Dysmenorrhea

Dysmenorrhea, also known as period pain, painful periods or menstrual cramps, is pain during menstruation.^[4][5][2] Its usual onset occurs around the time that menstruation begins.^[1] Symptoms typically last less than three days.^[1] The pain is usually in the pelvis or lower abdomen.^[1] Other symptoms may include back pain, diarrhea or nausea.^[1]

Dysmenorrhea can occur without an underlying problem.

The main symptom of dysmenorrhea is pain concentrated in the lower abdomen or pelvis.^[1] It is also commonly felt in the right or left side of the abdomen. It may radiate to the thighs and lower back.^[1]

Symptoms often co-occurring with menstrual pain include

Dysmenorrhea is associated with increased pain sensitivity and heavy menstrual bleeding.^[10][11]

For many women, primary dysmenorrhea gradually subsides in late second generation.^{[clarification needed]} Pregnancy has also been demonstrated to lessen the severity of dysmenorrhea, when menstruation resumes. However, dysmenorrhea can continue until menopause. 5–15% of women with dysmenorrhea experience symptoms severe enough to interfere with daily activities.^[12]

Causes

There are two types of dysmenorrhea, primary and secondary, based on the absence or presence of an underlying cause. Primary dysmenorrhea occurs without an associated underlying condition, while secondary dysmenorrhea has a specific underlying cause, typically a condition that affects the uterus or other reproductive organs.^[5]

Painful menstrual cramps can result from an excess of prostaglandins released from the uterus. Prostaglandins cause the uterine muscles to tighten and relax causing the menstrual cramps. This type of dysmenorrhea is called primary dysmenorrhea.^[5] Primary dysmenorrhea usually begins in the teens soon after the first period.^[13]

Secondary dysmenorrhea is the type of dysmenorrhea caused by another condition such as

Membranous dysmenorrhea is a type of secondary dysmenorrhea in which the entire lining of the uterus is shed all at once rather than over the course of several days as is typical.[15] Signs and symptoms include spotting, bleeding, abdominal pain, and menstrual cramps. The resulting uterine tissue is called a decidual cast and must be passed through the cervix and vagina.^[16] It typically takes the shape of the uterus itself. Membranous dysmenorrhea is extremely rare and there are very few reported cases. The underlying cause is unknown, though some evidence suggests it may be associated with ectopic pregnancy or the use of hormonal contraception.

When laparoscopy is used for diagnosis, the most common cause of dysmenorrhea is endometriosis, in approximately 70% of adolescents.^[17]

Other causes of secondary dysmenorrhea include leiomyoma,^[18] adenomyosis,^[19] ovarian cysts, pelvic congestion,^[20] and cavitated and accessory uterine mass.^[21]

Risk factors

Genetic factors, stress and depression are risk factors for dysmenorrhea.^[22] Risk factors for primary dysmenorrhea include: early age at menarche, long or heavy menstrual periods, smoking, and a family history of dysmenorrhea.^[12]

Dysmenorrhea is a highly

Three distinct possible phenotypes have been identified for dysmenorrhea which include "multiple severe symptoms", "mild localized pain", and "severe localized pain". While there are likely differences in genotypes underlying each phenotype, the specific correlating genotypes have not yet been identified. These phenotypes are prevalent at different levels in different population demographics, suggesting different allelic frequencies across populations (in terms of race, ethnicity, and nationality).^[25]

Polymorphisms in the ESR1 gene have been commonly associated with severe dysmenorrhea.^[23] Variant genotypes in the metabolic genes such as CYP2D6 and GSTM1 have been similarly been correlated with an increased risk of severe menstrual pain, but not with moderate or occasional phentoypes.^[26]

The occurrence and frequency of secondary dysmenorrhea (SD) has been associated with different alleles and genotypes of those with underlying pathologies, which can affect the pelvic region or other areas of the body. Individuals with disorders may have genetic mutations related to their diagnoses which produce dysmenorrhea as a symptom of their primary diagnosis. It has been found that those with fibromyalgia who have the ESR1 gene variation Xbal and possess the Xbal AA genotype are more susceptible to experiencing mild to severe menstrual pain resulting from their primary pathology.^[27] Commonly, genetic mutations which are a hallmark of or associated with specific disorders can produce dysmenorrhea as a symptom which accompanies the primary disorder.

In contrast with secondary dysmenorrhea, primary dysmenorrhea (PD) has no underlying pathology.^[28] Genetic mutation and variations have therefore been thought to underlie this disorder and contribute to the pathogenesis of PD.^[29] There are multiple single-nucleotide polymorphisms (SNP) associated with PD. Two of the most well studied include an SNP in the promoter of MIF and an SNP in the tumor necrosis factor (TNF-α) gene. When a cytosine 173 base pairs upstream of macrophage migration inhibitory factor (MIF) promoter was replaced by a guanine there was an associated increase in the likelihood of the individual experiencing PD. While a CC/GG genotype led to an increase in likelihood of the individual experiencing severe menstrual pain, a CC/GC genotype led to a more significant likelihood of the disorder impacting the individual overall and increasing the likelihood of any of the three phenotypes.^[30] A second associated SNP was located 308 base pairs upstream from the start codon of the TNF-α gene, in which guanine was substituted for adenine. A GG genotype at the loci is associated with the disorder and has been proposed as a possible genetic marker to predict PD.^[30]

There has also been an association with mutations in the MEFV gene and dysmenorrhea, which are considered to be causative.^[31] The phenotypes associated with these mutations in the MEFV genes have been better studied; individuals who are heterozygous for these mutations are more likely to be affected by PD which presents as a severe pain phenotype.^[23]

Genes related to immunity have been identified as playing a significant role in PD as well.

Two additionally well studied SNPs which are suspected to contribute to PD were found in ZM1Z1 (the mutant allele called rs76518691) and NGF (the mutant allele called rs7523831). Both ZMIZ1 and NGF are associated with autoimmune responses and diseases, as well as pain response.^[23] The implication of these genes impacting Dysmenorrhea is significant as it suggests mutations which affect the immune system (specifically the inflammatory response) and pain response may also be a cause of primary dysmenorrhea.

Mechanism

The underlying mechanism of primary dysmenorrhea is the contractions of the muscles of the uterus which induce a local ischemia.^[32]

During an individual's menstrual cycle, the

Prostaglandins and leukotrienes are released during menstruation, due to the build up of omega-6 fatty acids.^[33][34] Release of prostaglandins and other inflammatory mediators in the uterus cause the uterus to contract and can result in systemic symptoms such as nausea, vomiting, bloating and headaches or migraines.^[33] Prostaglandins are thought to be a major factor in primary dysmenorrhea.^[35] When the uterine muscles contract, they constrict the blood supply to the tissue of the endometrium, which, in turn, breaks down and dies. These uterine contractions continue as they squeeze the old, dead endometrial tissue through the cervix and out of the body through the vagina. These contractions, and the resulting temporary oxygen deprivation to nearby tissues, are thought to be responsible for the pain or cramps experienced during menstruation.

Compared with non-dysmnenorrhic individuals, those with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions.^[36]

Diagnosis

The diagnosis of dysmenorrhea is usually made simply on a

Further work-up includes a specific medical history of symptoms and menstrual cycles and a pelvic examination.^[6] Based on results from these, additional exams and tests may be motivated, such as:

• Gynecologic ultrasonography^[6]
• Laparoscopy^[6]

Management

Treatments that target the mechanism of pain include

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen are effective in relieving the pain of primary dysmenorrhea.^[39] They can have

A review indicated the effectiveness of transdermal nitroglycerin.^[48] Reviews indicated magnesium supplementation seemed to be effective.^[49][2] A review indicated the usefulness of using

Tamoxifen has been used effectively to reduce uterine contractility and pain in dysmenorrhea patients.^[51]

There is some evidence that exercises performed 3 times a week for about 45 to 60 minutes, without particular intensity, reduces menstrual pain.^[52]

Alternative medicine

There is insufficient evidence to recommend the use of many herbal or dietary supplements for treating dysmenorrhea, including melatonin, vitamin E, fennel, dill, chamomile, cinnamon, damask rose, rhubarb, guava, and uzara.^[1][53] Further research is recommended to follow up on weak evidence of benefit for: fenugreek, ginger, valerian, zataria, zinc sulphate, fish oil, and vitamin B₁. A 2016 review found that evidence of safety is insufficient for most dietary supplements.^[53] There is some evidence for the use of fenugreek.^[54]

One review found

A 2007 systematic review found some scientific evidence that behavioral interventions may be effective, but that the results should be viewed with caution due to poor quality of the data.[60]

Spinal manipulation does not appear to be helpful.^[55] Although claims have been made for chiropractic care, under the theory that treating subluxations in the spine may decrease symptoms,^[61] a 2006 systematic review found that overall no evidence suggests that spinal manipulation is effective for treatment of primary and secondary dysmenorrhea.^[62]

Valerian, Humulus lupulus and Passiflora incarnata may be safe and effective in the treatment of dysmenorrhea.^[10]

TENS

A 2011 review stated that high-frequency transcutaneous electrical nerve stimulation may reduce pain compared with sham TENS, but seems to be less effective than ibuprofen.^[55]

Surgery

One treatment of last resort is presacral neurectomy.^[63]

Epidemiology

Dysmenorrhea is one of the most common gynecological problems, regardless of age or race. It is one of the most frequently identified causes of pelvic pain in those who menstruate. Dysmenorrhea is estimated to affect between 50% and 90% of female adolescents and women of reproductive age.

A survey in Norway showed that 14 percent of females between the ages of 20 to 35 experience symptoms so severe that they stay home from school or work.^[69] Among adolescent girls, dysmenorrhea is the leading cause of recurrent short-term school absence.^[70]

References

External links

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