Primary Dysmenorrhea

Original Editor - Priya Gulla

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

Definition

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). With a prevalence of 20 to 90%, primary dysmenorrhea is by far the most common gynaecological problem. It is also the leading cause of recurrent absenteeism from school or work in adolescent girls and young women.Despite resulting in activity limitations, most women suffer silently and fail to report their symptoms to a healthcare provider.

Clinical Presentation

Primary dysmenorrhea usually presents at the age of adolescence within three years of menarche. 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.

Females suffering from primary dysmenorrhea may experience sharp, intermittent spasms of pain, usually centered in suprapubic (lower abdomen) area. Pain may radiate into the lower back and inner aspects of the thighs. 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. The severity of pain usually lasts for few hours, may extend up to a duration of 24 to 36 hours. This is consistent with when there is maximal prostaglandin release into the menstrual fluid during menstruation.

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

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). A paper by Coco (1999) listed several criteria indicative of secondary dysmenorrhea:

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

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)

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)).

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).

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).

Management

Pharmacological System:

NSAIDs, Diclofenac, etc.

Hormonal Treatments:

• Oral Contraceptive Pills, etc.

Physiotherapy Treatments:

• Heat Therapy,
• TENS: Review 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,
• Exercises like Kegel and pilates.

Surgical Intervention

• In rare cases.