In cervical spondylosis, primary degenerative processes are responsible for the ultimate secondary compressive phenomena. Both neural and vascular processes can become symptomatic. White and Panjabi (8) developed a theory of the biomechanical factors leading to cervical spondylotic myeloradiculopathy. They divided factors into static and dynamic groups. The static mechanisms relate to the primary degenerative processes that lead to a smaller canal diameter. These would include a congenitally small canal, osteophyte formation from the vertebral body or uncovertebral joint, disk herniation, hypertrophy of the facet joint, ligamentum flavum folding, and calcification
of the posterior longitudinal ligament or ligamentum flavum. Secondarily, the dynamic factors include abnormal forces on the spinal cord during loading and movement. Together, these mechanisms can lead to neurologic symptoms.

Reduction in the sagittal spinal canal size is the driving force behind the development of spondylotic symptoms. This process begins with cervical disk desiccation (9). The cervical disk is taller ventrally than it is dorsally, which effectively maintains lordosis. The ventral annulus fibrosus is made of type I collagen interweaved and multilayered, whereas the dorsal annulus is merely a thin layer of fibers (10). As the body ages, there is a progressive decline in the water content of the intervertebral disk. The nucleus pulposus is made of glycosaminoglycans, a proteoglycan core with many polysaccharide attachments of keratin sulfate and chondroitin sulfate, negatively charged to hold water. This unit gives the nucleus its elastic and viscous properties. With aging, the nucleus pulposus shows morphologically high cell activities near the cartilaginous end plate, including a process suggestive of regeneration. Eventually, it becomes an indistinct fibrocartilaginous mass (11). As a result, the disk loses its ability to retain water, its elasticity, and its ability to bear load. With no other options, the annulus fibrosis takes on the weight-bearing duties. As this degenerative process ensues, the contents of the disk can bulge into the spinal canal (1,9,12). Initially, the loss of height occurs ventrally and may lead to a loss of lordosis. Altered biomechanics lead to increased forces ventrally and may lead further to a kyphotic deformity (12). As the vertebral bodies subside toward one another, the facet joint capsule and the ligamentum flavum fold into the spinal canal, further reducing the canal diameter. Due to increased load bearing, osteophytes are formed at the edges of the vertebral body, facet joints, and uncovertebral joints.

All of the preceding effects of aging eventually lead to reduced spinal canal and encroachment on the neural elements. White and Panjabi (8) discovered that patients with a sagittal canal diameter less than 14.8 mm were more likely to develop cervical spondylotic myelopathy (CSM). Others reported 13 and 14 mm (1,9,13,14). The location of the compressive pathology (spinal cord, nerve root, or a combination of the two) determines the spectrum of symptoms. Compression between the uncovertebral joint and the facet joint may cause radicular symptoms, whereas compression from vertebral body osteophytes, bulging disks, ossified posterior longitudinal ligament, or infolded ligamentum flavum may cause myelopathy.

Cervical motion also affects the secondary compressive processes. Flexion may exacerbate or cause symptoms from ventral compression. Extension may induce compression from infolding of the ligamentum flavum. In addition, unstable cervical segments may result in a pincer phenomenon, during which flexion or extension may pinch the spinal cord between ventral and dorsal structures (8). Another biomechanical consideration is the “sagittal bowstring effect,” in which the cord is tethered over a ventral mass in a kyphotic spine. In this situation, a laminectomy may actually worsen the deformity, and an ventral approach to the pathology is warranted (12).

Not only do the compressive processes affect the spinal cord itself, they also may compress local blood supply to the cord, resulting in ischemia. Both arterial and venous vessels can be affected by the degenerative changes in the cervical spine. Necrosis and cavitation may be seen in the spinal gray matter, which seems to be more sensitive to ischemic events. The spinal cord has a more tenuous radicular blood supply to the C5 to C7 nerve roots (15) Additionally, it has been thought that acute presentation of cervical myelopathy may be due to the thrombosis of a compressed artery (16, 17, 18 and 19).

At the cellular and molecular level, recent literature has shed light on the pathobiologic mechanisms associated with the progressive loss of neural tissue in CSM. Yu et al. (20) used an animal model consisting of the twy/twy mutant mouse, which develops an ossified ligamentum flavum at C2-C3 and undergoes progressive paralysis, to show that chronic cord compression leads to Fas-mediated apoptosis of neurons and oligodendrocytes. This, in turn, is associated with activation of caspase-8, caspase-9, and caspase-3 and progressive neurologic deficits. They suggest that, eventually, molecular therapies could complement surgical decompression to help maximize neurologic recovery. In addition, free radical- and cation-mediated cell injury and glutamatergic toxicity may play a role in the pathophysiology of cervical myelopathy (21). It seems that there is early demyelination of the corticospinal tracts followed by destruction of the anterior horn cells. There is relative preservation of the anterior columns. Changes generally occur caudal to compressive lesions. Necrosis and cavitation in the central gray matter are seen late and suggest chronic disease (22).