Complete spontaneous resorption of a symptomatic L5–S1 lumbar disc herniation following conservative management despite an initial indication for surgery: a case report with a review of immunobiological mechanisms

Background Lumbar disc herniation (LDH) is among the leading causes of low back pain and lumbar radiculopathy. Although surgical discectomy is considered the standard treatment for patients with persistent disabling symptoms or neurological deficits, increasing evidence indicates that spontaneous regression of lumbar disc herniation may occur following conservative management, particularly in extruded and sequestrated discs. This phenomenon is believed to result from a coordinated inflammatory response involving macrophage infiltration, angiogenesis, cytokine release, extracellular matrix degradation, and phagocytosis of the herniated fragment. We report a case of complete spontaneous resorption of a symptomatic L5–S1 lumbar disc herniation and discuss the biological mechanisms underlying this remarkable process. Case presentation A 48-year-old woman presented with a three-month history of mechanical low back pain that progressively evolved into severe right-sided lumbosciatica associated with L5–S1 paresthesia and painful intermittent claudication. Pain intensity was 9/10 on the visual analogue scale. Neurological examination demonstrated a positive straight-leg-raising test at 30° and a diminished right Achilles tendon reflex without motor deficit or sphincter dysfunction. Lumbar magnetic resonance imaging revealed a right paramedian and foraminal L5–S1 disc herniation causing significant narrowing of the right neural foramen. Initial conservative management consisted of oral corticosteroids, analgesics, and muscle relaxants. Owing to persistent disabling pain, surgery was proposed. However, the patient declined surgical intervention and elected to continue conservative treatment. After gradual pain relief, a structured physiotherapy program was initiated. Follow-up magnetic resonance imaging performed eight months later demonstrated complete spontaneous disappearance of the herniated disc with restoration of the neural foramen, accompanied by marked clinical recovery. Conclusion This case highlights that spontaneous lumbar disc regression is an active immunobiological process rather than passive dehydration, supporting individualized treatment strategies in neurologically stable patients. In the absence of progressive neurological deficit or cauda equina syndrome, carefully selected patients may benefit from continued conservative treatment. Current evidence supports an active biological process driven by inflammation, neovascularization, macrophage-mediated phagocytosis, and extracellular matrix remodeling.