Spinal epidural lipomatosis: a case study.

Spinal epidural lipomatosis (SEDL), an abnormal localized or tumor-like accumulation of fat in the epidural space, is an infrequent complication of chronic steroid usage and an uncommon cause of spinal cord compression. A patient with a primary malignant brain tumor on chronic corticosteroids presented with a clinical picture of cord compression and was diagnosed with SEDL.

Symptomatic spinal epidural lipomatosis induced by a long-term steroid treatment. Review of the literature and report of two additional cases.

Spinal epidural lipomatosis associated with Cushing's syndrome is an uncommon complication (11 reported cases). Two additional symptomatic cases with neurologic deficit are described. Steroid treatment was systemic in the first case and local with epidural injections in the second. The second case is unique because no similar observations have yet been reported. In most cases, a preoperative computed tomographic scan establishes the diagnosis by demonstrating dural compression by an adipose mass. Myelography is far less specific. In some cases, the exact diagnosis is made at the time of surgery. The treatment is primarily surgical, with laminectomy over the length of the compression and the removal of the compressing fat. Neurologic recovery is dependent on two factors: the level of the compression and the adequacy of decompression.

Epidural lipomatosis as a cause of spinal cord compression in polymyalgia rheumatica.

Polymyalgia rheumatica (PMR) is a common rheumatologic disorder in older individuals that usually requires chronic, low dose corticosteroid therapy for adequate control of symptoms. Epidural lipomatosis is a rare complication of chronic corticosteroid use in which neurologic deficits occur due to extradural fat compression of the spinal cord. The author describes the first reported case of epidural lipomatosis occurring as a complication of corticosteroid therapy in a patient with PMR.

Idiopathic and glucocorticoid-induced spinal epidural lipomatosis.

Pathological overgrowth of the epidural fat in the spine has been described and reported nearly exclusively in patients either with Cushing's syndrome or on chronic intake of glucocorticoids for a variety of clinical disorders. The authors report four patients with documented spinal lipomatosis (three pathologically and one radiologically). Only one of these patients received corticosteroids, and none had an underlying endocrinological abnormality. All four patients were adult males with a mean age at onset of symptoms of 43 years (range from 18 to 60 years). The symptoms ranged from simple neurogenic claudication and radicular pain to frank myelopathy. Myelography followed by computerized tomography were instrumental in the diagnosis of the first three patients; the fourth was diagnosed by magnetic resonance imaging. The thoracic spine was involved in two cases and the lumbosacral area in the other two. The different treatment modalities were tailored according to the symptomatology of the patients. These included weight reduction of an overweight patient with minimal neurological findings in one case and decompressive laminectomy and fat debulking to achieve adequate cord decompression in the remaining three cases. Two patients improved significantly, the condition of one stabilized, and the fourth required a second decompression at other spinal levels. The various modalities of treatment and their potential complications are discussed.

[Epidural lipomatosis as a complication of a long-term glucocorticoid therapy]. / Epidurale Lipomatose als Komplikation einer chronischen Glucocorticoidmedikation.

In a 47-year-old patient with asymmetrical proximal paraparesis a long cervical and thoracic spinal epidural lipomatosis was found, by computed tomography and (the first such case) magnetic resonance imaging, to be the cause of the signs of a transverse cord lesion. Such a space-occupying mass is a rare complication of long-term corticosteroid medication--in this case administered for over seven years for bronchial asthma. Contrary to the majority of similar reported cases, no decompression operation was performed, because the neurological signs had not progressed and the clinical findings in fact quickly regressed once the steroid dosage had been reduced and they showed a clear dependence on the amount of steroid administered.