It has also been shown that the spinal cord, displaced posteriorly by osteophytes, is compressed by the infolding of the posterolateral ligamentum flavum each time the neck is extended (Stoltmann and Blackwood). Segmental ischemic necrosis resulting from intermittent compression of spinal arteries or from compression of the anterior spinal artery has also been postulated. Most neuropathologists favor the idea of intermittent cord compression between osteophytes anteriorly and ligamentum flavum posteriorly, with an added vascular element accounting for the scattered lesions deep in the cord. Trauma from sudden extreme extension, as in a fall, severe whiplash injury, or chiropractic manipulation, or from a lesser degree of retraction of the head during myelography, tooth extraction, or a tonsillectomy may be operative in individual cases, particularly in patients with congenitally narrow canals. The lateral extension of the osteophyte and hypertrophy of the adjacent facet joint together compress the nerve root as it is entering its spinal foramen. Sometimes these are the main changes and cause only a radiculopathy, as discussed in Chap. 10.
When pain and stiffness in the neck, brachialgia, either in the form of aching or a more distinctive radicular pain, and sensorimotor-reflex changes in the arms are combined with signs of myelopathy, there is little difficulty in diagnosis. When the neck and arm changes are inconspicuous or absent, the diagnosis becomes more difficult. The myelopathy must then be distinguished from the late, progressive form of spinal multiple sclerosis. Because posterior vertebral osteophytes and other bony alterations are frequent in the sixth and seventh decades of life, the question that must be answered in any given case is whether the vertebral changes are adequately severe to cause the neurologic abnormality. The finding of some degree of sensorimotor or reflex change corresponding only to the level of the spinal abnormalities is a point that always favors spondylotic myelopathy. A lack of such corresponding changes and the presence of oligoclonal bands and signs of lesions in the optic nerves and brain indicate demyelinating myelopathy.
The detailed findings on both MRI and CT myelography become critical in such cases (Fig. 42-9). The MRI may overestimate the degree of cord compression by an osteophyte, but clear deformation of the cord into the shape of a kidney bean and obliteration of the surrounding CSF spaces in the transverse image support the diagnosis of spondylotic compression. To confidently attribute neurologic symptoms to spondylosis there should be considerable encroachment on and obliteration of the circumferential CSF space at that level, not simply an impingement or slight deformation of the normal oval shape of the cord. Signal changes within the body of the cord underlying or within a half segment of the compression are seen in advanced cases and usually indicate a degree of irreversibility of at least the sensory symptoms. Curiously, these signal changes may be one or two levels above or below the site of main compression. A purportedly specific imaging sign of a transverse “pancake-like” gadolinium enhancement at and just caudal to the site of maximal compression has been suggested by Flanagan and colleagues (2014). However, serious symptoms may occur even without changes in the intrinsic MRI signal. Contrast myelography with the patient supine and lateral views taken during flexion and extension of the neck are useful diagnostic procedures in uncertain cases.