Pathogenesis

The exact pathogenetic mechanism of ossification of the ligamentum flavum is unclear.1 Dynamic, chronic, and excessive stresses on the ligamentum flavum have been suggested as causative factors.1 Trauma to the ligamentum flavum has been identified as an etiological factor.1 Systemic hyperostosis, endocrine abnormality, and a generalized aging process may also be responsible.1

Histological examination helps to differentiate calcified ligamentum flavum, ossified ligamentum flavum, and calcium pyrophosphate dihydrate crystal deposition disease.2–5 In calcification of the ligamentum flavum, calcified granules are deposited within the degenerated ligament fibers, with no mature bone formed within the ligament, which is a feature of ossified ligamentum flavum.6

Differences exist between the ossification of the posterior longitudinal ligament and ossified ligamentum flavum, but similarities exist at the molecular and possibly the genetic levels.1 The clinical presentation may be that of myelopathy or radiculomyelopathy, of acute or insiduous onset and progression. Based on the clinical presentation and radiological investigations, the differential diagnosis includes calcified ligamentum flavum, osteoid osteoma, and fracture or congenital anomalies of the lamina.1

Investigations

Computed tomography and magnetic resonance imaging provide definition of the extent, site, and nature of the disease.7–9 High-intensity intramedullary signal changes reflect edema or gliosis of the spinal cord and are generally associated with a poor prognosis.10–13 However, in patients with ossified ligamentum flavum, the high-intensity intramedullary signal may be due to reversible cord changes and are therefore not necessarily associated with a poor prognosis.2,14 In our patient, although the cord demonstrated a high signal intramedullary change on both preoperative and postoperative images, good clinical recovery was achieved.