Cervical stenosis in the context of herniated disc and injury refers to narrowing of the spinal canal that can result from both acute disc herniation and trauma superimposed on pre-existing degenerative changes. The stenosis may be developmental (congenital narrowing) or acquired through degenerative processes, and injury can precipitate symptomatic cord or nerve root compression in patients with pre-existing canal narrowing.

Herniated discs contribute to stenosis by causing the nucleus pulposus to protrude beyond the annulus fibrosus, directly compressing the spinal cord or nerve roots.

[1]

 This herniation results from degenerative changes that weaken the annular fibers through increased load sharing and decreased yield strength.

[1]

 The herniated disc material not only causes mechanical compression but also releases inflammatory mediators including matrix metalloproteinases, prostaglandin E2, and interleukin-6, which contribute to nerve root inflammation.

[2]

Injury can cause or worsen stenosis through several mechanisms. Minor trauma superimposed on chronic degenerative spondylosis can cause spinal cord damage even without fracture, particularly in patients with pre-existing canal narrowing.

[3]

 Acute traumatic compression results from combinations of fractured bone fragments, disc herniation, and vertebral subluxation.

[3]

 The severity of neurologic symptoms from cervical disc herniation is inversely related to the sagittal diameter of the bony spinal canal—patients with developmental stenosis (mean diameter 12.9 mm) are at higher risk for motor disturbances.

[4]

Static factors contributing to stenosis include disc collapse with posterior bulging, vertebral osteophytes, and ligamentous hypertrophy.

[5]

 Dynamic factors involve biomechanical changes during flexion and extension that cause compression, tethering, and shearing of the spinal cord.

[5]

 Spinal cord injury risk increases substantially with severe stenosis (6 mm canal diameter) during whiplash-type injuries.