A possible neurophysiological explanation is that menstrual pain is not confined to the uterus. Nociceptive signals arising from the uterus converge with somatic afferents within the spinal cord through viscerosomatic convergence, providing a plausible explanation for the characteristic distribution of pain beyond the uterus5,6.
Persistent visceral nociceptive input may subsequently influence muscle tone and alter the mechanical loading of surrounding fascial tissues. Such alterations in fascial biomechanics may function as secondary pain amplifiers, contributing to the propagation and persistence of menstrual pain rather than its initiation.
