The fundamental lesion of the spinal column is probably generated initially by a fraying of the annulus fibrosus with extrusion of disc material into the spinal canal. The disc becomes covered with fibrous tissue or partly calcified, thereby forming a transverse osteophytic “spondylitic bar” or there may be simply central bulging of the annulus without extrusion of nuclear material. The latter, unlike ruptured discs that occur mainly at the C5-C6 or C6-C7 interspace, often involve higher interspaces and may occur at several adjacent levels. The dura may be thickened and adherent to the posterior longitudinal ligament at affected levels. The underlying pia-arachnoid is also thickened and the adjacent ligamentous hypertrophy contributes to compression of the cord or the nerve roots. This series of pathologic changes is often ascribed to a type of hypertrophic osteoarthritis. However, osteophyte formation and ridging are so frequently observed in patients who have no other signs of arthritic disease that this explanation is surely not totally correct. Subclinical trauma in persons who are structurally susceptible to spondylosis is more likely to be the cause of bar formation, in the authors’ opinion.
When a cervical nerve root is compressed by lateral osteophytic overgrowth, the dural sleeve is thickened and truncated and the root fibers are damaged. Usually the fifth, sixth, or seventh cervical roots are affected in this way, both the anterior and posterior, or only the anterior, on one or both sides. A small neuroma may rarely appear proximal to the site of anterior root compression.
The dura is ridged and the underlying spinal cord is flattened. The root lesions may lead to secondary wedge-shaped areas of degeneration in the lateral parts of the posterior columns at higher levels. The most marked changes in the spinal cord are at the level(s) of compression. There are zones of demyelination or focal necrosis at the points of attachment of the dentate ligaments (which tether the spinal cord to the dura) and areas of rarefaction in the posterior and lateral columns, as well as loss of nerve cells. Ventral gray matter lesions, often asymmetrical, are attributed by Hughes to ischemia.
The vulnerability of the cervical spine to degenerative change has no ready explanation. Most likely it is related in some way to the high degree of mobility of the lower cervical vertebrae, which is accentuated by their location next to the relatively immobile thoracic spine.
The mechanism of spinal cord injury would seem to be one of simple compression and ischemia. When the spinal canal is developmentally narrow in its anteroposterior dimension at one or several points, the space available for the spinal cord becomes insufficient. A small canal certainly makes an individual more subject to the compressive effects of spondylosis. The range acquired of narrowing of the canal that produces symptomatic cervical spondylosis is generally from 7 to 12 mm (normal canal diameter: 17 to 18 mm). Consequently, one must consider several additional mechanisms by which the cord might be damaged. The effects of the natural motions of the spinal cord during flexion and extension of the neck are probably important in this respect. Adams and Logue confirmed the observation of O’Connell that, during full flexion and extension of the neck, the cervical cord and dura move up and down. The spinal cord is literally dragged over protruding osteophytes and hypertrophied ligaments; conceivably it is this type of intermittent trauma that causes progressive injury.