Bolesne miesiączkowanie
Patofizjologia i mechanizm

Bolesne miesiączkowanie (dysmenorrhea) jest powszechnym problemem ginekologicznym u kobiet w wieku rozrodczym, charakteryzującym się skurczowym bólem w dolnej części brzucha podczas menstruacji. Wyróżnia się bolesne miesiączkowanie pierwotne, bez patologii narządów miednicy, oraz wtórne, związane z chorobami takimi jak endometrioza, adenomioza czy mięśniaki macicy. Patofizjologia pierwotnego bolesnego miesiączkowania opiera się głównie na nadprodukcji prostaglandyn F2α (PGF2α) i E2 (PGE2) w endometrium, które indukują skurcze mięśniówki macicy i zwężenie naczyń, prowadząc do niedokrwienia, hipoksji i uwrażliwienia zakończeń nerwowych. Spadek poziomu progesteronu po degeneracji ciałka żółtego inicjuje kaskadę enzymatyczną (fosfolipaza A2, COX), skutkującą zwiększoną syntezą prostaglandyn. Wysokie stężenia PGF2α i PGE2 korelują z intensywnością bólu, co potwierdza skuteczność inhibitorów syntezy prostaglandyn (NLPZ) w terapii. Dodatkowo, leukotrieny i wazopresyna mogą modulować ból poprzez zwiększenie wrażliwości włókien nerwowych i zmniejszenie przepływu krwi w macicy, co może tłumaczyć oporność na NLPZ u niektórych pacjentek.

Bolesne miesiączkowanie – patogeneza i mechanizm

Bolesne miesiączkowanie (dysmenorrhea) to jeden z najczęstszych objawów ginekologicznych występujących u kobiet w wieku rozrodczym. Jest to dolegliwość charakteryzująca się kurczowym, skurczowym bólem w dolnej części brzucha, który pojawia się tuż przed lub podczas miesiączki i może utrzymywać się przez kilka dni. Istotne jest zrozumienie mechanizmów patofizjologicznych leżących u podstaw tego powszechnego problemu zdrowotnego, który dotyka około 42 miliony kobiet w Stanach Zjednoczonych, a u 3,5 miliona powoduje niezdolność do funkcjonowania przez jeden do dwóch dni w miesiącu z powodu silnego nasilenia objawów1.

Pierwotne i wtórne bolesne miesiączkowanie

Bolesne miesiączkowanie można podzielić na dwie kategorie: pierwotne i wtórne23. Pierwotne bolesne miesiączkowanie odnosi się do nawracającego bólu bez identyfikowalnej przyczyny patologicznej w narządach miednicy4. Występuje ono zazwyczaj 6-12 miesięcy po pierwszej miesiączce, gdy cykle stają się owulacyjne, a szczyt częstości występowania przypada na późne lata nastoletnie lub wczesne dwudzieste5. Wtórne bolesne miesiączkowanie jest związane z występowaniem choroby w narządach miednicy, takiej jak endometrioza, adenomioza, mięśniaki macicy czy inne schorzenia6. Ból związany z wtórnym bolesnym miesiączkowaniem często zaczyna się później w życiu, pogarsza się z czasem i może trwać dłużej niż ból związany z pierwotnym bolesnym miesiączkowaniem7.

Rola prostaglandyn w patogenezie bolesnego miesiączkowania

Badania eksperymentalne i kliniczne z ostatnich lat zidentyfikowały prostaglandyny maciczne jako istotny czynnik przyczyniający się do patogenezy pierwotnego bolesnego miesiączkowania8. Prostaglandyny są substancjami chemicznymi wytwarzanymi w wyściółce macicy, które odgrywają kluczową rolę w wywoływaniu skurczów macicy podczas miesiączki9.

Aktualnie wiadomo, że pod koniec cyklu miesiączkowego prostaglandyny zwiększają skurcze mięśniówki macicy i powodują zwężenie małych naczyń krwionośnych endometrium, co skutkuje niedokrwieniem tkanek, dezintegracją endometrium, krwawieniem i bólem10. Ból miesiączkowy może być spowodowany niedokrwieniem tkanek wynikającym ze zwiększonego ciśnienia wewnątrzmacicznego, zwężenia naczyń i zmniejszonego przepływu krwi w macicy11.

Mechanizm działania prostaglandyn

Obecne dowody sugerują, że patogeneza bolesnego miesiączkowania jest związana ze zwiększonym wydzielaniem prostaglandyny F2 (PGF2) i prostaglandyny E2 (PGE2) w macicy podczas złuszczania endometrium1213. Te prostaglandyny są zaangażowane w zwiększanie skurczów mięśniówki macicy i zwężanie naczyń krwionośnych, co prowadzi do niedokrwienia macicy i produkcji metabolitów beztlenowych14. Skutkuje to uwrażliwieniem włókien bólowych i ostatecznie bólem miednicy15.

Prostaglandyny są syntetyzowane w kaskadzie kwasu arachidonowego, za pośrednictwem szlaku cyklooksygenazy (COX)16. Synteza kwasu arachidonowego jest regulowana przez poziom progesteronu, poprzez aktywność enzymu lizosomalnegofosfolipazy A217. Poziom progesteronu osiąga szczyt w środkowej fazie lutealnej – późniejszej fazie cyklu miesiączkowego – która występuje po owulacji18.

Jeśli nie dojdzie do zapłodnienia, następuje degeneracja ciałka żółtego i spadek poziomu progesteronu we krwi19. Ten gwałtowny spadek poziomu progesteronu jest związany ze złuszczaniem endometrium, krwawieniem miesiączkowym i uwalnianiem enzymów lizosomalnych, prowadzącym do wytwarzania kwasu arachidonowego, a tym samym produkcji prostaglandyn20.

Poziom prostaglandyn a intensywność bólu

Kobiety z regularnymi cyklami miesiączkowymi mają podwyższony poziom prostaglandyn endometrialnych w późnej fazie lutealnej21. Jednak kilka badań, które mierzyły stężenie prostaglandyn w fazie lutealnej poprzez biopsje endometrium i płyny miesiączkowe, wykazało, że kobiety cierpiące na bolesne miesiączkowanie mają wyższy poziom prostaglandyn niż kobiety bez tej dolegliwości22. W konsekwencji skurcze miesiączkowe, intensywność bólu i towarzyszące objawy są bezpośrednio skorelowane z wyższymi stężeniami PGF2 i PGE2 w endometrium2324.

Najbardziej przekonującym dowodem na „teorię prostaglandynową” jest skuteczność inhibitorów syntezy prostaglandyn w leczeniu bolesnego miesiączkowania25. Ulga w bólu osiągnięta dzięki tym lekom wiąże się z zahamowaniem syntezy prostaglandyn i zmniejszeniem ciśnienia wewnątrzmacicznego26.

Dodatkowe mechanizmy bólu miesiączkowego

Rola leukotrienów

Poza prostaglandynami, leukotrieny również odgrywają rolę w patofizjologii bolesnego miesiączkowania27. Uważa się, że leukotrieny zwiększają wrażliwość włókien bólowych w macicy28. Role innych prostanoidów, takich jak tromboksan A2 i prostacyklina, w pierwotnym bolesnym miesiączkowaniu nie są dobrze poznane. Wstępne dowody sugerują, że prostacyklina jest zaangażowana w patofizjologię pierwotnego bolesnego miesiączkowania29.

Zwiększony poziom leukotrienów w macicy może być odpowiedzialny za niektóre formy pierwotnego bolesnego miesiączkowania, które nie reagują na terapię z zastosowaniem niesteroidowych leków przeciwzapalnych (NLPZ), ponieważ leukotrieny są produkowane przez szlak enzymatyczny 5-lipooksygenazy, a nie szlak cyklooksygenazy30.

Rola wazopresyny

Hormon tylnego przysadki, wazopresyna, może być zaangażowany w nadwrażliwość mięśniówki macicy, zmniejszony przepływ krwi w macicy i ból w pierwotnym bolesnym miesiączkowaniu31. Podwyższony poziom wazopresyny odnotowano u kobiet z pierwotnym bolesnym miesiączkowaniem32.

Hipoteza neuronalna

Oprócz teorii prostaglandynowej, istnieje również hipoteza neuronalna patogenezy pierwotnego bolesnego miesiączkowania33. Kobiety z bolesnym miesiączkowaniem wydają się mieć zwiększoną wrażliwość na ból w porównaniu do kobiet bez bolesnego miesiączkowania, nawet w fazach cyklu miesiączkowego, gdy nie doświadczają bólu miesiączkowego34. Ta zwiększona wrażliwość na ból może zwiększać ryzyko innych przewlekłych stanów (np. fibromialgii) u dotkniętych kobiet, a także negatywnie wpływać na jakość ich życia35.

Istnieją dowody sugerujące, że mózg odgrywa kluczową rolę w patofizjologii pierwotnego bolesnego miesiączkowania, a jego zaangażowanie obejmuje centralną sensytyzację, zmienione przetwarzanie bólu, regulację czynników neuroendokrynnych oraz interakcje z czynnikami psychologicznymi36.

Zmiany w pracy mózgu związane z bolesnym miesiączkowaniem

Badania z wykorzystaniem funkcjonalnego rezonansu magnetycznego (fMRI) wykazały, że mechanizm centralnej nadwrażliwości na ból w pierwotnym bolesnym miesiączkowaniu może być związany z zaburzeniami w połączeniach funkcjonalnych między istotą szarą okołowodociągową (PAG) a zstępującym systemem modulacji bólu, siecią domyślnego trybu pracy mózgu (DMN) i płatem potylicznym37.

Oscylacje theta (4-7 Hz) są dobrze udokumentowane pod względem ich związku z neuronalnymi procesami pamięci. Wyraźny wzrost aktywności theta jest powszechnie obserwowany u pacjentów z przewlekłym bólem neurogennym38.

Badania wykazały zwiększoną aktywność theta w regionach mózgu związanych z przetwarzaniem bólu u kobiet z pierwotnym bolesnym miesiączkowaniem, w tym w prawym zakręcie parahipokampalnym, prawej tylnej wyspie i lewym przednim/środkowym zakręcie obręczy podczas fazy miesiączkowej oraz lewej przedniej wyspie i lewym środkowym/dolnym zakręcie skroniowym podczas fazy okołoowulacyjnej39. Korelacje między aktywnością theta a miarami psychologicznymi związanymi z doświadczeniem bólu (depresja, lęk jako stan, indeks oceny bólu) wskazują na rolę oscylacji theta w emocjonalnym i sensorycznym przetwarzaniu bólu40.

Kompleksowy mechanizm bólu miesiączkowego

W pierwotnym bolesnym miesiączkowaniu istnieje bardzo złożona interakcja między hormonami i mediatorami, temperaturą ciała, wzorcami snu i ośrodkowym układem nerwowym (OUN), której zakres nie jest w pełni zrozumiały41.

Podwyższone prostaglandyny mogą również odgrywać rolę we wtórnym bolesnym miesiączkowaniu, ale z definicji musi występować jednocześnie patologia miednicy42. Prawie każdy proces, który może wpływać na narządy miednicy, może wywoływać cykliczny ból miednicy43.

Czynniki behawioralne i psychologiczne, niedokrwienie macicy, zwężenie lub zwężenie szyjki macicy, zwiększone uwalnianie wazopresyny, zwiększona aktywność macicy oraz zwiększona produkcja i uwalnianie prostanoidów macicznych zostały wymienione jako przyczyny pierwotnego bolesnego miesiączkowania44. Dowody sugerują, że większość kobiet z pierwotnym bolesnym miesiączkowaniem ma zwiększoną lub nieprawidłową produkcję i uwalnianie prostanoidów macicznych, co prowadzi do nieprawidłowej aktywności macicy, a tym samym do bólu45.

Uwarunkowania genetyczne

Najnowsze badania wykazały macierzyńską transmisję pierwotnego bolesnego miesiączkowania u nastolatek i młodych kobiet, z istotnym wpływem genów na bolesne miesiączkowanie46. Uważa się, że komponenta genetyczna ma również wpływ na patofizjologię pierwotnego bolesnego miesiączkowania47.

Wtórne bolesne miesiączkowanie i jego przyczyny

Wtórne bolesne miesiączkowanie jest spowodowane przez choroby w narządach rozrodczych48. Ból ma tendencję do pogarszania się z czasem i często trwa dłużej niż normalne skurcze miesiączkowe49.

Niektóre z chorób, które mogą powodować wtórne bolesne miesiączkowanie, obejmują:

  • Endometriozę – stan, w którym tkanka podobna do wyściółki macicy rośnie w innych obszarach ciała, takich jak jajniki i jajowody, za macicą oraz na pęcherzu moczowym50
  • Mięśniaki macicy – są to niezłośliwe guzy, które mogą tworzyć się na zewnątrz, wewnątrz lub w ścianach macicy. Mięśniaki zlokalizowane w ścianie macicy mogą powodować ból51
  • Adenomiozę – rozwija się, gdy tkanka normalnie wyściełająca macicę zaczyna rosnąć w ścianie mięśniowej macicy52
  • Wrodzone wady anatomiczne – niektóre wady, z którymi kobieta się rodzi, mogą powodować ból podczas miesiączki53
  • Zapalenie narządów miednicy mniejszej (PID) – stan zapalny narządów rozrodczych54
  • Wkładkę domaciczną (IUD) – może również powodować ból miesiączkowy, szczególnie w pierwszych 3-6 miesiącach po jej założeniu55

Podsumowanie mechanizmów bólu miesiączkowego

Bolesne miesiączkowanie jest złożonym procesem, który może zależeć od wielu czynników56. Wiadomo, że cykl miesiączkowy jest zależny od cyklicznych zmian stężenia hormonów jajnikowych, a zatem również od cyklicznych zmian poziomu prostaglandyn i aktywności kurczliwej macicy57.

Mechanizmy, które następują po spadku stężenia progesteronu, są złożonymi reakcjami między układem endokrynnym, naczyniowym i immunologicznym58. Prostaglandyny powodują zwężenie naczyń krwionośnych zaopatrujących macicę, nieprawidłową aktywność kurczliwą macicy, co prowadzi do niedokrwienia, hipoksji macicy i zwiększonej wrażliwości zakończeń nerwowych59.

Zrozumienie patofizjologii pierwotnego bolesnego miesiączkowania umożliwiło racjonalne stosowanie niesteroidowych leków przeciwzapalnych w leczeniu pierwotnego bolesnego miesiączkowania, a nie farmakoterapii, która jedynie hamuje skurcze macicy, na przykład za pomocą środków betamimetycznych60.

Pomimo licznych badań patomechanizm bolesnego miesiączkowania nie jest w pełni zrozumiały61. Wcześniejsze badania wykazały, że bolesne miesiączkowanie jest złożonym procesem, który może zależeć od wielu czynników62. Kontynuacja badań nad mechanizmami bólu miesiączkowego jest niezbędna dla opracowania bardziej skutecznych i ukierunkowanych terapii tego powszechnego problemu zdrowotnego63.

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Painful Periods (Dysmenorrhea)
    https://studenthealth.ucsd.edu/resources/health-topics/painful-periods/index.html
    Dysmenorrhea is the most common cause of lost work and school hours among women in the United States. In fact, 42 million women in the United States suffer from painful menstrual symptoms. Of these, about 3 1/2 million are unable to function for one to two days each month because the condition is so severe. […] In some cases, the cause of dysmenorrhea is an actual disease or some physical abnormality. These conditions may sometimes be difficult to diagnose but they can often be managed with medication and/or surgical intervention. The causes of dysmenorrhea in a normal, healthy woman are not so clear. It has long been believed that heredity, psychological well-being, and environment are important influences. However, the most up-to-date thinking indicates that a group of chemicals in your body called „prostaglandins” may be the most direct influence.
  • #2 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. It is one of the most common gynecologic complaints in young women who present to clinicians. Optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea can be divided into two broad categories: primary and secondary. […] Evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2 (PGF2), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium. […] The response to prostaglandin inhibitors in patients with dysmenorrhea supports the assertion that dysmenorrhea is prostaglandin-mediated. Substantial evidence attributes dysmenorrhea to prolonged uterine contractions and decreased blood flow to the myometrium. […] Elevated prostaglandin levels have been found in the endometrial fluid of women with dysmenorrhea and correlate well with the degree of pain.
  • #3 Dysmenorrhea: Menstrual Cramps, Causes & Treatments
    https://my.clevelandclinic.org/health/diseases/4148-dysmenorrhea
    Dysmenorrhea is the medical term for painful menstrual periods. It happens because your uterus contracts to shed its lining. […] Primary dysmenorrhea refers to recurrent pain with no identifiable cause. Secondary dysmenorrhea results from conditions like endometriosis. […] Menstrual cramps happen when a chemical called prostaglandin makes your uterus contract (tighten up). During menstruation, prostaglandin levels are higher, which means your uterus contracts more strongly. This is the cramping and discomfort you feel. […] Experts arent entirely sure why some people have more painful periods, but they think it may be because they have higher levels of prostaglandins. […] Menstrual pain from secondary dysmenorrhea is a result of a condition affecting your reproductive organs. Conditions that can cause cramping include: Endometriosis: A condition where the tissue lining your uterus (the endometrium) grows outside of your uterus. […] Adenomyosis: A condition where the lining of your uterus grows into the muscle of your uterus. […] If testing shows that you have secondary dysmenorrhea, your provider will discuss treatment for the condition causing you pain. This might mean oral contraceptives, other types of medications or surgery.
  • #4 Painful menstrual periods: MedlinePlus Medical EncyclopediaLock
    https://medlineplus.gov/ency/article/003150.htm
    Painful menstrual periods are periods in which a woman has crampy lower abdominal pain, which can be sharp or aching and come and go. […] The medical term for painful menstrual periods is dysmenorrhea. […] Painful menstrual periods fall into two groups, depending on the cause: Primary dysmenorrhea and Secondary dysmenorrhea. […] Primary dysmenorrhea is menstrual pain that occurs around the time that menstrual periods first begin in otherwise healthy young women. In most cases, this pain is not related to a specific problem with the uterus or other pelvic organs. Increased activity of the hormone prostaglandin, which is produced in the uterus, is thought to play a role in this condition. […] Secondary dysmenorrhea is menstrual pain that develops later in women who have had normal periods. It is often related to problems in the uterus or other pelvic organs, such as endometriosis, fibroids, pelvic inflammatory disease, and premenstrual syndrome (PMS).
  • #5 Diagnosis and Initial Management of Dysmenorrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2014/0301/p341.html
    Dysmenorrhea is one of the most common causes of pelvic pain. It negatively affects patients’ quality of life and sometimes results in activity restriction. Primary dysmenorrhea is menstrual pain in the absence of pelvic pathology. […] Endometriosis is the most common cause of secondary dysmenorrhea. Symptoms and signs of adenomyosis include dysmenorrhea, menorrhagia, and a uniformly enlarged uterus. […] Dysmenorrhea is considered primary in the absence of underlying pathology. Onset is typically six to 12 months after menarche, with peak prevalence occurring in the late teens or early twenties. Secondary dysmenorrhea results from specific pelvic pathology. […] Endometriosis is the most common cause of secondary dysmenorrhea. The incidence is highest among women 25 to 29 years of age and lowest among women older than 44 years.
  • #6 Period Pain | Menstrual Cramps | MedlinePlus
    https://medlineplus.gov/periodpain.html
    Menstruation, or period, is normal vaginal bleeding that happens as part of a woman’s monthly cycle. Many women have painful periods, also called dysmenorrhea. The pain is most often menstrual cramps, which are a throbbing, cramping pain in your lower abdomen. […] Primary dysmenorrhea is the most common kind of period pain. It is period pain that is not caused by another condition. The cause is usually having too many prostaglandins, which are chemicals that your uterus makes. These chemicals make the muscles of your uterus tighten and relax, and this causes the cramps. […] Secondary dysmenorrhea often starts later in life. It is caused by conditions that affect your uterus or other reproductive organs, such as endometriosis and uterine fibroids. This kind of pain often gets worse over time. It may begin before your period starts and continue after your period ends.
  • #7 Got period pain or cramps? What to eat and avoid – School of Public Health – University of Queensland
    https://public-health.uq.edu.au/article/2024/01/got-period-pain-or-cramps-what-eat-and-avoid
    Painful periods are common. More than half of people who menstruate have some pain for up to three days a month, typically throbbing or cramping in the lower abdomen. […] There are many treatments for period pain (known medically as dysmenorrhoea). Not all these treatments are well-tolerated or work for everyone. […] Omega-3 fatty acids affect how our cells function and the signalling pathways associated with inflammation and pain. […] Vitamin D may help reduce the factors that cause inflammation in the uterus. This includes levels of hormone-like molecules called prostaglandins. […] There is some evidence vitamin E supplements reduce period pain. […] Caffeine intake is associated with menstrual pain. Although we dont know the precise underlying mechanism, researchers think caffeine may narrow blood vessels, which limits blood flow, leading to stronger cramps. […] Having a healthy, balanced diet is one of the best ways we can support our own health and prevent future chronic conditions. This can help reduce inflammation in our bodies, thought to be the main way diet can help people with painful periods.
  • #8 Menstrual pain: its origin and pathogenesis.
    https://vivo.weill.cornell.edu/display/pubid7001019
    A variety of misconceptions about the etiology of dysmenorrhea have existed in the past. Experimental and clinical research of the last 15 years, however, has identified uterine prostaglandins as substantially contributing to the pathogenesis of primary dysmenorrhea. […] It is now known that at the end of the menstrual cycle, prostaglandins increase myometrial contractions and cause constriction of small endometrial blood vessels, with consequent tissue ischemia, endometrial disintegration, bleeding and pain. Dysmenorrhea may be due to tissue ischemia resulting from increased intrauterine pressure, vessel constriction and decreased uterine blood flow. […] The most compelling evidence for the „prostaglandin theory” is the success of prostaglandin synthesis inhibitors in the treatment of dysmenorrhea. The pain relief achieved with these drugs is accompanied by a suppression of prostaglandin synthesis and a decrease in intrauterine pressure.
  • #9 Prostaglandins: What It Is, Function & Side Effects
    https://my.clevelandclinic.org/health/articles/24411-prostaglandins
    Prostaglandins are responsible for uterine contractions during menstruation. These contractions help release the uterine lining (endometrium) from your uterus, thus producing a period. […] Prostaglandins have a lot of influence over key natural bodily processes, including pain levels and inflammation. The normal inflammatory process is your body’s way of protecting itself from further damage. […] While prostaglandins are necessary for menstruation, for example, excess prostaglandins can cause painful and heavy periods (menorrhagia). […] Sometimes, your body produces too many prostaglandins, which leads to unwanted and unhelpful inflammation in your body. Excessive levels of prostaglandins can cause or contribute to a variety of health conditions, including painful menstruation or menstrual cramps (dysmenorrhea).
  • #10 Menstrual pain: its origin and pathogenesis – PubMed
    https://pubmed.ncbi.nlm.nih.gov/7001019/
    A variety of misconceptions about the etiology of dysmenorrhea have existed in the past. […] Experimental and clinical research of the last 15 years, however, has identified uterine prostaglandins as substantially contributing to the pathogenesis of primary dysmenorrhea. […] It is now known that at the end of the menstrual cycle, prostaglandins increase myometrial contractions and cause constriction of small endometrial blood vessels, with consequent tissue ischemia, endometrial disintegration, bleeding and pain. […] Dysmenorrhea may be due to tissue ischemia resulting from increased intrauterine pressure, vessel constriction and decreased uterine blood flow. […] The most compelling evidence for the „prostaglandin theory” is the success of prostaglandin synthesis inhibitors in the treatment of dysmenorrhea. […] The pain relief achieved with these drugs is accompanied by a suppression of prostaglandin synthesis and a decrease in intrauterine pressure.
  • #11 Menstrual pain: its origin and pathogenesis.
    https://vivo.weill.cornell.edu/display/pubid7001019
    A variety of misconceptions about the etiology of dysmenorrhea have existed in the past. Experimental and clinical research of the last 15 years, however, has identified uterine prostaglandins as substantially contributing to the pathogenesis of primary dysmenorrhea. […] It is now known that at the end of the menstrual cycle, prostaglandins increase myometrial contractions and cause constriction of small endometrial blood vessels, with consequent tissue ischemia, endometrial disintegration, bleeding and pain. Dysmenorrhea may be due to tissue ischemia resulting from increased intrauterine pressure, vessel constriction and decreased uterine blood flow. […] The most compelling evidence for the „prostaglandin theory” is the success of prostaglandin synthesis inhibitors in the treatment of dysmenorrhea. The pain relief achieved with these drugs is accompanied by a suppression of prostaglandin synthesis and a decrease in intrauterine pressure.
  • #12 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8943241/
    Primary dysmenorrhea (PD) is characterized by painful cramps in the lower abdomen, which start shortly before or at the onset of menses and which could last for 3 days. […] It is suggested that increased intrauterine secretion of prostaglandins F2 and E2 are responsible for the pelvic pain associated with this disorder. […] Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #13 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. […] These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. […] This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Prostaglandins are synthesized through the arachidonic acid cascade, mediated by the cyclooxygenase (COX) pathway. […] Arachidonic acid synthesis is regulated by the level of progesterone, through the activity of the lysosomal enzyme phospholipase A2. […] The progesterone level peaks during the middle of the luteal phase—the latter phase of the menstrual cycle—that occurs after ovulation.
  • #14 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. […] These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. […] This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Prostaglandins are synthesized through the arachidonic acid cascade, mediated by the cyclooxygenase (COX) pathway. […] Arachidonic acid synthesis is regulated by the level of progesterone, through the activity of the lysosomal enzyme phospholipase A2. […] The progesterone level peaks during the middle of the luteal phase—the latter phase of the menstrual cycle—that occurs after ovulation.
  • #15 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8943241/
    Primary dysmenorrhea (PD) is characterized by painful cramps in the lower abdomen, which start shortly before or at the onset of menses and which could last for 3 days. […] It is suggested that increased intrauterine secretion of prostaglandins F2 and E2 are responsible for the pelvic pain associated with this disorder. […] Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #16 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. […] These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. […] This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Prostaglandins are synthesized through the arachidonic acid cascade, mediated by the cyclooxygenase (COX) pathway. […] Arachidonic acid synthesis is regulated by the level of progesterone, through the activity of the lysosomal enzyme phospholipase A2. […] The progesterone level peaks during the middle of the luteal phase—the latter phase of the menstrual cycle—that occurs after ovulation.
  • #17 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. […] These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. […] This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Prostaglandins are synthesized through the arachidonic acid cascade, mediated by the cyclooxygenase (COX) pathway. […] Arachidonic acid synthesis is regulated by the level of progesterone, through the activity of the lysosomal enzyme phospholipase A2. […] The progesterone level peaks during the middle of the luteal phase—the latter phase of the menstrual cycle—that occurs after ovulation.
  • #18 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. […] These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. […] This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Prostaglandins are synthesized through the arachidonic acid cascade, mediated by the cyclooxygenase (COX) pathway. […] Arachidonic acid synthesis is regulated by the level of progesterone, through the activity of the lysosomal enzyme phospholipase A2. […] The progesterone level peaks during the middle of the luteal phase—the latter phase of the menstrual cycle—that occurs after ovulation.
  • #19 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    If conception does not occur, this results in degeneration of the corpus luteum and a decline in the circulating progesterone level. […] This rapid decline in the progesterone level is associated with endometrial sloughing, menstrual bleeding, and the release of lysosomal enzymes, leading to the generation of arachidonic acid, and therefore, the production of prostaglandins. […] Females with regular menstrual cycles have elevated endometrial prostaglandin levels during the late luteal phase. […] However, several studies that measured prostaglandin concentrations in the luteal phase, through endometrial biopsies and menstrual fluids, revealed that dysmenorrheic females have higher levels of prostaglandins than eumenorrheic females. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #20 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    If conception does not occur, this results in degeneration of the corpus luteum and a decline in the circulating progesterone level. […] This rapid decline in the progesterone level is associated with endometrial sloughing, menstrual bleeding, and the release of lysosomal enzymes, leading to the generation of arachidonic acid, and therefore, the production of prostaglandins. […] Females with regular menstrual cycles have elevated endometrial prostaglandin levels during the late luteal phase. […] However, several studies that measured prostaglandin concentrations in the luteal phase, through endometrial biopsies and menstrual fluids, revealed that dysmenorrheic females have higher levels of prostaglandins than eumenorrheic females. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #21 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    If conception does not occur, this results in degeneration of the corpus luteum and a decline in the circulating progesterone level. […] This rapid decline in the progesterone level is associated with endometrial sloughing, menstrual bleeding, and the release of lysosomal enzymes, leading to the generation of arachidonic acid, and therefore, the production of prostaglandins. […] Females with regular menstrual cycles have elevated endometrial prostaglandin levels during the late luteal phase. […] However, several studies that measured prostaglandin concentrations in the luteal phase, through endometrial biopsies and menstrual fluids, revealed that dysmenorrheic females have higher levels of prostaglandins than eumenorrheic females. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #22 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    If conception does not occur, this results in degeneration of the corpus luteum and a decline in the circulating progesterone level. […] This rapid decline in the progesterone level is associated with endometrial sloughing, menstrual bleeding, and the release of lysosomal enzymes, leading to the generation of arachidonic acid, and therefore, the production of prostaglandins. […] Females with regular menstrual cycles have elevated endometrial prostaglandin levels during the late luteal phase. […] However, several studies that measured prostaglandin concentrations in the luteal phase, through endometrial biopsies and menstrual fluids, revealed that dysmenorrheic females have higher levels of prostaglandins than eumenorrheic females. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #23 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://kjfm.or.kr/journal/view.php?number=4607
    If conception does not occur, this results in degeneration of the corpus luteum and a decline in the circulating progesterone level. […] This rapid decline in the progesterone level is associated with endometrial sloughing, menstrual bleeding, and the release of lysosomal enzymes, leading to the generation of arachidonic acid, and therefore, the production of prostaglandins. […] Females with regular menstrual cycles have elevated endometrial prostaglandin levels during the late luteal phase. […] However, several studies that measured prostaglandin concentrations in the luteal phase, through endometrial biopsies and menstrual fluids, revealed that dysmenorrheic females have higher levels of prostaglandins than eumenorrheic females. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #24 Primary Dysmenorrhea: Pathophysiology, Diagnosis, and Treatment Updates
    https://pmc.ncbi.nlm.nih.gov/articles/PMC8943241/
    Primary dysmenorrhea (PD) is characterized by painful cramps in the lower abdomen, which start shortly before or at the onset of menses and which could last for 3 days. […] It is suggested that increased intrauterine secretion of prostaglandins F2 and E2 are responsible for the pelvic pain associated with this disorder. […] Although the pathophysiology of dysmenorrhea has not been fully elucidated, current evidence suggests that the pathogenesis of dysmenorrhea is due to the increased secretion of prostaglandin F2 (PGF2) and prostaglandin E2 (PGE2) in the uterus during endometrial sloughing. These prostaglandins are involved in increasing myometrial contractions and vasoconstriction, leading to uterine ischemia and production of anaerobic metabolites. This results in the hypersensitization of pain fibers, and ultimately pelvic pain. […] Consequently, menstrual cramps, pain intensity, and associated symptoms are directly correlated with higher concentrations of PGF2 and PGE2 in the endometrium.
  • #25 Menstrual pain: its origin and pathogenesis.
    https://vivo.weill.cornell.edu/display/pubid7001019
    A variety of misconceptions about the etiology of dysmenorrhea have existed in the past. Experimental and clinical research of the last 15 years, however, has identified uterine prostaglandins as substantially contributing to the pathogenesis of primary dysmenorrhea. […] It is now known that at the end of the menstrual cycle, prostaglandins increase myometrial contractions and cause constriction of small endometrial blood vessels, with consequent tissue ischemia, endometrial disintegration, bleeding and pain. Dysmenorrhea may be due to tissue ischemia resulting from increased intrauterine pressure, vessel constriction and decreased uterine blood flow. […] The most compelling evidence for the „prostaglandin theory” is the success of prostaglandin synthesis inhibitors in the treatment of dysmenorrhea. The pain relief achieved with these drugs is accompanied by a suppression of prostaglandin synthesis and a decrease in intrauterine pressure.
  • #26 Menstrual pain: its origin and pathogenesis – PubMed
    https://pubmed.ncbi.nlm.nih.gov/7001019/
    A variety of misconceptions about the etiology of dysmenorrhea have existed in the past. […] Experimental and clinical research of the last 15 years, however, has identified uterine prostaglandins as substantially contributing to the pathogenesis of primary dysmenorrhea. […] It is now known that at the end of the menstrual cycle, prostaglandins increase myometrial contractions and cause constriction of small endometrial blood vessels, with consequent tissue ischemia, endometrial disintegration, bleeding and pain. […] Dysmenorrhea may be due to tissue ischemia resulting from increased intrauterine pressure, vessel constriction and decreased uterine blood flow. […] The most compelling evidence for the „prostaglandin theory” is the success of prostaglandin synthesis inhibitors in the treatment of dysmenorrhea. […] The pain relief achieved with these drugs is accompanied by a suppression of prostaglandin synthesis and a decrease in intrauterine pressure.
  • #27 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction. […] Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. […] The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea. […] In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. […] Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain. […] This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.
  • #28 Dysmenorrhea | GLOWM
    https://www.glowm.com/section-view/heading/Dysmenorrhea/item/9
    The roles of prostanoids, such as thromboxane A2 and prostacyclin, and leukotrienes in primary dysmenorrhea are not well understood. Preliminary evidence suggests that prostacyclin is involved in the pathophysiology of primary dysmenorrhea. Increased uterine leukotriene may be responsible for some forms of primary dysmenorrhea that do not respond to therapy with NSAIDs, because leukotrienes are produced through the 5-lipoxygenase enzyme pathway rather than the cyclooxygenase pathway. […] The postulated mechanisms for the generation of pain from pelvic structures in primary dysmenorrhea are summarized in Figure 4. The increased uterine production and release of prostaglandins at menstruation give rise to increased abnormal uterine activity, which then causes uterine hypoxia and pain. Increased uterine activity and uterine ischemia or hypoxia are two major factors in the causation of the pain. Prostaglandins, such as prostaglandin E2, and cyclic endoperoxides hypersensitize pain fibers in the pelvis and uterus to the action of pain-inducing substances or factors. This understanding of the pathophysiology of primary dysmenorrhea has enabled the rational use of nonsteroidal antiinflammatory drugs for the relief of primary dysmenorrhea rather than pharmacotherapy, which merely inhibits uterine contractions, such as with betamimetic agents.
  • #29 Dysmenorrhea | GLOWM
    https://www.glowm.com/section-view/heading/Dysmenorrhea/item/9
    The roles of prostanoids, such as thromboxane A2 and prostacyclin, and leukotrienes in primary dysmenorrhea are not well understood. Preliminary evidence suggests that prostacyclin is involved in the pathophysiology of primary dysmenorrhea. Increased uterine leukotriene may be responsible for some forms of primary dysmenorrhea that do not respond to therapy with NSAIDs, because leukotrienes are produced through the 5-lipoxygenase enzyme pathway rather than the cyclooxygenase pathway. […] The postulated mechanisms for the generation of pain from pelvic structures in primary dysmenorrhea are summarized in Figure 4. The increased uterine production and release of prostaglandins at menstruation give rise to increased abnormal uterine activity, which then causes uterine hypoxia and pain. Increased uterine activity and uterine ischemia or hypoxia are two major factors in the causation of the pain. Prostaglandins, such as prostaglandin E2, and cyclic endoperoxides hypersensitize pain fibers in the pelvis and uterus to the action of pain-inducing substances or factors. This understanding of the pathophysiology of primary dysmenorrhea has enabled the rational use of nonsteroidal antiinflammatory drugs for the relief of primary dysmenorrhea rather than pharmacotherapy, which merely inhibits uterine contractions, such as with betamimetic agents.
  • #30 Dysmenorrhea | GLOWM
    https://www.glowm.com/section-view/heading/Dysmenorrhea/item/9
    The roles of prostanoids, such as thromboxane A2 and prostacyclin, and leukotrienes in primary dysmenorrhea are not well understood. Preliminary evidence suggests that prostacyclin is involved in the pathophysiology of primary dysmenorrhea. Increased uterine leukotriene may be responsible for some forms of primary dysmenorrhea that do not respond to therapy with NSAIDs, because leukotrienes are produced through the 5-lipoxygenase enzyme pathway rather than the cyclooxygenase pathway. […] The postulated mechanisms for the generation of pain from pelvic structures in primary dysmenorrhea are summarized in Figure 4. The increased uterine production and release of prostaglandins at menstruation give rise to increased abnormal uterine activity, which then causes uterine hypoxia and pain. Increased uterine activity and uterine ischemia or hypoxia are two major factors in the causation of the pain. Prostaglandins, such as prostaglandin E2, and cyclic endoperoxides hypersensitize pain fibers in the pelvis and uterus to the action of pain-inducing substances or factors. This understanding of the pathophysiology of primary dysmenorrhea has enabled the rational use of nonsteroidal antiinflammatory drugs for the relief of primary dysmenorrhea rather than pharmacotherapy, which merely inhibits uterine contractions, such as with betamimetic agents.
  • #31 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction. […] Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. […] The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea. […] In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. […] Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain. […] This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.
  • #32 Dysmenorrhea | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0115/p285.html
    Dysmenorrhea is thought to be caused by the release of prostaglandins in the menstrual fluid, which causes uterine contractions and pain. Vasopressin also may play a role by increasing uterine contractility and causing ischemic pain as a result of vasoconstriction. Elevated vasopressin levels have been reported in women with primary dysmenorrhea. […] The relationship between endometriosis and dysmenorrhea is not clear. Endometriosis may be asymptomatic, or it may be associated with pelvic pain that is not limited to the menstrual period and the low anterior pelvis. In one study of women undergoing elective sterilization, no difference was found in the prevalence of dysmenorrhea in women with and women without an incidental finding of endometriosis. However, an observational study of women undergoing laparoscopy for infertility supported a relationship between dysmenorrhea and the severity of endometriosis.
  • #33 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction. […] Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. […] The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea. […] In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. […] Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain. […] This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.
  • #34 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction. […] Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. […] The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea. […] In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. […] Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain. […] This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.
  • #35 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction. […] Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. […] The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea. […] In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. […] Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain. […] This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.
  • #36 Revealing the mechanism of central pain hypersensitivity in primary dysmenorrhea: evidence from neuroimaging – Jin – Quantitative Imaging in Medicine and Surgery
    https://qims.amegroups.org/article/view/122997/html
    Primary dysmenorrhea (PDM) is the most common problem in menstruating women. A number of functional magnetic resonance imaging (fMRI) study have revealed that the brain plays a crucial role in the pathophysiology of PDM. […] However, recent studies indicate that the brain plays a crucial role in the pathophysiology of PDM, with its involvement encompassing central sensitization, altered pain processing, regulation of neuroendocrine factors, and interactions with psychological factors. […] The results from this study suggest that the mechanism of central pain hypersensitivity of PDM may be related to the disorder of the FC between the PAG and descending pain modulation system, default mode network (DMN), and occipital lobe. […] The findings revealed that there were no functional or structural differences between patients in the PDM-NP and HCs. However, there was evidence of altered brain function and FC patterns of the PAG during the pain phase.
  • #37 Revealing the mechanism of central pain hypersensitivity in primary dysmenorrhea: evidence from neuroimaging – Jin – Quantitative Imaging in Medicine and Surgery
    https://qims.amegroups.org/article/view/122997/html
    Primary dysmenorrhea (PDM) is the most common problem in menstruating women. A number of functional magnetic resonance imaging (fMRI) study have revealed that the brain plays a crucial role in the pathophysiology of PDM. […] However, recent studies indicate that the brain plays a crucial role in the pathophysiology of PDM, with its involvement encompassing central sensitization, altered pain processing, regulation of neuroendocrine factors, and interactions with psychological factors. […] The results from this study suggest that the mechanism of central pain hypersensitivity of PDM may be related to the disorder of the FC between the PAG and descending pain modulation system, default mode network (DMN), and occipital lobe. […] The findings revealed that there were no functional or structural differences between patients in the PDM-NP and HCs. However, there was evidence of altered brain function and FC patterns of the PAG during the pain phase.
  • #38 Encoding of menstrual pain experience with theta oscillations in women with primary dysmenorrhea | Scientific Reports
    https://www.nature.com/articles/s41598-017-16039-4
    Theta oscillation (47Hz) is well documented for its association with neural processes of memory. Pronounced increase of theta activity is commonly observed in patients with chronic neurogenic pain. However, its association with encoding of pain experience in patients with chronic pain is still unclear. […] Our results revealed increased theta activity in brain regions of pain processing in women with PDM, including the right parahippocampal gyrus, right posterior insula, and left anterior/middle cingulate gyrus during the menstrual phase and the left anterior insula and the left middle/inferior temporal gyrus during the periovulatory phase. The correlations between theta activity and the psychological measures pertaining to pain experience (depression, state anxiety, and pain rating index) implicate the role of theta oscillations in emotional and sensory processing of pain. The present study provides evidence for the role of theta oscillations in encoding the immediate and sustained effects of pain experience in young women with PDM.
  • #39 Encoding of menstrual pain experience with theta oscillations in women with primary dysmenorrhea | Scientific Reports
    https://www.nature.com/articles/s41598-017-16039-4
    Theta oscillation (47Hz) is well documented for its association with neural processes of memory. Pronounced increase of theta activity is commonly observed in patients with chronic neurogenic pain. However, its association with encoding of pain experience in patients with chronic pain is still unclear. […] Our results revealed increased theta activity in brain regions of pain processing in women with PDM, including the right parahippocampal gyrus, right posterior insula, and left anterior/middle cingulate gyrus during the menstrual phase and the left anterior insula and the left middle/inferior temporal gyrus during the periovulatory phase. The correlations between theta activity and the psychological measures pertaining to pain experience (depression, state anxiety, and pain rating index) implicate the role of theta oscillations in emotional and sensory processing of pain. The present study provides evidence for the role of theta oscillations in encoding the immediate and sustained effects of pain experience in young women with PDM.
  • #40 Encoding of menstrual pain experience with theta oscillations in women with primary dysmenorrhea | Scientific Reports
    https://www.nature.com/articles/s41598-017-16039-4
    Theta oscillation (47Hz) is well documented for its association with neural processes of memory. Pronounced increase of theta activity is commonly observed in patients with chronic neurogenic pain. However, its association with encoding of pain experience in patients with chronic pain is still unclear. […] Our results revealed increased theta activity in brain regions of pain processing in women with PDM, including the right parahippocampal gyrus, right posterior insula, and left anterior/middle cingulate gyrus during the menstrual phase and the left anterior insula and the left middle/inferior temporal gyrus during the periovulatory phase. The correlations between theta activity and the psychological measures pertaining to pain experience (depression, state anxiety, and pain rating index) implicate the role of theta oscillations in emotional and sensory processing of pain. The present study provides evidence for the role of theta oscillations in encoding the immediate and sustained effects of pain experience in young women with PDM.
  • #41 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basal body temperature, sleep patterns, and the central nervous system (CNS), the extent of which is not completely understood. […] Elevated prostaglandins may also play a role in secondary dysmenorrhea, but by definition, concomitant pelvic pathology must be present. […] Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.
  • #42 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basal body temperature, sleep patterns, and the central nervous system (CNS), the extent of which is not completely understood. […] Elevated prostaglandins may also play a role in secondary dysmenorrhea, but by definition, concomitant pelvic pathology must be present. […] Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.
  • #43 Dysmenorrhea: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/253812-overview
    In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basal body temperature, sleep patterns, and the central nervous system (CNS), the extent of which is not completely understood. […] Elevated prostaglandins may also play a role in secondary dysmenorrhea, but by definition, concomitant pelvic pathology must be present. […] Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.
  • #44 Dysmenorrhea | GLOWM
    https://www.glowm.com/section-view/heading/Dysmenorrhea/item/9
    Dysmenorrhea, one of the most frequently encountered gynecologic disorders, refers to painful menstruation. Dysmenorrhea is classified as primary or secondary dysmenorrhea. Primary dysmenorrhea is defined as painful menstrual cramps in the absence of any visible pelvic pathology that could account for it. In secondary dysmenorrhea, the painful menstruation is accompanied by visible pelvic pathology that accounts for the pain. Such a classification allows practical differentiation in the management approach, which is based on the causal mechanism. […] Behavioral and psychologic factors, uterine ischemia, cervical stenosis or narrowing, increased vasopressin release, increased uterine activity, and increased uterine prostanoid production and release have been implicated in the cause of primary dysmenorrhea. Evidence suggests that most women with primary dysmenorrhea have increased or abnormal uterine prostanoid production and release, giving rise to abnormal uterine activity and therefore to pain.
  • #45 Dysmenorrhea | GLOWM
    https://www.glowm.com/section-view/heading/Dysmenorrhea/item/9
    Dysmenorrhea, one of the most frequently encountered gynecologic disorders, refers to painful menstruation. Dysmenorrhea is classified as primary or secondary dysmenorrhea. Primary dysmenorrhea is defined as painful menstrual cramps in the absence of any visible pelvic pathology that could account for it. In secondary dysmenorrhea, the painful menstruation is accompanied by visible pelvic pathology that accounts for the pain. Such a classification allows practical differentiation in the management approach, which is based on the causal mechanism. […] Behavioral and psychologic factors, uterine ischemia, cervical stenosis or narrowing, increased vasopressin release, increased uterine activity, and increased uterine prostanoid production and release have been implicated in the cause of primary dysmenorrhea. Evidence suggests that most women with primary dysmenorrhea have increased or abnormal uterine prostanoid production and release, giving rise to abnormal uterine activity and therefore to pain.
  • #46 Dysmenorrhea: Epidemiology, Causes and Current State of the Art for Treatment
    https://www.imrpress.com/journal/CEOG/50/12/10.31083/j.ceog5012274/htm
    After ovulation and before menstruation, progesterone withdrawal stimulates a huge release of arachidonic acid, an omega-6 fatty acid located among the phospholipids of cell membranes, that promotes the activation of prostaglandins and leukotrienes in the uterus. […] Thus, increased estrogen production, after progesterone withdrawal, increases prostaglandin (PG) production in the endometrium through the activation of cyclooxygenase-2 (COX-2) and nuclear factor kappa B (NF-kB), a nuclear transcription factor responsible for the activation of genes involved in the inflammatory cascade. […] This strong inflammatory response is thought to cause dysmenorrhea symptoms, such as nausea, vomiting, bloating, headache, and affects the intensity of dysmenorrhea and bleeding. […] Pain fibers are excited by leukotrienes also; these fibers in the uterus activate the afferent pain pathways to the central nervous system. […] A recent study demonstrated maternal transmission of primary dysmenorrhea in adolescent and young women, with an important gene influence on dysmenorrhea. […] Genetic component is also thought to have an impact on PD pathophysiology.
  • #47 Dysmenorrhea: Epidemiology, Causes and Current State of the Art for Treatment
    https://www.imrpress.com/journal/CEOG/50/12/10.31083/j.ceog5012274/htm
    After ovulation and before menstruation, progesterone withdrawal stimulates a huge release of arachidonic acid, an omega-6 fatty acid located among the phospholipids of cell membranes, that promotes the activation of prostaglandins and leukotrienes in the uterus. […] Thus, increased estrogen production, after progesterone withdrawal, increases prostaglandin (PG) production in the endometrium through the activation of cyclooxygenase-2 (COX-2) and nuclear factor kappa B (NF-kB), a nuclear transcription factor responsible for the activation of genes involved in the inflammatory cascade. […] This strong inflammatory response is thought to cause dysmenorrhea symptoms, such as nausea, vomiting, bloating, headache, and affects the intensity of dysmenorrhea and bleeding. […] Pain fibers are excited by leukotrienes also; these fibers in the uterus activate the afferent pain pathways to the central nervous system. […] A recent study demonstrated maternal transmission of primary dysmenorrhea in adolescent and young women, with an important gene influence on dysmenorrhea. […] Genetic component is also thought to have an impact on PD pathophysiology.
  • #48 Dysmenorrhea: Painful Periods | ACOG
    https://www.acog.org/womens-health/faqs/dysmenorrhea-painful-periods
    Pain associated with menstruation is called dysmenorrhea. […] Primary dysmenorrhea is the cramping pain that comes before or during a period. This pain is caused by natural chemicals called prostaglandins that are made in the lining of the uterus. Prostaglandins cause the muscles and blood vessels of the uterus to contract. On the first day of a period, the level of prostaglandins is high. As bleeding continues and the lining of the uterus is shed, the level goes down. This is why pain tends to lessen after the first few days of a period. […] Secondary dysmenorrhea is caused by a disorder in the reproductive organs. The pain tends to get worse over time and it often lasts longer than normal menstrual cramps. […] Some of the conditions that can cause secondary dysmenorrhea include the following: Endometriosis happens when tissue similar to the lining of the uterus grows in other areas of the body, such as on the ovaries and fallopian tubes, behind the uterus, and on the bladder. Like the lining of the uterus, this tissue breaks down and bleeds in response to changes in hormones. This bleeding can cause pain, especially around the time of a period.
  • #49 Dysmenorrhea: Painful Periods | ACOG
    https://www.acog.org/womens-health/faqs/dysmenorrhea-painful-periods
    Pain associated with menstruation is called dysmenorrhea. […] Primary dysmenorrhea is the cramping pain that comes before or during a period. This pain is caused by natural chemicals called prostaglandins that are made in the lining of the uterus. Prostaglandins cause the muscles and blood vessels of the uterus to contract. On the first day of a period, the level of prostaglandins is high. As bleeding continues and the lining of the uterus is shed, the level goes down. This is why pain tends to lessen after the first few days of a period. […] Secondary dysmenorrhea is caused by a disorder in the reproductive organs. The pain tends to get worse over time and it often lasts longer than normal menstrual cramps. […] Some of the conditions that can cause secondary dysmenorrhea include the following: Endometriosis happens when tissue similar to the lining of the uterus grows in other areas of the body, such as on the ovaries and fallopian tubes, behind the uterus, and on the bladder. Like the lining of the uterus, this tissue breaks down and bleeds in response to changes in hormones. This bleeding can cause pain, especially around the time of a period.
  • #50 Dysmenorrhea: Painful Periods | ACOG
    https://www.acog.org/womens-health/faqs/dysmenorrhea-painful-periods
    Pain associated with menstruation is called dysmenorrhea. […] Primary dysmenorrhea is the cramping pain that comes before or during a period. This pain is caused by natural chemicals called prostaglandins that are made in the lining of the uterus. Prostaglandins cause the muscles and blood vessels of the uterus to contract. On the first day of a period, the level of prostaglandins is high. As bleeding continues and the lining of the uterus is shed, the level goes down. This is why pain tends to lessen after the first few days of a period. […] Secondary dysmenorrhea is caused by a disorder in the reproductive organs. The pain tends to get worse over time and it often lasts longer than normal menstrual cramps. […] Some of the conditions that can cause secondary dysmenorrhea include the following: Endometriosis happens when tissue similar to the lining of the uterus grows in other areas of the body, such as on the ovaries and fallopian tubes, behind the uterus, and on the bladder. Like the lining of the uterus, this tissue breaks down and bleeds in response to changes in hormones. This bleeding can cause pain, especially around the time of a period.
  • #51 Dysmenorrhea: Painful Periods | ACOG
    https://www.acog.org/womens-health/faqs/dysmenorrhea-painful-periods
    Fibroids are growths that form on the outside, on the inside, or in the walls of the uterus. Fibroids located in the wall of the uterus can cause pain. […] Adenomyosis develops when tissue that normally lines the uterus begins to grow in the muscle wall of the uterus. […] Certain defects that a woman is born with can result in pain during menstruation. […] Medications are usually the first step when treating painful periods. Certain pain relievers target prostaglandins. These medications, called nonsteroidal anti-inflammatory drugs (NSAIDs), reduce the prostaglandins made by the body and lessen their effects. This in turn makes menstrual cramps less severe. […] Birth control methods that contain estrogen and progestin, such as the pill, the patch, and the vaginal ring, can be used to treat painful periods.
  • #52 Dysmenorrhea: Painful Periods | ACOG
    https://www.acog.org/womens-health/faqs/dysmenorrhea-painful-periods
    Fibroids are growths that form on the outside, on the inside, or in the walls of the uterus. Fibroids located in the wall of the uterus can cause pain. […] Adenomyosis develops when tissue that normally lines the uterus begins to grow in the muscle wall of the uterus. […] Certain defects that a woman is born with can result in pain during menstruation. […] Medications are usually the first step when treating painful periods. Certain pain relievers target prostaglandins. These medications, called nonsteroidal anti-inflammatory drugs (NSAIDs), reduce the prostaglandins made by the body and lessen their effects. This in turn makes menstrual cramps less severe. […] Birth control methods that contain estrogen and progestin, such as the pill, the patch, and the vaginal ring, can be used to treat painful periods.
  • #53 Dysmenorrhea: Painful Periods | ACOG
    https://www.acog.org/womens-health/faqs/dysmenorrhea-painful-periods
    Fibroids are growths that form on the outside, on the inside, or in the walls of the uterus. Fibroids located in the wall of the uterus can cause pain. […] Adenomyosis develops when tissue that normally lines the uterus begins to grow in the muscle wall of the uterus. […] Certain defects that a woman is born with can result in pain during menstruation. […] Medications are usually the first step when treating painful periods. Certain pain relievers target prostaglandins. These medications, called nonsteroidal anti-inflammatory drugs (NSAIDs), reduce the prostaglandins made by the body and lessen their effects. This in turn makes menstrual cramps less severe. […] Birth control methods that contain estrogen and progestin, such as the pill, the patch, and the vaginal ring, can be used to treat painful periods.
  • #54 Menstrual pain Information | Mount Sinai – New York
    https://www.mountsinai.org/health-library/condition/menstrual-pain
    Primary dysmenorrhea is caused by strong contractions of the uterus triggered by prostaglandins, chemicals in the body that are involved in inflammation and pain. Generally, the higher the levels of prostaglandins, the more menstrual pain. […] Secondary dysmenorrhea can be caused by: […] Uterine infections […] PID […] Intrauterine device (IUD).
  • #55 Period pain
    https://www.nhs.uk/conditions/period-pain/
    Period pain usually happens when your womb tightens during your period. It’s often a normal part of the menstrual cycle. […] Sometimes painful periods can be caused by a condition such as womb tissue growing in other places (endometriosis and adenomyosis). […] An intrauterine device (IUD) can also cause period pain, particularly during the first 3 to 6 months after it’s put in. […] If you have severe period pain, a GP may recommend anti-inflammatory medicines like naproxen, flurbiprofen or mefenamic acid. […] The GP may refer you to a specialist (gynaecologist) if your period pain does not get better. […] You might need tests, such as an ultrasound scan, to find out what’s causing your period pain. If a condition is found, treating it will help.
  • #56 Inflammatory Markers in Dysmenorrhea and Therapeutic Options
    https://www.mdpi.com/1660-4601/17/4/1191
    Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. […] Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous studies have shown that dysmenorrhea is a complex process that may depend on many factors. It is known that the menstrual cycle is dependent on cyclic changes in ovarian hormone concentrations, and therefore also on cyclic changes in prostaglandin level and uterine contractile activity. As early as in 1965, Pickles et al. noted that one of the factors contributing to dysmenorrhea may be an increase in prostaglandin concentration before menstruation. These suggestions were confirmed in subsequent years by other authors who have demonstrated that prostaglandins are overproduced in dysmenorrhea. This is also indicated by the symptoms that co-occur with dysmenorrhea during menstruation. Prostaglandins cause narrowing of the blood vessels supplying the uterus, abnormal contractile activity of the uterus, which leads to ischemia, hypoxia of the uterus and increased sensitivity of the nerve endings. […] The mechanisms that follow a decrease in progesterone concentration are complex reactions between the endocrine, vascular and immune systems.
  • #57 Inflammatory Markers in Dysmenorrhea and Therapeutic Options
    https://www.mdpi.com/1660-4601/17/4/1191
    Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. […] Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous studies have shown that dysmenorrhea is a complex process that may depend on many factors. It is known that the menstrual cycle is dependent on cyclic changes in ovarian hormone concentrations, and therefore also on cyclic changes in prostaglandin level and uterine contractile activity. As early as in 1965, Pickles et al. noted that one of the factors contributing to dysmenorrhea may be an increase in prostaglandin concentration before menstruation. These suggestions were confirmed in subsequent years by other authors who have demonstrated that prostaglandins are overproduced in dysmenorrhea. This is also indicated by the symptoms that co-occur with dysmenorrhea during menstruation. Prostaglandins cause narrowing of the blood vessels supplying the uterus, abnormal contractile activity of the uterus, which leads to ischemia, hypoxia of the uterus and increased sensitivity of the nerve endings. […] The mechanisms that follow a decrease in progesterone concentration are complex reactions between the endocrine, vascular and immune systems.
  • #58 Inflammatory Markers in Dysmenorrhea and Therapeutic Options
    https://www.mdpi.com/1660-4601/17/4/1191
    Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. […] Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous studies have shown that dysmenorrhea is a complex process that may depend on many factors. It is known that the menstrual cycle is dependent on cyclic changes in ovarian hormone concentrations, and therefore also on cyclic changes in prostaglandin level and uterine contractile activity. As early as in 1965, Pickles et al. noted that one of the factors contributing to dysmenorrhea may be an increase in prostaglandin concentration before menstruation. These suggestions were confirmed in subsequent years by other authors who have demonstrated that prostaglandins are overproduced in dysmenorrhea. This is also indicated by the symptoms that co-occur with dysmenorrhea during menstruation. Prostaglandins cause narrowing of the blood vessels supplying the uterus, abnormal contractile activity of the uterus, which leads to ischemia, hypoxia of the uterus and increased sensitivity of the nerve endings. […] The mechanisms that follow a decrease in progesterone concentration are complex reactions between the endocrine, vascular and immune systems.
  • #59 Inflammatory Markers in Dysmenorrhea and Therapeutic Options
    https://www.mdpi.com/1660-4601/17/4/1191
    Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. […] Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous studies have shown that dysmenorrhea is a complex process that may depend on many factors. It is known that the menstrual cycle is dependent on cyclic changes in ovarian hormone concentrations, and therefore also on cyclic changes in prostaglandin level and uterine contractile activity. As early as in 1965, Pickles et al. noted that one of the factors contributing to dysmenorrhea may be an increase in prostaglandin concentration before menstruation. These suggestions were confirmed in subsequent years by other authors who have demonstrated that prostaglandins are overproduced in dysmenorrhea. This is also indicated by the symptoms that co-occur with dysmenorrhea during menstruation. Prostaglandins cause narrowing of the blood vessels supplying the uterus, abnormal contractile activity of the uterus, which leads to ischemia, hypoxia of the uterus and increased sensitivity of the nerve endings. […] The mechanisms that follow a decrease in progesterone concentration are complex reactions between the endocrine, vascular and immune systems.
  • #60 Dysmenorrhea | GLOWM
    https://www.glowm.com/section-view/heading/Dysmenorrhea/item/9
    The roles of prostanoids, such as thromboxane A2 and prostacyclin, and leukotrienes in primary dysmenorrhea are not well understood. Preliminary evidence suggests that prostacyclin is involved in the pathophysiology of primary dysmenorrhea. Increased uterine leukotriene may be responsible for some forms of primary dysmenorrhea that do not respond to therapy with NSAIDs, because leukotrienes are produced through the 5-lipoxygenase enzyme pathway rather than the cyclooxygenase pathway. […] The postulated mechanisms for the generation of pain from pelvic structures in primary dysmenorrhea are summarized in Figure 4. The increased uterine production and release of prostaglandins at menstruation give rise to increased abnormal uterine activity, which then causes uterine hypoxia and pain. Increased uterine activity and uterine ischemia or hypoxia are two major factors in the causation of the pain. Prostaglandins, such as prostaglandin E2, and cyclic endoperoxides hypersensitize pain fibers in the pelvis and uterus to the action of pain-inducing substances or factors. This understanding of the pathophysiology of primary dysmenorrhea has enabled the rational use of nonsteroidal antiinflammatory drugs for the relief of primary dysmenorrhea rather than pharmacotherapy, which merely inhibits uterine contractions, such as with betamimetic agents.
  • #61 Inflammatory Markers in Dysmenorrhea and Therapeutic Options
    https://www.mdpi.com/1660-4601/17/4/1191
    Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. […] Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous studies have shown that dysmenorrhea is a complex process that may depend on many factors. It is known that the menstrual cycle is dependent on cyclic changes in ovarian hormone concentrations, and therefore also on cyclic changes in prostaglandin level and uterine contractile activity. As early as in 1965, Pickles et al. noted that one of the factors contributing to dysmenorrhea may be an increase in prostaglandin concentration before menstruation. These suggestions were confirmed in subsequent years by other authors who have demonstrated that prostaglandins are overproduced in dysmenorrhea. This is also indicated by the symptoms that co-occur with dysmenorrhea during menstruation. Prostaglandins cause narrowing of the blood vessels supplying the uterus, abnormal contractile activity of the uterus, which leads to ischemia, hypoxia of the uterus and increased sensitivity of the nerve endings. […] The mechanisms that follow a decrease in progesterone concentration are complex reactions between the endocrine, vascular and immune systems.
  • #62 Inflammatory Markers in Dysmenorrhea and Therapeutic Options
    https://www.mdpi.com/1660-4601/17/4/1191
    Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. […] Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous studies have shown that dysmenorrhea is a complex process that may depend on many factors. It is known that the menstrual cycle is dependent on cyclic changes in ovarian hormone concentrations, and therefore also on cyclic changes in prostaglandin level and uterine contractile activity. As early as in 1965, Pickles et al. noted that one of the factors contributing to dysmenorrhea may be an increase in prostaglandin concentration before menstruation. These suggestions were confirmed in subsequent years by other authors who have demonstrated that prostaglandins are overproduced in dysmenorrhea. This is also indicated by the symptoms that co-occur with dysmenorrhea during menstruation. Prostaglandins cause narrowing of the blood vessels supplying the uterus, abnormal contractile activity of the uterus, which leads to ischemia, hypoxia of the uterus and increased sensitivity of the nerve endings. […] The mechanisms that follow a decrease in progesterone concentration are complex reactions between the endocrine, vascular and immune systems.
  • #63
    https://research-archive.org/index.php/rars/preprint/view/1569
    The prevalence of menstrual pain is high yet there is a lack of research and understanding of it. […] Much research has been dedicated to understanding the biochemistry of the mechanisms of these medicines and how pain is generated at a molecular level. […] I argue that future research should focus on menstrual pain specifically and how to alleviate it with more targeted therapies. […] These broad efforts will enhance our understanding of reproductive health sciences and have a significant impact on a large portion of the human population.