Spinal Epidural Lipomatosis Due to Excess Steroid Intake Leading to Spinal Cord Compression

Presentation Number: SAT-402
Date of Presentation: March 7th, 2015

Niki Margari*1, Alison Butler2, Jonathan Benjamin2, Sanjiv Chawda2, Zahra Khatami3, Eltayab Marouf4 and Nemanja D Stojanovic5
1University College London Partners, United Kingdom, 2Queens Hospital, 3Barking, Havering & Redbridge University Hospitals NHS Trust, London, United Kingdom, 4Barking, Havering & Redbridge University Hospitals NHS Trust, 5Queen's Hosp, London, United Kingdom


Background: Spinal epidural lipomatosis (SEL), a rare but well recognized complication of excessive steroid intake or production, is characterized by overgrowth of adipose tissue into the extradural space. Ultimately this pathological process can lead to spinal cord compression.

Clinical case: A 63-year old man presented with a two-month history of progressive bilateral leg weakness on a background of chronic back pain secondary to spinal canal stenosis from L2 to S1. He also suffered from Addison’s disease for which he had been taking hydrocortisone in a total dose of 100 mg daily since the diagnosis was made over 40 years ago. His steroid replacement therapy was managed by his primary care physician.  

Examination revealed an obese patient with marked centripetal fat deposition and Cushingoid features. A working diagnosis of proximal myopathy due to long-term steroid intake was made and the steroid dose was slowly tapered down.

Soon after the admission he developed an acute spastic paraparesis with loss of sensation restricted to the S1 distribution of the left leg. An MRI spine revealed SEL extending throughout the mid/lower thoracic and mid to lower lumbar spine causing multilevel compression of the cord from T4-5 to T9-10 as well as L2-3 to L4-5 levels. He underwent urgent T5-T8 thoracic laminectomy. Power in the lower limbs significantly improved thereafter to 4/5 over the next 10 days.

At discharge oral hydrocortisone had been reduced to the total dose of 60 mg daily, and the patient was advised to taper it down further to 25 mg daily in divided doses. He was given an outpatient endocrine follow up. 

Discussion:  SEL was first reported in 1975. Since then there have been 111 cases of SEL reported of which 49 cases were idiopathic and 62 were due to secondary causes. From the idiopathic cases 16 were noted in non-obese patients, 46 cases have been associated with exogenous steroid use while 16 were due to Cushing disease, hypothyroidism and prolactinoma.

Most patients are obese and more males than females are affected. SEL is caused by adipose tissue dysfunction mediated by insulin resistance. Secretion of proinflammatory adipokines by large adipocytes ultimately leads to spinal fat deposition. Weight reduction appears to be beneficial only to those with mild symptoms and no significant neurological signs. Surgical laminectomy is the treatment of choice when patients develop spinal cord compression. SEL should be considered in any patient on long-term steroids or active Cushing’s disease that develops neurological signs consistent with spinal cord compression or persistent back pain.


Nothing to Disclose: NM, AB, JB, SC, ZK, EM, NDS