Inflammatory and Analgesic Profiles in Intervertebral Disc Herniation: Variability with Respect to Neurological Deficit.

Background: Disc herniation is both a mechanical and biochemical process in which contact between intervertebral discs and spinal nerves causes compression, chemical irritation, inflammation, and pain. The inflammatory process is known to vary depending on pain duration, herniation type, and pain severity, but the relationship with neurological deficits remains unknown.

Objective: This study aimed to compare individuals with lumbar disc herniation with and without neurological deficits (WND/WOND) and healthy individuals in terms of serum levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 4 (IL-4), interleukin 1 beta (IL-1β), beta-endorphin, anandamide, and 2-arachidonoylglycerol (2-AG).

Methods: The study included 37 lumbar disc herniation patients WND (22 female, 15 male), 37 patients WOND (22 female, 15 male), and 35 healthy individuals (18 female, 17 male). TNF-α, IL-6, IL-4, IL-1β, beta-endorphin, anandamide, and 2-AG serum levels were analyzed using commercial enzyme-linked immunosorbent assay kits.

Results: There was no difference in TNF-α levels between the WOND, WND, and control groups (P = 0.383). The WOND and WND groups showed significantly higher expression of IL-1β (P < 0.001) and IL-4 (P = 0.034, P < 0.001) when compared with healthy controls. IL-6 expression was lower in the WND group than in the control group (P < 0.001). Beta-endorphin, anandamide, and 2-AG levels did not differ significantly between the WOND, WND, and control groups (P = 0.888, P = 0.247, P = 0.433, respectively).

Conclusions: This study is the first to demonstrate the effect of the presence of a neurological deficit on serum biomarker levels in patients with lumbar disc herniation. Even in the presence of neurological deficit, decreased levels of proinflammatory cytokines and increased levels of anti-inflammatory cytokines indicated regression of the disc herniation. These results suggest the need to establish new and improved treatment protocols to target the inflammatory process in individuals with lumbar disc herniation.