Primary Dysmenorrhea: Difference between revisions

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== Etiology ==
== Etiology ==
Primary dysmenorrhea is thought to be caused by excessive levels of prostaglandins, which are hormones that stimulate the uterus to contract during menstruation and childbirth (Coco 1999, Dawood 2006, Durian 2004). It has been found that women with dysmenorrhea have higher levels of prostaglandins in their menstrual fluid than women who do not experience menstrual pain (Bieglmayer 1995,Pickles 1979) . Furthermore, a study by Dawood and colleagues(2006) stated that the intensity of menstrual cramps is directly proportional to the amount of prostaglandins that is released (Dawood 2006)
Primary dysmenorrhea is thought to be caused by excessive levels of prostaglandins, which are hormones that stimulate the uterus to contract during menstruation and childbirth.<ref name=":0" /><ref name=":3" /><ref name=":4" />It has been found that women with dysmenorrhea have higher levels of prostaglandins in their menstrual fluid than women who do not experience menstrual pain.<ref>Bieglmayer C, Hofer G, Kainz C, Reinthaller A, Kopp B, Janisch H. Concentrations of various arachidonic acid metabolites in menstrual fluid are associated with menstrual pain and are influenced by hormonal contraceptives. Gynecological endocrinology. 1995 Jan 1;9(4):307-12.</ref><ref>Pickles VR. Prostaglandins and Dysmenorrhea Historical survey. Acta Obstetricia et Gynecologica Scandinavica. 1979 Jan 1;58(sup87):7-12.</ref>  Furthermore, a study by Dawood and colleagues (2006)<ref name=":4" /> stated that the intensity of menstrual cramps is directly proportional to the amount of prostaglandins that is released.<ref name=":4" />


During endometrial sloughing of menstruation, disintegrating endometrial cells increase the release of prostaglandins (PGF-2 alpha)(Coco 1999, Durian 2004). The excessive release of prostaglandins stimulates the myometrium (or middle layer of muscles of the uterine wall) to contract excessively (Coco 1999). Hypercontractility of the uterus elevates intrauterine pressure (Lefebvre 2005, Elboim 2020) and decreases blood flow in the uterus (Kannon and Claydon 2014;Elboim 2020)), ultimately resulting in uterine hypoxia and ischemia (Kannon and Claydon 2014;Elboim 2020)). The resulting hypoxia and ischemia is believed to be the cause for the pain and cramps (Kannon and Claydon 2014;Elboim 2020)).  
During endometrial sloughing of menstruation, disintegrating endometrial cells increase the release of prostaglandins (PGF-2 alpha).<ref name=":0" /><ref name=":3" /> The excessive release of prostaglandins stimulates the myometrium (or middle layer of muscles of the uterine wall) to contract excessively.<ref name=":0" /> Hyper-contractility of the uterus elevates intrauterine pressure<ref name=":1">Elboim-Gabyzon M, Kalichman L. Transcutaneous Electrical Nerve Stimulation (TENS) for Primary Dysmenorrhea: An Overview. International Journal of Women's Health. 2020;12:1.</ref><ref name=":6">Lefebvre G, Pinsonneault O, Antao V, Black A, Burnett M, Feldman K, Lea R, Robert M. Primary dysmenorrhea consensus guideline. J Obstet Gynaecol Can. 2005 Dec 1;27(12):1117-46.</ref>  and decreases blood flow in the uterus<ref name=":2" /><ref name=":1" />, ultimately resulting in uterine hypoxia and ischemia.<ref name=":2" /><ref name=":1" /> The resulting hypoxia and ischemia is believed to be the cause for the pain and cramps.<ref name=":2" /><ref name=":1" />


Although still being debated in the literature, vasopressin has also been implicated in the etiology of primary dysmenorrhea (Dawood 2006).  Levels of circulating vasopressin  are elevated in women with primary dysmenorrhea (Valentin 2000, Akerlund 1979). Elevated vasopressin levels can lead to irregular uterine contractions that decrease blood flow to the uterus, ultimately resulting in uterine hypoxia (Dawood 2006).
Although still being debated in the literature, vasopressin has also been implicated in the etiology of primary dysmenorrhea.<ref name=":4" />  Levels of circulating vasopressin  are elevated in women with primary dysmenorrhea.<ref>Valentin L, Sladkevicius P, Kindahl H, Broeders A, Marsal K, Melin P. Effects of a vasopressin antagonist in women with dysmenorrhea. Gynecologic and obstetric investigation. 2000;50(3):170-7.</ref><ref>Åkerlund M. Pathophysiology of dysmenorrhea. Acta Obstetricia et Gynecologica Scandinavica. 1979 Jan 1;58(sup87):27-32.</ref> Elevated vasopressin levels can lead to irregular uterine contractions that decrease blood flow to the uterus, ultimately resulting in uterine hypoxia.<ref name=":4" />


It is important to note that menstrual pain can not be attributed to the cyclic production of only a few hormones (Durrain). Women with primary dysmenorrhea are more susceptible to depression, anxiety and somatization (Bancroft 1993). For this reason, it has been proposed in the literature that dysmenorrheic women have an alternative mode of systemic pain processing(Garnot 2001), whereby the pain induced by uterine contractions during menstruation may be perceived as more severe than in non-dysmenorrheic women. A study by Granot and colleagues (2001) reported that dysmenorrheic women had a longer latency period of pain,  a higher rating of pain as measured by the visual analogue scale (VAS), and higher levels of anxiety. For this reason, Granot and colleagues proposed that this augmentation of pain perception may be part of the development of dysmenorrhea. This can be supported by the work of Walsh and colleagues (2003) who suggest that there is an association between pain catastrophizing and the  severity of menstrual pain (Walsh 2003).  
It is important to note that menstrual pain can not be attributed to the cyclic production of only a few hormones.<ref name=":3" /> Women with primary dysmenorrhea are more susceptible to depression, anxiety and somatization.<ref>Bancroft J, Williamson L, Warner P, Rennie D, Smith SK. Perimenstrual complaints in women complaining of PMS, menorrhagia, and dysmenorrhea: toward a dismantling of the premenstrual syndrome. Psychosomatic Medicine. 1993 Mar.</ref> For this reason, it has been proposed in the literature that dysmenorrheic women have an alternative mode of systemic pain processing, whereby the pain induced by uterine contractions during menstruation may be perceived as more severe than in non-dysmenorrheic women.<ref name=":7">Granot M, Yarnitsky D, Itskovitz-Eldor J, Granovsky Y, Peer E, Zimmer EZ. Pain perception in women with dysmenorrhea. Obstetrics & Gynecology. 2001 Sep 1;98(3):407-11.</ref> A study by Granot and colleagues (2001)<ref name=":7" /> reported that dysmenorrheic women had a longer latency period of pain, a higher rating of pain as measured by the visual analogue scale (VAS), and higher levels of anxiety.<ref name=":7" /> For this reason, Granot and colleagues proposed that this augmentation of pain perception may be part of the development of dysmenorrhea.<ref name=":7" /> This can be supported by the work of Walsh and colleagues (2003)<ref name=":8">Walsh TM, LeBlanc L, McGrath PJ. Menstrual pain intensity, coping, and disability: The role of pain catastrophizing. Pain Medicine. 2003 Dec 1;4(4):352-61.</ref> who suggest that there is an association between pain catastrophizing and the  severity of menstrual pain.<ref name=":8" />


== Management ==
== Management ==


==== Pharmacological System: ====
=== Pharmacological Treatment  ===
NSAIDs, Diclofenac, etc.
NSAIDs along with oral contraceptives help to relieve symptoms of primary dysmenorrhea by decreasing the excessive levels of prostaglandins present during menstruation. <ref name=":4" />


==== Hormonal Treatments: ====
=== Physiotherapy Treatments ===
* Oral Contraceptive Pills, etc.


==== Physiotherapy Treatments: ====
==== Transcutaneous Electrical Nerve Stimulation (TENS) ====
* Heat Therapy,
[https://www.physio-pedia.com/Transcutaneous_Electrical_Nerve_Stimulation_(TENS) TENS], which delivers electrical currents through the skin via electrodes, provides a non-invasive pharmacological intervention to treat primary dysmenorrhea.<ref name=":1" /><ref name=":9">Proctor M, Farquhar C, Stones W, He L, Zhu X, Brown J. Transcutaneous electrical nerve stimulation for primary dysmenorrhoea. Cochrane Database of Systematic Reviews. 2002(1).</ref> . Specifically, high frequency TENS, which involves electrical pulses delivered between 50 and 120 Hz) is most effective.<ref name=":1" /><ref name=":9" /> TENS poses several advantages including that it is safe, portable and inexpensive.<ref name=":1" /> TENS can be self-administered regularly during the time of menstruation following appropriate education.<ref name=":1" /> Intensity should be set to a non-painful, maximum tolerable intensity level and then increased continually throughout each session to avoid habituation.<ref name=":1" /> More research regarding dosing of TENS (ii.e. Duration, frequency and number of treatments) is still required.<ref name=":1" /><ref name=":9" />
* [[Transcutaneous Electrical Nerve Stimulation (TENS)|TENS]]: Review<ref name=":1">Elboim-Gabyzon M, Kalichman L. [[Transcutaneous Electrical Nerve Stimulation (TENS) for Primary Dysmenorrhea: An Overview]]. International Journal of Women's Health. 2020;12:1.</ref> suggests that Primary Dysmenorrhea can be effectively managed with Transcutaneous Electrical Nerve Stimulation (TENS) as it is safe, portable, battery-operated, and relatively inexpensive.
 
* Kinesio-Taping,  
==== Thermotherapy ====
* Exercises like [[Kegel's Exercise : Females|Kegel]] and [[pilates]].
Heat therapies have been supported in the literature as an effective non-pharmacological method to decrease menstrual pain in women with primary dysmenorrhea.<ref name=":6" /><ref name=":10">Igwea SE, Tabansi-Ochuogu CS, Abaraogu UO. TENS and heat therapy for pain relief and quality of life improvement in individuals with primary dysmenorrhea: a systematic review. Complementary therapies in clinical practice. 2016 Aug 1;24:86-91. </ref><ref name=":11">Jo J, Lee SH. Heat therapy for primary dysmenorrhea: A systematic review and meta-analysis of its effects on pain relief and quality of life. Scientific reports. 2018 Nov 2;8(1):1-8.</ref>. In two systematic reviews<ref name=":10" /><ref name=":11" />, heat therapies ranged from heated wraps, belts, patches and pillows ranging from 38 to 40 degrees with placement over the lower abdomen for a minimum duration of 30 minutes and a maximum duration 8 -12 hours.<ref name=":10" /><ref name=":11" /> The proposed mechanism behind heat therapy is through the reduction of muscle tension and promotion of abdominal muscle relaxation.<ref name=":11" /> More research is still required regarding which heating modalities are most beneficial and cost-effectiveness of each modality.<ref name=":11" />
 
==== Exercise ====
Several studies have reported beneficial effects of exercise, including stretching, aerobic exercise (i.e jogging), yoga and kegel exercises, to treat primary dysmenorrhea.<ref name=":2" /><ref name=":12">Brown J, Brown S. Exercise for dysmenorrhoea. Cochrane Database of Systematic Reviews. 2010(2).</ref><ref name=":13">Billig HE. Dysmenorrhea: the result of a postural defect. Archives of Surgery. 1943 May 1;46(5):611-3.</ref><ref>Prior JC, Vigna Y. Conditioning exercise and premenstrual symptoms. The Journal of Reproductive Medicine. 1987 Jun 1;32(6):423-8.</ref><ref>Israel RG, Sutton M, O'Brien KF. Effects of aerobic training on primary dysmenorrhea symptomatology in college females. Journal of american college health. 1985 Jun 1;33(6):241-4.</ref><ref>Ortiz MI, Cortés-Márquez SK, Romero-Quezada LC, Murguía-Cánovas G, Jaramillo-Díaz AP. Effect of a physiotherapy program in women with primary dysmenorrhea. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2015 Nov 1;194:24-9.</ref><ref>Kannan P, Claydon LS, Miller D, Chapple CM. Vigorous exercises in the management of primary dysmenorrhea: a feasibility study. Disability and rehabilitation. 2015 Jul 17;37(15):1334-9.</ref> Stretching exercises may help to reduce the amount of pain that radiates into the lumbar area and the adductors.<ref name=":12" /><ref name=":13" /> [https://www.physio-pedia.com/Kegel%27s_Exercise_:_Females Kegel exercises] may help to increase local blood supply to the uterus, allowing for rapid elimination of prostaglandins and a decreased intensity of menstrual pain.<ref>Harvey MA. Pelvic floor exercises during and after pregnancy: a systematic review of their role in preventing pelvic floor dysfunction. Journal of Obstetrics and Gynaecology Canada. 2003 Jun 1;25(6):487-98.</ref><ref>Beales D, Hope JB, Hoff TS, Sandvik H, Wergeland O, Fary R. Current practice in management of pelvic girdle pain amongst physiotherapists in Norway and Australia. Manual therapy. 2015 Feb 1;20(1):109-16.</ref>
 
A review by Armour and colleagues (2019)<ref name=":14">Armour M, Ee CC, Naidoo D, Ayati Z, Chalmers KJ, Steel KA, de Manincor MJ, Delshad E. Exercise for dysmenorrhoea. Cochrane Database of Systematic Reviews. 2019(9).</ref> suggests that exercise, performed for approximately 45 to 60 minutes per session, 3 or more times per week, regardless of intensity may provide a significant reduction in menstrual pain intensity of around 25 mm on a 100 mm visual analogue scale (VAS).<ref name=":14" /> Although this evidence was low in quality, women should consider using exercise alone or in conjunction with other modalities to manage menstrual pain given the health benefits of exercise and the relatively low side effects associated with exercise.<ref name=":14" />


==== Diet Supplements ====
==== Diet Supplements ====

Revision as of 16:55, 23 June 2020

Original Editor - Priya Gulla

Top Contributors - Priya Gulla, Vidya Acharya, Victoria Geropoulos, Franca Ebomah, Funmilayo Adepeju Aregbeshola, Oyemi Sillo, Nicole Hills and Sehriban Ozmen;


Definition[edit | edit source]

Primary dysmenorrhea, commonly referred to as menstrual cramps, is defined as the pain occurring in the lower abdomen before or during menstrual cycle, in the absence of any other pelvic pathology (i.e. endometriosis).[1][2][3] With a prevalence of 20 to 90%,[4][5][6] primary dysmenorrhea is by far the most common gynaecological problem.[1] It is also the leading cause of recurrent absenteeism from school or work in adolescent girls and young women.[2]Despite resulting in activity limitations, most women suffer silently and fail to report their symptoms to a healthcare provider.[1][3][7]

Clinical Presentation[edit | edit source]

Primary dysmenorrhea usually presents at the age of adolescence within three years of menarche.[1] However, it is unusual for symptoms to start within the first six months after menarche as it is in sync with a female's ovulatory cycles.[1]

Females suffering from primary dysmenorrhea may experience sharp, intermittent spasms of pain, usually centered in suprapubic (lower abdomen) area.[1] Pain may radiate into the lower back and inner aspects of the thighs.[1] Pain usually begins a few hours before or at the onset of menstrual flow, reaching a peak when flow becomes the heaviest at day one or two of the cycle.[8] The severity of pain usually lasts for few hours, may extend up to a duration of 24 to 36 hours.[8] This is consistent with when there is maximal prostaglandin release into the menstrual fluid during menstruation.[8]

Systematic symptoms of primary dysmenorrhea may include nausea, vomiting, diarrhoea, fatigue, fever, headache or light-headedness.[1] Symptoms may be accompanied by vasomotor changes that causes pallor, cold sweats and occasional fainting.[9] Although rare, syncope and collapse may occur in severe cases.[9]

Primary dysmenorrhea can be distinguished from secondary dysmenorrhea by number of factors. Secondary dysmenorrhea occurs years after painless menstruation and is typically associated with another medical or gynaecological conditions (i.e. endometriosis, chronic pelvic inflammatory disease, fibroids, inflammatory bowel disease, etc).[1][3] A paper by Coco (1999)[1] listed several criteria indicative of secondary dysmenorrhea:

    1. Dysmenorrhea occurring during the first one or two cycles after menarche[1]
    2. Dysmenorrhea occurring after 25 years[1]
    3. Late onset of dysmenorrhea after a history of painless menstruation (consider complications of pregnancy : ectopic or threatened spontaneous abortion)[1]
    4. Pelvic abnormality on physical examination, infertility heavy menstrual flow or irregular menstrual cycle[1]
    5. Little or no response to therapy with drugs like NSAIDs, oral contraceptives or both[1]

Etiology[edit | edit source]

Primary dysmenorrhea is thought to be caused by excessive levels of prostaglandins, which are hormones that stimulate the uterus to contract during menstruation and childbirth.[1][3][8]It has been found that women with dysmenorrhea have higher levels of prostaglandins in their menstrual fluid than women who do not experience menstrual pain.[10][11] Furthermore, a study by Dawood and colleagues (2006)[8] stated that the intensity of menstrual cramps is directly proportional to the amount of prostaglandins that is released.[8]

During endometrial sloughing of menstruation, disintegrating endometrial cells increase the release of prostaglandins (PGF-2 alpha).[1][3] The excessive release of prostaglandins stimulates the myometrium (or middle layer of muscles of the uterine wall) to contract excessively.[1] Hyper-contractility of the uterus elevates intrauterine pressure[12][13] and decreases blood flow in the uterus[2][12], ultimately resulting in uterine hypoxia and ischemia.[2][12] The resulting hypoxia and ischemia is believed to be the cause for the pain and cramps.[2][12]

Although still being debated in the literature, vasopressin has also been implicated in the etiology of primary dysmenorrhea.[8]  Levels of circulating vasopressin  are elevated in women with primary dysmenorrhea.[14][15] Elevated vasopressin levels can lead to irregular uterine contractions that decrease blood flow to the uterus, ultimately resulting in uterine hypoxia.[8]

It is important to note that menstrual pain can not be attributed to the cyclic production of only a few hormones.[3] Women with primary dysmenorrhea are more susceptible to depression, anxiety and somatization.[16] For this reason, it has been proposed in the literature that dysmenorrheic women have an alternative mode of systemic pain processing, whereby the pain induced by uterine contractions during menstruation may be perceived as more severe than in non-dysmenorrheic women.[17] A study by Granot and colleagues (2001)[17] reported that dysmenorrheic women had a longer latency period of pain, a higher rating of pain as measured by the visual analogue scale (VAS), and higher levels of anxiety.[17] For this reason, Granot and colleagues proposed that this augmentation of pain perception may be part of the development of dysmenorrhea.[17] This can be supported by the work of Walsh and colleagues (2003)[18] who suggest that there is an association between pain catastrophizing and the  severity of menstrual pain.[18]

Management[edit | edit source]

Pharmacological Treatment[edit | edit source]

NSAIDs along with oral contraceptives help to relieve symptoms of primary dysmenorrhea by decreasing the excessive levels of prostaglandins present during menstruation. [8]

Physiotherapy Treatments[edit | edit source]

Transcutaneous Electrical Nerve Stimulation (TENS)[edit | edit source]

TENS, which delivers electrical currents through the skin via electrodes, provides a non-invasive pharmacological intervention to treat primary dysmenorrhea.[12][19] . Specifically, high frequency TENS, which involves electrical pulses delivered between 50 and 120 Hz) is most effective.[12][19] TENS poses several advantages including that it is safe, portable and inexpensive.[12] TENS can be self-administered regularly during the time of menstruation following appropriate education.[12] Intensity should be set to a non-painful, maximum tolerable intensity level and then increased continually throughout each session to avoid habituation.[12] More research regarding dosing of TENS (ii.e. Duration, frequency and number of treatments) is still required.[12][19]

Thermotherapy[edit | edit source]

Heat therapies have been supported in the literature as an effective non-pharmacological method to decrease menstrual pain in women with primary dysmenorrhea.[13][20][21]. In two systematic reviews[20][21], heat therapies ranged from heated wraps, belts, patches and pillows ranging from 38 to 40 degrees with placement over the lower abdomen for a minimum duration of 30 minutes and a maximum duration 8 -12 hours.[20][21] The proposed mechanism behind heat therapy is through the reduction of muscle tension and promotion of abdominal muscle relaxation.[21] More research is still required regarding which heating modalities are most beneficial and cost-effectiveness of each modality.[21]

Exercise[edit | edit source]

Several studies have reported beneficial effects of exercise, including stretching, aerobic exercise (i.e jogging), yoga and kegel exercises, to treat primary dysmenorrhea.[2][22][23][24][25][26][27] Stretching exercises may help to reduce the amount of pain that radiates into the lumbar area and the adductors.[22][23] Kegel exercises may help to increase local blood supply to the uterus, allowing for rapid elimination of prostaglandins and a decreased intensity of menstrual pain.[28][29]

A review by Armour and colleagues (2019)[30] suggests that exercise, performed for approximately 45 to 60 minutes per session, 3 or more times per week, regardless of intensity may provide a significant reduction in menstrual pain intensity of around 25 mm on a 100 mm visual analogue scale (VAS).[30] Although this evidence was low in quality, women should consider using exercise alone or in conjunction with other modalities to manage menstrual pain given the health benefits of exercise and the relatively low side effects associated with exercise.[30]

Diet Supplements[edit | edit source]

Surgical Intervention[edit | edit source]

References[edit | edit source]

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 Coco AS. Primary Dysmenorrhea. American Family Physician. 1999,60(2):489-96
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Kannan P, Claydon LS. Some physiotherapy treatments may relieve menstrual pain in women with primary dysmenorrhea: a systematic review. Journal of physiotherapy. 2014 Mar 1;60(1):13-21.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Durain D. Primary dysmenorrhea: assessment and management update. Journal of midwifery & women's health. 2004 Nov 1;49(6):520-8.
  4. ↑ Ortiz MI, Rangel-Flores E, Carrillo-Alarcón LC, Veras-Godoy HA. Prevalence and impact of primary dysmenorrhea among Mexican high school students. International Journal of Gynecology & Obstetrics. 2009 Dec 1;107(3):240-3.
  5. ↑ Ortiz MI. Primary dysmenorrhea among Mexican university students: prevalence, impact and treatment. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2010 Sep 1;152(1):73-7.
  6. ↑ Latthe PM, Champaneria R. Dysmenorrhoea. BMJ clinical evidence. 2011;2011.
  7. ↑ Niven CA, Walker A. Reproductive potential and fertility control. Butterworth Heineman, Oxford. 1996.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 Dawood MY. Primary dysmenorrhea: advances in pathogenesis and management. Obstetrics & Gynecology. 2006 Aug 1;108(2):428-41
  9. ↑ 9.0 9.1 Dutta DC, Konar H. DC Dutta's textbook of gynecology. JP Medical Ltd; 2014 Apr 30.
  10. ↑ Bieglmayer C, Hofer G, Kainz C, Reinthaller A, Kopp B, Janisch H. Concentrations of various arachidonic acid metabolites in menstrual fluid are associated with menstrual pain and are influenced by hormonal contraceptives. Gynecological endocrinology. 1995 Jan 1;9(4):307-12.
  11. ↑ Pickles VR. Prostaglandins and Dysmenorrhea Historical survey. Acta Obstetricia et Gynecologica Scandinavica. 1979 Jan 1;58(sup87):7-12.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 12.9 Elboim-Gabyzon M, Kalichman L. Transcutaneous Electrical Nerve Stimulation (TENS) for Primary Dysmenorrhea: An Overview. International Journal of Women's Health. 2020;12:1.
  13. ↑ 13.0 13.1 Lefebvre G, Pinsonneault O, Antao V, Black A, Burnett M, Feldman K, Lea R, Robert M. Primary dysmenorrhea consensus guideline. J Obstet Gynaecol Can. 2005 Dec 1;27(12):1117-46.
  14. ↑ Valentin L, Sladkevicius P, Kindahl H, Broeders A, Marsal K, Melin P. Effects of a vasopressin antagonist in women with dysmenorrhea. Gynecologic and obstetric investigation. 2000;50(3):170-7.
  15. ↑ Åkerlund M. Pathophysiology of dysmenorrhea. Acta Obstetricia et Gynecologica Scandinavica. 1979 Jan 1;58(sup87):27-32.
  16. ↑ Bancroft J, Williamson L, Warner P, Rennie D, Smith SK. Perimenstrual complaints in women complaining of PMS, menorrhagia, and dysmenorrhea: toward a dismantling of the premenstrual syndrome. Psychosomatic Medicine. 1993 Mar.
  17. ↑ 17.0 17.1 17.2 17.3 Granot M, Yarnitsky D, Itskovitz-Eldor J, Granovsky Y, Peer E, Zimmer EZ. Pain perception in women with dysmenorrhea. Obstetrics & Gynecology. 2001 Sep 1;98(3):407-11.
  18. ↑ 18.0 18.1 Walsh TM, LeBlanc L, McGrath PJ. Menstrual pain intensity, coping, and disability: The role of pain catastrophizing. Pain Medicine. 2003 Dec 1;4(4):352-61.
  19. ↑ 19.0 19.1 19.2 Proctor M, Farquhar C, Stones W, He L, Zhu X, Brown J. Transcutaneous electrical nerve stimulation for primary dysmenorrhoea. Cochrane Database of Systematic Reviews. 2002(1).
  20. ↑ 20.0 20.1 20.2 Igwea SE, Tabansi-Ochuogu CS, Abaraogu UO. TENS and heat therapy for pain relief and quality of life improvement in individuals with primary dysmenorrhea: a systematic review. Complementary therapies in clinical practice. 2016 Aug 1;24:86-91.
  21. ↑ 21.0 21.1 21.2 21.3 21.4 Jo J, Lee SH. Heat therapy for primary dysmenorrhea: A systematic review and meta-analysis of its effects on pain relief and quality of life. Scientific reports. 2018 Nov 2;8(1):1-8.
  22. ↑ 22.0 22.1 Brown J, Brown S. Exercise for dysmenorrhoea. Cochrane Database of Systematic Reviews. 2010(2).
  23. ↑ 23.0 23.1 Billig HE. Dysmenorrhea: the result of a postural defect. Archives of Surgery. 1943 May 1;46(5):611-3.
  24. ↑ Prior JC, Vigna Y. Conditioning exercise and premenstrual symptoms. The Journal of Reproductive Medicine. 1987 Jun 1;32(6):423-8.
  25. ↑ Israel RG, Sutton M, O'Brien KF. Effects of aerobic training on primary dysmenorrhea symptomatology in college females. Journal of american college health. 1985 Jun 1;33(6):241-4.
  26. ↑ Ortiz MI, Cortés-Márquez SK, Romero-Quezada LC, Murguía-Cánovas G, Jaramillo-Díaz AP. Effect of a physiotherapy program in women with primary dysmenorrhea. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2015 Nov 1;194:24-9.
  27. ↑ Kannan P, Claydon LS, Miller D, Chapple CM. Vigorous exercises in the management of primary dysmenorrhea: a feasibility study. Disability and rehabilitation. 2015 Jul 17;37(15):1334-9.
  28. ↑ Harvey MA. Pelvic floor exercises during and after pregnancy: a systematic review of their role in preventing pelvic floor dysfunction. Journal of Obstetrics and Gynaecology Canada. 2003 Jun 1;25(6):487-98.
  29. ↑ Beales D, Hope JB, Hoff TS, Sandvik H, Wergeland O, Fary R. Current practice in management of pelvic girdle pain amongst physiotherapists in Norway and Australia. Manual therapy. 2015 Feb 1;20(1):109-16.
  30. ↑ 30.0 30.1 30.2 Armour M, Ee CC, Naidoo D, Ayati Z, Chalmers KJ, Steel KA, de Manincor MJ, Delshad E. Exercise for dysmenorrhoea. Cochrane Database of Systematic Reviews. 2019(9).
  31. ↑ Linda French. Dysmenorrhea. American Family Physician. 2005; 71(2): 285-91
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