Spine strangler: A case of spinal epidural lipomatosis in a young male

Abstract

Introduction: Spinal stenosis is the narrowing of intervertebral foramina most commonly caused by degenerative changes in the vertebral bodies. Other common causes include achondroplasia, ankylosing spondylitis, or Paget disease. We report a case of a 32-year-old male who presented with difficulty walking and was found to have a rare culprit, spinal epidural lipomatosis (SEL). Case Description: A 32-year-old obese male presented with an eight-month history of progressive bilateral leg weakness and back pain, with acute worsening in the past two weeks. He also had associated bilateral lower extremity pain, weakness, numbness, and multiple mechanical falls in the past six months. On physical exam, he was afebrile and normotensive with BMI of 38. He was A/A/O x 4, with neurologic exam significant for muscle strength 2/5 in left leg, 3/5 in right leg, and 5/5 in bilateral upper extremities. He had diminished sensation below L3 in both legs, +4 bilateral patellar reflex with clonus, and upgoing bilateral plantar reflexes. Labs showed normal levels of cholesterol, triglycerides, hbA1C, and TSH. MRI thoracic and lumbar spine revealed spinal cord stenosis with cord compression and myelopathy at T5-T6 due to left central disc extrusion, thickening of ligamentum flavum, and diffuse dorsal epidural lipomatosis. Neurosurgery was consulted, and he underwent urgent T5-T6 decompressive laminectomy with partial T4-T7 laminectomies for evacuation of epidural lipomatosis. At the time of discharge to a rehabilitation facility, his weakness improved in lower extremities with 4/5 muscle strength bilaterally. Discussion: Spinal epidural lipomatosis is seen in 2.5% of population and is caused by excessive adipose tissue in the epidural space. The exogenous steroid group represents 55.3% cases, while obesity-associated disease represents 24.5%. In our patient, obesity may be a driving factor for SEL. SEL is most common in patients taking exogenous steroids, such as post-transplant patients. SEL is also seen in people with type 2 diabetes mellitus, increased production of endogenous steroids, HIV on protease inhibitor therapy, Scheuermann's disease, and those on androgen antagonist therapy. Management of SEL depends on the presentation. With acute neurologic deficits, the first-line treatment is urgent surgical decompression. Conservative management of inciting features is recommended if there is a slowly progressive disease. It includes cessation of steroids and treatment of endocrinopathies. Weight reduction has been shown to significantly reduce SEL in obese patients, with one report recommending at least 15 kgs of weight loss to help control symptoms. If conservative therapy is not successful, decompressive surgery such as laminectomy with or without removal of fatty tissue can be considered. Removing as much fatty tissue as possible avoids post-surgical complications. Unfortunately, mortality rate within one year after surgical decompression is as high as 22%.