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  • Title: Symptomatic Idiopathic Spinal Epidural Lipomatosis in 9 Patients: Clinical, Radiologic, and Pathogenetic Features.
    Author: Kellett CG, Siva V, Norman ICF, Jung J, Grahovac G, Minhas P.
    Journal: World Neurosurg; 2019 Jun; 126():e33-e40. PubMed ID: 30708081.
    Abstract:
    BACKGROUND: Symptomatic spinal epidural lipomatosis (SSEL) is characterized by hypertrophy of adipose tissue within the spinal canal and consequent neural compromise. The exact pathogenesis remains enigmatic. The authors describe a retrospective case series, define the full clinical spectrum, and discuss possible pathogenetic mechanisms. METHODS: The medical notes and imaging of 9 patients with SSEL undergoing surgery from 2008-2018 were analyzed. Seven patients presented secondary to lumbosacral spinal epidural lipomatosis (SEL); 3 patients with chronic incomplete cauda equina syndrome (CES), 3 patients with acute CES (including a 25-week gravid patient and a 40-year-old patient with intravenous leiomyomatosis, both of whom had mild SEL) and 1 patient with chronic lumbar radiculopathy. In addition, 2 patients presented with progressive myelopathy secondary to thoracic SEL. RESULTS: Patients presenting with acute CES had a mean age of 37 years (range 23-49 years) and mean extradural fat (EF)-to-spinal canal (SC) ratio of 47% (range 41%-58%), in comparison with patients with chronic CES; mean age 61 years (range 58-65 years) and EF:SC ratio 72% (range 65%-80%). Patients underwent laminectomy and resection of EF at compressive levels. All patients with CES experienced complete resolution of symptoms at follow-up (range 1-48 months). CONCLUSIONS: The clinician should be astute to the radiologic features of SEL, particularly in patients presenting with CES in the absence of acute disk herniation. The outcome of patients with CES and SEL after surgery is excellent regardless of symptom duration. Venous impedance related to increased body mass index and EF deposition may play the predominant role in addition to mechanical compression in the pathogenesis of SSEL.
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