• Family history

• Frequent life changes

• Young age

• Few social supports

• Precocious menarche

• Stressful close relationships

• Heavy and prolonged menstrual flows

• Low socioeconomic level

• Nulliparity

• Low fish intake

• Smoking and exposure to environmental tobacco smoking

• Poor physical activity

• Underweight and overweight

• Marked uterine retroversion

• Low intake of polyunsaturated fatty acids

• Vitamin D deficiency

Balbi et al. [11], Dei and Bruni [12]

Two different main clinical pictures exist among affected teenagers:

  • Primary Dysmenorrhea: at postmenarchal onset, it accounts for the 90% of cases in teenagers and typically comprises recurrent abdominal painful cramps occurring with menses without any identifiable pelvic pathology.

  • Secondary Dysmenorrhea, in 10% adolescent cases, at late onset depending on the underlying disease, with menstrual pains associated with well-defined pelvic pathologies, such as:

– Endometriosis

– Interstitial cystitis

– Mullerian obstructive anomalies

– Adenomyosis


– Pedunculate submucous myomas

– STDs

– Endometrial polyps

– Early pregnancy complications

– Pelvic adhesions

– Cervical stenosis

– Bowel inflammatory diseases

– Ovarian cysts and dermoids

– Pelvic tuberculosis

– Sequelae of genital mutilations

– Large ovarian cysts

Dei and Bruni [12], Harel [13], Sanfilippo, and Erb [14]

Secondary dysmenorrhea may be accompanied by other gynecological symptoms, such as intermenstrual bleeding and menorrhagia; moreover, the timing and intensity of pain during the menstrual cycle may be constant or diffuse, and not necessarily associated with menses [4].

Affecting 8–10% women of reproductive age, endometriosis, that is endometrial tissue in extrauterine locations, is the most frequent etiology of secondary dysmenorrhea and it is associated with obstructive genital anomalies in 11% cases [14, 15]. Another possible cause of secondary dysmenorrhea is adenomyosis, that is endometrial tissue within the myometrium, recently detected also in adolescents and more frequently than previously expected [16].

All Mullerian anomalies may give rise to secondary dysmenorrhea because of altered vascularity. Nevertheless, heavier and worsening clinical pictures may occur in obstructed uterine and/or vaginal anomalies, such as noncommunicating functioning rudimentary uterine horn and obstructed hemivagina. Most cases are part of complex asymmetrical uro-genital malformations with duplex uteri and vaginae with unilateral renal agenesis [12].

The pathophysiology of primary dysmenorrhea shows different steps, with a major role of defined inflammatory lesions occurring in the menstruating womb:

  • Increase of ω-6 fatty acids (mainly arachidonic acid) in endometrial cell membrane after ovulation and their release with premenstrual progesterone withdrawal which activates lysosomal phospholipase.

  • ω-3 fatty acids/ω-6 fatty acids ratio may play a role in the release of algogenic factors.

  • Activation of prostaglandins (PGs) and leukotrienes (LTs) cascade in the uterine wall, with subsequent inflammation giving rise to cramps and systemic symptoms.

  • Myometrial contractions, then ischemia and pain in the uterine muscle [17].

  • Higher vasopressin and low nitric oxide blood levels may induce vasoconstriction and myometrial contractions [18, 19].

  • Uterine flexion may play a pathogenetic role in dysmenorrhea: if the best condition is uterine body and cervix on the same axis, with an angle of 180° + 30°, greater or lesser angles could impede menstruation with stronger myometrial contractions and pains: marked anteflexion and retroflexion both may rise menstrual pains [20].

Up to now, the overproduction of uterine prostaglandins is the most widely accepted explanation for primary dysmenorrhea. The severity of menstrual pain and associated symptoms is directly proportional to the amount of prostaglandins released, and their production is strictly connected to the endometrial exposure to luteal phase progesterone and therefore to ovulation. Among all prostaglandins, PgE2 and PgF are mainly involved in the pathogenesis of dysmenorrhea. While the former may result in either myometrial contraction or relaxation, the latter elicits both strong vasoconstriction of uterine blood vessels and myometrial contractions, lowering also pain threshold by sensitizing nerve endings to pain. In the pathogenesis of dysmenorrhea, a more and more relevant role of central factors was shown, even if their relationship with peripheral factors has still to be fully clarified. Unknown genetic or environmental factors and congenital variants in the pain processing of the central nervous system may predispose dysmenorrheic women to a greater pain perception, being mainly hypersensitive to deep muscle pain [4]. Dysmenorrheic women displayed a shift in the balance between pro-inflammatory cytokines and anti-inflammatory transforming growth factor-β, with up-regulation of genes coding for cytokines and down-regulation of the ones coding for transforming growth factor-β; therefore in dysmenorrheic women, the inflammatory response is different even without pain, with distorted hormonal and cytokine profiles [21]. Recurrent monthly dysmenorrhea may lead to the development of a central sensitivity to pain, with an abnormal augmentation of pain perception by mechanisms within the central nervous system [22]. Dysmenorrheic women are supposed to have central changes which persist beyond menses being possibly induced by the recurrent nociceptive stimuli into the central nervous system. Primary dysmenorrhea may therefore raise the risk for the development of other painful diseases later in life [23].

Signs and symptoms of primary dysmenorrhea are:

• Cramps

• Loss of appetite

• Diarrhea

• Nausea

• Weakness

• Facial blemishes

• Vomiting

• Headache

• Abdominal pains

• Bloating

• Backache

• Dizziness

• Flushing

• Depression

• Sleeplessness

• Irritability

• General aching

• Nervousness

• Leg aches

The relationship between sleep and pain may be bidirectional, with pain disrupting sleep and disrupted sleep heightening pain perception [4].

Secondary dysmenorrhea more often shows

  • Chronic pelvic pains

  • Mid-cycle pains

  • Dyspareunia

  • Metrorrhagia

    Harel [13]

The main diagnostic symptom of primary dysmenorrhea is a colicky suprapubic abdominal pain, occurring as follows:

  • Along the lower abdomen midline

  • Also described as a “dull” pain in both lower abdominal quadrants, lumbar areas, and thighs

  • Appearing with the onset of ovulatory cycles

  • Starting just few hours before or after the onset of menses

  • With frequent associated symptoms such as diarrhea, nausea, vomiting, weakness, lightheadedness, headache, dizziness, lipothymia, fever, etc.

Associated symptoms peak with maximum blood flow and usually last less than 1 day. Pains may last 2–3 days at most and are quite similar in every menstrual period [5]. Being a subjective symptom, the quantification of dysmenorrhea is difficult. Its intensity may be:

  • Mild, not disturbing daily activities nor requiring painkillers

  • Moderate, slightly interfering with daily routines but manageable with pain killers

  • Severe, markedly preventing daily life activities [24]

To measure and to grade dysmenorrhea, the two most common tools currently in use rely upon girls’ self-reporting, which is unavoidably subjective and inaccurate:

  1. (a)

    A verbal multidimensional scoring system, such as the “Menstrual Distress Questionnaire” and the “Menstrual Symptom Questionnaire,” both considering the impacts of pain on daily activities, systemic symptoms, and analgesic requirements (Table 5.1);


Table 5.1
Verbal multidimensional scoring system (VMS)


Working ability

Systemic symptoms


Grade 0: Non-painful menstruation



Not required

        Unaffected daily activity

Grade 1: Painful menstruation seldom inhibiting the woman’s normal activity

Rarely affected


Rarely required

        Analgesics seldom required. Mild pain

Grade 2: Daily activity affected. Moderate pain

Moderately affected


Moderately required

        Analgesics required giving relief

        Absence from school/work is unusual

Grade 3: Activity clearly inhibited. Severe pain

Clearly affected


Poor effect

        Poor effect of analgesics. Vegetative symptoms (headache, tiredness, nausea, vomiting, diarrhea)

Gamit KS, et al. “International Journal of Medical Science and Public Health,” (2014)

  1. (b)

    A linear visual analogue scale (VAS): a 10 cm line drawn on a sheet of paper, representing a continuum of severity of pain from “no pain at all” at one extreme till “unbearable pain” at the opposite one. The patient is asked to rate pain with a mark on the line and the result is achieved by measuring the distance from zero to the mark (Fig. 5.1).



Fig. 5.1
Linear Visual Analogue Scale (VAS) (www.​researchgate.​net/​publication/​259499877)

Both tools lack validation and cannot be trustfully employed in teens [8].

Taking into account the onset of dysmenorrhea, different clinical pictures may be identified:

  • Early onset dysmenorrhea, appearing within 6 postmenarchal months or in clearly non-ovulatory patients, it is very likely due to an underlying obstructive genital anomaly, and mainly Wunderlich/OHVIRA syndrome (uterus didelphys with obstructed hemivagina and ipsilateral renal agenesis).

  • Late onset dysmenorrhea, arising after some years of painless periods, highly suggests secondary dysmenorrhea.

  • Sudden onset dysmenorrhea, suddenly arising in non-symptomatic or oligo-symptomatic patients, makes PID and early pregnancy complications (miscarriage or ectopic pregnancy) suspected [25].

Clinical approach to dysmenorrheic patients must follow good medical practice recommendations:

MEDICAL HISTORY, properly focused on menstruation, allows for differential diagnosis between primary and secondary dysmenorrhea by considering:

– Age at menarche

– Associated symptoms

– Length and regularity of cycles

– Chronology of associated symptoms related to menses

– Dates of the last two menses

– Severity and duration of associated symptoms

– Duration and amount of flows

– Progression of associated symptoms over time

– Type, location, and radiation of pain

– Time between menarche and onset of symptoms

– Worsening of pain over time

– Degree of patient’s disability

– Gastrointestinal and urinary functions

– Lifestyle (food, smoking, physical activity)

Bettendorf et al. [26]

Other items to be considered in medical history:

  • Sexual activity, dyspareunia, contraception

  • Past obstetric and gynecologic events, and mainly STDs, PID, pelvic surgery, infertility

  • Other medical problems

  • Family history of endometriosis in first degree relatives

  • All previous treatments, ways of administration, and outcomes

  • Other ongoing medical treatments

    Dei and Bruni [12], Harel [13]

  • Meal skipping

  • Less sleep

  • Higher sugar intake

are other important risk factors for the occurrence of dysmenorrhea [6].

PHYSICAL EXAMINATION must follow several steps.

  • Abdominal evaluation is always indicated to detect palpable masses.

  • Inspection of external genitalia is mandatory in young girls to rule out abnormal hymens.

  • Pelvic exam (vaginal or rectal), not indicated in virgins with mild to moderate dysmenorrhea, must be performed:

    • In sexually active girls

    • If organic diseases or genital anomalies are suspected

    • With no response to conventional treatments of primary dysmenorrhea

LABORATORY TESTING OR IMAGING, not required to diagnose primary dysmenorrhea, are advisable if secondary dysmenorrhea is suspected. Laboratory testing are not resolving, and they may be useful if a pelvic inflammatory disease is suspected, with a slight increase of both erythrocyte sedimentation rate (ESR) and protein C reactive and possible positive cervical swabs [12].

  • Ultrasonography, first-step diagnostic tool to image the pelvis, including also the assessment of number and location of kidneys in girls, is widely performed even if no evidence exists about its routine application in primary dysmenorrhea. On the contrary, pelvic ultrasonography is mandatory:

    • In the diagnostic workup of secondary dysmenorrhea

    • With no response to first-line treatments

    • With an abnormal, impossible, or unsatisfactory pelvic exam

      The transabdominal approach is usually preferred in young patients. Nevertheless, it must be borne in mind that ultrasonography can never replace physical exam.

  • Magnetic resonance imaging is unnecessary in the diagnosis of primary dysmenorrhea while it may be useful to detect adenomyosis, Mullerian anomalies, andbladder lesions [27].

  • Hysteroscopy and sonohysterography can highlight congenital anomalies of the uterine cavity and endometrial polyps and submucous myomas as well.

  • Laparoscopy is still the gold standard in the diagnostic workup of secondary dysmenorrhea due to endometriosis, PID, and pelvic adhesions. It must be performed

    • With highly suspected organic pathologies

    • With failed first-line treatments.

    It is not to be delayed in refractory to therapy teens if endometriosis is suspected; biopsies of lesions are mandatory if endometriosis is diagnosed [28].

5.1 Treatments

Different therapeutic approaches to dysmenorrhea exist, and they may be grouped as follows:

  • Non-medical options

  • Medical options, both hormonal and nonhormonal ones

  • Surgical options

  • Complementary and alternative medicine

Treatments of dysmenorrhea may also be classified into

Conventional therapies:

 Non-steroidal anti-inflammatory drugs (NSAIDs)

 Oral contraceptives (OCs)


Nonconventional therapies:

 Behavioral treatments

 Physical exercise

 Manipulation of the spine


 Heat therapy




 Alternative medicine

Nonmedical treatments include:

  • Diet: by lowering animal fats intake in favor of ω-3 fatty acids provided food, such as fish [12].

  • Physical exercise may act on dysmenorrhea by enhancing β-endorphins release and by bettering pelvic blood flows. The results are controversial but it must always be advised as a first-step therapy.

  • Transcutaneous electrical nerve stimulation (TENS) may be distinguished in

    • High frequency TENS (50–120 Hz): with low effect, it is more effective than placebo

    • Low frequency TENS: not effective at all in fact

    Self-regulated by the patient, it is a non-medicinal-no-risk procedure acting by activation of the large-diameter Aβ proprioceptive nerve fibers of the skin with no activation of both finer Αδ fibers and pain C fibers. TENS effectiveness relies on the rise of pain threshold, preventing pelvic painful stimuli to reach the spinal cord. Furthermore, it enhances β-endorphins secretion and it betters uterine blood flow. Positive effects, if present, are perceivable within few minutes from the application of the device [13, 29, 30].

  • Acupuncture: well tolerated without side effects procedure, it has been approved by FDA. It significantly lowers pain in mild-to-severe dysmenorrhea, with a long-acting effect. More expensive than NSAIDs and OCs, it may be recommended when first-line treatments are rejected or contraindicated. To establish proper recommendations and administration, further data are required [29, 31, 32].

  • Manipulation of the spine: as some Authors suggest, the rationale of this procedure relies upon the existing close relationship of pelvic sympathetic and parasympathetic nerve pathways with spine segments T10-2L and S2–S4. Possible vertebral mechanical dysfunctions, with lowered mobility of the spine, could alter sympathetic pathways regulating blood supply in pelvic organs, with subsequent vasoconstriction and dysmenorrhea. Vertebral manipulation could improve spine mobility and increase pelvic blood supply by action on vessels innervation, thus bettering dysmenorrhea. According to Cochrane Library, the efficacy of this procedure has no evidence [33].

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Jul 27, 2018 | Posted by in GYNECOLOGY | Comments Off on Dysmenorrhea
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