Subluxation degeneration has been described as a
progressive process associated with abnormal spinal mechanics. The degenerative changes
are associated with various mechanisms of neurological dysfunction. (1)
Progressive degeneration of the cervical spine is thought to begin with the
intervertebral discs, progressing to changes in the cervical vertebrae and contiguous soft
tissues. (2)
Several early investigators explored the relationship of spinal degenerative disease to
neurological compromise.
In 1838, Key described a case of cord pressure due to degenerative changes causing
spinal canal stenosis. (3)
Bailey and Casamajor reported that cord compression could result from spinal
osteoarthritis. They suggested that disc thinning was the basic pathology underlying
degenerative change. (4)
As early as 1926, Elliott gave an account of how radicular symptoms could be caused by
foraminal stenosis secondary to arthritic changes. (5)
Several mechanisms have been suggested which may be operative in cervical spine
degeneration.
Resnick and Niwayama used the term "intervertebral (osteo)chondrosis" to
describe abnormalities which predominate in the nucleus pulposus. (6)
Osteoarthritis of the uncovertebral and zygapophyseal joints is another manifestation
of cervical spine degeneration. Spondylosis is the term these authors applied to
degenerative changes which occur as a result of enlarging annular defects which lead to
disruption of the attachment sites of the disc to the vertebral body. This leads to the
appearance of osteophytes.
O'Connell employed the term "spondylosis" in a broader context. Three lesions
were described: disc protrusion into the intervertebral canal; primary spondylosis,
characterized by degenerative changes between the vertebral bodies and zygapophyseal
joints; and secondary spondylosis, associated with disc protrusion at a single spinal
level. (7)
In the lumbar spine, pathomechanics and torsional stress have been implicated as
etiological factors in spinal degeneration. (8,9)
It is likely that these factors are operative in the pathogenesis of cervical spine
degeneration as well. Although it has been suggested that aging is responsible for
degenerative changes in the spine, this appears to be an oversimplification. (10)
For example, Lestini and Weisel report that there is a high statistical correlation
between disc degeneration and posterior osteophyte formation. (2)
Furthermore, it is noted that the incidence of degenerative changes varies from one
segmental level to another. The C5/C6 level is most frequently involved, with C6/C7 being
the level next most frequently affected. The C2/C3 level is the one least likely to
exhibit degenerative changes. (11)
Since the prevalence of cervical spine degenerative change is not uniform throughout
the region, the hypothesis that degenerative change is associated with spinal
pathomechanics deserves consideration.
Hadley suggests that both aging and pathomechanics are operative in the pathogenesis of
cervical spine degeneration. Age related disc degeneration causes hypermobilty, resulting
in greater tractional forces on ligaments. This is said to result in the formation of
reactive osteophytes. Trauma can result in local spondylotic changes. (11)
This is similar to MacNab's description of traction spur formation in the lumbar spine.
(12)
Pesch et al measured the dimensions of the fifth, sixth, and seventh cervical vertebral
bodies in 105 cadavers aged 16 to 91 years. Similar measurements were made on the third,
fourth, and fifth lumbar vertebral bodies.
The authors suggest that dynamic stressing of the cervical vertebral bodies leads
laterally to friction between vertebral bodies at the uncovertebral joints, causing
osteophytosis. Anteriorly, osteophytic formation is attributed weakness of the anterior
longitudinal ligament, leading to anterior disc protrusion. (13)
Neurological consequences of spinal degeneration
Neurological manifestations of spinal degeneration may be due to a variety of
mechanisms. These include:
1. Cord compression. Compression of the spinal cord may result from disc
protrusion, ligamentum flavum hypertrophy/corrugation, or osteophytosis. Myelopathy may
result in cord pressure and/or pressure which interferes with the arterial supply.
(7,14,15,16)
Payne and Spillane found that myelopathy was more likely to occur in persons with
congenitally small spinal canals who subsequently develop spondylosis. (17)
Hayashi et al report that in the cervical region, dynamic canal stenosis occurs most
commonly in the upper disc levels of C3/C4 and C4/C5. (18)
2. Nerve root compression. Compromise of the nerve roots may develop
following disc protrusion or osteophytosis. Symptoms are related to the nerve root(s)
involved. (19)
3. Local irritation. This includes irritation of mechanoreceptive and
nociceptive fibers within the intervertebral motion segments. MacNab reports that arm pain
may occur without evidence of root compression. The pain is attributed to cervical disc
degeneration associated with segmental instability. (19)
4. Vertebral artery compromise. MacNab advises that osteophytes may cause
vertebral artery compression. (19)
Furthermore, Smirnov studied 145 patients with pathology of the cervical spine and
cerebral symptoms. 59% had vertebrobasilar circulatory disorders. (20)
5. Autonomic dysfunction. Symptoms associated with the autonomic nervous
system have been reported. The Barre'-Lieou syndrome includes blurred vision, tinnitus,
vertigo, temporary deafness, and shoulder pain. This phenomenon occurs following some
cervical injuries, and is also known as the posterior cervical syndrome. (21)
Stimulation of sympathetic nerves has been implicated in the pathogenesis of this
syndrome. (22)
Another manifestation of autonomic involvement, reflex sympathetic dystrophy, results
in shoulder and arm pain accompanied by trophic changes. (23)
References
1. Flesia J: "Renaissance -- A Psychoepistemological Basis for the New Renaissance
Intellectual." Renaissance International, Colorado Springs, CO, 1982.
2. Lestini WF, Wiesel SW: "The pathogenesis of cervical spondylosis." Clin
Orthop (1989 Feb) 238:69.
3. Key CA: "On paraplegia depending on the ligaments of the spine." Guy's
Hosp Rep (1838) 3:17.
4. Bailey P, Casamajor L: "Osteoarthritis of the spine as a cause of compression
of the spinal cord and its roots." J Nerv Ment Dis (1911) 38:588.
5. Elliott GR: "A contribution to spinal osteoarthritis involving the cervical
region." J Bone Joint Surg (1926) 8:42.
6. Resnick D, Niwayama G: "Diagnosis of Bone and Joint Disorders, Volume 3."
WB Saunders Co., Philadelphia, PA, 1988.
7. O'Connell JE: "Involvement of the spinal cord by intervertebral disc
protrusions." Br J Surg (1955) 43:225.
8. Miller J, Schmatz B, Schultz A: "Lumbar disc degeneration: Correlation with
age, sex, and spine level in 600 autopsy specimens." Spine (1988) 13:173.
9. Farfan HF, Cossette JW, Robertson GH, Wells RV: "The effects of torsion on the
lumbar intervertebral joints: The role of torsion in the production of disc
degeneration." J Bone Joint Surg (Am) (1970) 52A(3):468.
10. Kent C, Holt F, Gentempo P: "Subluxation degeneration in the lumbar spine:
Plain film and MR imaging considerations." ICA Review (Jan/Feb 1991) 47(1):55.
11. Hadley LA: "Anatomico-Roentgenographic Studies of the Spine." Charles C.
Thomas, Springfield, IL. 1981. Chapters IV and IX.
12. MacNab I: "The traction spur: An indicator of segmental instability." J
Bone Joint Surg (1971) 53A:663.
13. Pesch HJ, Bischoff W, Becker T, Seibold H: "On the pathogenesis of spondylosis
deformans and arthrosis uncovertebralis: comparative form- analytical radiological and
statistical studies on lumbar and cervical vertebral bodies." Arch Orthop Trauma
Sur (1984) 103(3):201.
14. Taylor AR: "Mechanism and treatment of spinal cord disorders associated with
cervical spondylosis." Lancet (1953) 1:717.
15. Mair WG, Druckman R: "The pathology of spinal cord lesions and their relations
to the clinical features in protrusion of cervical intervertebral discs." Brain
(1953) 76:70.
16. Maiuri F, Gangemi M, Gambardella A, Simari R, D'Andrea F: "Hypertrophy of the
ligamenta flava of the cervical spine. Clinico- radiological correlations." J
Neurosurg Sci (1985) 29(2):89.
17. Payne EE, Spillane JD: "The cervical spine. An anatomico- pathological study
of 70 specimens (using a special technique) with particular reference to the problem of
cervical spondylosis." Brain (1957) 80:571.
18. Hayashi H, Okada K, Ueno R: "Etiologic factors of cervical spondylitic
myelopathy in aged patients -- clinical and radiological studies." Nippon
Seikeigeka Gakkai Zasshi (1987) 61(10):1015. (Published in Japanese--English
abstract).
19. MacNab I: "Cervical spondylosis." Clin Orthop (1975) 109:69.
20. Smirnov VA: "The clinical picture and pathogenesis of cerebral symptomatology
in diseases of the cervical region of the spine." Zh Nervopatol Psikhiatr
(1976) 76(4):523. Published in Russian -- English abstract).
21. Barre' JA: "Sur un syndrome sympathique cervical posterieur et sa cause
frequente, 1, artrite cervicale." Rev Neurol (Paris) (1926) 1:1246. Published
in French.
22. Watanuki A: "The effect of the sympathetic nervous system on cervical
spondylosis." Nippon Seikeigeka Gakkai Zasshi (1981) 55(4):371. Author's
translation.
23. Wainapel SF: "Reflex sympathetic dystrophy following traumatic myelopathy. Pain
(1984) 18:345.
(Dr. Christopher Kent, president of the Council on Chiropractic Practice, is a 1973
graduate of Palmer College of Chiropractic. Named "Chiropractic Researcher of the
Year" in 1991 by the ICA and in 1994 by the WCA, Dr. Kent is director of research for
EMG Consultants, Inc., and co-founder of Paradigm Partners, Inc. With Dr. Patrick
Gentempo, Jr., Dr. Kent produces a monthly audio tape journal, "On Purpose,"
covering current events in science, philosophy, and politics of vital interest to the
practicing chiropractor. For subscription information call 1-800-892-6463.)