Symptomatic spinal epidural lipomatosis is a rare disorder characterized by overgrowth of fat in the extradural space. Most
patients have an underlying endocrine disorder, such as Cushing’s syndrome, or have taken exogenous steroids chronically.
Although less common, obesity alone is thought to be a cause of spinal epidural lipomatosis, representing <25% of reported
cases. Patients rarely become symptomatic before middle age without chronic exogenous steroid use. The usual clinical manifestations
are similar to degenerative lumbar stenosis with neurogenic claudication, resulting in decreased walking and standing endurance
with variable neurological deficits.
This article describes 2 unique cases of spinal epidural lipomatosis, both in young patients with underlying morbid obesity
who presented with acute progressive leg weakness and urinary retention. The patients had no underlying endocrinopathy, nor
any history of exogenous steroid use. They underwent emergency laminectomy and removal of epidural fat, and histopathological
examination confirmed the diagnosis of epidural lipomatosis. Postoperatively, the patients demonstrated significant improvement.
We conducted a review of the available English literature and compared the age distribution in each group. Based on our review,
our 2 patients are considerably younger than those in past reports, especially in the patient group to which the steroid was
not administered. In addition, few cases exist of spinal epidural lipomatosis with acute sphincter dysfunction and paraparesis.
Our cases suggest that morbid obesity can lead to juvenile spinal epidural lipomatosis with acute neurological changes.
Drs Ohba, Saito, Kawasaki, Maekawa, and Haro are from the Department of Orthopedic Surgery, University of Yamanashi, Japan.
Drs Ohba, Saito, Kawasaki, Maekawa, and Haro have no relevant financial relationships to disclose.
Spinal epidural lipomatosis is a rare condition characterized by an excessive deposition of mature a dipose tissue that proliferates
in an infiltrative manner. Most patients have an underlying endocrine disorder, such as Cushing’s syndrome, or have taken
exogenous steroids chronically.
1,2
Although less common, obesity alone is thought to be a cause of spinal epidural lipomatosis, representing <25% of reported
cases.
1
The majority of these patients are middle-aged or elderly.
2–5
Juvenile spinal epidural lipomatosis is especially rare in the absence of exogenous steroid use.
This article describes 2 unique cases of spinal epidural lipomatosis, both in young patients with underlying morbid obesity
who presented with acute progressive weakness and urinary retention. The patients had no underlying endocrinopathy, nor any
history of exogenous steroid use. They underwent emergency laminectomy and removal of epidural fat. Postoperatively, both
patients demonstrated significant improvement.
A 19-year-old man presented with a 1-year history of low back pain and bilateral thigh numbness. Prior to his visit to our
hospital, he had developed progressive bilateral lower extremity weakness over 1 week, with 48 hours of urinary retention.
The patient was obese (body mass index [BMI]=45.4) and had no evidence of clinical spinal deformity. Neurological examination
revealed bilateral lower extremity weakness throughout (power 2/5), numbness on the anterior thighs, and symmetric hyporeflexia.
Magnetic resonance imaging (MRI) of the lumbosacral spine revealed multilevel degenerative changes and spinal stenosis. An
axial view revealed epidural fat extending from L1 to S1 (Figure ).
Figure 1:. Sagittal (A) and Axial (B) MRIs Showing Epidural Lipomatosis Compressing the Spinal Cord.
An urgent laminectomy was performed from L1 to S1. Intraoperatively, the thecal sac and bilateral L5 nerve roots were seen
to have excessive focal compression because of adipose tissue. Epidural fat was completely removed, and histopathological
examination confirmed our diagnosis of epidural lipomatosis (Figure ).
Figure 2:. Photomicrograph Showing Mature Adipocytes. Hematoxylin-Eosin Staining.
Postoperatively, the patient demonstrated gradual improvement and recovered bladder function in 2 weeks. At 12-month follow-up, the patient demonstrated normal muscular strength and bladder function with…