Abstract

BackgroundLumbar epidural lipomatosis (LEL) is characterized by abnormal accumulation of unencapsulated adipose tissue in the spinal epidural space. Such accumulation compresses the dural sac and nerve roots, and results in various neurological findings. However, the pathophysiology of LEL remains unclear. This study examined the associations between imaging and clinical findings in detail, and investigated the mechanisms underlying symptom onset by measuring intraoperative epidural pressures in LEL.MethodsSixteen patients (all men; mean age, 68.8 years) were enrolled between 2011 and 2015. Mean body mass index was 26.5 kg/m2. Four cases were steroid-induced, and the remaining 12 cases were idiopathic. All patients presented with neurological deficits in the lower extremities. Cauda equina syndrome (CES) alone was seen in 8 patients, radiculopathy alone in 4, and both radiculopathy and CES (mixed CES) in 4. All patients subsequently underwent laminectomy with epidural lipomatosis resection and were followed-up for more than 1 year. We investigated the clinical course and imaging and measured epidural pressures during surgery.ResultsSubjective symptoms improved within 1 week after surgery. Mean Japanese Orthopaedic Association (JOA) score was 15.2 ± 2.8 before surgery, improving to 25.4 ± 2.5 at 1 year after surgery. On magnetic resonance imaging, all lipomatosis lesions included the L4–5 level. On preoperative computed tomography, saucerization of the laminae was not observed in radiculopathy cases, whereas saucerization of the posterior vertebral body was observed in all radiculopathy or mixed CES cases. Intraoperative epidural pressures were significantly higher than preoperative subarachnoid pressures. The results suggest that high epidural pressure resulting from the proliferation of adipose tissue leads to saucerization of the lumbar spine and subsequent symptoms.ConclusionsClinical courses were satisfactory after laminectomy. In LEL, epidural pressure increases and symptoms develop through the abnormal proliferation of adipose tissue. Higher epidural pressures induce saucerization of the laminae and/or posterior vertebral body. Furthermore, the direction of proliferative adipose tissue (i.e., site of saucerization) might be related to the types of neurological symptoms.

Highlights

  • Lumbar epidural lipomatosis (LEL) is characterized by abnormal accumulation of unencapsulated adipose tissue in the spinal epidural space

  • Spinal epidural lipomatosis (SEL) is defined as the abnormal accumulation of unencapsulated adipose tissue in the spinal epidural space, and causes various neurological symptoms [2]

  • This study suggests that high epidural pressure resulting from the proliferation of adipose tissue leads to saucerization of the lumbar spine and subsequent symptoms

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Summary

Introduction

Lumbar epidural lipomatosis (LEL) is characterized by abnormal accumulation of unencapsulated adipose tissue in the spinal epidural space. Such accumulation compresses the dural sac and nerve roots, and results in various neurological findings. SEL is defined as the abnormal accumulation of unencapsulated adipose tissue in the spinal epidural space, and causes various neurological symptoms [2]. Secondary SEL occurs in relation to exogenous steroid treatment [2, 3], endocrinopathies such as Cushing syndrome [4], and hypothyroidism [5]. Idiopathic SEL may occur without any history of steroid use or endocrine disorder [6, 7]. Factors involved in the onset of SEL remain unclear

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