Dysmenorrhea and related disorders

Introduction

Dysmenorrhea is defined as the presence of painful cramps of uterine origin that occur during menstruation and represents one of the most common causes of pelvic pain and menstrual disorder. The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”¹. In particular, chronic pelvic pain is located in the pelvic area and lasts for 6 months or longer².

The burden of dysmenorrhea is greater than any other gynecological complaint³: dysmenorrhea is the leading cause of gynecological morbidity in women of reproductive age regardless of age, nationality, and economic status^4–7. The effects extend beyond individual women to society, resulting annually in an important loss of productivity^8,9. Thus, the World Health Organization estimated that dysmenorrhea is the most important cause of chronic pelvic pain¹⁰.

The estimated prevalence of dysmenorrhea is high, although it varies widely, ranging from 45 to 93% of women of reproductive age^3,10, and the highest rates are reported in adolescents^11,12. Because it is accepted as a normal aspect of the menstrual cycle and therefore is tolerated, women do not report it¹³ and do not seek medical care^13,14. Some women (3 to 33%) have very severe pain, severe enough to render them incapacitated for 1 to 3 days each menstrual cycle, requiring absence from school or work^15,16. Indeed, dysmenorrhea has a high impact on women’s lives, resulting in a restriction of daily activities^17,18, a lower academic performance in adolescents^19,20, and poor quality of sleep²¹, and has negative effects on mood, causing anxiety and depression²².

Definition and pathogenesis

On the basis of pathophysiology, dysmenorrhea is classified as primary dysmenorrhea (menstrual pain without organic disease) or secondary dysmenorrhea (menstrual pain associated with underlying pelvic pathology)²³. The cause of primary dysmenorrhea is not well established. However, the responsible cause has been identified on the hyper-production of uterine prostaglandins, particularly of PGF_2a and PGF₂, thus resulting in increased uterine tone and high-amplitude contractions²⁴. Women with dysmenorrhea have higher levels of prostaglandins, which are highest during the first two days of menses²⁵. Prostaglandin production is controlled by progesterone: when progesterone levels drop, immediately prior to menstruation, prostaglandin levels increase^13,24. If the exposure of endometrium to luteal phase is crucial for the increased production of progesterone, dysmenorrhea occurs only with ovulatory cycles. This could explain why primary dysmenorrhea onset is shortly after menarche and why dysmenorrhea responds well to ovulatory inhibition. However, multiple other factors may play a role in the perception and the severity of pain, which does not depend only on endocrine factors²⁶.

The recurrent menstrual pain is associated with central sensitization, which is associated with structural and functional modification of the central nervous system^24,27. Given that dysmenorrhea might led to important long-term consequences and may be increasing women’s susceptibility to others chronic pain conditions later in life, it is mandatory to treat menstrual pain in order to limit the noxious input into the central nervous system²⁴. The most common causes of secondary dysmenorrhea in young women are endometriosis and adenomyosis.

Risk factors

Heavy menstrual bleeding and longer menstrual bleeding duration are often associated with dysmenorrhea^3,20. Childbearing is a very influential factor for the decrease of dysmenorrhea⁵. Increasing age is also associated with less severe dysmenorrhea¹², although a longitudinal study found that the proportion of women with moderate to severe dysmenorrhea remained constant with increasing age⁵.

The early onset of pain is associated with more severe pain³, and a family history of dysmenorrhea is associated with a significantly higher prevalence of dysmenorrhea²⁰. Since anxiety and depression are often associated, dysmenorrhea may be part of a somatoform syndrome³.

Diagnosis

A focused history and physical examination are usually sufficient for making a diagnosis of primary dysmenorrhea^23,26. The onset of primary dysmenorrhea is usually 6 to 12 months after menarche. The typical pain is sharp and intermittent, is located in the suprapubic area, and develops within hours of the start of menstruation and peaks with maximum blood flow²³. The physical examination is completely normal, and the menstrual pain may be associated with systemic symptoms, such as nausea, vomiting, diarrhea, fatigue, fever, headache, and insomnia^11,16,40. There is no evidence for routine use of ultrasound in the evaluation of primary dysmenorrhea, although ultrasound is very useful in excluding the secondary causes of dysmenorrhea, such as endometriosis and adenomyosis²⁶ (Figure 1).

Dysmenorrhea that occurs any time after menarche, that is associated with other gynecological symptoms such as dyspareunia, heavy menstrual bleeding, AUB, and infertility, and that does not respond to treatment with NSAIDs or OCs might be suspicious for secondary dysmenorrhea^23,24. In particular, the analysis of menstrual bleeding abnormalities associated with dysmenorrhea might be helpful for the diagnosis of adenomyosis (Figure 1).

Figure 1. Flowchart for the management of patients with dysmenorrhea.

Flowchart for the management of patients with dysmenorrhea.

Treatment

The aim of the treatment for primary dysmenorrhea is pain relief.