What is the pathophysiology of a sequestrated disc?

Pathophysiology of Sequestrated Disc

A sequestrated disc occurs when a fragment of the nucleus pulposus herniates through the annulus fibrosus and becomes completely separated from the parent disc, migrating into the epidural space as a free fragment. 1, 2

Mechanical Process of Sequestration

The pathophysiological cascade begins with herniation of the nucleus pulposus through a defect in the fibrous outer covering (annulus fibrosus) of the intervertebral disc. 1 In sequestration specifically, the herniated fragment loses all continuity with the disc of origin and becomes a free-floating fragment in the epidural space. 2, 3

• The sequestered fragment can migrate considerable distances from the parent disc level, sometimes moving posteriorly into the epidural space or even to adjacent vertebral levels. 2, 3
• This migration pattern distinguishes sequestration from other disc herniation subtypes (protrusion, extrusion) where some connection to the parent disc remains. 4
• The fragment typically consists of nucleus pulposus material with varying amounts of cartilaginous endplate and annular tissue. 3, 5

Inflammatory Response and Biological Cascade

The most critical pathophysiological feature of sequestrated discs is the robust inflammatory response triggered when disc material loses contact with the parent disc and enters the epidural space. 4, 6

• The sequestered fragment elicits an intense inflammatory reaction because the immune system recognizes the disc material as foreign once it enters the vascular epidural space. 4, 6
• This inflammatory cascade involves neovascularization, macrophage infiltration, and production of inflammatory mediators including matrix metalloproteinases, interleukins, and tumor necrosis factor. 4, 6
• The inflammatory response serves dual purposes: it causes acute neural compression and radicular pain, but paradoxically also facilitates spontaneous resorption of the fragment. 4, 6
• Sequestrated fragments have higher water content compared to contained herniations, making them more susceptible to both inflammatory-mediated resorption and dehydration. 6

Neural Compression Mechanisms

Sequestrated fragments cause neural compression through both mechanical mass effect and chemical irritation of nerve roots. 1, 2

• The free fragment can compress nerve roots from the lower cord segments, potentially causing cauda equina syndrome with urinary retention, bilateral motor weakness, and saddle anesthesia. 1, 2
• Posterior epidural migration of sequestrated fragments is particularly dangerous, as 77.8% of such cases present with cauda equina syndrome. 2
• The compression results in radiculopathy with pain, sensory impairment, weakness, or diminished deep tendon reflexes in the affected nerve root distribution. 1
• Chemical radiculitis from inflammatory mediators released by the sequestered fragment contributes significantly to pain beyond pure mechanical compression. 4, 6

Degenerative and Pseudoneoplastic Changes

Sequestrated disc fragments undergo degenerative changes that can create diagnostic confusion with neoplastic processes. 3, 5

• Pathologically, the sequestered fragment may show clustering of chondrocytes, prominent neovascularization, and granulation tissue formation that mimics cartilaginous neoplasms. 3
• The fragment becomes surrounded by granulation tissue and demonstrates prominent peripheral contrast enhancement on MRI, which can be mistaken for abscess, hematoma, or tumor. 3, 5
• These pseudoneoplastic features result from the reparative inflammatory response and should not be confused with true malignancy. 3, 5

Natural History and Resorption Potential

Sequestrated discs have the highest likelihood among all disc herniation subtypes to undergo spontaneous regression, with symptomatic resolution occurring in a mean of 1.33 months and radiographic resolution in 9.27 months. 4, 6

• The mechanism for spontaneous resorption involves both dehydration of the water-rich fragment and inflammation-mediated enzymatic degradation by macrophages and inflammatory cells. 4, 6
• Conservative management for at least 2 months is appropriate in the absence of cauda equina syndrome, intractable pain, inability to walk, or progressive weakness. 4, 6
• The robust inflammatory response that causes acute symptoms paradoxically facilitates faster resorption compared to contained herniations. 4, 6

Critical Clinical Pitfall

The most dangerous pitfall is delayed recognition of cauda equina syndrome, which requires emergency surgical decompression to prevent permanent neurological deficits including bladder/bowel dysfunction and lower extremity paralysis. 1, 2 Early surgical treatment within 12 hours of symptom onset is critical when cauda equina syndrome develops, as outcomes deteriorate significantly with delayed intervention. 1, 2