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

Two different main clinical pictures exist among affected teenagers:

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:

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_2α 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:

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

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

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:

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:

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:

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:

Bettendorf et al. [26]

Other items to be considered in medical history:

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

PHYSICAL EXAMINATION must follow several steps.

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].