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A REVIEW ON HORMONAL SIGNALING, NEUROINFLAMMATION AND SCIATIC NERVE INJURY IN CATAMENIAL SCIATICA
Authors/Creators
- 1. Senior Lecturer in Zoology, Government Degree College, Vizianagaram (Nellimarla) Andhra Pradesh, India
Description
Catamenial sciatica is a rare and often overlooked manifestation of endometriosis in which sciatic-type pain shows a characteristic relationship with the menstrual cycle. Pain may occur or become more severe just before or during menstruation and can range from buttock and posterior thigh pain to numbness, tingling and, in advanced cases, motor weakness. Although the condition is uncommon, its distinctive cyclical pattern provides an important clinical clue and may reflect a complex interaction between ovarian hormones, inflammation and peripheral nerve function. This review explores the biological mechanisms that may connect menstrual-cycle changes with sciatic pain and nerve injury.
Focus is given to hormonal signaling, especially the changing influence of estrogen and progesterone on endometriotic tissue and pain-related pathways. Altered steroid responsiveness in endometriosis may contribute to a local inflammatory environment involving cytokines, prostaglandins, chemokines and neurotrophic factors. At the pelvic–sciatic interface, these inflammatory signals may interact with sensory nerves and contribute to peripheral sensitization. When endometriotic lesions involve, surround or compress the lumbosacral plexus or sciatic nerve, repeated inflammation and tissue remodeling may further increase neural vulnerability.
The review also considers how recurrent menstrual-associated inflammation may progress from intermittent pain to more persistent neuropathic symptoms and sciatic nerve dysfunction. A proposed hormone–inflammation–nerve axis provides an integrated framework in which hormonal fluctuations influence endometriotic activity, inflammatory signaling alters neural sensitivity, and repeated neural irritation may contribute to longer-lasting pain and, in some patients, structural nerve injury. However, because direct molecular studies of sciatic endometriosis are limited, several components of this model remain mechanistic hypotheses derived from broader endometriosis and neuropathic-pain research. Understanding these interactions may improve recognition of catamenial sciatica and encourage earlier investigation of patients with menstrual-patterned sciatic pain, while also highlighting the need for further research into biomarkers, nerve imaging and strategies for preventing progressive neurological damage.
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01-Dr. Y. Shanti Prabha - Online - IERJ1156951473.pdf
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- Journal: 2454-9916 (EISSN)
References
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