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Steroid induced spinal epidural lipomatosis--case report and review of the literature.


Steroids are one of the most commonly prescribed medications for a variety of medical conditions, often long term. Spinal epidural lipomatosis (SEL) is a state of pathological fatty tissue overgrowth in the vertebral canal. It is a rare and dangerous complication of chronic steroid therapy that may lead to back pain, radiculopathy, or paraparesis. We describe a patient that was taking long term steroids and presented with progressively worsening weakness of the lower extremities. On the MRI scan, a long segment of unusual accumulation of fatty deposits in the posterior aspect of the spinal canal resulting in canal stenosis extending from C7 to the T10 level was observed. Despite an appropriate diagnosis and surgical intervention, his weakness did not resolve. We discuss the implications of this case in the primary care practice.


Spinal epidural lipomatosis is an excessive deposition of unencapsulated fat in the epidural space. It is most commonly observed in patients receiving long-term exogenous steroid therapy, but can also be seen in patients with endogenous steroid overproduction, obesity, or idiopathic disease. As hypertrophy of the epidural adipose tissue occurs, it causes a narrowing of the spinal canal resulting in compression of the surrounding neural structures.

Case Report

A 46-year-old white male with significant past medical history of rheumatoid arthritis and hypertension was admitted for 2 weeks duration of progressive weakness and numbness of both lower extremities. Two weeks prior to admission, the patient was in his usual state when he noticed numbness, weakness and tingling sensation in his lower extremities which gradually progressed. Three days prior to admission he was lying in bed when he realized that he was unable to rise up or move his lower extremities. He also noticed a loss of control over his bladder and hadn't had a bowel movement since. The patient denied an upper respiratory tract infection in preceding weeks. His medical history also included emphysema for several years due to smoking. His only medication was prednisone 20 mg daily for the past 1.5 years for rheumatoid arthritis which was diagnosed several years prior.

Physical examination revealed a well developed, cushingoid appearing overweight male (BMI = 29) with normal vital signs. Neurological examination demonstrated several symmetrical abnormalities below the level of umbilicus. Lower extremities exhibited muscle strength reduced to 1/5 with increased tone. Sensory examination revealed a loss of sensations in lower extremities up to the level of T10. Deep tendon reflexes in the lower extremities were increased with bilateral ankle clonus. Chest examination revealed few late inspiratory crackles, and abdominal examination was unremarkable except for obesity. Rest of the exam was normal.

Initial laboratory test results revealed white blood count of 13x[10.sup.9] cells/L, with 76% neutrophils. MRI of the spine with contrast revealed acute vertebral body compression of T5 and a long segment of fatty deposition in the posterior aspect of the spinal canal which was attributed to the unusual accumulation of fat in this area resulting in canal stenosis which extended from C7-T1 to the T9-10 level. Lumbar spine was normal (See Figures 1, 2). Vitamin B12 and folic acid levels were normal and Cushing's disease was ruled out. Lyme disease antibody titer and HIV test were negative. Diagnosis of Spinal Epidural Lipomatosis (SEL) secondary to the chronic use of steroids was made and the patient underwent T5-7 laminectomy with removal of the epidural fat. The patient recovered well with return of sensory function but there was no benefit in the motor weakness of the lower extremities at discharge 4 weeks after surgery. In the long term, while minimal improvement in the motor function of lower extremities did occur, the patient was still not able to bear weight and continued to require an indwelling catheter. The steroids were discontinued permanently and the patient was prescribed alternative regimen for management of his rheumatoid arthritis.


SEL is a condition in which an abnormal excess adipose tissue is deposited circumferentially around the spinal cord in the epidural space. Exogenous steroid administration remains the main etiology while endogenous steroid production, obesity, hypothyroidism, pituitary prolactinoma and idiopathic causes may also occur. (1, 2, 3) When it presents with features of spinal cord compression it may be initially misdiagnosed with other common spine conditions, like spinal stenosis and degenerative joint disease.

SEL occurs more commonly in men than women, with 75% of reported cases involving male patients. (4, 5) While it can occur in younger age groups, the mean age of patients with SEL is 43 years. (4, 5) It usually affects either the thoracic spine or the lumbar spine and is always posterior to the spinal cord. Obese patients tend to develop SEL in the lumbar region three times more often than the thoracic region although this was not the case in our patient. Steroids by contrast tend to cause SEL in the thoracic region slightly less than twice as often as in the lumbar region. (6) The clinical presentation may include progressive and longstanding complaints of pain, weakness, numbness, incontinence, abnormal reflexes and even paralysis. Our initial differential diagnoses included transverse myelitis, epidural abscess, neoplasm, Vitamin B12 deficiency and Lyme disease. These were ruled out based on both clinical features and the laboratory results until finally a diagnosis of SEL was made on MRI.

In the steroid induced SEL case reports described to date, the duration and dosage of the steroid therapy administered has varied, but in the majority of the cases the patient received moderate to high doses of steroids for years prior to the development of symptoms. (1, 6) Since our patient had reported receiving steroids at a moderate dose for only 18 months this was somewhat unusual. However, upon further follow up questioning it was revealed that he was administered additional steroid injections in his physician's office intermittently for several years.

MRI is considered the most sensitive and specific modality for diagnosing SEL. (7) The high contrast between adipose tissue and the thecal sac on T1-weighted MRI permits an accurate evaluation of the extent of pathologic epidural tissue overgrowth in the spinal canal. The normal range for sagittal epidural fat thickness is 3 to 6 mm while in symptomatic SEL, the sagittal epidural fat thickness may approach 7 to 15 mm.8 Our patient's epidural fat thickness was measured at 11 mm.



The appropriate recognition of SEL is critical as timely intervention can avert considerable disability. Treatment options include surgical or conservative methods depending upon the patient's neurological assessment. Surgical treatment consists of decompression laminectomy and fat debulking while medical management consists of weight reduction and discontinuing steroids.9 The indication for surgical decompression is determined by the patient's neurological status and failure to respond to initial conservative treatment. Similar to our patient, presentation with a significant neurological deficit or progressive neurological symptoms of cord compression may be an indication to proceed with spinal decompression with excision of the excess fatty tissue. While a majority of such patients experience improvement or resolution of their neurological symptoms after surgical intervention or conservative management, some, similar to our patient, may suffer permanent neurological damage related to cord compression and infarct. (10, 11)

In conclusion, symptomatic SEL is an uncommon but important cause of compression of the spinal cord with progressive neurological symptoms and should be considered in the differential diagnosis of any patient who is on long term corticosteroid therapy.


(1.) Fassett DR, Schmidt MH. Spinal epidural lipomatosis: a review of its causes and recommendations for treatment. Neurosurg Focus 2004;16(4):E11.

(2.) Stambough JL, Cheeks ML, Keiper GL. Nonglucocorticoidinduced lumbar epidural lipomatosis: a case report and review of literature. J Spinal Disord 1989;2:201-7.

(3.) Fujisawa H, Hasegawa M, Tachibana O, et al. Spinal epidural lipomatosis associated with pituitary macroprolactinoma. Acta Neurochir 2002;144:213-14.

(4.) Robertson SC, Traynelis VC, Follett KA, et al. Idiopathic spinal epidural lipomatosis. Neurosurgery 1997;41:68-75.

(5.) Roy-Camille R, Mazel C, Husson JL, et al. Symptomatic spinal epidural lipomatosis induced by a long-term steroid treatment. Review of the literature and report of two additional cases. Spine 1991;16:1365-71.

(6.) Fogel GR, Cunnigham PY 3rd, Esses SI. Spinal epidural lipomatosis: case reports, literature review and meta-analysis. Spine J 2005;5(2):202-11.

(7.) Hierholzer J, Vogl T, Hosten N, Lanksch W, Felix R. Imaging in epidural lipomatosis. Crit Rev Neurosurg 1998;8(5):279-81.

(8.) Quint DJ, Boulos RS, Sanders WP, Mehta BA, Patel SC, Tiel RL. Epidural lipomatosis. Radiology 1988;169(2):485-90.

(9.) Borre DG, Borre GE, Aude F, Palmieri GN. Lumbosacral epidural lipomatosis: MRI grading. Eur Radiol 2003; 13(7):1709-21.

(10.) Archer CR, Smith KR Jr. Extradural lipomatosis simulating an acute herniated nucleus pulposus. J Neurosurg. 1982;57(4):559-62.

(11.) Sandberg DI, Lavyne MH. Symptomatic spinal epidural lipomatosis after local epidural corticosteroid injections: case report. Neurosurgery. 1999;45(1):162-5.

Rahul Gupta, MD, MPH, FACP

Health Officer and Executive Director, Kanawha Charleston Health Department, Charleston

Mobin Shah, MD

Department of Internal Medicine, York Hospital, York, PA

Carla M. Reese, MD

Department of Psychiatry, University of Maryland, Baltimore, MD
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Title Annotation:Scientific Article
Author:Gupta, Rahul; Shah, Mobin; Reese, Carla M.
Publication:West Virginia Medical Journal
Article Type:Case study
Date:Jul 1, 2011
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