CT Evaluation of Intervertebral Disc Herniation and Degenerative Change
Intervertebral disc herniation represents displacement of nucleus pulposus material through defects or weakened regions of the annulus fibrosus, most often in the posterior or posterolateral direction where the annulus is biomechanically vulnerable. The posterior longitudinal ligament (PLL) partially reinforces the midline but tapers laterally, explaining the frequency of paracentral herniations that impinge on traversing nerve roots while sparing exiting roots. True central herniations may narrow the thecal sac, whereas far-lateral (extraforaminal) protrusions contact the exiting nerve root at or just beyond the foramen. Bilateral symmetric herniations are less common and usually reflect broad-based disc pathology (bulge) rather than focal extrusion.
Lumbar disc herniation is most prevalent because of cumulative axial load and mobility demands; cervical herniation follows, while thoracic involvement remains rare due to relative immobility and the stabilizing rib cage. On CT, the direct sign of a lumbar herniation is a focal, crescentic, or lobulated soft tissue density extending beyond the expected posterior disc margin. Its attenuation exceeds cerebrospinal fluid but is lower than cortical bone. Secondary signs include effacement of normally lucent epidural fat, indentation or deformation of the dural sac, and displacement, compression, or tapering of nerve root sleeves. Foraminal or extraforaminal components narrow or obliterate the fat plane within the foramen, and in severe cases may remodel adjacent osseous margins.
Disc material traversing a complete annular fissure and PLL tear may sequester. A sequestered (free) fragment migrates cranially or caudally within the canal, sometimes remote from the index disc space, appearing as an irregular, discrete soft tissue focus that maintains similar attenuation to the parent disc and produces localized dural contour deviation. Differentiating retained fragment from postoperative fibrosis relies partly on contrast-enhanced CT or CT myelography: fibrous scar enhances due to vascular granulation tissue, whereas residual or recurrent disc fragment typically remains non-enhancing or only minimally reactive peripherally.
Degenerative changes frequently coexist and modify imaging appearance. Marginal osteophytes, endplate sclerosis, vacuum phenomenon (intragas collection within degenerated nucleus or clefts), and calcification may be evident. Posterior osteophytic ridging, ossified PLL, and facet joint hypertrophy contribute to central, lateral recess, or foraminal stenosis that can amplify clinical symptomatology beyond the contribution of soft disc material alone. Vacuum phenomenon appears as sharply marginated very low attenuation linear or focal collections, confirming chronic degenerative disc desiccation and fissuring rather than acute herniation.
Important mimics of disc herniation must be excluded. Enlarged epidural venous plexuses can simulate soft tissue protrusion but often enhance and display tubular or serpiginous morphology. Conjoined nerve roots, most commonly at lumbosacral junction, create asymmetric lateral recess fullness with smooth margins and continuity to the dural sac. Foraminal nerve sheath tumors (e.g., schwannoma, neurofibroma) are typically round or fusiform, may cause osseous remodeling or enlargement of the foramen, and can enhance following contrast. Metastatic or primary vertebral neoplasms generate destructive bone change and associated epidural soft tissue that differs from the relatively preserved osseous cortex in uncomplicated disc extrusion. Facet synovial (juxtafacet) cysts arise adjacent to degenerated facet joints, projecting posteriorly or posterolaterally into the canal as low-attenuation lesions; peripheral calcification, gas inclusion, or a thin enhancing wall may be present. Epidural abscess presents as a lenticular or crescent soft tissue collection that may displace the thecal sac, often with adjacent bone or disc inflammatory changes and systemic clinical context. Postoperative enhancement patterns, surgical hardware artifact, and scar planes further complicate evaluation and necessitate correlation with operative history.
Cervical disc herniation appears as a focal or broad-based soft tissue prominence indenting the anterior subarachnoid space or contacting the spinal cord. The relative paucity of epidural fat and thinner discs reduce inherent contrast, making subtle lesions harder to perceive; thin-section acquisition and multiplanar reconstructions increase detection sensitivity. Large central or paracentral cervical protrusions can flatten or displace the cord, and chronic compression may correlate clinically with myelopathic signs—although MRI is superior for direct cord signal evaluation. Coexistent uncovertebral joint osteophytes and ligamentum flavum thickening narrow the canal and foramina, leading to combined static and dynamic stenotic effects.
Thoracic disc herniations, while uncommon, often occur centrally or paracentral and may calcify, particularly in middle-aged adults. Their clinical relevance ranges from incidental to causative in myelopathy. CT delineates calcified components that influence surgical planning, especially when ventral to the cord where anterior approaches are challenging.
Generalized disc degeneration manifests as symmetric circumferential extension of disc material beyond the vertebral ring apophyses (disc bulge) without focal disruption of annulus continuity. This contrasts with a focal protrusion (broad base narrower than outward extension) or extrusion (neck narrower than displaced fragment). Recognizing these morphological distinctions standardizes reporting and guides management algorithms. Uniform annular bulging commonly accompanies loss of disc height, vacuum changes, and facet arthropathy in multilevel degenerative cascade.
Accurate CT interpretation benefits from a structured checklist: confirm vertebral numbering; assess alignment for listhesis that alters biomechanical load; inspect disc height, contour, attenuation, and presence of gas or calcification; evaluate canal dimensions and lateral recess patency; scrutinize foraminal fat planes; identify facet joint degeneration and juxtafacet cysts; search for sequestered fragments; and differentiate mimics using enhancement characteristics, morphology, and osseous reaction patterns. When uncertainty persists—especially regarding neural element compression severity—MRI or CT myelography provides complementary evaluation of intradural and parenchymal detail.
In conclusion, CT characterization of intervertebral disc herniation hinges on recognizing focal contour abnormalities, secondary epidural space effacement, and associated degenerative context while avoiding diagnostic pitfalls posed by mimics. A disciplined, anatomy‑focused approach optimizes sensitivity, specificity, and clinical relevance in reporting.
Disclaimer: Educational overview; integrate with MRI findings and clinical correlation for definitive management decisions.