Cervical and lumbar spinal stenosis are the most common causes of neck and back pain and spinal cord and cauda equina or nerve root dysfunction and represent the most frequent indications for spinal surgery in adults older than the age of 55 years.

The term spinal stenosis describes an acquired condition of progressive narrowing of the spinal canal usually due to age-related progressive arthritic degeneration of the intervertebral disks and facet joints. This process results in disk bulging, facet overgrowth, synovial cyst development, and bone spur formation, as well as ligamentum flavum and facet joint capsule hypertrophy. These proliferative, so-called spondylotic, changes that occur in response to accumulated mechanical stress in the spine lead to progressive narrowing of the spinal canal and/or foramina. In some patients, these degenerative changes may compromise the mechanical integrity of the spine leading to deformity (e.g., degenerative scoliosis, kyphosis) or spondylolisthesis that may further exacerbate the clinical condition produced by spinal stenosis. In a smaller subset of patients, narrowing of the spinal canal may be due to degenerative and/or destructive changes to the articulating joints from systemic conditions such as rheumatoid arthritis, or enthesopathies such as ossification of the posterior longitudinal ligament (OPLL), ankylosing spondylitis, or diffuse idiopathic skeletal hyperostosis (DISH). OPLL may be focal or diffuse and seems to be most common in people of Asian heritage. These conditions much more commonly affect the cervical spine.

Progressive stenosis of the cervical, or rarely thoracic, spinal canal from these conditions may damage the spinal cord producing a condition known as cervical spondylotic myelopathy (CSM). Such myelopathy is attributed to one or more of three possible mechanisms: (1) direct compression of the spinal cord by bony or fibrous tissue overgrowth, (2) ischemia caused by compromise of the vascular supply to the cord, and (3) repeated trauma in the course of normal neck movement. Similarly, ongoing progressive or intermittent narrowing of the nerve root foramen may cause injury to the cervical nerve roots. Although the cauda equina seems less susceptible than the spinal cord to permanent injury from lumbar spinal stenosis, advanced, nontreated severe stenosis may result in irreversible injury to these nerve roots similar to cervical myelopathy.

In the cervical spine, spondylotic bars may leave deep indentations (e.g., visible at autopsy) on the ventral surface of the spinal cord. At what may be several levels of lesions, there is degeneration of the gray matter, sometimes with necrosis and cavitation. Above the compression, there is degeneration of the posterior columns; below the compression, corticospinal tracts are demyelinated. A similar process occurs in the lumbar spine where the proliferative changes due to the normal aging process produces progressive narrowing of the lumbar spinal canal and compression of the cauda equina.

Normal, albeit accentuated, wear and tear degenerative changes in the spine is the most common cause of spinal stenosis both in the cervical and lumbar spine. The water content of the intervertebral disk and annulus fibrosus declines progressively with advancing age. Concomitantly, there are degenerative changes in the disk. The intervertebral space narrows and may be obliterated, and the annulus fibrosus protrudes into the spinal canal. Osteophytes form at the margins of the vertebral body, converge on the protruded annulus, and may convert it into a bony ridge or bar. The bar may extend laterally into the intervertebral foramen; there is also fibrosis of the dural sleeves of the nerve roots. All these changes narrow the canal, a process that may be aggravated by fibrosis and hypertrophy of the ligamenta flava. In some cases, this narrowing may be exacerbated by acute or chronic disk herniation, synovial cyst development from the facet joint, or degenerative spondylolisthesis. These last two conditions are much more common in the lumbar spine of women, especially at the L4-L5 level. The likelihood of spinal cord or cauda equina compression or vascular compromise increases in direct relation to the decrease in the original diameter of the spinal canal.

Most cases of degenerative cervical or lumbar stenosis are sporadic in occurrence, although there may be a family history in some patients. The term congenital spinal stenosis is a bit of a misnomer because stenosis connotes an acquired narrowing. A developmentally small spinal canal is a more accurate term than congenital stenosis. Patients with a developmentally small canal, a familial characteristic, may be more susceptible to develop symptomatic stenosis simply because they have less capacity to accommodate the proliferative degenerative changes associated with the progressive arthritic process of the spine. Spinal stenosis tends to develop at the most mobile and mechanically stressed spinal levels. The C5-C6 and C6-C7 levels are most commonly involved in the cervical spine, whereas L4-L5 and L3-L4 are the most commonly affected lumbar levels. Both C4-C5 and L5-S1 are slightly less commonly involved. Concomitant symptomatic cervical and lumbar stenosis can be seen in up to 15% of patients. Patients who have either congenital (i.e., Klippel-Feil syndrome) or previously performed surgical spinal fusion may be prone to develop spinal stenosis at levels adjacent to the fused level.

Systemic conditions such as rheumatoid arthritis may cause destructive changes of synovial joints, especially in the upper cervical spine leading to cervical instability and stenosis with spinal cord compression. The term enthesis describes the site where ligaments or tendons attach to bone. In the spine, a number of different enthesopathies may involve the spine to produce spinal stenosis. The most common of these is OPLL, where calcification of the posterior longitudinal ligament can produce progressive spinal stenosis, particularly in the cervical spine, and myelopathy. Less commonly, diffuse idiopathic skeletal hyperostosis or ankylosing spondylitis may result in excessive ossification of either the posterior or anterior longitudinal spinal ligaments leading to spinal rigidity, fragility, and spinal stenosis.