Epidural Lipomatosis

Pathophysiology

• Mechanism of fat accumulation:
  • Hypertrophy of normal epidural adipose tissue rather than neoplastic proliferation
  • Steroid-induced lipogenesis and redistribution of body fat
  • Increased adipocyte differentiation and proliferation
• Distribution patterns:
  • Predominantly posterior epidural space
  • Can extend along multiple vertebral levels
  • May cause "Y-sign" configuration of compressed thecal sac on axial imaging
• Secondary effects:
  • Mechanical compression of thecal sac and nerve roots
  • Potential venous congestion from epidural venous plexus compression
  • Progressive spinal stenosis if untreated

Demographics

• Age: Most common in 5th-7th decades; can occur at any age including paediatric population
• Gender: Male predominance (M:F ratio approximately 3:1)
• Risk factors:
  • Chronic corticosteroid therapy (most common cause)
  • Cushing's syndrome or disease
  • Morbid obesity (BMI >30)
  • Hypothyroidism
  • Idiopathic (approximately 17% of cases)
• Location preference:
  • Thoracic spine (60%)
  • Lumbar spine (40%)
  • Rarely cervical spine

Diagnosis

• Clinical presentation:
  • Back pain (most common symptom)
  • Progressive neurogenic claudication
  • Radiculopathy with dermatomal distribution
  • Myelopathy in severe cases (weakness, sensory changes, bowel/bladder dysfunction)
  • Cauda equina syndrome (rare but serious complication)
• Laboratory findings:
  • Elevated cortisol levels (if endogenous hypercortisolism)
  • No specific biomarkers
• Grading system (Borré classification based on epidural fat thickness):
  • Grade 0: Normal epidural fat
  • Grade I: Mild (<40% canal compromise)
  • Grade II: Moderate (40-50% canal compromise)
  • Grade III: Severe (>50% canal compromise with thecal sac compression)

Imaging

• MRI (modality of choice):
  • T1: Hyperintense epidural fat signal matching subcutaneous fat
  • T2: Hyperintense epidural fat (may be less conspicuous than T1)
  • T1 + C: No enhancement (distinguishes from epidural neoplasms)
  • Fat-suppressed sequences (STIR/T2FS): Complete signal suppression confirms fat
  • Sagittal images: Posterior epidural fat accumulation over multiple levels
  • Axial images: "Y-sign" or stellate appearance of compressed thecal sac
• CT:
  • Hypodense epidural tissue (-80 to -120 HU) consistent with fat attenuation
  • Spinal canal narrowing with posterior epidural fat accumulation
  • Less sensitive than MRI for neural compression assessment
• Myelography (rarely used):
  • Extradural compression with smooth indentation of contrast column
  • "Featureless" thecal sac compression

Treatment

• Conservative management:
  • Weight reduction program for obese patients
  • Gradual corticosteroid tapering or discontinuation when possible
  • Physical therapy and activity modification
  • Epidural steroid injections (paradoxical but may provide temporary relief)
• Medical management:
  • Treatment of underlying endocrinopathy
  • Pain management with NSAIDs or neuropathic pain medications
  • Metabolic optimization
• Surgical intervention:
  • Indications:
  • Progressive neurological deficit
  • Cauda equina syndrome
  • Failure of conservative management (3-6 months)

Differential diagnosis