Steroid-induced Spinal Epidural Lipomatosis after Suprasella Tumor Resection
A 32-year-old woman was admitted in a wheelchair. She presented with leg weakness and radiating pain on both buttock, posterior thigh & calf for 1 year. Because pain and weakness in both legs was gradually aggravated during 4 months, she could not walk or stand when she was admitted. Prior to admission, she underwent an operation for a suprasellar tumor resection in our hospital when she was 14 years old. At that time, the pathologic diagnosis was pilocytic astrocytoma. After the operation, panhypopituitarism occurred, so steroid hormone replacement therapy was started in 1993. For a period of 19 years, exogenous steroid maintenance had been administrated (median dose of prednisolon 7.5mg). The neurologic examination revealed both legs weakness (motor grade IV/IV) and radiating pain on the L5 and S1 dermatomes. The straight leg raising test was negative, but the bilateral knee jerk and ankle jerk were slightly hyperreflexive. A magnetic resonance imaging (MRI) study showed severe compression of the lumbar spinal cord by epidural fat tissue. At the dorsum of the spinal cord from the L1 to L5 levels, high signal lesions on T1- and T2-weighted images were checked. The longest length from the dorsum of the spinal cord to the ligamentum flavum was 11.4mm on the L3 level and the median length was 9.2mm at the L1-L5 levels. Fat suppression MR imaging showed low signal intensity at the same lesion () as well. In the enhanced T1-weighted MRI, the epidural vessels were more developed than in a normal person's MRI. The engorged epidural vessels were positioned beneath the nerve root exit site, bilaterally ().\nConsidering the long-term exogenous steroid administration, her neurologic symptoms and MR images, we could make the diagnosis of spinal epidural lipomatosis. Because she complained of radiating pain on the bilateral L5 and S1 dermatomes, she had an operation to decompress the L5 and S1 nerve roots. In the operation field, fat tissue compressed the dorsum of the thecal sac and engorged epidural vessels were found on nerve root exit sites (). We removed the epidural fat tissue and coagulated the engorged epidural vessels for nerve root decompression. The postoperative course was good. The radiating pain in both legs was dramatically relieved and motor power was slightly improved. She was admitted in a wheelchair but discharged walking. After 1 month, we did a follow-up MRI. On the follow-up MRI, the epidural fat tissue did not compress the thecal sac and the courses of nerve roots were not interrupted.