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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 the menstrual cycle, in the absence of any other pelvic pathology (e.g., 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[edit | edit source]
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 supra-pubic (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 a few hours, but 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 a number of factors. Secondary dysmenorrhea occurs years after painless menstruation and is typically associated with another medical or gynaecological condition (i.e. endometriosis, chronic pelvic inflammatory disease, fibroids, inflammatory bowel disease, etc). A paper by Coco (1999) listed several criteria indicative of secondary dysmenorrhea:
- Dysmenorrhea occurring during the first one or two cycles after menarche
- Dysmenorrhea occurring after 25 years
- Late-onset of dysmenorrhea after a history of painless menstruation (consider complications of pregnancy: ectopic or threatened spontaneous abortion)
- Pelvic abnormality on physical examination, infertility heavy menstrual flow or irregular menstrual cycle
- Little or no response to therapy with drugs like NSAIDs, oral contraceptives or both
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.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. 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.
During endometrial sloughing of menstruation, disintegrating endometrial cells increase the release of prostaglandins (PGF-2 alpha). The excessive release of prostaglandins stimulates the myometrium (or middle layer of muscles of the uterine wall) to contract excessively. Hyper-contractility of the uterus elevates intrauterine pressure and decreases blood flow in the uterus, ultimately resulting in uterine hypoxia and ischemia. The resulting hypoxia and ischemia is believed to be the cause of the pain and cramps experienced in primary dysmenorrhea.
Although still debated in the literature, vasopressin has been implicated in the etiology of primary dysmenorrhea. Levels of circulating vasopressin are elevated in women with primary dysmenorrhea. Elevated vasopressin levels can lead to irregular uterine contractions that decrease blood flow to the uterus, ultimately resulting in uterine hypoxia.
It is important to note that menstrual pain can not be attributed to the cyclic production of only a few hormones. Women with primary dysmenorrhea are more susceptible to depression, anxiety and somatization. For this reason, it has been proposed in the literature that women with primary dysmenorrhea 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 women without primary dysmenorrhea. A study by Granot and colleagues (2001) reported that women with primary dysmenorrhea 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 (2001) 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.
Management[edit | edit source]
Pharmacological Treatment[edit | edit source]
Nonsteroidal anti-inflammatory drugs (NSAIDs) along with oral contraceptives help to relieve symptoms of primary dysmenorrhea by decreasing the excessive levels of prostaglandins present during menstruation. 
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. . Specifically, high-frequency TENS, which involves electrical pulses delivered between 50 and 120 Hz has been found to be most effective. TENS poses several advantages including that it is safe, portable and inexpensive. TENS can be self-administered regularly during the time of menstruation following appropriate education. Intensity should be set to a non-painful, maximum tolerable intensity level and then increased continually throughout each session to avoid habituation. More research regarding the appropriate TENS parameters (e.g., duration, frequency and number of treatments) in this population is still required.
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.. In two systematic reviews, 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. The proposed mechanism behind heat therapy is through the reduction of muscle tension and the promotion of abdominal muscle relaxation. More research is still required regarding which heating modalities are most beneficial and cost-effective.
Exercise[edit | edit source]
Several studies have reported beneficial effects of exercise, including stretching, aerobic exercise (e.g., jogging), yoga and kegel exercises, to treat primary dysmenorrhea. Stretching exercises may help to reduce the amount of pain that radiates into the lumbar area and the adductors. Kegel exercises may help to increase local blood supply to the uterus, allowing for the rapid elimination of prostaglandins and a decreased intensity of menstrual pain.
A review by Armour and colleagues (2019) 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). 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.
Kinesio Taping[edit | edit source]
Several studies support the use of Kinesio taping to relieve the pain associated with primary dysmenorrhea. Specifically, the application of Kinesio tape over the T11-T12 dermatome, over the supra-pubic region or lower abdomen, the sacral region and lower back has shown benefits. Kinesio tape can be applied from the estimated day of ovulation (~ day 14) until the end of menstruation, ranging from a minimum of 2 to 6 days per week.
The proposed mechanism behind Kinesio tape's benefits is through the reduction of tension. Kinesio tape can lift the skin microscopically, reducing the tension in the pelvic area, and increasing the interstitial space in the skin. This helps to drain lymphatic fluid and decrease the inflammatory responses that may aggravate the nociceptors during menstruation. Kinesio tape also helps to increase blood supply to the uterus by stimulating the vasomotor reflex, which allows for the vasodilation of the arterioles in the uterus and removal of prostaglandins from the area.
Surgical Intervention[edit | edit source]
Surgeries, such as laparoscopies, hysterectomies, presacral neurectomies may be considered in women whose symptoms persist despite medical management.
References[edit | edit source]
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