Dysmenorrhea, the term for painful periods, is derived from the Greek words dys (difficult, painful, or abnormal), meno (month), and rrhea (flow). Cathleen Morrow and Betsy Naumburg, authors of the excellent chapter “Dysmenorrhea” in Women’s HealthPrimary Care: Clinics in Office Practice, offer a thorough introduction to the topic.
Primary dysmenorrhea is a gynecological condition characterized by painful cramps accompanying menstruation in the absence of any underlying abnormality. Secondary dysmenorrheic pain, on the other hand, originates from a handful of identifiable pathological conditions including endometriosis, adenomyosis, fibroids (myomas) and pelvic inflammatory disease. Primary dysmenorrhea is more common in adolescents, while secondary dysmenorrhea manifests later in life.14
The adverse symptoms of dysmenorrhea typically begin with the onset of menstrual flow and can persist for up to 72 hours, frequently peaking in the first 24 to 48 hours of the menstrual cycle. Dysmenorrhea is often associated with not only pelvic pain, but also nausea, vomiting, diarrhea, headache, malaise, insomnia, and fatigue. These symptoms throw a monkey wrench in well-being, sabotaging sleep quality, daily physical activities, and mood. There’s a high comorbidity between dysmenorrhea and chronic pelvic pain. Primary dysmenorrhea is a global phenomenon, with high rates of incidence.
One research team consolidated data on the prevalence of primary dysmenorrhea worldwide and found the following frequencies: 70.2% in India, 89.1% in Iran, 52.07% in Georgia, 64% in Mexican university students, 87.8 in Turkish university students, 48.4% in Mexican high school students, 60% in Canada, and 80% in Australian high school girls. The incidence of dysmenorrhea in menstruating US citizens between the ages of 18 and 45 years was reported at 90%. The researchers conclude: “The high prevalence of primary dysmenorrhea among girls represents a significant public health problem” . Another team reports on the prevalence of primary dysmenorrhea in Asia: 83% among college students in Korea, 55.5% among university students in Turkey, 65.6% among high school students in Anatolia, and over 60% among college students in Taiwan .
One group of Dutch researchers conducted an investigation via questionnaire of 947 individuals and found that those who had a history of self-reported sexual abuse had significantly higher rates of dysmenorrhea . Additional risk factors for dysmenorrhea include adolescence, anxiety or stress, body mass index less than 20 or greater than 30 kg/m2 , depression (particularly if associated with an eating disorder), disrupted social networks, family history (especially in a first-degree relative), menarche at a young age, menorrhagia, metrorrhagia, nulliparity, and smoking. The severity of symptoms of PD tends to dwindle with age and following childbirth. Primary dysmenorrhea is predominantly a disorder of the young – Morrow and Naumburg report on a cohort study of the natural history of dysmenorrhea in nulliparous women in China, and note that researchers symptoms diminished in those who had more frequent intercourse, less frequent associated symptoms, and increased age. By age 40, symptoms of primary dysmenorrhea had essentially abated. These findings, however, are complicated by other studies which found conflicting results. The lack of consensus indicates the need for further research .
Half the humans of reproductive age menstruate, yet it is a process shrouded in secrecy. Studies show that menarche is a mystery to many, and that the topic goes generally undiscussed. Of the information that is shared, much is inaccurate and negatively biased.
These erroneous attitudes towards women and their normal – let me rephrase that – extremely adaptive biological processes profoundly influence the scientific research and medical care available for women’s health. As Maybin et al. explain in their insightful article “Menstrual physiology: implications for endometrial pathology and beyond” published in Oxford Academic’s 2015 Human Reproduction
“Currently, global differences in women’s rights and status have a dramatic impact on reproductive health and consequently their morbidity and mortality.” Shifting reproductive practices and increased female participation in the workplace define modern menstrual complexities.
Maybin et al. elaborate:
As women undertake positions of responsibility in the workplace and home, abnormal menstruation can cause significant socio-economic problems. Abnormal menstrual bleeding affects 20-30% of premenopausal women (RCOG, 2011), and more than 800,000 women seek treatment annually in the UK (NICE, 2007). A US study demonstrated financial losses of >$2000 per patient each year due to work absence and home management costs (Fricket al., 2009). Although time has proven that physiological menstruation is not a barrier to female success; family and career responsibilities may become impossible if heavy or painful bleeding occurs. Due to advances in family planning, women in developed countries now can expect greater than 400 episodes of menstruation in their lifetime. This is in stark contrast to our ancestors and women in very underdeveloped countries, who have ∼40 menstrual bleeds due to multiple pregnancy and long spells of lactational amenorrhoea (Short, 1976).
Indeed, the socio-economic repercussions are legion. Over 35% of menstruating high school students report missing school due to pain, while 15% of working Hungarian women of reproductive age reported that it limited their daily activity . Menstrual cramps experienced by those with dysmenorrhea can be markedly disabling, and have been likened to re nal colic pain . In large cross-sectional studies conducted worldwide of hundreds-to-thousands of people, it was found that menstrual pain has a multidimensional negative impact on the personal lives of those affected, including family relationships, friendships, school/work performance, and social and recreational activities. Cyclic pain is associated with a restriction of physical activity, and dysmenorrheic pain is the leading cause of recurrent short-term school or work absenteeism among those of child-bearing age. Longitudinal studies indicate that rates of absenteeism in those with dysmenorrhea range from 34 to 50%, with approximately 10 to 30% of all people working or studying with dysmenorrhea losing 1 to 2 working days per month, for an annual loss of ∼600 million working hours, or up to $2 billion annually in the USA. In Sweden, a country with a population of only 4 million, primary dysmenorrhea is the cause of 230,000 lost working days per year, with >50% of women claiming absenteeism from work or school at least once due to dysmenorrhea. Furthermore, as most people don’t seek medical care for dysmenorrhea as it is commonly believed to be a normal part of the menstrual cycle, these numbers are likely to be underestimates. Dysmenorrhea makes a serious impact on productivity with global economic consequences .
Primary dysmenorrhea is the most common gynecological condition regardless of nationality, and carries significant medical and psychosocial implications.
Current prevalence estimates vary between 45 and 95% of those who menstruate, with severe primary dysmenorrhea estimated to effect ∼10-25% of women of reproductive age. Inconsistent definitions of the condition and varying methods of assessment, however, are roadblocks to accurate estimation . Despite its ubiquity, the risk of gross under-diagnosis is high due to pervasive social perceptions about the burdens of menstruation, and lack of viable treatment options. Women often do not seek medical evaluation for their symptoms of dysmenorrhea, even when their quality of life is severely impacted; many consider the pain to be a normal part of the menstrual cycle rather than a disorder .
The Physiology of Pain
After capacious debate, dismissal, and claims of “psychosomatic” causes, researchers have more or less concluded that dysmenorrhea is the result of an excess or imbalance of prostaglandins, vasopressin, and chemical substances derived from phospholipids. The current theory is that increased prostaglandin (PG) release from endometrial sloughing causes myometrial hypercontractility, which results in ischemia and hypoxia of the uterine muscle, leading to pain. Iacovides et al., in their superb 2015 article “What we know about primary dysmenorrhea today: a critical review” published in Human Reproduction Update, elucidate the mechanisms of pain in dysmenorrhea. According to their research, PGs (intracellular substances distributed through the whole body) are derived from long-chain polyunsaturated fatty acids such as arachidonic acid, a common component of cell membrane phospholipids. PGs play a role in a wide variety of physiological processes such as body temperature and sleep regulation, as well as pathological manifestations of pain and inflammation. Phospholipids are broken down into arachidonic acid by the lysosomal enzyme phospholipase A2. The stability of this lysosomal enzyme is contingent on a number of factors, one of which is progesterone levels. High progesterone levels stabilize the activity of lysosomes, and once they fall lysosome activity is labilized. The drop in progesterone caused by the regression of the corpus luteum in the late luteal phase of the menstrual cycle therefore allows increased activity of the endometrial lysosomes, the release of phospholipase A2, menstrual flow, and hydrolysis of phospholipids from the cell membrane to produce additional arachidonic acid. The intracellular destruction and tissue trauma of menstruation together with increased availability of arachidonic acid favors the production of prostaglandins.
Everyone who menstruates has increased levels of PGs during the luteal phase as compared to the follicular phase of the ovulatory cycle, but those with dysmenorrhea have higher levels than those with eumenorrhea (normal/regular menstruation). PG levels are highest during the first 48 h of menstruation, when symptoms are at their worst. In fact, the severity of dysmenorrhea symptoms were found to be directly proportional to the amount of PGs released. Blocking the synthesis of prostaglandins with cyclooxygenase (COX) inhibitors lowered the levels of prostaglandins present in menstrual fluid and resulted in a clinically significant reduction of symptoms. Researchers found that clinical administration of exogenous PGs results in uterine contraction, and often produces the same systemic symptoms of dysmenorrhea including nausea, vomiting and diarrhea.
These findings support the theory that PGs are responsible for the painful uterine contractions and systemic symptoms of dysmenorrhea.
In addition to higher levels of PGs, or likely as a result of this increased activity, individuals with dysmenorrhea exhibit higher levels of uterine activity during menstruation compared with asymptomatic individuals. These contractions are not only stronger, but also more frequent, and uncoordinated. Studies of uterine blood flow using Doppler ultrasonography revealed that the strong and abnormal menstrual uterine contractions in those with dysmenorrhea were associated with reduced uterine blood flow and subsequent myometrial ischemia. To sum it up, excessive release of PGs by the endometrium triggers hypercontractility of the uterus, leading to uterine muscle ischemia, hypoxia, and ultimately pain. The role of vasopressin remains controversial, with some studies showing higher levels of arginine vasopressin resulting in dysrhythmical uterine contractions, while other studies found equal plasma vasopressin levels in those with dysmenorrhea and eumenorrhea. A vasopressin antagonist had no effect on menstrual pain, intrauterine pressure, and uterine blood flow.
Another avenue of investigation in dysmenorrhea has to do with central pain sensitization. Central sensitization is defined as an abnormal amplification of pain by the central nervous system (CNS), representing a state wherein the response to normal peripheral stimuli is significantly enhanced. This occurs in such clinical conditions as fibromyalgia and tension-type headaches, and can be triggered by repeated monthly episodes of painful menstruation. The conditions are defined by pain hypersensitivity in the absence of tissue injury, inflammation, or mechanical damage to the nervous system. Increasing evidence indicates that those with dysmenorrhea manifest a mode of divergent systemic pain processing where the peripheral nociceptive message generated by the reproductive organs during menstruation is enhanced, leading to increased excitability of somatovisceral convergent neurons in the spinal cord to produce amplified pain perception. Prolonged afferent visceral barrage of the CNS can lead to functional and structural changes in the CNS, of which central sensitization to pain is one dimension. Abnormal metabolic changes in pain-processing regions of the brain have also been observed .
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