Menopause-Associated Anterior Cutaneous Nerve Entrapment Syndrome: A Case Highlighting Perineural Microenvironmental Pathology

Anterior cutaneous nerve entrapment syndrome (ACNES) is an underrecognized cause of abdominal wall pain and is commonly diagnosed based on localized physical findings and response to local anesthetic nerve block. While this approach is clinically practical, it provides limited insight into the underlying pathophysiology and may contribute to diagnostic delay and repeated unnecessary investigations. ACNES represents a form of localized chronic compressive neuropathy characterized by perineural fibrosis and vascular involvement; however, little attention has been paid to systemic conditions that may influence nerve vulnerability or modulate the perineural environment. We report a case of menopause-associated ACNES in a woman presenting with severe abdominal pain that led to multiple emergency visits and extensive negative visceral evaluations. Definitive diagnosis was established based on physical findings and response to nerve block. Preoperative rehabilitation resulted in partial symptom improvement, followed by surgical resection. Operative findings revealed localized adhesions surrounding the cutaneous nerve. Histopathological examination demonstrated preservation of intrafascial nerve architecture. In contrast, no clearly identifiable peripheral nerve structure was observed in the extrafascial region. Instead, elongated fibrous structures extended longitudinally through the tissue, lacking normal nerve fascicular organization and surrounded by densely packed, irregularly arranged, curled collagen fibers. In addition, marked vascular wall thickening with severe luminal narrowing was observed, predominantly within the subcutaneous tissue. These layer-specific findings indicate pathological alteration of the perineural microenvironment. The temporal association with the menopausal transition provides a biologically plausible systemic background for these changes, given the known effects of estrogen deficiency on vascular remodeling, connective tissue metabolism, and pain modulation. This case extends the current understanding of ACNES by highlighting menopause as a potential systemic modifier of disease expression and underscores the limitations of relying solely on physical examination and nerve block response for diagnosis. Integrating systemic background with histopathological insight may help refine current conceptual and diagnostic frameworks for ACNES.