Several mechanisms are likely to activate the thoracolumbar and pelvic afferents invoking dysmenorrhea. These include: (1) myometrial contractions leading to intense intrauterine pressure and uterine hypoxia; (2) hyperproduction of prostaglandins and leukotrienes and other hormonal factors which increase afferent terminal excitability; (3) altered CNS processing of the afferent barrage possibly mediated by opioid or gamma aminobutyric acid (GABA)-ergic mediations; and (4) environmental and behavioral factors.12 In primary dys-menorrhea, an increase in endometrial prostaglandin production is seen in the secretory phase of the cycle.12

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