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CHAPTER 36 Cervical Spondylosis
Pathophysiology, Natural History, and Clinical Syndromes of Neck Pain, Radiculopathy, and Myelopathy
Degenerative changes at the cervical discs and facet joints are ubiquitous in the adult population; these changes are a natural consequence of aging and are asymptomatic in most of the population. Spondylosis refers to these age-related degenerative changes within the spinal column.121
Degenerative changes within the cervical disc lead to loss of disc height, arthrosis in the uncovertebral and facet joints, and motion aberrations between two vertebral bodies.3414
As the disc loses height, the vertebral bodies approach each other, causing infolding of the ligamentum flavum and facet joint capsule and reducing the dimensions of the canal and the foramen.5647
Axial neck pain results from a multitude of potential causes and can be divided geographically into anterior neck pain, which usually stems from sprains and strains of the sternocleidomastoid and other strap muscles and their attachments, and posterior neck pain, which can be subdivided further into subaxial and suboccipital locations.85
The physiology of this pain process is not yet fully delineated. Patients with chronic myofascial pain have significantly lower levels of high-energy phosphates in the involved muscle tissue.9
Axial neck pain should be attributed to degenerative changes in the cervical discs or facet joints only after careful consideration, owing to the ubiquitous nature of these changes in the spine. Nevertheless, multiple studies suggest that cervical discs and facet joints can generate pain.10–14Fig. 36–110Fig. 36–214
FIGURE 36–1 Cross-sectional anatomy showing dorsal and ventral primary branches of cervical nerve root, origin of sinuvertebral nerve (also known as recurrent meningeal nerve) from the nerve root, and sympathetic plexus. Note proximity of disc, uncovertebral and facet joints, and vertebral artery.
FIGURE 36–2 Axial pain patterns provoked during discography at each cervical level. A, C2-3. B, C3-4. C, C4-5. D, C5-6. E, C6-7.
(From Grubb SA, Kelly CK, Bogduk N: Cervical discography: Clinical implications from 12 years of experience. Spine [Phila Pa 1976] 25:1382-1389, 2000.)
Degenerative changes at a cervical facet joint can be a source of axial neck pain. Provocative injections into the facet joints of asymptomatic volunteers result in a reproducible pattern of axial neck pain and shoulder girdle pain (Fig. 36–3121115
FIGURE 36–3 Composite map of axial pain patterns from facet joints at C2-3 to C6-7.
(From Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns. I. A study in normal volunteers. Spine [Phila Pa 1976] 15:453-457, 1990.)
Suboccipital pain radiating down into the neck or to the back of the ear may be a manifestation of degenerative arthritis in the upper cervical spine. Injection of the atlanto-occipital and atlantoaxial joints results in a reproducible pain pattern in this region, with the atlanto-occipital joints showing the capacity to generate intense and diffuse pain.16 Wächli and colleagues171810
Radicular findings in the arm originate from the cervical nerve roots at some point between their origins as nerve rootlets from the spinal cord and their transition into peripheral nerves as they emerge from the neural foramen. Degenerative changes at the cervical motion segment, soft disc herniations, stenosis, intrinsic nerve root pathology, and trauma all can result in these symptoms. Loss of disc height leads to impingement on the nerve root origins from disc bulging, infolding of the facet joint capsule and ligamentum flavum, and osteophyte formation at the disc margins (hard disc formation) and at the uncovertebral and facet joints, all of which result in foraminal stenosis and radiculopathy (Fig. 36–419
FIGURE 36–4 Nerve root compression in lateral spinal canal from disc, uncovertebral joint, or facet joint pathology can lead to cervical radiculopathy.
Mechanical deformation of the nerve root may lead to motor weakness or sensory deficits. The exact pathogenesis of radicular pain is unclear, but the general belief exists that in addition to the compression, an inflammatory response must occur for pain to develop. Within the compressed nerve root, intrinsic vessels show increased permeability, secondarily resulting in edema of the nerve root. Chronic edema and fibrosis (scar) within the nerve root play a role in altering the response threshold and heighten the sensitivity of the nerve root to pain.20Table 36–121,22
Neurogenic | Non-neurogenic |
---|---|
Substance P | Bradykinin |
Somatostatin | Serotonin |
Cholecystokininlike substance | Histamine |
Vasoactive intestinal peptide | Acetylcholine |
Calcitonin gene-related peptide | Prostaglandin E1 |
Gastrin-releasing peptide | Prostaglandin E2 |
Dynorphin | Leukotrienes |
Enkephalin | diHETE |
Gelanin | |
Neurotensin | |
Angiotensin II |
diHETE, dihydroxyeicosatetraenoic acid
From Chabot MC, Montgomery DM: The pathophysiology of axial and radicular neck pain. Semin Spine Surg 7:2-8, 1995.
Dynamic factors in the cervical spinal column affect the amount of nerve root compression. Flexion of the cervical spine lengthens the cervical neural foramina 18% to 31%, whereas extension shortens the foramina 16% to 22%.23
Changes in intrinsic tension within the nerve root have the ability to alter radicular pain. Davidson and colleagues2425
Often, patients present with radicular pain in an atypical distribution.2627
Although it is generally agreed that mechanical compression of the spinal cord is the primary pathophysiologic mechanism resulting in myelopathy, in many patients a combination of this static compression with dynamic factors secondary to motion between the vertebral bodies, a congenitally stenotic canal, changes in the intrinsic morphology of the spinal cord, and vascular factors contributes to the development of myelopathy. A developmentally narrow spinal canal in the anteroposterior plane can contribute to the development of cervical myelopathy. The normal anteroposterior diameter of the cervical spine measures 17 to 18 mm in adults, and the anteroposterior diameter of the spinal cord in the cervical region measures approximately 10 mm. An anteroposterior diameter of the spinal canal less than 13 mm defines congenital cervical stenosis, whereas a diameter greater than 16 mm suggests a relatively low risk of myelopathy (Fig. 36–5A28,2930
FIGURE 36–5 Radiographic criteria important in pathogenesis of cervical spondylotic myelopathy. A, Mid-sagittal diameter of spinal canal is measured as distance from middle of dorsal surface of vertebral body to nearest point on spinolaminar line. Patients in whom osseous canal measures less than 13 mm are considered developmentally stenotic. B, Distance of less than 12 mm from posteroinferior corner of vertebral body to anterosuperior edge of lamina of immediately caudal vertebra with neck in extension is suggestive of dynamic stenosis. C, Olisthesis (retrolisthesis or anterolisthesis) of greater than 3.5 mm is measure of excessive translation between vertebral bodies. Signal changes within substance of spinal cord, noted on T1-weighted and T2-weighted MRI in some patients, are represented diagrammatically with gray lines.
(From Rao RD, Gourab K, David KS: Operative treatment of cervical spondylotic myelopathy. J Bone Joint Surg Am 88:1619-1640, 2006.)
A strong association exists between flattening of the cord within the narrowed spinal canal and the development of cervical myelopathy. Penning and colleagues312323330,34
Segmental motion of the cervical spinal column affects the development of cervical myelopathy. Hyperextension of the neck narrows the spinal canal by shingling the laminae and buckling the ligamentum flavum ventrally into the canal. Extension and flexion of the neck may alter the diameter of the canal by 2 mm.35 Angulation or translation between vertebral bodies in flexion or extension may result in narrowing of the space available for the cord (Fig. 36–5B30Fig. 36–5C28,363738
Cervical spine flexion and extension cause morphologic changes within the spinal cord itself. Breig and colleagues3940
The classic study by Breig and colleagues39454640,47
Severe compression results in pathologic changes within the spinal cord. The central gray matter and the lateral columns show the most changes, with cystic cavitation, gliosis, and demyelination most pronounced caudad to the compression site. The posterior columns and posterolateral tracts show wallerian degeneration cephalad to the site of compression. The irreversibility of these changes may explain why some patients fail to recover after decompressive surgery. The anterior white columns are relatively resistant to infarction, even in cases of severe compression.48
Neck pain commonly affects adults of all ages and both sexes almost equally. Few population-based studies exist on the prevalence of neck pain. A study of the Saskatchewan adult population showed that neck pain is more prevalent than commonly thought, with 66% of adults experiencing neck pain during their lifetime and 5% highly disabled by it.495051
No true natural history studies of axial neck pain exist; all published studies involve some form of treatment in most patients. DePalma and Subin525353
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