Background: Deep gluteal syndrome (DGS) is an underdiagnosed cause of sciatica-like pain, involving the entrapment of the sciatic nerve by various structures within the subgluteal space. While cases of ossification or calcification in the context of severe pelvic imbalance have been rarely reported, isolated SSL calcification as a primary cause of DGS remains largely unexplored and undocumented. This case report presents the first documented instance of sacrospinous ligament (SSL) calcification identified as the primary cause of DGS and its successful management with ultrasound-guided prolotherapy. Case Presentation: A 51-year-old female presented with severe, worsening left-sided sciatica of several months’ duration. Physical examination revealed an antalgic gait, positive sacroiliac joint tests, and multiple positive DGS-specific provocative tests (FAIR, Pace sign, Seated Piriformis Stretch). Radiographs and musculoskeletal ultrasound (MSK-US) confirmed calcification within the left sacrospinous ligament, with associated sciatic nerve swelling. The patient underwent three sessions of ultrasound-guided prolotherapy (dextrose 10% with lidocaine) targeting the calcification site, followed by a structured rehabilitation program. Results: The patient reported a significant reduction in pain, from a Visual Analog Scale (VAS) score of 10/10 to 1/10 within one month. All previously positive provocative tests converted to negative, indicating a resolution of the nerve entrapment. Functional mobility was fully restored. Conclusions: This case highlights isolated sacrospinous ligament calcification as a potential and previously overlooked pathological entity responsible for deep gluteal syndrome. To our knowledge, this is the first report to implicate ligamentous calcification as a primary etiological factor in DGS. Musculoskeletal ultrasound proved indispensable for both diagnosis and treatment guidance. Furthermore, ultrasound-guided prolotherapy emerged as a successful and minimally invasive therapeutic option in this case, potentially by stabilizing the ligament and reducing neurogenic inflammation. This case expands the differential diagnosis of sciatica, introduces a new target for intervention in refractory cases, and underscores the need for future studies in larger patient cohorts to validate these findings.
Yoon et al. (2025) studied this question.