neoplasm, and pelvic inflammatory disease must be considered as causes. The diagnosis is made by the history, physical examination, and review of symptoms.
Today physicians are generally more aware that after menarche the budding young adult is prone to the various systemic and local organic diseases that can confuse and delay the diagnosis of primary or acquired dysmenorrhea, so a telephone diagnosis of primary dysmenorrhea should not be made. It is only after eliciting a complete and comprehensive history and conducting a complete physical examination that a diagnosis of acquired dysmenorrhea can be made. A logical and appropriate treatment regimen can then be implemented.
Dysmenorrhea is a symptom complex including premenstrual tension and degrees of menstrual pain, and not a disease. There is convincing evidence that the menarche is ovulatory and that the subsequent cycles are more normal than was previously thought. Dysmenorrhea might very well be associated with dysmaturity of the cycle instead of with complete normal menstruation. During the past decade numerous authors have proposed the prostaglandin theory for primary dysmenorrhea. Intelligent, logical, and effective treatment should therefore be directed towards a three-pronged course - symptomatic relief, maturity of the cycle, and stabilization of the full impact of the prostaglandin or prostaglandinlike effect.
The full socioeconomic impact of the menstrual molimina should be appreciated. Acquired dysmenorrhea, although more often a problem in later years, can indeed have its early manifestations in the adolescent years. Before treatment the patient should properly have a complete history taken and be given a complete physical examination, with such ancillary investigations as endoscopy, in order to establish an accurate diagnosis.
1. Oriatti, M.D. Unpublished data. Pediatric Gynecology Clinic, Cook County Hospital.
2. Pickles, Hall, and Best as quoted by Butram, V., and Kaufman, R. Texas Med. Ix: 5 (August, 1969), 52-55.
3. Bickers, W. Menorrhagia: Menstrual Distress. Springfield, III.: Charles C Thomas, 1954, pp. 12-16.