Abstract

INTRODUCTION: Laminectomy is the standard of treatment in Lumbar Spinal Stenosis(LSS). Multiple studies (Mariconda;Boden;Schonstrom;Matsumoto;Herno;Webber.) have not found relationship between spinal canal widening and symptoms improvement in LSS. Neurogenic compression and rootlets hypoxia theories try to explain pathophysiology of LSS. We propose Epidural Hypertension (EH) as a new paradigm that explains dynamic stress of neural structures involved in LSS. METHODS: Group A: single-segment LSS diagnosed by magnetic resonance (n = 4). Group B: Patients without LSS requiring surgery for another diagnosis (spinal cord stimulation, foraminotomy) (n = 3). Laminectomy was performed, previously, flavum ligament was meticulously dissected and a pressure microsensor was inserted in epidural space in stenotic segment. EP was measured in 0 and 50° extension in order to extrapolate EP in standing position. RESULTS: EP in LSS patients was 18,5 mmHg at 0° (IQR 16.5-37.5 mmHg) and 26 mmHg at 50° (IQR 20-34.5 mmHg). In patients without LSS, EP was 8mmHg at 0° (IQR 1-8 mmHg) and 3 mmHg at 50° (IQR 1-12 mmHg). We found differences using Wilcoxon's test. EP was greater in patients with LSS at 0° (p = 0.031) y 50° (p = 0.034). CONCLUSIONS: EH may play a foundamental role in pathophysiology of LSS. In Patients without LSS we found a drop in EP at 50° possibly secondary to caudal CSF displacement. In LSS patients we found a raise in EP at 50° possibly secondary to spinal canal narrowing impeding normal CSF flow increasing hydrostatic pressure in the stenotic segment. This results might be the first step to consider EH as a treatment target in LSS and determine its relationship with LSS symptoms.

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