Journal of Vertebral Subluxation Research 1996; 1 (1): 1-6 ~ FULL TEXT
By Christopher Kent, D.C.
Thanks to Matthew McCoy DC, MPH for permission to reproduce this Full-Text article, exclusively on Chiro.Org!
Basic science and clinical models of the vertebral subluxation are reviewed. Neurobiological
mechanisms associated with these models are described. Models reviewed include the subluxation complex
model, subluxation degeneration, nerve compression, dysafferentation, the neurodystrophic model
and segmental facilitation. Clinical models, including the segmental, postural, and tonal approaches are
Key words: Vertebral Subluxation, Models of Vertebral Subluxation, Subluxation Complex, Subluxation
Degeneration, Nerve Compression, Dysafferentation, Segmental Facilitation.
The FULL TEXT Article
The term “subluxation” has a long history in the healing arts
literature. According to Haldeman  it was used at the time of
Hippocrates,  while the earliest English definition is attributed
to Randall Holme in 1688. Holme  defined subluxation as “a
dislocation or putting out of joynt.”Watkins  and Terrett  refer to
a 1746 definition of the term. The matter is further complicated
by the diverse array of alternative terms used to describe subluxations.
Rome  listed 296 variations and synonyms used by
medical, chiropractic, and other professions. Rome concluded
the abstract of his paper by stating, “It is suggested that, with so
many attempts to establish a term for such a clinical and biological
finding, an entity of some significance must exist.”
The possible neurological consequences of subluxation were
described by Harrison in 1821, as quoted by Terrett :
“When any of the vertebrae become displaced or too prominent, the patient experiences inconvenience from a local derangement in the nerves of the part. He, in consequence, is tormented with a train of nervous symptoms, which are as obscure in their origin as they are stubborn in their nature...”
Although medical authorities
acknowledge that neurological complications may result
from subluxation,  classical chiropractic definitions mandate the
presence of a neurological component. D. D. Palmer and B. J.
Palmer  defined subluxation as follows: “A (sub)luxation of a
joint, to a Chiropractor, means pressure on nerves, abnormal
functions creating a lesion in some portion of the body, either in
its action, or makeup.” According to Stephenson’s 1927 text,  the
following must occur for the term “vertebral subluxation” to be
Loss of juxtaposition of a vertebra with the one above, the one below, or both.
Occlusion of an opening.
Interference with the transmission of mental impulses.
As Lantz  noted, “Common to all concepts of subluxation
are some form of kinesiologic dysfunction and some form of
Component Models of Subluxation
Dishman11 and Lantz [12–13] developed and popularized the five
component model of the “vertebral subluxation complex”
attributed to Faye.  However, the model was presented in a text
by Flesia1  dated 1982, while the Faye notes bear a 1983 date.
The original model has five components:
The “vertebral subluxation complex” model includes tissue
specific manifestations described by Herfert  which include:
Connective tissue involvement, including disc, other ligaments,
fascia, and muscles
The neurological component, including nerve roots and spinal cord
Advancing complications in the innervated tissues and/or the patient’s symptoms.
This is sometimes termed the “end
tissue phenomenon” of the vertebral subluxation complex.
Lantz [10,16] has since revised and expanded the “vertebral subluxation
complex” model to include nine components:
Connective tissue physiology
Lantz  summarized his objectives in expanding the model:
“The VSC allows for every aspect of chiropractic clinical management to be integrated into a single conceptual model, a sort
of ‘unified field theory’ of chiropractic... Each component can, in turn, be described in terms of precise details of anatomic, physiologic,
and biochemical alterations inherent in subluxation degeneration and parallel changes involved in normalization of structure and function through adjustive procedures.”
this model will realize these objectives remains to be seen.
Subluxation Degeneration Model
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.  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.
 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. Bailey and Casamajor 
reported that cord compression could result from spinal
osteoarthritis. They suggested that disc thinning was the basic
pathology underlying degenerative change. As early as 1926,
Elliott  gave an account of how radicular symptoms could be
caused by foraminal stenosis secondary to arthritic changes.
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.
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.
In the lumbar spine, pathomechanics and torsional stress have
been implicated as etiological factors in spinal degeneration. [22–23]
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.  For example,
Lestini and Weisel  report that there is a high statistical correlation
between disc degeneration and posterior osteophyte formation.
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.  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. This is similar to MacNab’s description of
traction spur formation in the lumbar spine. 
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
Neurological Consequences of Spinal Degeneration
Neurological manifestations of spinal degeneration may be
due to a variety of mechanisms.These include:
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. [21, 28–30] Payne and Spillane  found
that myelopathy was more likely to occur in persons with
congenitally small spinal canals who subsequently develop
spondylosis. 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.
Nerve root compression. Compromise of the nerve roots may develop following disc protrusion or osteophytosis. 
Symptoms are related to the nerve root(s) involved.
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
Vertebral artery compromise. MacNab  advises that osteophytes may cause vertebral artery compression.
Furthermore, Smirnov  studied 145 patients with pathology
of the cervical spine and cerebral symptoms. Fifty nine
percent had vertebrobasilar circulatory disorders.
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.  Stimulation of sympathetic
nerves has been implicated in the pathogenesis of
this syndrome.  Another manifestation of autonomic
involvement, reflex sympathetic dystrophy, results in shoulder
and arm pain accompanied by trophic changes. 
Nerve Root Compression Model
Compression of spinal nerves has traditionally been proposed
as a mechanism associated with spinal subluxation,  although
attempts have been made to discredit the premise that subluxations
cause nerve interference by mechanical compression. 
Results of early animal studies of nerve compression reported
that pressures ranging from 130 mm Hg to over 1000 mm Hg
were required to produce a significant compression block. [40–42]
However, these older studies dealt with peripheral nerves, not
Sunderland and Bradley  reported that spinal roots may be
more susceptible to mechanical effects because of their lack of
the perineurium and funicular plexus formations present in
peripheral nerves. However, few experimental studies involving
compression of nerve roots were reported in the literature. 
Those which were reported were criticized. 
In 1975, Sharpless  reported the results of a series of animal
experiments to determine the susceptibility of spinal roots to
compression block. These investigations were supported by the
ICA and the ACA. The results were published in a monograph
by the National Institutes of Health. Sharpless described his
results as “astonishing” and “spectacular.” According to the
“A pressure of only 10 mm Hg produced a significant conduction block, the potential falling to 60% of its initial value
in 15 minutes, and to half of its initial value in 30 minutes. After such a small compressive force is removed, nearly complete
recovery occurs in 15 to 30 minutes. With higher levels of pressure, we have observed incomplete recovery after many hours of
Korr  listed factors which render nerve roots more
vulnerable to mechanical effects than peripheral nerves:
Their location within the intervertebral foramen is in itself
a great hazard.
Spinal roots lack the protection of epineurium and perineurium.
Since each root is dependent on a single radicular artery
entering via the foramen, the margin of safety provided by
collateral pathways is minimal.
Venous congestion may be more common in the roots
because the radicular veins would probably be immediately
compressed by any reduction in foraminal diameter.
There is also the possibility of reflux from the segmental
veins through pressure damaged valves; and venous congestion
would have additional consequences because the
swelling, being within the foramen, would contribute to
compression of the other intraforaminal structures.
Circulation to the dorsal root ganglion is especially vulnerable.
Contemporary papers have been published concerning nerve
root compression. In 1995, Konno et al.  reported results similar
to those of Sharpless, noting that compression of the nerve
roots of the cauda equina with as little as 10 mm Hg of pressure
resulted in decreased action potentials. Rydevik  described
other adverse effects of nerve root compression:
“Venous blood flow to spinal roots was blocked with 5–10 mm Hg of pressure. The resultant retrograde venous stasis due to venous congestion is suggested as a significant cause of nerve root compression. Impairment of nutrient flow to spinal nerves is present with
similar low pressure.”
Hause  observed that compressed nerve
roots can exist without causing pain. Also described in the paper
was a proposed mechanism of progression, where mechanical
changes lead to circulatory changes, and inflammatogenic agents
may result in chemical radiculitis. This may be followed by disturbed
CSF flow, defective fibrinolysis and resulting cellular
changes. The influence of the sympathetic system may result in
synaptic sensitization of the CNS and peripheral nerves, creating
a “vicious circle” resulting in radicular pain.
Kuslich, Ulstrom, and Michael  discussed the importance of
mechanical compromise of nerve roots in the production of
radicular symptoms. Their human surgical studies revealed that
“Stimulation of compressed or stretched nerve roots consistently produced the same sciatic distribution of pain as the patient
experienced preoperatively...we were never able to reproduce a patient’s sciatica except by finding and stimulating a stretched, compressed, or swollen nerve root.”
The importance of asymptomatic
lesions was reported by Wilberger and Pang  who followed
108 asymptomatic patients with evidence of herniated
discs. They reported that within three years, 64% of these
patients developed symptoms of lumbosacral radiculopathy.
Schlegal et al.,  Kirkaldy-Willis  and Manelfe  noted that subluxation
of the facet joints may be associated with nerve root
entrapment and spinal stenosis, particularly when degenerative
disease is present. The degenerative changes are described as a
progressive “cascade.” Nerve root compression is one of many
mechanisms of neural disruption which may be associated with
vertebral subluxation. While some may criticize the “garden
hose” model as being overly simplistic, the nerve root compression
hypothesis is far from obsolete.
The neurological dysfunction associated with the vertebral
subluxation may take other forms. The intervertebral motion
segment is richly endowed by nociceptive and mechanoreceptive
structures. As a consequence, biomechanical dysfunction
may result in an alteration in normal nociception and/or
mechanoreception. Aberrated afferent input to the CNS may
lead to dysponesis. To use the contemporary jargon of the computer
industry, “garbage in—garbage out.” Appreciation of these
processes begins with an understanding of the neuroanatomy of
the tissues of the intervertebral motion segment.
Several papers have described the innervation of human cervical
and lumbar intervertebral discs. Bogduk et al.  observed
that the lumbar intervertebral discs are supplied by a variety of
nerves. According to Bogduk, the sinuvertebral nerve supplies
the posterior aspect of the disc and the posterior longitudinal
ligament. The posterolateral aspects are innervated by adjacent
ventral primary rami and from the grey rami communicantes.
The lateral aspects of the disc are innervated by the rami communicantes.
The anterior longitudinal ligament is innervated by
recurrent branches of rami communicantes. Clinically, Bogduk 
stated that intervertebral discs can be a source of pain without
rupture or herniation. Torsional stress may result in circumferential
tears in the innervated outer third of the annulus.
Compression injuries may lead to internal disruption of the disc,
resulting in mechanical or chemical stimulation of the nerve
endings in the annulus.
Nakamura et al.  reported that the anterior portion of lumbar
intervertebral discs is innervated by sympathetic fibres alone.
Sympathetic afferents return through the sympathetic trunks
and the rami communicantes and pass through the same dorsal
horn as the somatosensory afferents. The posterior portion of
the disc is innervated by sinuvertebral nerves derived from the
recurrent branch of the spinal nerve, or both the recurrent spinal
nerve and sympathetic nerve. These authors observed that dual
innervation exists in the intervertebral discs of the lumbar
region, and that no other organs are known to have such dual
Bogduk et al.  examined the nerve supply to the cervical
intervertebral discs. The sinuvertebral nerves were found to supply
the disc at their level of entry as well as the disc above. Nerve
fibers were found as deeply as the outer third of the annulus.
Mendel  et al. stated that nerves were seen throughout the
annulus. In addition, receptors resembling Pacinian corpuscles
and Golgi tendon organs were seen in the posterolateral region
of the disc. The authors conclude that human cervical intervertebral
discs are supplied with both nerve fibers and mechanoreceptors.
Human cervical facet joints are also equipped with
mechanoreceptors. McLain  found Type I,Type II, and Type III
mechanoreceptors, as well as unencapsulated nerve endings in
the cervical facet joints of normal subjects. The author stated,
“The presence of mechanoreceptive and nociceptive nerve endings in cervical facet capsules proves that these tissues are monitored by the central nervous system and implies that neural input from the facets is important to proprioception and pain sensation in the cervical spine. Previous studies have suggested that protection muscular reflexes modulated by these types of mechanoreceptors are important in preventing joint instability and degeneration.”
Wyke [61–62] has described articular mechanoreceptors,
and explored the clinical implications of dysafferentation
in pain perception.
Besides the discs and articular capsules, mechanoreceptors
and other neural tissues have been described in the ligaments
attached to the spine. Jiang et al.  noted that Pacinian corpuscles
were scattered randomly, close to blood vessels, whereas
Ruffini corpuscles were seen in the periphery of human
supraspinal and interspinal ligaments. Rhalmi et al.  found
nerve fibers in the ligamentum flavum, the supraspinal ligament,
and the lumbodorsal fascia.
Alterations in mechanoreceptor function may affect postural
tone. Murphy  summarized the neurological pathways associated
with the maintenance of background postural tone:
“Weight bearing disc and mechanoreceptor functional integrity regulates and drives background postural neurologic information and function (muscular) through the unconscious mechanoreception anterior and posterior spinocerebellar tract, cerebellum, vestibular nuclei, descending medial longitudinal fusciculus (medial and lateral vestibulospinal tracts), regulatory anterior horn cell pathway.”
The anterior horn cells provide motor output
which travels via motor nerves to muscle fibres.
Although stimulation of articular mechanoreceptors may
exert an analgesic effect, use of manipulation for the episodic,
symptomatic treatment of pain is not chiropractic. The authors
of the remarkable book Segmental Neuropathy,  published in
the 1960’s by Canadian Memorial Chiropractic College, proposed
the concept of a “neural image,” dependent upon the
integrity of neural receptors and afferent pathways. If afferent
input is compromised, efferent response may be qualitatively and
quantitatively compromised. Correcting the specific vertebral
subluxation cause is paramount to restoring normal afferent
input to the CNS, and allowing the body to correctly perceive
itself and its environment.
The “neurodystrophic” model suggests that neural dysfunction
is stressful to body tissues and that “lowered tissue resistance”
can modulate specific and nonspecific immune responses
and may alter the trophic function of the involved nerves. A
growing number of investigators are exploring the common
denominators in disease processes, and the role of the nervous,
immune, and endocrine systems in pathogenesis. 
Korr  proposed that spinal “lesions” (analogous to the vertebral
subluxation) are associated with exaggerated sympathetic
activity as well as exaggerated paraspinal muscle tone. It is interesting
that Korr, like D.D. Palmer, employed the term “tone” in
reference to ambient nervous system activity. According to Korr,
“High sympathetic tone may alter organ and tissue responses to
hormones, infectious agents, and blood components.” The
mechanism postulated by Korr was one of segmental facilitation.
Decreased thresholds in efferent neurons arising from the anterior
and lateral horn cells are postulated to result in increased
impulse traffic to the somatic and visceral structures innervated
by the affected neurons.
More recently, other authors have explored the relationship
of sympathetic activity to immune system function in greater
depth. Murray et al.  examined the effect of sympathetic stimulation
on the immune system. Sympathetic stimulation was
induced in human volunteers by exhaustive exercise. They found
that acute sympathetic stimulation leads to selective release of
immunoregulatory cells into the circulation, with subsequent
alterations in cellular immune function. These authors stated,
“Growing evidence suggests that immune function is regulated in part by the sympathetic nervous system. Sympathetic nerve
endings densely innervate lymphoid tissue such as the spleen, lymph nodes and thymus, and lymphoid cells have beta 2 adregenergic receptors.”
In their experiments, there was a sharp
rise in T suppressor/cytotoxic cells and natural killer cells following
sympathetic stimulation. However, only modest rises
were seen in T helper and B cells. The cells most affected, the T
suppressor/cytotoxic cells and the natural killer cells, are those
with the largest density of beta receptors.
Felten et al.  reported that the neurotransmitter norepinephrine
is present in postganglionic sympathetic fibers which innervate
lymphoid organs and act on the spleen. Furthermore, there
are available receptors on cells in the white pulp and the localized
neurotransmitter terminal which directly contact T lymphocytes
in the periarticular lymphatic sheath. The authors propose that
norepinephrine in lymphoid organs fulfills the criteria for neurotransmission,
and plays a significant role in the modulation of
immune responses. They state,
“Stressful conditions lead to altered measures of immune function, and altered susceptibility to a variety of diseases. Many stimuli, which primarily act on the central nervous system, can profoundly alter immune responses. The two routes available to the central nervous system for communication with peripheral organs are neuroendocrine channels and autonomic nerve channels.”
In a more recent paper, Felten’s team 
reviewed aspects of neural-immune signaling. Noradrenergic and
peptidergic nerve fibers abundantly innervate the parenchyma of
both primary (bone marrow) and secondary (spleen, lymph
nodes) lymphoid organs. Nerve fibers distribute within the
parenchyma of these organs, as well as along smooth muscle compartments.
Both noradrenaline and peptides such as substance P
have been shown to fulfill the basic criteria for neurotransmission
with lymphocytes, macrophages, and other immunocytes as targets.
Denervation or pharmacological manipulation of these neurotransmitters
can profoundly alter immunological reactivity at
the individual cellular level, at the level of complex multicellular
interactions (such as antibody response), and at the level of host
responses to a disease-producing challenge.”
The relationship between the nervous system and the
immune system has attracted the attention of the popular press.
An article in the New York Times  stated,
“Scientists have found the first evidence of an anatomical connection between the nervous system and the immune system. Nerve cell endings in the skin and white blood cells of the immune system are in intimate contact, and chemicals secreted by the nerves can shut down
immune system cells nearby.”
The New York Times author was
describing the findings of a paper written by Hossi et al. 
Inflammatory disease is influenced by the nervous system.
Undem  noted that nerve stimulation can affect the growth and
function of inflammatory cells. Sternberg et al.  stated, “The
central nervous system may coordinate both behavioral and
immunologic adaptation during stressful situations. The pathophysiologic
perturbation of this feedback loop, through various
mechanisms, results in the development of inflammatory syndromes,
such as rheumatoid arthritis, and behavioral syndromes,
such as depression. Thus, diseases characterized by both inflammatory
and emotional disturbances may derive from common
alteration in specific central nervous system pathways.
Fricchoine and Stefano  also reviewed what they termed the
“neuroendocrine-neuroimmune stress response system.” 
Central nervous system influences on lymphocyte migration
was addressed by Ottaway and Husband.  These authors suggested
“Many of the alterations in immunity resulting from CNS activity may be explained in terms of changes in lymphocyte
migration patterns in response to endocrine signals, neural signals via neurotransmitter release, or direct contacts between nerves and cells of the immune system.”
Weihe and Krekel 
“peptides, being present in small-diameter nerve fibers, could exert an indirect immunoregulatory role by influencing
vascular tone and/or permeability.”
A very interesting hypothesis proposed by Grossman et al. 
is that cells can learn to associate responsiveness to antigens and
other immunoactive agents, with responsiveness to signals originating
in the CNS delivered via neuroendocrine or autonomic
nervous channels. They propose storage (memory) of stimuli in
the immune system rather than in the brain. Just what does this
mean to the chiropractor? Can spinal adjustments alter immune
system activity? Brennan et al.  found that when a thoracic
“manipulation” was applied, the response of polymorphonuclear
neutrophils isolated from blood collected 15 minutes after the
manipulation was significantly higher than blood collected 15
minutes before and 30 and 45 minutes after manipulation. A
slight, but significant rise in substance P was also observed.
What are the clinical implications of the nervous system—immune system link? A small controlled study of HIV positive
patients was conducted by Selano et al.  The effects of specific
upper cervical adjustments on the immune system CD4 cell
counts of HIV positive individuals was studied. Half the patients
received atlas adjustments based upon Grostic upper cervical
analysis. The other half received a placebo in the form of an
inactive adjusting instrument applied to the mastoid bone. Over
the six month period of the study, the control group experienced
a 7.96% decrease in CD4 cell counts, while the adjusted
group experienced a 48% increase in CD4 cell counts over the
Contemporary research is beginning to shed light
on the neurobiological mechanisms which may explain the outstanding
clinical results chiropractors have experienced when
managing patients with infectious diseases. The popular press has
been filled with stories describing the emergence of antibiotic
resistant pathogens, and the futility of the long term strategy of
developing new, stronger antibiotics. [82–83] As author Geoffrey
“Drug resistant microbes don’t threaten us all equally. A healthy immune system easily repels most bacterial
invaders, regardless of their susceptibility to drugs.” 
Maintaining a healthy immune system depends upon maintaining
a healthy nervous system.
It is obvious that these neurobiological models are not mutually
exclusive, and that any or all may be operative in a given
patient. Clinical practice requires that theoretical models of
nerve dysfunction be operationalized. This process has resulted
in the development of clinical operational models. Selection of
outcomes assessments is dependent upon the nature of the
model employed by the practitioner.
Cooperstein  described two broad approaches to chiropractic technique, the segmental approach and the postural approach. Murphy  added a third, the tonal approach. These conceptual models determine the nature of the analytical procedures employed, the type of adjustments applied, and the criteria for determining the success or failure of a given intervention.
A summary of each follows:
The segmental model. Subluxation is described in terms of
alterations in specific intervertebral motion segments. In
segmental approaches, the involved motion segments may
be identified by radiographic procedures which assess intersegmental
disrelationships, or by clinical examination procedures
such as motion palpation. Examples of segmental
approaches are the Gonstead  and Diversified techniques. 
Postural approaches. In postural approaches, subluxation is
seen as a postural distortion. Practitioners of postural
approaches assess “global” subluxations using postural
analysis and radiographic techniques which evaluate spinal
curves and their relationship to the spine as a whole.
Examples of techniques emphasizing a postural approach
are Pettibon Spinal Biomechanics  and Applied Spinal
Tonal approaches. In 1910, D. D. Palmer  wrote, “Life is an
expression of tone. Tone is the normal degree of nerve tension.
Tone is expressed in function by normal elasticity,
strength, and excitability... the cause of disease is any variation
in tone.” Tonal approaches tend to view the spine and
nervous system as a functional unit. Tonal approaches
emphasize the importance of functional outcomes, and
acknowledge that clinical objectives may be achieved using
a variety of adjusting methods. Examples of tonal
approaches include Network Spinal Analysis [92–93] and
Torque-release Technique. 
In reviewing the preceeding basic science and clinical models
of the subluxation, it may be seen that the wide diversity of
techniques in chiropractic may use different methods, but generally
share the common objective of correcting spinal nerve
interference caused by vertebral subluxation. Commonality and
accountabiliy may be achieved through the development of
models which emphasize clinical outcomes, yet afford the practitioner
flexibility in determing how those objectives are
achieved. Such outcomes include, but are not limited to, evidence
of functional integrity of the nervous system, and
improvement in general health and quality of life indicators.
Research resources should be directed toward the development
of models and clinical strategies which result in more predictable
and more efficient practice procedures.
Address reprint requests to:
Christopher Kent, D.C., 714 Broadway Paterson, NJ 07514 (201) 523-1397
1. Haldeman S. The pathophysiology of the the spinal subluxation. In:
Goldstein M, ed. The Research Status of Spinal Manipulative Therapy.
Bethesda, MD: DHEW publication no. (NIH) 76-998, 1975
2. Adams F (trans). The Genuine Works of Hippocrates.Volume 2. London:
Sydenham Society, 1849
3. Holme R.Academy of Armory. Menston, England: Published by the author
in 1688. Reprinted by The Scholar Press, Ltd., 1972
4.Watkins RJ. Subluxation terminology since 1746.
J Can Chiro Assoc 1968;
5.Terrett AJC.The search for the subluxation: an investigation of medical literature
Chiro History 1987; 7:29
6. Rome PL. Usage of chiropractic terminology in the literature: 296 ways to
say “subluxation”: complex issues of the vertebral subluxation.
Technique 1996; 8(2):49
7. Evans DK. Anterior cervical subluxation.
J Bone Joint Surg (Br) 1976;
8. Palmer DD, Palmer BJ. The Science of Chiropractic. Davenport, IA: The
Palmer School of Chiropractic, 1906
9. Stephenson RW. Chiropractic Text-book. Davenport, IA: Palmer School of
10. Lantz CA. The subluxation complex. In: Gatterman MI,ed. Foundations of
Chiropractic Subluxation. St. Louis, MO: Mosby, 1995
11. Dishman R.Review of the literature supporting a scientific basis for the chiropractic
J Manipulative Physiol Ther 1985; 8(3):163
12. Lantz CA. The vertebral subluxation complex part 1: introduction to the
model and the kinesiological component.
Chiropractic Research Journal
13. Lantz CA.The vertebral subluxation complex part 2: neuropathological and
Chiropractic Research Journal 1990; 1(4):19
14. Flesia J. Renaissance:A Psychoepistemological Basis for the New Renaissance
Intellectual. Renaissance International, Colorado Springs, CO, 1982
15. Herfert R. Communicating the Vertebral Subluxation Complex, Herfert
Chiropractic Clinics, East Detroit, MI, 1986
16. Lestini WF,Wiesel SW.The pathogenesis of cervical spondylosis. Clin Orthop
1989; Feb. 238:69
17. Key CA. On paraplegia depending on the ligaments of the spine.
Rep 1838; 3:17
18. 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
19. Elliott GR. A contribution to spinal osteoarthritis involving the cervical
J Bone Joint Surg 1926; 8:42
20. Resnick D, Niwayama G. Diagnosis of Bone and Joint Disorders, Volume 3.
Philadelphia, PA:WB Saunders Co., 1988
21. O’Connell JE. Involvement of the spinal cord by intervertebral disc protrusions.
Br J Surg 1955; 43:225
22. Miller J, Schmatz B, Schultz A. Lumbar disc degeneration: Correlation with
age, sex, and spine level in 600 autopsy specimens.
Spine 1988; 13:173
23. 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
J Bone Joint Surg (Am) 1970; 52A(3):468
24. Kent C, Holt F, Gentempo P. Subluxation degeneration in the lumbar spine:
Plain film and MR imaging considerations.
ICA Review 1991; 47(1):55
25. Hadley LA.Anatomico-Roentgenographic Studies of the Spine. Chapters IV
and IX. Springfield, IL: Charles C.Thomas, 1981
26. MacNab I. The traction spur: An indicator of segmental instability.
Joint Surg 1971; 53A:663
27. 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
28.Taylor AR. Mechanism and treatment of spinal cord disorders associated
with cervical spondylosis.
Lancet 1953; 1:717
29. 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
30. 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
31. 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
32. Hayashi H, Okada K, Ueno R. (Etiologic factors of cervical spondylotic
myelopathy in aged patients—clinical and radiological studies).
Seikeigeka Gakkai Zasshi 1987; 61(10):1015. (Published in Japanese—
33. MacNab I. Cervical spondylosis. Clin Orthop 1975; 109:69
34. 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)
35. Barre’ JA. Sur un syndrome sympathique cervical posterieur et sa cause frequente,
1, artrite cervicale.
Rev Neurol (Paris) 1926; 1:1246. Published in
36.Watanuki A. (The effect of the sympathetic nervous system on cervical
spondylosis). Nippon Seikeigeka Gakkai Zasshi 1981; 55(4):371. Author’s
37.Wainapel SF. Reflex sympathetic dystrophy following traumatic myelopathy.
Pain 1984; 18:345
38. Palmer BJ. Chiropractic Proofs. Davenport, IA, 1903. Reproduced in
Peterson D,Wiese G, eds. Chiropractic:An Illustrated History. St. Louis,MO:
39. Crelin ES.A scientific test of the chiropractic theory.
Am Sci 1973; 61(5):574
40. Meek WJ, Leaper WE.The effect of pressure on conductivity of nerve and
Amer J Physiol 1911; 27:308
41. Bentley FH, Schlapp W.The effects of pressure on conduction in peripheral
J Physiol 1943; 102:72
42. Causey G, Palmer E.The effect of pressure on nerve conduction and nerve
J Physiol 1949; 109:220
43. Sunderland S, Bradley L. Stress-strain phenomena in human spinal roots.
Brain 1961; 84:121
44. Gelfan S, Tarlov IM. Physiology of spinal cord, nerve root and peripheral
Amer J Physiol 1956; 185:217
45. Sharpless SK. Susceptibility of spinal roots to compression block. In:
Goldstein M, ed. The Research Status of Spinal Manipulative Therapy.
Bethesda, MD: DHEW publication (NIH) 76-998, 1975
46.Korr IM. Discussion. In: Goldstein M, ed. The Research Status of Spinal
Manipulative Therapy. Bethesda,MD:DHEW publication (NIH) 76-998, 1975
47. Konno S, Olmarker K, Byrod G et al. Intermittent cauda equina compression.
Spine 1995; 20(1):1223
48. Rydevik BL.The effects of compression on the physiology of nerve roots.
Manipulative Physiol Ther 1992; 15(1):62
49. Hause M. Pain and the nerve root.
Spine 1993; 18(14):2053
50. Kuslich S, Ulstrom C, Michael C.The tissue origin of low back pain and sciatica:
a report of pain response to tissue stimulation during operations on the
Ortho Clinics of North America 1991; 22(2):181
51.Wilberger JE Jr, Pang D. Syndrome of the incidental herniated lumbar disc.
J Neurosurg 1983; 59(1):137
52. Schlegel JD, Champine J,Tayler MS et al.The role of distraction in improving
the space available in the lumbar stenotic canal and foramen.
53. Kirkaldy-Willis WH.The relationship of structural pathology to the nerve
Spine 1984; 9(1):49
54. Manelfe C. Imaging of the Spine and Spinal Cord. New York, NY: Raven
55. Bogduk N, Tynan W,Wilson AS. The nerve supply to the human lumbar
J Anat 1981; 132(Pt 1):39
56. Bogduk N. Pathology of lumbar disc pain.
Manual Medicine 1990; 5(2):72
57. Kakamura S,Takahashi K,Takahashi Y, et al. Origin of nerves supplying the
posterior portion of lumbar intervertebral discs.
Spine 1996; 21(8):917
58. Bogduk N,Winsor M, Inglis A.The innervation of the cervical intervertebral
Spine 1988; 13(1):2
59. Mendel T,Wink CS, Zimny ML. Neural elements in human cervical intervertebral
Spine 1992; 17(2):132
60. McLain RF. Mechanoreceptor endings in human cervical facet joints.
61.Wyke B.The neurology of joints.
Ann R Coll Surg (Br) 1967;:25
62.Wyke B. Neurology of the cervical spinal joints.
Physiother 1979; 65:72
63. Jiang H, Russell G, Raso VJ et al.The nature and distribution of the innervation
of human supraspinal and interspinal ligaments.
Spine 1995; 20(8):869
64. Rhalmi S,Yahia LH, Newman N, Isler M. Immunohistochemical study of
nerves in lumbar spine ligaments.
Spine 1993; 18(2):264
65. Murphy DJ. Neurogenic posture.
Am J of Clinical Chiropractic 1995; 5(1):16
66. Segmental Neuropathy. Canadian Memorial Chiropractic College.Toronto,
Ontario. No date
67. Leach RA.The Chiropractic Theories. St. Louis, MO:Williams and Wilkins,
68. Korr IM. Andrew Taylor Still memorial lecture: research and practice—a
J Am Osteopath Assoc 1974; 73:362
69. Murray DR, Irwin M, Reardon CA, et al. Sympathetic and immune interactions
during dynamic exercise. Mediation via a beta 2 -andrenergic-dependent
Circulation 1992; 86(1):203
70. Felten DL, Felten SY, Bellinger DL, et al. Norandrenergic sympathetic neural
interactions with the immune system: structure and function.
Rev 1987; 100:225
71. Felten DL, Felten SY, Bellinger DL, Madden KS. Fundamental aspects of
Psychother Psychosom 1993; 60(1):46
72. Kolata G. Nerve cells tied to immune system. New York Times.May 13, 1993
73. Hosoi J, Murphy GF, Egan CL et al. Regulation of Langerhans cell function
by nerves containing calcination gene-related peptide.
74. Undem BJ. Neural-immunologic interactions in asthma.
Hosp Pract (Off
Ed) 1994; 29(2):59
75. Sternberg EM, Chrousos GP,Wilder RL, Gold PW.The stress response and
the regulation of inflammatory disease.
Ann Intern Med 1992; 117(10):854
76. Fricchoine GL, Stefano GB.The stress response and autoimmunoregulation.
Adv Neuroimmunol 1994; 4(1):13
77.Ottaway CA, Husband AJ. Central nervous system influences on lymphocyte
Brain Behav Immun 1992; 6(2):97
78.Weihe E, Krekel J. The neuroimmune connection in human tonsils.
Behav Immun 1991; 5(1):41
79. Grossman Z, Heberman RB, Livnat S. Neural modulation of immunity: conditioning
phenomena and the adaptability of lymphoid cells.
Int J Neurosci
80. Brennan PC,Triano JJ, McGregor M, et al. Enhanced neutrophil respiratory
burst as a biological marker for manipulation forces: duration of the effect
and association with substance P and tumor necrosis factor.
Physiol Ther 1992; 15(2):83
81. Selano JL, Hightower BC, Pfleger B, et al.The effects of specific upper cervical
adjustments on the CD4 counts of HIV positive patients.
Research Journal 1994; 3(1):32
82.The end of antibiotics. Newsweek. March 28, 1994
83. Revenge of the killer microbes.Time. September 12, 1994
84. Cowley G.Too much of a good thing. Newsweek. March 28, 1994
85. Cooperstein R. Contemporary approach to understanding chiropractic
technique. In: Lawrence DJ, ed.
Advances in Chiropractic, Volume 2. St.
Louis, MO: Mosby, 1995
86. Murphy D. Seminar notes. 1995
87. Plaugher G ed).Textbook of Clinical Chiropractic:A Specific Biomechanical
Approach. Baltimore, MD:Williams and Wilkins, 1993
88. States AZ. Spinal and Pelvic Techniques. Lombard, IL: National College of
89. Pettibon B. Introduction to Spinal Biomechanics. Tacoma, WA: Pettibon
Spinal Biomechanics Institute, 1989
90. Speiser R, Aragona R, Heffernan J. The application of therapeutic exercises
based upon lateral flexion roentgenography to restore biomechanical function
in the lumbar spine.
Chiropractic Research Journal 1990; 1(4):7
91. Speiser R, Aragona R. Applied spinal bioengineering (ASBE) methodology
utilizing pre- and post- stress loading roentgenographs and biomechanical
physiological rehabilitative spinal exercises.
Proceedings of the International
Conference on Spinal Manipulation. Arlington,VA, 1989
92. Palmer DD.Textbbok of the Art, Science, and Philosophy of Chiropractic.
The Chiropractor’s Adjuster. Portland,OR:Portland Publishing House, 1910
93. Epstein D. The spinal meningeal functional unit: tension and stress adaptation.
Digest of Chiropractic Economics 1986; 29(3):58
94. Epstein D. Network chiropractic explores the meningeal critical. Part 1:
anatomy and physiology of the meningeal functional unit.
Chiropractic Economics 1994; 26(4):78
95. Holder JM,Talsky M.Torque-release Technique. Seminar notes. 1995
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