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Dysmenorrhea
Dysmenorrhea
Dysmenorrhea
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Dysmenorrhea
Other namesDysmenorrhoea, period pain, painful periods, menstrual cramps
Menstrual cycle and changes in hormone production
SpecialtyGynecology
SymptomsPain during first few days of menstruation, diarrhea, nausea[1][2]
Usual onsetWithin a year of the first menstrual period[1]
DurationLess than 5 days (primary dysmenorrhea)[1]
CausesNo underlying problem, uterine fibroids, adenomyosis, endometriosis[3]
Diagnostic methodPelvic exam, ultrasound[1]
Differential diagnosisEctopic pregnancy, pelvic inflammatory disease, interstitial cystitis, chronic pelvic pain[1]
TreatmentHeating pad, medication[3]
MedicationNSAIDs such as ibuprofen, hormonal birth control, IUD with progestogen[1][3]
PrognosisOften improves with age[2]
Frequency50–90% female adolescents and women of reproductive age[4]

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.[3][6] Underlying issues that can cause dysmenorrhea include uterine fibroids, adenomyosis, and most commonly, endometriosis.[3] It is more common among those with heavy periods, irregular periods, those whose periods started before twelve years of age and those who have a low body weight.[1] A pelvic exam and ultrasound in individuals who are sexually active may be useful for diagnosis.[1] Conditions that should be ruled out include ectopic pregnancy, pelvic inflammatory disease, interstitial cystitis and chronic pelvic pain.[1]

Dysmenorrhea occurs less often in those who exercise regularly and those who have children early in life.[1][7] Treatment may include the use of a heating pad.[3] Medications that may help include NSAIDs such as ibuprofen, hormonal birth control and the IUD with progestogen.[1][3] Taking vitamin B1 or magnesium may help.[2] Evidence for yoga, acupuncture and massage is insufficient.[1] Surgery may be useful if certain underlying problems are present.[2]

Estimates of the percentage of female adolescents and women of reproductive age affected are between 50% and 90%,[4][6] and the Women's Health Concern estimates it to be around 80%.[8] It is the most common menstrual disorder.[2] Typically, it starts within a year of the first menstrual period.[1] When there is no underlying cause, often the pain improves with age or following having a child.[2]

Signs and symptoms

[edit]
Illustration of menstrual cramps

The main symptom of dysmenorrhea is pain concentrated in the lower abdomen or pelvis.[1][9] 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 nausea and vomiting, diarrhea, headache, dizziness, disorientation, fainting and fatigue.[10] Symptoms of dysmenorrhea often begin immediately after ovulation and can last until the end of menstruation. This is because dysmenorrhea is often associated with changes in hormonal levels in the body that occur with ovulation. In particular, prostaglandins induce abdominal contractions that can cause pain and gastrointestinal symptoms.[11][12] The use of certain types of birth control pills can prevent the symptoms of dysmenorrhea because they stop ovulation from occurring.

Dysmenorrhea is associated with increased pain sensitivity and heavy menstrual bleeding.[13][14]

For many, primary dysmenorrhea symptoms gradually subside after their mid-20s. 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.[15]

Causes

[edit]

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.[16]

Secondary dysmenorrhea is the type of dysmenorrhea caused by another condition such as endometriosis, uterine fibroids,[5] uterine adenomyosis, and polycystic ovary syndrome. Rarely, birth defects, intrauterine devices, certain cancers, and pelvic infections cause secondary dysmenorrhea.[15] If the pain occurs between menstrual periods, lasts longer than the first few days of the period, or is not adequately relieved by the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or hormonal contraceptives, this could indicate another condition causing secondary dysmenorrhea.[17]

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.[18] 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.[19] 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.[20]

Other causes of secondary dysmenorrhea include leiomyoma,[21] adenomyosis,[22] ovarian cysts, pelvic congestion,[23]and cavitated and accessory uterine mass.[24]

Risk factors

[edit]

Genetic factors, stress and depression are risk factors for dysmenorrhea.[25] Risk factors for primary dysmenorrhea include: early age at menarche, long or heavy menstrual periods, smoking, and a family history of dysmenorrhea.[15]

Dysmenorrhea is a highly polygenic and heritable condition.[26] There is strong evidence of familial predisposition and genetic factors increasing susceptibility to dysmenorrhea. There have been multiple polymorphisms and genetic variants in both metabolic genes and genes responsible for immunity which have been associated with the disorder.[27]

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).[28]

Polymorphisms in the ESR1 gene have been commonly associated with severe dysmenorrhea.[26] 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 phenotypes.[29]

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.[30] 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.[31] Genetic mutation and variations have therefore been thought to underlie this disorder and contribute to the pathogenesis of PD.[32] 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.[33] 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.[33]

There has also been an association with mutations in the MEFV gene and dysmenorrhea, which are considered to be causative.[34] 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.[26]

Genes related to immunity have been identified as playing a significant role in PD as well. IL1A was found to be the gene most associated with primary dysmenorrhea in terms of its phenotypic impact.[26] This gene encodes a protein essential for the regulation of immunity and inflammation. While the mechanism of how it influences PD has yet to be discovered, it is assumed that possible mutations in IL1A or genes which interact with it impact the regulation of inflammation during menstruation. These mutations may therefore affect pain responses during menstruation which lead to the differing phenotypes associated with dysmenorrhea.

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.[26] 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

[edit]

The underlying mechanism of primary dysmenorrhea is the contractions of the muscles of the uterus which induce a local ischemia.[35]

During an individual's menstrual cycle, the endometrium thickens in preparation for potential pregnancy. After ovulation, if the ovum is not fertilized and there is no pregnancy, the built-up uterine tissue is not needed and thus shed.

Prostaglandins and leukotrienes are released during menstruation, due to the build up of omega-6 fatty acids.[36][37] 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.[36] Prostaglandins are thought to be a major factor in primary dysmenorrhea.[38] 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-dysmenorrheic individuals, those with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions.[39]

Diagnosis

[edit]

The diagnosis of dysmenorrhea is usually made simply on a medical history of menstrual pain that interferes with daily activities. However, there is no universally accepted standard technique for quantifying the severity of menstrual pains.[40] There are various quantification models, called menstrual symptometrics, that can be used to estimate the severity of menstrual pains as well as correlate them with pain in other parts of the body, menstrual bleeding and degree of interference with daily activities.[40]

Further work-up

[edit]

Once a diagnosis of dysmenorrhea is made, further workup is required to search for any secondary underlying cause of it, in order to be able to treat it specifically and to avoid the aggravation of a perhaps serious underlying cause.

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:

Management

[edit]

Treatments that target the mechanism of pain include non-steroidal anti-inflammatory drugs (NSAIDs) and hormonal contraceptives. NSAIDs inhibit prostaglandin production. With long-term treatment, hormonal birth control reduces the amount of uterine fluid/tissue expelled from the uterus. Thus resulting in shorter, less painful menstruation.[41] These drugs are typically more effective than treatments that do not target the source of the pain (e.g. acetaminophen).[42] Regular physical activity may limit the severity of uterine cramps.[15][43]

NSAIDs

[edit]

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen are effective in relieving the pain of primary dysmenorrhea.[42] They can have side effects of nausea, dyspepsia, peptic ulcer, and diarrhea.[44][42]

Hormonal birth control

[edit]

Use of hormonal birth control may improve symptoms of primary dysmenorrhea.[45][36] A 2009 systematic review (updated in 2023) found evidence that the low or medium doses of estrogen contained in the birth control pill reduces pain associated with dysmenorrhea.[46] In addition, no differences between different birth control pill preparations were found.[46] The review did not determine if the estrogen in birth control pills was more effective than NSAIDs.[46]

Norplant[47] and Depo-provera[48][49] are also effective, since these methods often induce amenorrhea. The intrauterine system (Mirena IUD) may be useful in reducing symptoms.[50]

Other

[edit]

A review indicated the effectiveness of transdermal nitroglycerin.[51] Reviews indicated magnesium supplementation seemed to be effective.[52][2]A review indicated the usefulness of using calcium channel blockers.[35] Heat is effective compared to NSAIDs and is a preferred option by many patients, as it is easy to access and has no known side effects.[53]

Tamoxifen has been used effectively to reduce uterine contractility and pain in dysmenorrhea patients.[54]

There is some evidence that exercise performed three times a week for about 45 to 60 minutes, without particular intensity, reduces menstrual pain.[43]

Alternative medicine

[edit]

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][55] A 2016 review found that evidence of safety is insufficient for most dietary supplements.[55] There is some evidence for the use of fenugreek.[56] A 2019 study found that herbal treatments using Valerian, Humulus lupulus and Passiflora incarnata may be safe and effective in the treatment of dysmenorrhea.[13]

One review found thiamine and vitamin E to be likely effective.[57] It found the effects of fish oil and vitamin B12 to be unknown.[57] Reviews found tentative evidence that ginger powder may be effective for primary dysmenorrhea.[58] Reviews have found promising evidence for Chinese herbal medicine for primary dysmenorrhea, but that the evidence was limited by its poor methodological quality.[59][60]

A 2016 Cochrane review of acupuncture for dysmenorrhea concluded that it is unknown if acupuncture or acupressure is effective.[61] There were also concerns of bias in study design and in publication, insufficient reporting (few looked at adverse effects), and that they were inconsistent.[61] There are conflicting reports in the literature, including one review which found that acupressure, topical heat, and behavioral interventions are likely effective.[57] It found the effect of acupuncture and magnets to be unknown.[57]

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.[62]

Spinal manipulation does not appear to be helpful.[57] Although claims have been made for chiropractic care, under the theory that treating subluxations in the spine may decrease symptoms,[63] a 2006 systematic review found that overall no evidence suggests that spinal manipulation is effective for treatment of primary and secondary dysmenorrhea.[64]

TENS

[edit]

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.[57]

Surgery

[edit]

One treatment of last resort is presacral neurectomy.[65]

Epidemiology

[edit]

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.[4] Another report states that estimates can vary between 16% and 91% of surveyed individuals, with severe pain observed in 2% to 29% of menstruating individuals.[53] Reports of dysmenorrhea are greatest among individuals in their late teens and 20s, with reports usually declining with age. The prevalence in adolescent females has been reported to be 67.2% by one study[66] and 90% by another.[67] It has been stated that there is no significant difference in prevalence or incidence between races,[67] although one study of Hispanic adolescent females indicated an elevated prevalence and impact in this group.[68] Another study indicated that dysmenorrhea was present in 36.4% of participants, and was significantly associated with lower age and lower parity.[69] Childbearing is said to relieve dysmenorrhea, but this does not always occur. One study indicated that in nulliparous individuals with primary dysmenorrhea, the severity of menstrual pain decreased significantly after age 40.[70]

A survey in Norway showed that 14 percent of females between the ages of 20 and 35 experience symptoms so severe that they stay home from school or work.[71] Among adolescent girls, dysmenorrhea is the leading cause of recurrent short-term school absence.[72]

A study from India conducted by Dr RimJhim Kumari found that painful menstruation affected 66.7% of adolescent girls studied, of which 27% sought medical advice from a doctor.[73]

References

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Dysmenorrhea

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from Grokipedia
Dysmenorrhea, commonly known as menstrual cramps or painful periods, is defined as cramping pain in the lower that occurs just before or during , often radiating to the lower back and thighs. It is one of the most prevalent gynecological disorders among women of reproductive age, affecting 16% to 91% globally, with severe symptoms impacting 2% to 29% and leading to missed school or work in up to 12% of cases. Dysmenorrhea is classified into two types: primary dysmenorrhea, which involves recurrent pain without underlying pathology and typically begins in adolescence, and secondary dysmenorrhea, which arises from identifiable conditions such as , uterine fibroids, or . The hallmark symptom of dysmenorrhea is a throbbing or cramping pain in the lower that is often perceived as stomach pain or discomfort, that may start one to three days before the menstrual period and peak within 24 hours of onset, usually subsiding after two to three days. Accompanying symptoms can include , , , , , , bloating, and water retention attributed to hormonal changes, which may interfere with daily activities. In primary dysmenorrhea, the pain results from excessive production, which triggers strong leading to reduced blood flow and tissue ischemia. Secondary dysmenorrhea, often starting later in life, is linked to underlying reproductive tract disorders; for instance, affects up to 10% of women and is a leading cause. Risk factors include age under 30, before age 11, heavy or irregular menstrual bleeding, family history, nulliparity, and . Diagnosis of dysmenorrhea begins with a detailed and , including a pelvic exam to rule out secondary causes. For suspected secondary dysmenorrhea, imaging such as or MRI may be used, and in some cases, is performed to identify conditions like . Treatment for primary dysmenorrhea focuses on symptom relief through nonsteroidal drugs (NSAIDs) like ibuprofen, which inhibit synthesis and are effective in reducing pain for most women when started just before . Hormonal contraceptives, including oral pills, patches, or intrauterine devices, suppress and thin the uterine lining to alleviate cramps. Lifestyle measures, including regular exercise (identified in recent systematic reviews and network meta-analyses as one of the most effective non-pharmacological interventions for reducing pain intensity), application of heat to the abdomen, and dietary adjustments (e.g., increasing omega-3 fatty acids, consuming ginger or peppermint tea, or high-cocoa dark chocolate, with preliminary evidence from small randomized controlled trials suggesting it may help reduce pain intensity) can provide additional relief. For secondary dysmenorrhea, management targets the underlying condition, potentially involving surgery like laparoscopic removal of fibroids or, in severe refractory cases, . Women should seek medical evaluation if menstrual cramps are severe enough to interfere with daily activities, are not relieved by over-the-counter pain medications, are worsening or have changed significantly, or are accompanied by heavy bleeding, bleeding between periods, pain during sex, unusual vaginal discharge, nausea/vomiting, fever, or persistent severe bloating, particularly if symptoms begin or worsen after age 25, to rule out underlying conditions such as endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, or ovarian cysts.

Introduction

Definition

Dysmenorrhea is the medical term for the crampy pain in the lower that occurs immediately before or during , typically lasting 8 to 72 hours. The term derives from words dys- (meaning difficult or painful), men- (meaning month), and -rrhea (meaning flow), literally translating to "difficult monthly flow." While some degree of menstrual discomfort is common, dysmenorrhea is distinguished by pain that is severe enough to interfere with daily activities, affecting approximately 2% to 29% of menstruating individuals. It is broadly classified into primary dysmenorrhea, which is not associated with underlying pelvic pathology, and secondary dysmenorrhea, which stems from identifiable disorders. The condition typically begins within 1 to 2 years after , with symptoms peaking in prevalence during the late teens or early twenties. It often improves with age or following , although for some individuals, symptoms may intensify during perimenopause due to hormonal fluctuations (particularly periods of high estrogen increasing prostaglandin production and uterine contractions) before generally ceasing after menopause once menstruation stops.

Classification

Dysmenorrhea is classified into primary and secondary types based on the presence or absence of underlying pelvic , with diagnostic criteria emphasizing age of onset, pain characteristics, and clinical evaluation for organic disease. Primary dysmenorrhea is characterized by crampy, lower occurring during without identifiable pelvic , typically manifesting as a related to normal uterine . In contrast, secondary dysmenorrhea involves menstrual pain attributable to an identifiable gynecological condition, such as or uterine fibroids, and requires exclusion of through or for confirmation. Primary dysmenorrhea generally begins 1 to 2 years after , coinciding with the establishment of ovulatory cycles, and affects adolescents and young adults without evidence of structural abnormalities on or diagnostic tests. The pain is typically colicky, confined to the lower , and follows a predictable cyclic pattern aligned with menses, often improving or resolving by age 25 to 30 or following in many cases. relies on a history of pain starting soon after , absence of abnormal pelvic findings, and normal menstrual flow without . Secondary dysmenorrhea, by comparison, often emerges later in the reproductive years, typically after age 25 or following a period of painless menses, and may progressively worsen over time due to the advancing underlying disorder. Pain patterns may deviate from strict cyclicity, potentially including non-menstrual pelvic discomfort, heavy or irregular , or , prompting further investigation to identify . Classification as secondary requires clinical correlation with risk factors, such as prior pelvic surgery or , and confirmation via , MRI, or to rule out conditions like . A rare subtype, membranous dysmenorrhea, involves the periodic shedding of the entire endometrial lining as a single cast, leading to intense colicky pain from , though it is not always distinguished as a separate category and may overlap with primary or secondary forms. Overall, hinges on a thorough history assessing onset timing (early for primary, later for secondary), pain reproducibility with menses, and exclusion of through targeted diagnostics, ensuring appropriate differentiation for .

Clinical Presentation

Signs and Symptoms

Dysmenorrhea manifests primarily as crampy, colicky pain in the lower abdomen, often perceived as stomach pain or discomfort, particularly on the first day of menstruation. This pain is the most common cause of such stomach discomfort on the first day of a period in primary dysmenorrhea, where elevated prostaglandins trigger strong uterine contractions to shed the endometrial lining, causing lower abdominal cramps that often feel like stomach pain and radiate to the lower back and thighs. This pain typically begins at the onset of , peaks within 24 hours, and is intermittent in nature. In primary dysmenorrhea, the discomfort is usually relieved by heat or nonsteroidal anti-inflammatory drugs (NSAIDs). The pain episode typically lasts 12 to 72 hours, resolving as menstrual flow diminishes, though individual experiences vary, with some reporting milder cramps that come and go throughout the menstrual period. Dysmenorrhea affects 45% to 95% of women of reproductive age, with 5% to 30% reporting severe symptoms that significantly disrupt daily activities. Accompanying symptoms are common and include , , or loose stools, bloating, water retention, , , and , which can further impair during menses. These effects often arise from hormonal changes and prostaglandin release. While primary dysmenorrhea presents with these characteristic cyclic symptoms in the absence of pelvic pathology, secondary dysmenorrhea may involve similar pain but often with additional features like persistent discomfort or abnormal bleeding indicative of an underlying condition.

Complications

Dysmenorrhea, especially in its severe form, profoundly affects by interfering with daily functioning, social interactions, and emotional well-being. Affected individuals often experience reduced at work or school, with —attending activities while impaired—common during episodes. School and work absenteeism is particularly notable, with approximately 12% of women missing monthly activities due to pain, and up to 14% of adolescents absent from school. This leads to broader psychological impacts, including heightened risks of anxiety and depression, as severe pain disrupts normal routines and exacerbates vulnerabilities. Untreated or severe dysmenorrhea can progress to physical complications that extend beyond menstrual cycles. Chronic develops in many cases, with studies showing a significant association between dysmenorrhea and persistent syndromes, potentially due to central sensitization or underlying pathologies. Sleep disturbances are prevalent, manifesting as , reduced sleep efficiency, and prolonged , which further compound and daytime impairment. Gastrointestinal issues, such as persistent or altered bowel habits, may continue outside of menses, often co-occurring with conditions like that amplify overall discomfort. In secondary dysmenorrhea, failure to address the root cause heightens reproductive risks, including progression to or . Conditions like , a frequent , impair ovarian and tubal function, reducing rates by up to 30-50% in affected individuals if untreated. , another common cause, can scar fallopian tubes, elevating risk through impaired embryo transport. Globally, 5-15% of cases are severe enough to cause substantial , contributing to significant disability-adjusted life years (DALYs) lost through chronic impairment and productivity deficits; dysmenorrhea imposes a greater than any other gynecologic complaint.

Etiology and Pathophysiology

Causes

Dysmenorrhea is categorized into primary and secondary types, with primary dysmenorrhea arising without any identifiable pelvic or structural abnormality in the reproductive organs. It is linked to the normal physiological release of prostaglandins from the during , which occurs in otherwise healthy individuals. This form typically manifests shortly after and is considered a after ruling out other conditions. In contrast, secondary dysmenorrhea results from an underlying gynecological disorder or anatomical issue that disrupts normal menstrual function. The most common cause is , a condition where endometrial-like tissue grows outside the , accounting for 62-75% of cases identified in adolescents undergoing for chronic . Other frequent secondary causes include uterine fibroids (leiomyomas), which are benign growths in the uterine wall; , involving the invasion of endometrial tissue into the ; (PID), an infection of the upper genital tract; and the presence of intrauterine devices (IUDs), which can provoke inflammatory responses. Rarer etiologies of secondary dysmenorrhea encompass , which obstructs menstrual flow; ovarian cysts, particularly functional or endometriotic types; and obstructive congenital anomalies such as , transverse vaginal septum, or other uterine malformations that impede menstrual flow. Primary dysmenorrhea is distinguished by the absence of any detectable organic on clinical evaluation, whereas secondary forms are characterized by anatomical alterations, inflammatory processes, or neoplastic changes that can be identified through diagnostic investigation.

Mechanism

Dysmenorrhea pain primarily arises from excessive production of prostaglandins, particularly prostaglandin F2α (PGF2α), during the . As the sheds, membrane phospholipids release , which is then metabolized by (COX) enzymes—primarily COX-2—into prostaglandins. These prostaglandins bind to receptors on uterine cells, inducing myometrial hypercontractility and increasing uterine tone. In primary dysmenorrhea, the elevated prostaglandins trigger strong uterine contractions necessary to shed the uterine lining, resulting in lower abdominal cramps that are frequently perceived as stomach pain or discomfort. These cramps typically peak within the first 24 hours of menstrual onset. The resulting strong, dysrhythmic contractions elevate intrauterine pressure, compressing endometrial blood vessels and causing transient uterine ischemia. This ischemic state sensitizes nociceptors, particularly type unmyelinated pain fibers in the and , to anaerobic metabolites like and produced during hypoxia. Activation of these nociceptors transmits signals via visceral afferent nerves through the sympathetic plexus to the (T10-L1 levels), where they are perceived as cramping lower that may radiate to the back or thighs. Women with primary dysmenorrhea exhibit higher endometrial prostaglandin levels, correlating with more intense contractions and greater severity. Women with primary dysmenorrhea often exhibit heightened pain sensitivity during menstruation, characterized by lower pain thresholds to experimental stimuli such as pressure, cold, and ischemic pain. This heightened sensitivity, observed both at sites of referred pain and remote areas, is attributed to prostaglandin-induced peripheral sensitization of nociceptors and may involve potential central sensitization mechanisms. In secondary dysmenorrhea, underlying pathologies amplify these mechanisms through additional pathways. promotes chronic pelvic , with ectopic endometrial implants releasing pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), and IL-8, which enhance local synthesis and sensitize nociceptors independently of menstrual contractions. Uterine fibroids contribute via mechanical distortion, as their growth—especially of submucosal or intramural types—increases myometrial rigidity and disrupts normal peristaltic waves, leading to prolonged contractions, heightened intrauterine pressure, and exacerbated ischemic pain during menses. Emerging research suggests an association between dysmenorrhea and alterations in the gut microbiome. Mendelian randomization studies have provided causal evidence that dysmenorrhea influences gut microbiota composition, with reductions in genera such as the Eubacterium xylanophilum group and Roseburia (within the Lachnospiraceae family) and increases in Erysipelotrichaceae. Beneficial taxa such as Blautia and Bifidobacterium have been negatively associated with pain severity. In animal models of primary dysmenorrhea, microbiome-targeted interventions, such as the traditional Chinese medicine Wenjing Zhitong Decoction, have been shown to restore these beneficial taxa and alleviate symptoms. Some studies have also linked specific taxa like Escherichia/Shigella to broader menstrual disorders via pathways involving inflammation and estrogen metabolism.

Risk Factors and Epidemiology

Risk Factors

Risk factors for dysmenorrhea can be categorized as non-modifiable, modifiable, and those specific to secondary dysmenorrhea. Non-modifiable factors include early age at , nulliparity, and family history, often linked to genetic predispositions such as polymorphisms in the ESR1 encoding . Early , defined as onset before age 12, is associated with increased odds of dysmenorrhea, with studies reporting adjusted odds ratios ranging from 1.22 to 4.67 depending on the and used. Nulliparity, or lack of prior , elevates risk compared to parous women, as parity shows an inverse association with dysmenorrhea prevalence. Family history strongly predicts dysmenorrhea, with odds ratios varying from 1.68 to as high as 20.7 in affected lineages, and genetic studies have identified ESR1 polymorphisms, such as PvuII variants, as significantly more common in primary dysmenorrhea patients than controls. Modifiable risk factors encompass lifestyle and physiological elements that can influence dysmenorrhea onset or severity. Heavy or prolonged menstrual bleeding (menorrhagia) substantially heightens , with one reporting an adjusted of 10.28 for those with heavy flows. is a well-established , increasing the of primary dysmenorrhea ( 1.45, 95% CI: 1.30–1.61). Low (BMI) is linked to higher incidence, potentially due to associated hormonal imbalances, alongside behaviors like attempts to lose weight. elevates , with high stress levels showing a positive association independent of other factors. or lack of regular exercise also contributes, as physical inactivity correlates with greater symptom burden compared to active individuals. For secondary dysmenorrhea, risk factors often relate to underlying gynecological conditions. Prior pelvic infections, such as , predispose individuals by promoting intrauterine adhesions or chronic inflammation that intensifies menstrual pain. Use of copper intrauterine devices (IUDs) can worsen or induce symptoms due to increased release, though this varies by device type. Obesity raises the likelihood of secondary causes like uterine fibroids, with elevated BMI identified as a key modifiable risk for fibroid development and associated dysmenorrhea.

Prevalence and Demographics

Dysmenorrhea affects a significant proportion of menstruating individuals worldwide, with estimates ranging from 50% to 90%. A and of studies across 70 countries reported a pooled global of 71.3% (95% CI 68.7%-73.8%), including 73% for primary dysmenorrhea and 35% for secondary dysmenorrhea. Severe cases, which substantially impair daily activities, occur in 10% to 25% of affected individuals, with one global estimate indicating 10%-20% reporting debilitating pain. These figures highlight dysmenorrhea as a common gynecological issue, though underreporting remains prevalent due to stigma and limited healthcare access. Prevalence varies notably by age, peaking during and early adulthood before declining. Among adolescents, rates reach up to 90%, with studies showing 60% to 93% affected in this group. In young women under 25 years, prevalence is similarly high at around 70%-80%, but it decreases with advancing age, becoming less common after 30 and rare post-menopause due to the cessation of . Severe dysmenorrhea is most frequent among those aged 18-28, affecting over 50% in some cohorts. Geographically and racially, dysmenorrhea is largely consistent across diverse populations, with no major disparities by race or in overall occurrence. However, minoritized racial and ethnic groups may experience worse outcomes, including higher intensity, in certain contexts. Reporting rates tend to be higher in urban settings compared to rural areas, attributed to greater health awareness and access to medical services, though actual shows minimal urban-rural differences in many studies (e.g., 52.5% urban vs. 55.7% rural in one comparison). Epidemiological trends indicate relative stability in prevalence over time, with no major shifts observed in 2025 data from recent global reviews. However, rates have increased, particularly since 2020, driven by improved healthcare access and reduced stigma, as evidenced by rising self-reported cases and treatment market growth.

Diagnosis

Clinical Assessment

The clinical assessment of dysmenorrhea begins with a thorough to characterize the and identify potential underlying causes. Key elements include the age of onset, with primary dysmenorrhea typically starting within 6-12 months after , often coinciding with the establishment of ovulatory cycles, whereas secondary dysmenorrhea may emerge later, such as after age 25. The history should detail the pain's location, usually in the lower with possible radiation to the back or thighs, its duration (typically 8-72 hours for primary dysmenorrhea, peaking 24-48 hours after menses onset), and associated symptoms such as or . Relieving and aggravating factors are evaluated, including responses to , , or over-the-counter analgesics, alongside menstrual patterns like cycle regularity and flow volume. The sexual and reproductive history is essential, encompassing details on parity, contraceptive use, , and symptoms like . A comprehensive physical examination follows to rule out structural abnormalities. Vital signs are assessed as part of the initial evaluation to detect any systemic issues. Abdominal palpation is performed to identify tenderness, guarding, or masses in the lower quadrants. The pelvic examination, when appropriate (e.g., in post-pubertal patients), includes bimanual palpation to evaluate uterine size, position, tenderness, adnexal masses, or cervical abnormalities such as friability or discharge. In primary dysmenorrhea, the exam is typically normal, with a nontender, normal-sized uterus. Certain historical features serve as red flags suggesting secondary dysmenorrhea, warranting further evaluation. These include pain onset after age 25, irregular menstrual cycles, dyspareunia, post-coital bleeding, intermenstrual bleeding, unusual vaginal discharge, severe pain that is unresponsive to over-the-counter pain medications (such as ibuprofen or naproxen), interferes with daily activities or work/school, is worsening or has changed significantly, or is accompanied by persistent severe bloating, heavy bleeding, bleeding between periods, nausea, vomiting, fever, or other concerning symptoms. These red flags may indicate underlying conditions such as endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, or ovarian cysts. Patients experiencing these symptoms should consult a healthcare provider, preferably a gynecologist, for evaluation. Diagnosis of primary dysmenorrhea is clinical, relying on a characteristic history of crampy, cyclical lower starting at menses onset in the absence of pelvic , with exclusion of secondary causes through the aforementioned history and physical findings. This approach aligns with guidelines emphasizing functional pain syndromes, where the assessment prioritizes symptom pattern and ruling out organic disease without initial invasive testing.

Further Investigations

Further investigations are warranted when the clinical history suggests secondary dysmenorrhea, such as progressively worsening pain, onset after age 25, or associated symptoms like . These evaluations aim to identify or exclude underlying pelvic pathologies, which are suspected in approximately 10% of dysmenorrhea cases among adolescents and young adults. Imaging modalities are the cornerstone of further assessment. Transvaginal ultrasound serves as the initial noninvasive test to evaluate for uterine fibroids, ovarian endometriomas, and early signs of , offering high sensitivity (up to 91%) and specificity (up to 98%) for certain features like bowel involvement. If ultrasound findings are inconclusive or is suspected, (MRI) provides superior characterization, with a sensitivity of 77% and specificity of 89% for detecting myometrial . Laboratory studies support imaging by screening for systemic effects or specific markers. A (CBC) helps detect secondary to or chronic inflammation. Serum CA-125 levels may be assessed in cases of suspected , though its diagnostic utility is limited by moderate sensitivity (61.1%) and specificity (87.5%). Hormonal assays, including and levels, are indicated if irregular cycles accompany the pain, to rule out endocrine disorders contributing to secondary causes. Invasive procedures are reserved for confirmatory when noninvasive tests are nondiagnostic or when therapeutic intervention is planned. remains the gold standard for definitively diagnosing endometriosis through direct visualization and , particularly in women with persistent symptoms or concerns. is employed to investigate intrauterine abnormalities, such as polyps or adhesions, that may contribute to dysmenorrhea.

Management

Prior to seeking professional medical evaluation, temporary self-management strategies for menstrual pain may include initiating nonsteroidal anti-inflammatory drugs such as ibuprofen or naproxen 1-2 days before the expected onset of menses—consulting a pharmacist or healthcare provider if uncertain about suitability—applying a hot water bag or heating pad to the lower abdomen, engaging in light exercise or yoga, and reducing stress through relaxation techniques. These first-line measures provide initial relief and align with clinical recommendations.

Pharmacological Treatments

Pharmacological treatments for dysmenorrhea (痛经, menstrual cramps) primarily target the underlying mechanisms of , such as excessive production, and are considered first-line options for managing symptoms in both primary and secondary cases. These therapies include nonsteroidal anti-inflammatory drugs (NSAIDs), hormonal contraceptives, and select alternatives for specific scenarios or when primary options are contraindicated. from systematic reviews supports their use, with varying by agent and patient response, though approximately 18% of women report minimal or no relief with NSAIDs, possibly due to central mechanisms on which NSAIDs have limited effect. Nonsteroidal drugs (NSAIDs) are the cornerstone of pharmacological for dysmenorrhea due to their ability to inhibit (COX) enzymes, thereby reducing synthesis responsible for , nociceptor sensitization, and . Ibuprofen (芬必得) is generally recommended as a preferred NSAID over acetaminophen (泰诺林) for menstrual cramps, as it more effectively targets the prostaglandin-mediated mechanism underlying dysmenorrhea. Common examples include ibuprofen and naproxen, which provide relief in approximately 82% of cases when initiated at the onset of symptoms or preemptively 1-2 days prior to menses. A of randomized controlled trials demonstrated that NSAIDs are over four times more effective than for relief (odds ratio 4.37, 95% CI 3.76-5.09), outperforming acetaminophen, which provides general pain relief but is less targeted and effective for dysmenorrhea. Typical dosing involves ibuprofen at 400-600 mg every 6-8 hours or naproxen at 500-550 mg initially followed by 250 mg every 6-12 hours, continued for 2-3 days as needed, preferably taken with food to minimize gastrointestinal upset. Patients should consult a healthcare professional for personalized dosing and to assess for contraindications prior to use. Side effects are primarily gastrointestinal, such as dyspepsia or ulceration (odds ratio 1.58, 95% CI 1.12-2.23), with rare renal or cardiovascular risks at short-term use; COX-2 selective inhibitors like celecoxib are generally avoided due to heightened thrombotic concerns. Hormonal contraceptives, particularly combined oral contraceptive pills (COCs), offer effective symptom control by suppressing ovulation, thinning the endometrium, and decreasing prostaglandin release, making them suitable for primary dysmenorrhea especially in patients seeking contraception. These agents provide pain relief in approximately 80% of responsive cases, with continuous rather than cyclic regimens often yielding faster and more sustained benefits. A Cochrane review confirmed that COCs significantly reduce dysmenorrhea severity compared to placebo, though evidence quality is moderate due to study limitations. Standard dosing follows typical COC schedules (e.g., 21 days active followed by 7 days placebo, or continuous), with alternatives like progestin-only implants or intrauterine systems for those intolerant to estrogen. Potential side effects include nausea, mood changes, and an elevated risk of venous thromboembolism (particularly with higher estrogen doses), necessitating individualized risk assessment. For patients with milder symptoms or NSAID contraindications (e.g., ), acetaminophen (泰诺林) serves as a less potent alternative, weakly inhibiting COX and providing moderate relief though inferior to NSAIDs in comparative trials. , another NSAID with specific affinity for uterine tissue, is dosed at 500 mg initially followed by 250 mg every 6 hours for up to 3 days and shares similar efficacy and gastrointestinal risks. In refractory cases accompanied by heavy menstrual flow, may be considered adjunctively to reduce bleeding volume by 40-50% per cycle via action, though it does not directly target ; dosing is typically 1,300 mg three times daily for up to 5 days during menses, with monitoring for thrombotic events in at-risk individuals.

Non-Pharmacological Interventions

Non-pharmacological interventions for dysmenorrhea encompass a range of lifestyle modifications, physical therapies, and complementary approaches aimed at alleviating menstrual pain without the use of medications. These methods focus on reducing uterine muscle contractions, improving blood flow, and modulating pain perception through natural mechanisms. Long-term strategies, such as maintaining regular sleep and exercise routines, staying warm, and managing stress to support overall well-being, can help prevent recurrent pain by reducing severity and frequency, based on clinical observations and studies linking these factors to symptom improvement. Common strategies include adequate hydration, heat application, regular , dietary adjustments, and neuromodulation techniques such as (TENS). Evidence from systematic reviews indicates that these interventions can provide moderate to significant pain relief, particularly when initiated before or during the onset of symptoms. Recent systematic reviews and network meta-analyses (2024–2025) identify regular exercise, topical heat therapy, and acupuncture as among the most effective evidence-based non-pharmacological interventions for relieving menstrual cramps in primary dysmenorrhea. A 2024 Bayesian network meta-analysis ranked exercise highest (rank probability 30.0%, mean difference -3.20 on VAS), followed by topical heat (26.0%, -2.97) and acupuncture (16.0%, -2.90). A 2025 systematic review and meta-analysis further supports heat therapy, showing significant pain reduction comparable to NSAIDs with fewer adverse effects. These interventions are recommended for their efficacy, safety, accessibility, and low risk profile. Ensuring adequate hydration through increased water intake serves as a simple, low-risk measure to alleviate dysmenorrhea symptoms, including bloating and gut discomfort such as diarrhea. Clinical studies demonstrate that higher water consumption can reduce pain intensity, shorten menstrual bleeding duration, and decrease reliance on pain relievers by supporting fluid balance and mitigating inflammatory responses. Heat therapy, often delivered via heating pads or patches, is a simple and accessible option for managing dysmenorrhea symptoms. Applied to the lower at temperatures of 40–45°C, it promotes , enhances pelvic blood circulation, and relaxes tense uterine muscles, thereby reducing intensity. Long-term practices like staying warm may contribute to fewer recurrent episodes. A of randomized controlled trials demonstrated that superficial significantly lowers scores compared to no treatment, with a mean difference of -4.04 on the visual analog scale (VAS), and shows comparable efficacy to analgesics with fewer side effects. A 2025 systematic review and meta-analysis confirmed that heat therapy significantly reduces pain intensity compared to no treatment (weighted mean difference -1.85 over 3 months) and provides comparable relief to NSAIDs (weighted mean difference -1.10) with reduced risk of adverse effects (relative risk 0.30). Application for 15–20 minutes per session during menstrual episodes is typically recommended, with studies reporting consistent relief across multiple cycles. Regular exercise, particularly aerobic activities such as walking (including walking a dog), , or , has been shown to mitigate dysmenorrhea by stimulating endorphin release and improving overall circulation. Light to moderate exercise, such as walking a dog, is generally recommended during menstruation, even when experiencing emotional symptoms such as mood swings, irritability, or discomfort, as it can help relieve these symptoms by releasing endorphins, reducing stress, and improving overall mood. Individuals should listen to their body and opt for lighter activity or rest if feeling too fatigued or experiencing severe cramps, though most women benefit from staying active. Engaging in moderate-intensity sessions of at least 30 minutes per day, ideally three to five times weekly, can decrease pain severity and duration. Incorporating stress management techniques alongside exercise supports positive mood and may further reduce symptom frequency. Systematic reviews highlight large effect sizes for in reducing menstrual pain compared to no intervention, attributing benefits to enhanced progesterone levels and stress reduction. This aligns with its ranking as the most effective non-pharmacological intervention in a 2024 network meta-analysis. , in particular, combines stretching and breathing to further alleviate symptoms, with meta-analyses confirming its role in improving and . Physical affection, such as hugging, releases oxytocin, known as the "cuddle hormone," which has general pain-relieving effects by modulating pain signals, potentially through inhibition in the spinal cord. Studies have shown that women with primary dysmenorrhea have significantly lower serum oxytocin concentrations during menses compared to healthy controls, with lower levels associated with greater menstrual pain severity. This association suggests that higher oxytocin levels may help reduce pain, but no clinical trials have directly confirmed that hugs or oxytocin released from hugging specifically relieve menstrual cramps or dysmenorrhea. As such, this remains a potential complementary lifestyle approach alongside established methods like exercise and heat application. Dietary modifications, including doctor-guided supplementation with omega-3 fatty acid, vitamin E, or vitamin B1 (thiamine), and adoption of low-fat, high-fiber diets, target associated with dysmenorrhea. Omega-3s, found in or supplements at doses of 1–2 g per day for two to three months, inhibit production, leading to reduced pain intensity. Vitamin E supplementation has been shown in meta-analyses to significantly reduce pain intensity in primary dysmenorrhea. Vitamin B1 at 100 mg daily demonstrates efficacy in clinical trials for alleviating symptoms after consistent use. Clinical trials indicate that such supplementation is as effective as nonsteroidal drugs in some cases, with benefits accumulating over cycles. Low-fat diets similarly lower inflammatory markers by decreasing intake, promoting overall symptom relief. Conversely, high-fat red meats such as steak, which are rich in arachidonic acid, may increase prostaglandin production and inflammation, potentially worsening dysmenorrhea symptoms. Consumption of dark chocolate with high cocoa content (e.g., 70% cocoa) has also been investigated in small randomized controlled trials. In a 2023 single-blind RCT, 35 g of 70% dark chocolate significantly reduced pain intensity in primary dysmenorrhea, with efficacy comparable to 400 mg ibuprofen (no significant difference in pain reduction, p = 0.490), likely due to its magnesium content (59.5 mg per 35 g) and flavonoids exerting anti-inflammatory effects by inhibiting prostaglandin production. However, these findings are preliminary, and larger-scale studies are needed for confirmation. In addition to dietary modifications, herbal teas such as chamomile combined with cinnamon are used as popular home remedies to help alleviate dysmenorrhea symptoms. Chamomile is traditionally recognized for its anti-inflammatory, antispasmodic, and calming properties, which may help relax uterine muscles and reduce pain. Cinnamon has anti-inflammatory effects, and some small randomized controlled trials have indicated that its consumption (as tea or supplements) can reduce the intensity of menstrual pain and the volume of menstrual bleeding. However, the scientific evidence for these herbs—particularly in combination—is limited, primarily from small-scale studies, and further high-quality research is required to establish efficacy and safety. These remedies are not substitutes for evidence-based medical treatments such as NSAIDs or hormonal therapies, and individuals with severe or persistent symptoms should consult a healthcare provider. For managing nausea associated with menstruation, common self-care strategies include consuming ginger tea or peppermint tea to soothe the stomach and potentially reduce nausea, drawing on their traditional use and evidence for antiemetic effects in general contexts. Ginger has demonstrated effectiveness for nausea in various settings and may also contribute to overall menstrual symptom relief, while peppermint tea may aid in relieving digestive discomfort. Additionally, eating small, frequent meals of bland, easy-to-digest foods, staying hydrated with regular sips of clear fluids, and avoiding greasy, fried, strong-smelling, or spicy foods that may exacerbate symptoms are recommended measures. These approaches are based on general nausea management guidelines, with limited specific evidence for their use in menstrual contexts; they are best used as complementary strategies alongside other treatments, and consultation with a healthcare provider is advised for persistent or severe symptoms. Transcutaneous electrical nerve stimulation (TENS) involves applying low-frequency electrical impulses (typically 2–10 Hz) to the lower back or via skin electrodes, interrupting signals and promoting endorphin release. Trials report 60–80% of users experiencing substantial relief, with reduction often exceeding 50% within 20 minutes of application. High-quality reviews support its use as a safe, non-invasive option, particularly for those seeking immediate symptom control during . A 2024 Cochrane review supports its for control in primary dysmenorrhea based on moderate-quality . Acupressure and abdominal massage are complementary approaches derived from traditional practices that may help alleviate menstrual pain in primary dysmenorrhea. Acupressure involves applying pressure to specific points such as Sanyinjiao (SP6), Guanyuan (CV4), and Qihai (CV6). Gentle abdominal massage, typically involving light circular motions on the lower abdomen, can promote blood circulation, relax pelvic and uterine muscles, and reduce discomfort, thereby alleviating pain. However, vigorous or forceful pressing or rubbing should be avoided, as it may exacerbate cramps and increase pain. When performed by partners or others, light circular motions should be employed, with ongoing communication to identify painful areas and adjust pressure based on feedback. These techniques are often combined with deep breathing and heat application. Some clinical studies and systematic reviews suggest potential benefits for pain reduction, though the evidence is generally limited or moderate in quality. Individuals should use these methods gently and consult a healthcare provider, particularly if pain is severe, prolonged, or accompanied by other symptoms, to rule out underlying pathological conditions. Overall evidence for these interventions is moderate, with and exercise demonstrating reliable benefits in meta-analyses of randomized trials, including their top rankings in recent network meta-analyses. also shows short-term pain reduction in network meta-analyses, though long-term effects require further study. Moxibustion, a traditional Chinese medicine technique involving the burning of mugwort near acupoints, has demonstrated potential benefits for pain relief in primary dysmenorrhea according to systematic reviews and meta-analyses, but evidence quality varies and consultation with a healthcare provider is advised. These approaches are best integrated into a personalized plan, often yielding additive effects when combined.

Surgical and Emerging Options

Surgical interventions for dysmenorrhea are typically reserved for refractory cases where medical therapies have failed and an underlying pathology, such as , is confirmed. , the surgical removal of the , is considered a definitive treatment for severe secondary dysmenorrhea, particularly when associated with conditions like fibroids or , as it eliminates menstrual cycles and associated pain. This procedure is most appropriate for women who have completed childbearing, with studies indicating high satisfaction rates among those with chronic heavy bleeding and pain. However, it carries risks including hemorrhage, , and injury to adjacent organs like the or bowel, with infection rates reported in approximately 5-10% of cases depending on surgical approach. Laparoscopic excision of endometriotic lesions is a targeted surgical option for secondary dysmenorrhea caused by , involving the precise removal of abnormal tissue to reduce pain and improve . Prospective studies have demonstrated significant pain reduction lasting up to 5 years post-procedure, with a lower likelihood of recurrence compared to ablative techniques. This minimally invasive method preserves potential and is preferred over more radical surgeries when possible. Uterine nerve , also known as laparoscopic uterosacral nerve (LUNA), involves interrupting pain-transmitting nerves near the and has been explored for primary and secondary dysmenorrhea unresponsive to other treatments. While early reports suggested potential alleviation of symptoms in outpatient settings, randomized trials have shown mixed results, with no consistent improvements in pain or compared to diagnostic alone, limiting its routine use. Emerging therapies focus on non-invasive or minimally invasive innovations for both primary and secondary dysmenorrhea, often targeting pain pathways or without systemic side effects. Low-level light therapy (LLLT), using wavelengths such as 630-940 nm, has shown promise in recent randomized controlled trials for primary dysmenorrhea, with a indicating a mean difference of -4.02 points on the visual analog scale (VAS) after 12 weeks compared to sham treatment (n=150, 95% CI -7.21 to -0.82). These 2024-2025 studies highlight LLLT's safety profile, though larger randomized controlled trials (RCTs) are needed to confirm long-term efficacy. Photodynamic therapy (PDT), particularly low-power visible-light-activated variants, represents another investigational approach for primary dysmenorrhea, activating photosensitizers to modulate inflammatory responses and reduce . Multicenter double-blind trials have reported effective relief without impacting normal ovarian function, and when combined with oral contraceptives, it enhances symptom control over either alone. Safety data support its use, but further RCTs are required to establish optimal protocols. Core stability exercises, emphasizing strengthening of abdominal and pelvic muscles, have emerged as a novel , with 2025 studies, including comparative trials, showing significant pain reduction and functional improvements with exercises after 8-week programs, comparable to other physical therapies. These exercises enhance pelvic support and reduce cramping intensity, though head-to-head trials against or indicate similar overall benefits. Long-term acupuncture effects have been documented in cohort studies, providing sustained relief from primary dysmenorrhea symptoms for up to three menstrual cycles post-treatment through modulation of inflammatory cytokines and pain pathways. A 2024 analysis further noted reduced depression risk as a secondary benefit, underscoring its role in holistic management. Indications for these surgical and emerging options generally include persistent symptoms despite optimized medical and diagnostic confirmation of via or . In 2024, introduced a hormonal therapy offering dual contraception and dysmenorrhea relief, expanding options for women seeking integrated . Risks for emerging therapies primarily involve the need for additional high-quality RCTs to validate durability and safety across diverse populations.

History and Societal Impact

Historical Perspectives

The recognition of dysmenorrhea dates back to ancient civilizations, where it was often attributed to imbalances in bodily fluids or obstructions in the . In the 5th century BCE, described painful menstruation as resulting from a "uterine flux" or retention of menstrual blood due to cervical obstruction, positing that this blockage caused distension and pain in the ; he recommended interventions like early marriage and physical activity to promote flow. Similarly, , as documented in texts like the from around 200 BCE, addressed menstrual disorders through concepts of stagnation and , employing to alleviate pain associated with irregular or painful periods since the (206 BCE–220 CE). By the , dysmenorrhea began to be acknowledged as a distinct clinical entity separate from general menstrual irregularities, with physicians documenting it as a common yet debilitating condition warranting specific treatments such as herbal remedies and uterine dilations. The groundwork for understanding its was laid in with the discovery of prostaglandins by Ulf von Euler, who identified these compounds in seminal fluid and later linked them to , though their direct role in dysmenorrhea was not established until the when elevated levels were found in menstrual fluid of affected women. Key milestones in the advanced both and . In the 1970s, the introduction of nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit synthesis, revolutionized treatment by providing effective relief for primary dysmenorrhea in 70–90% of cases, shifting focus from symptomatic palliation to . The into primary dysmenorrhea (crampy pain without underlying ) and secondary dysmenorrhea (pain due to conditions like ) became standardized in medical practice during the , aiding in . Prior to 2025, emphasis on secondary causes remained limited until the 1990s, when rising awareness of —through groups and highlighting its in 10–15% of reproductive-age women—prompted greater investigation of dysmenorrhea as a potential symptom of pelvic .

Societal and Cultural Aspects

Dysmenorrhea imposes a substantial economic burden globally, primarily through lost productivity and healthcare expenditures. In , the annual economic cost of menstrual symptoms, including dysmenorrhea, reaches approximately $8.6 billion (as of recent estimates), with 72% attributed to productivity losses such as and reduced work efficiency, and 28% to direct medical costs. This burden is amplified in low-income settings, where untreated cases lead to higher rates of work and school ; for instance, surveys in and indicate that up to one in five female workers miss work monthly due to menstrual disorders like dysmenorrhea. In developing countries, limited access to affordable treatments exacerbates these losses, contributing to broader economic disparities for women and girls. Cultural stigma surrounding significantly hinders the recognition and management of dysmenorrhea, particularly in conservative societies where it is viewed as taboo or unclean. In many developing countries, such as those in and , period poverty—defined as the inability to afford menstrual products—intersects with these norms, leading to isolation, , and underreporting of symptoms. For example, in rural , deep-rooted cultural taboos discourage open discussion of menstrual pain, resulting in harmful practices like using inadequate materials and avoiding medical consultation. This stigma fosters a cycle of silence, where women and girls in conservative cultures often endure severe dysmenorrhea without seeking help, perpetuating health inequities. Dysmenorrhea contributes to gender inequities in the workplace by reducing women's participation and productivity, widening economic gaps. Menstrual pain leads to absenteeism and presenteeism, with studies showing associations between menstrual disorders and lower workforce engagement, particularly in environments lacking supportive policies like menstrual leave. The (WHO) addresses this through ongoing advocacy for menstrual health as a issue, emphasizing to combat stigma and promote ; in 2022, WHO called for menstruation-responsive workplaces and schools, with continued initiatives in 2024–2025 highlighting access to products and information as key to equitable opportunities, including an August 2024 statement affirming menstrual health as a fundamental human right and a May 2024 report revealing gaps in school-based menstrual health (only 39% of schools worldwide provide it). Access to dysmenorrhea treatment remains uneven, with significant disparities affecting adolescents in rural and low-resource areas. In , many adolescent girls lack effective pain relief due to limited availability of medications and healthcare facilities, compounded by stigma that deters seeking care. Rural-urban divides are evident; for instance, in , rural adolescent girls report lower treatment-seeking rates compared to urban peers, often relying on traditional remedies amid barriers like distance to clinics and . These gaps disproportionately impact young girls in developing countries, where untreated dysmenorrhea can lead to chronic educational and economic disadvantages.

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