J Electromyography and Kinesiology 2012 (Oct); 22 (5): 632–642 ~ FULL TEXT
Charles N.R. Henderson
Palmer Center for Chiropractic Research,
FL, United States.
It is reasonable to think that patients responding to spinal manipulation (SM), a mechanically based therapy, would have mechanical derangement of the spine as a critical causal component in the mechanism of their condition. Consequently, SM practitioners routinely assess intervertebral motion, and treat patients on the basis of those assessments. In chiropractic practice, the vertebral subluxation has been the historical raison d'etre for SM. Vertebral subluxation is a biomechanical spine derangement thought to produce clinically significant effects by disturbing neurological function. This paper reviews the putative mechanical features of the subluxation and three theories that form the foundation for much of chiropractic practice. It concludes with discussion of subluxation as an indicator for SM therapy, particularly from the perspective that subluxation may be one contributory cause of ill-health within a "web of causation".
It is reasonable to think that patients responding to spinal
manipulation (SM), a mechanically based therapy, would have
mechanical derangement of the spine as a critical causal component.
Consequently, SM practitioners routinely assess intervertebral
motion, and treat patients on the basis of those assessments
(Abbott et al., 2009; Hengeveld et al., 2005; van Trijffel et al.,
2010; Leach, 2004).
In chiropractic practice, the vertebral subluxation has been the
historical raison d’etre for SM. Vertebral subluxation (or simply
‘‘subluxation’’) is a biomechanical spine derangement thought to
produce clinically significant effects by disturbing neurological
function (Henderson, 2005b; Triano, 2005). Joint misalignment
may be determined by palpation or radiographic examination,
but it is substantially less than that seen with a luxation (dislocation).
This minimal joint misalignment was the first reported characteristic
of subluxation, and hence the origin of the term. Given
the semantic link to the term luxation, it is sometimes confusing
to clinicians that subluxations are mechanically characterized by
hypomobility, rather than the hyper-mobility observed with
luxations. In addition, the biomechanical features characterizing
the subluxation are subtle, lacking the gross mechanical disruption and manifest microanatomical ligamentous and capsular discontinuities that are common to luxation.
Chiropractic perspective is an evolving synthesis of historical
chiropractic thought, clinical observations, and research. In this
paper, I introduce the historical origins of chiropractic, review
putative mechanical features of subluxation as it relates to three
foundational theories of chiropractic practice, and present related
research. I conclude with a discussion of subluxation as an indicator
for spinal manipulation.
2. Biomechanical features of the vertebral subluxation
D.D. Palmer, the originator of chiropractic, considered vertebral
misalignment to be the hallmark feature of subluxation (Palmer
and Palmer, 1906). However, Smith et al., early chiropractic practitioners,
educators, and publishers of the first chiropractic textbook,
asserted that intervertebral hypomobility, not misalignment, was
subluxation’s cardinal feature (Smith et al., 1906). This contrasting
mechanistic emphasis, intervertebral misalignment vs. hypomobility,
formed the basis for a heated polemic. It was maintained by B.J.
Palmer, the son of D.D. Palmer, a contemporary of Smith et al., and
the most widely acknowledged pioneer developer of chiropractic.
B.J. vigorously supported D.D. Palmer’s original assertion that
vertebral misalignment was the critical feature of subluxation
(Palmer, 1934). Although both misalignment and hypomobility
are currently recognized as biomechanical features of subluxation,
hypomobility has garnered much more attention in recent years. In
addition, chiropractors appreciate that vertebrae may be
hyper-mobile. Intervertebral hyper-mobility may result from frank trauma, advanced connective tissue pathology, or as a mechanical compensation to intervertebral hypomobility.
2.1. Intervertebral hypomobility
Patients reporting headache, neck, back, or limb pain often have
demonstrable altered spine mobility (Fernandez-de-las-Penas,
2009; Langevin and Sherman, 2007; Ssavedra-Hernandez et al.,
2011; Triano, 2005; Zito et al., 2006). And, intervertebral hypomobility
has been identified as a key prognostic factor in studies
developing clinical prediction rules for neck pain (Puentedura
et al., 2011; Raney et al., 2009; Ssavedra-Hernandez et al., 2011),
headache (Fernandez-de-las-Penas et al., 2011), and low back pain
(Childs et al., 2004; Cleland et al., 2009; Fritz et al., 2011). In early
studies, intervertebral hypomobility was implicated as a clinically
important factor in neck pain. For example, Norlander and
Nordgren (1998) conducted a cross-sectional study of 142 male
and 139 female workers to evaluate the influence of segmental
mobility in neck-shoulder pain (Norlander and Nordgren, 1998).
They observed reduced relative mobility at levels C7–T1 and
T1–T2 and reported that it was a significant predictor of neckshoulder
pain. In their study, reduced mobility explained 14% of
neck-shoulder pain (r2 = 0.14, p < 0.001) and 15% of weakness in
the hands (r2 = 0.15, p < 0.001).
In a recent randomized clinical trial examining the predictive
validity of manual, posterior–anterior mobility testing in 131 low
back pain patients, Fritz et al. reported finding both hypomobile
and hyper-mobile lumbar segments, with a prevalence of 71%
and 12% respectively (Fritz et al., 2005). And, in a study of 607
women working as homecare personnel, it was reported that a
combination of positive pain provocation tests and reduced lumbar
sagittal mobility was associated with particularly high disability
levels (Lundberg and Gerdle, 2000). Finally, in 30 human spine
specimens, investigators examined the effect of degenerative
changes in lumbar discs on intervertebral mobility (Thompson et
al., 2000). They reported that degenerative spine changes are associated
with intersegmental hypomobility, even when the individuals
have no history of low back pain complaints.
This conclusion highlights a well known clinical paradox; the
severity and disability of neck and back pain do not correspond
to the degree of spinal degeneration observed with plain film radiography
(Gore et al., 1986; van Tulder et al., 1997; Witt et al., 1984)
or the presence and magnitude of disc herniations demonstrated
with discograms (Holt, 1968; Walsh et al., 1990), myelograms (Hitselberger
and Witten, 1968), computerized tomography scans
(Wiesel et al., 1984), or magnetic resonance images (Boden et al.,
1990; Borenstein et al., 2001). Researchers have observed a high
incidence (24–37%) of abnormal findings on advanced imaging
studies in patients that have never had low back pain or sciatica
(Boden et al., 1990). Boden et al. found that 57% of individuals sixty
years old or older had degenerative spine problems (21% had intervertebral
foramen stenosis and 36% had one or more herniated
discs) (Boden et al., 1990). Similarly, a 7-year follow-up study on
a group of 67 individuals who were asymptomatic with no history
of back pain at an initial MRI, demonstrated that MRI had no predictive
value in forecasting the development or duration of low
back pain. This finding was underscored by the observation that
21 (31%) of these individuals had an identifiable disc or spinal
canal abnormality in the initial MRI (Borenstein et al., 2001). The
effect of this clinical paradox on current research efforts is discussed
in the final section of this paper.
2.2. Intervertebral hyper-mobility
Hyper-mobile spine segments are not primary therapeutic targets
for chiropractic SM (Peterson and Gatterman, 2005). But,
compensatory (secondary) intervertebral hyper-mobility may occur
as a mechanical response to hypomobility in other spine segments.
In the spine literature, this is often described as a
component of ‘‘adjacent segment disease,’’ which may be observed
after spine fusion or with rigid and semirigid spine instrumentation
(Cakir et al., 2009; Panjabi et al., 2007; Shono et al., 1998). This
mechanism has been directly observed in intervertebral hypomobility
studies with the External Link Model in my lab (Figure 1,
unpublished observation). Similarly, it may occur as a compensatory
response to physiologically developed intervertebral hypomobility
(DeStefano and Greenman, 2011; Lewit, 2010). Chiropractors
treat compensatory intervertebral hyper-mobility with SM directed
to hypomobile spine segments, often with adjunctive active
stabilization exercise programs (Hicks et al., 2005; Peterson and
Adjacent segment intervertebral hyper-mobility.
2.3. Intervertebral dyskinesia
Intervertebral mobility is often discussed as if the articulation
between two vertebrae comprised a single normally mobile, hypomobile,
or hyper-mobile joint. This is the simple mechanistic
approach presented above. In actuality, intervertebral articulations
are quite complex, being composed of synovial joints, a symphysis
(with the notable exception of C1–C2), and a compound syndesmosis
(Cramer and Darby, 2005). Consequently, clinicians and spine
researchers observe that a given intervertebral articulation may
be hypomobile on one side and normally mobile, or hyper-mobile
on the contralateral side.
Some chiropractic scholars suggest that features other than
misalignment or hypomobility characterize a subluxation. Perhaps
the quality, rather than the quantity, of intervertebral motion is
modified with a resulting loss of load bearing efficiency (Enebo
and Gatterman, 2005). Triano notes that the spine tissues are
dependent on regular movement to retain their integrity (Triano,
2005). Immobility, sustained or excessive loading, and repetitive
loads may all lead to tissue changes and failure under subsequent
loads. Prolonged static postures, even without additional loads,
become uncomfortable because of tissue deformation (creep) with
concentration of local tissue stresses. Concomitant muscle fatigue
is thought to aggravate this situation by altering muscle recruitment
patterns and redistributing loads to auxiliary muscles and
ligaments. Consequently, load bearing efficiency is lost with an increase
in the magnitude of coupled motions and an increased likelihood
It is increasingly suggested by SM therapists that a synovial
joint may demonstrate normal range of motion but have aberrant
motion within the joint’s motion-path and distorted coupled motion
patterns (Abbott et al., 2009; Enebo and Gatterman, 2005;
Lund et al., 2002). As a result of the complex intervertebral articulation,
as well as paraspinal muscle activity, coupled motions are
known to occur throughout the spine (Cholewicki et al., 1996;
Panjabi et al., 2001; Steffen et al., 1997). Many SM therapists incorporate
the concept of coupled motion into their therapeutic rationale.
However, the clinical implications of coupled intersegmental
motions is presently unclear. A recent critical review of the literature
examined 24 articles on coupled motion in the lumbar spine,
but found little agreement concerning its specific characteristics or
correlation with back pain (Legaspi and Edmond, 2007).
Lastly, two new kinematic phenomena have garnered increasing
interest in the manual therapy community. These are ‘‘spine
buckling’’ and the notion of a dynamically changing ‘‘neutral zone’’
existing within the range of motion of any given synovial joint.
Buckling is the rapidly developing spine instability characterized
by sudden bending under loads that are far lower than those
required to disrupt the connective tissues of the multijoint, multimuscle
spinal column. It is thought to result from a failure to maintain coordinated timing and contraction strength between the
large postural muscles that span many spinal segments and the
small, intrinsic muscles that coordinate intersegmental motions
(Preuss and Fung, 2005).
For each of a joint’s six degrees of freedom, the neutral zone is a
portion of a joint’s total range of motion around its neutral position,
up to the beginning of some resistance to physiological motion
(White and Panjabi, 1990). This is the inherent play in a
joint as it moves within its range of motion. The size of the neutral
zone changes with physiological or surgical modification of joint
stabilizing structures, and it has proven to be a more sensitive indicator
of intervertebral dyskinesia then the more familiar, total
range-of-motion (Busscher et al., 2009; Panjabi, 2003; Smit et al.,
2.4. Intervertebral misalignment
Static palpation and static X-ray films are used by many manual
therapists, including chiropractors, to assess intervertebral
misalignment (Christensen and National Board of Chiropractic
Examiners, 2010; Fryer et al., 2009; van Trijffel et al., 2009). However,
static palpation methods have not demonstrated acceptable
intra-examiner and inter-examiner reliability (French et al.,
2000; Haneline and Young, 2009; Holmgren and Waling, 2008;
Stovall and Kumar, 2010). Similarly, there is little evidence that
static radiographic analysis for spinal misalignment is reliable or
that misalignments alone will produce clinically relevant symptoms
or pathology requiring therapeutic intervention (Haas et
al., 1999). However, it is interesting that in his original operational
definition of the neutral-zone, Panjabi based his definition on the
observation that a given joint does not return to its initial position
after loading in a particular direction (White and Panjabi, 1990).
He measured this residual displacement from its starting position
30 s after removal of the load and equated this with the magnitude
of the neutral-zone. These static residual joint displacements
are responsive to visco- and poro-elastic properties of the intervertebral
support tissues (Smit et al., 2011). Future studies on
long-term, rather than the short-term displacements observed to
date, may provide mechanistic support for early chiropractic arguments
asserting the clinical significance of intervertebral
It is highly relevant that several studies report poor inter-examiner
reliability identifying specific anatomical spine landmarks
(Billis et al., 2003; Harlick et al., 2007; Snider et al., 2011). Studies
examining the reliability of spine assessment procedures also
required examining clinicians to identify the specific anatomical
level of misalignment or altered mobility. In effect, this ‘‘double
jeopardy’’ may confound examiner agreement studies. Actual
agreement on the location of intervertebral misalignment or
mobility changes may be obscured because study clinicians incorrectly
identify the spinal level of the involved segment.
3. Theoretical mechanisms of effect for subluxation
Although many theories have been put forth to explain the
putative effects of subluxation that are reported in clinical practice,
they may be broadly classified into three mechanism-oriented categories
that are not mutually exclusive (Henderson, 2005b):
Encroachment of the intervertebral foramen (IVF) or spinal canal,
the oldest and most widely known of these theories, proposes
that subluxations cause bulging intervertebral discs, hypertrophied
facet joint capsules, or enlarged intra-foraminal ligaments
that encroach on pressure-sensitive IVF contents (e.g., dorsal root ganglia, nerve roots, and associated vascular elements)
or the spinal canal and its contents (spinal cord, nerve
roots and vascular plexus).
Altered afferent input from spinal and paraspinal tissues is
thought to attend subluxations and produce lasting and farreaching
effects via neuroplastic changes in the peripheral
and central nervous systems.
Dentate ligament mediated cord distortion has been proposed as
a mechanism by which misaligned cervical vertebrae can
directly stress sensitive brainstem and upper cervical cord
structures, thereby disrupting critical neural processes.
Chiropractic clinicians, educators, and researchers use these
three theories as a framework for organizing and interpreting clinical
observations, as inspiration for new treatment approaches, and
as a source of testable research hypotheses. Each theory has garnered
some support in the research literature, but shortcomings
have also been identified. In this section I discuss the theories, their
research support, and their strengths and weaknesses in explaining
the clinical effects of SM. Lastly, I consider SM from the perspective
that subluxation may be one contributory cause of ill-health within
a “web of causation”.
3.1. Encroachment of IVF or spinal canal
In a historical speech, The Hour Has Arrived, B.J. Palmer provided
an ‘‘intensional’’ (necessary and sufficient) definition for subluxation
(Palmer, 1931). He identified six elements:
It [subluxation] must be out of relationship to its correspondents
above and below.
There must be an occlusion of a foramin sic or spinal canal.
There must exist a pressure or tension upon spinal nerves or
There must be present an interference to transmission of
mental impulse supply.
Resistance of that transmission is always present.
An increased abnormal local resistance heat is present in
adjacent immediate tissues.
It is readily appreciated that the 1st element requires demonstration
of misalignment, which chiropractors have historically attempted
with static palpation or plain radiographs. The 2nd
element requires encroachment of the intervertebral foramen or
the spinal canal, a pathoanatomical relationship that may be best
demonstrated with specialized imaging studies such as CT or
MRI. The 3rd through 5th elements identify the nervous system
as the critical mediator of subluxation effects.
Narrowing of the spinal canal and intervertebral foramen has
been demonstrated in association with vertebral misalignments
(Frymoyer and Wiesel, 2004; Hasegawa et al., 1995; Inufusa et
al., 1996). In a cryomicrotome study of human cadavers
(35–80 yrs, mean age = 60 yrs) examining foraminal stenosis and
critical heights of the associated intervertebral discs and foramina,
Hasegawa et al. observed nerve root compression in 21 of the 100
foramina studied. All 21 stenotic foramina were compressed by the
articular processes of subluxated vertebrae with concurrent anterior
bulging of the ligamentum flavum (Figure 2) (Hasegawa et al.,
1995). Cadaveric and animal studies have shown that intervertebral
foramen encroachment can produce sufficient pressure on
neural contents to retard axoplasmic flow and the latency and
amplitude of action potential transmission (Howe et al. 1977;
Morishita et al., 2006; Wall and Devor, 1983; Winkelstein and
DeLeo, 2004). Axoplasmic flow and action potential transmission
are generally considered to be the modern-day equivalents to Palmer’s
‘‘mental impulse.’’ However, the magnitude and longevity of
these neurophysiological effects, the 5th element, as well as the
actual clinical consequences are largely unknown. It is now appreciated
that even severe anatomical stenosis of the IVF or spinal
canal can be present in asymptomatic individuals, and up to 20%
of asymptomatic patients have imaging findings consistent with
stenosis (Boden et al., 1990; Borenstein et al., 2001; Genevay and
Atlas, 2010). The 6th element in B.J. Palmer’s subluxation definition,
‘‘an increased abnormal local resistance heat is present in
adjacent immediate tissues’’ is ambiguous, possibly referring to
heat produced by local inflammation or reflex vasomotor changes.
Intervertebral foramen encroachment.
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Several small animal models were developed to examine the
putative neurophysiological consequences of IVF encroachment
(Gu et al., 2008; Song et al., 1999, 2006). Gu et al. developed and
tested a rat model using a 60 ll, unilateral IVF injection of a hemostatic
gelatin matrix (SURGIFLOW™), which they argued was close
in texture to soft tissues such as herniated discs that are commonly
associated with IVF encroachment and radicular pain (Gu et al.,
2008). They reported that chronic compression (3–4 weeks) of
the left L5 lumbar dorsal root ganglion resulted in persistent ipsilateral
hindpaw mechanical allodynia and thermal hyperalgesia for
up to 4 or 5 postoperative weeks and a 1 week up-regulation of
N-methyl-D-aspartate (NMDA) receptor and inhibitory factor jba
(Ijb-a, an inflammatory marker) within the ipsilateral L5 dorsal
root ganglion and spinal cord dorsal horn. In addition, epidural
administration of a commonly used glucocorticoid steroid, triamcinolone,
on postoperative day 3 produced a transient (1–9 days),
dose-dependent attenuation of both the thermal hyperalgesia
and the mechanical allodynia. In this study, SURGIFLOW™ injected
into the tissue immediately external to the IVF did not produce
behavioral changes indicative of hyperalgesia or allodynia. In addition,
the behavioral changes considerably outlasted expression of
the inflammatory marker Ijb-a. Therefore, these investigators concluded
that the behavioral changes observed in their study were
related to mechanical compression of the DRG within the IVF,
not simply inflammation effects.
Song et al. evaluated behavioral and electrophysiological consequences
of chronic IVF encroachment in a rat model that used surgically
implanted stainless steel rods (4 mm long, 0.63 mm
diameter) to reduce the dimensions of the left L4 or L5 IVF (Song
et al., 2006). They reported hindpaw hyperalgesia and allodynia
restricted to the side ipsilateral to the IVF encroachment as well
as spontaneous extracellular discharges in the dorsal roots ipsilateral
to the compressed DRG. In contrast, there was no hyperalgesia
or allodynia in sham operated rats and only a transient (1 day)
mechanical hyperalgesia observed in a group of rats receiving an
acute injury (rods inserted and then removed within 5 s). They
concluded that chronic compression of the DRG within the IVF
may produce, in neurons with intact axons, abnormal ectopic discharges
originating in the DRG that may contribute to low back
pain, sciatica, hyperalgesia, and tactile allodynia.
Vertebral canal and IVF stenosis, with encroachment upon neural
structures can occur as a result of vertebral subluxation with
osseous degeneration and/or soft-tissue changes; such as disc thinning
and bulging; ligament laxity, fibrosis, bucking; and joint capsule
hypertrophy (Alyas et al., 2008; Genevay and Atlas, 2010;
Giles, 2000; Hansson et al., 2009; Hasegawa et al., 1995). In an
examination of the degenerative effects of experimentally induced
intervertebral hypomobility in the rat, Cramer et al. observed substantial
increased zygapophysial articular cartilage erosion and
hypertrophic spur formation associated with hypomobile vertebrae
(Cramer et al., 2004).
The upper cervical spine (occiput – C2) lacks intervertebral
foramina. Consequently, a subgroup of chiropractic practitioners
that place particular therapeutic focus on the upper cervical spine
region emphasize the altered afferent input and cord distortion
theories discussed below to explain clinical results they regularly
observe. Moreover, sacroiliac joints are commonly manipulated
in the treatment of low back pain. Encroachment of the IVF or
spinal canal can be invoked only indirectly as an explanation for
clinical effects observed after manipulation of these joints and
clearly cannot explain effects observed following manipulation of
3.2. Altered afferent input
This widely held chiropractic theory posits that long-term
changes in intervertebral mobility or alignment provides altered
afferent input to the central nervous system, causing neuroplastic
changes that impact biological function (also called the Dysafferentation
Theory) (Haavik-Taylor and Murphy, 2010; Henderson,
2005b; Seaman and Winterstein, 1998). This theory is generally extended
to explain that SM normalizes spine biomechanics, and as a
consequence, normalizes afferent input to the central nervous system
– resulting in normalized neurological function and improved
Activity dependent plasticity at the synaptic level is known to
occur in the spinal cord throughout life (Latremoliere and Woolf,
2009; Wolpaw and Tennissen, 2001) and it has been proposed as
an important mechanism by which mechanical perturbations in
the spine produce pain and disability (Boal and Gillette, 2004;
Giesbrecht and Battie, 2005). Neuroplastic changes occur at all levels
of the neuraxis, with the most caudal levels (spinal cord)
producing more focused effects and progressively cephalic levels
(brainstem and cerebral cortex) producing more widespread
effects (Latremoliere and Woolf, 2009; Schaible et al., 2009).
Several investigators have noted that afferent inputs from deep tissues
(e.g., joint capsules, ligaments, and muscles) are uniquely
capable of inducing central sensitization, with longer lasting
effects than that produced by cutaneous inputs (Sluka, 2002;
Woolf and Wall, 1986). Moreover, most dorsal horn neurons
receiving deep tissue input have convergent inputs from the skin.
This provides a strong neuroanatomical explanation for referred
pain patterns associated with deep tissue pathology.
Receptors in joint ligaments, capsules, and fascia contribute
influential input to critical neural circuitry that control spine stabilizing
muscles (Benjamin, 2009; Holm et al., 2002; Kang et al.,
2002; Le et al., 2009; Stubbs et al., 1998; Yahia et al., 1992). A team
of electrophysiologists have examined these substantial sensory
innervations in the spinal and paraspinal tissues (Minaki et al.,
1996; Sakamoto et al., 2001; Yamashita, 1990; Yamashita et al.,
1993). They reported nociceptive afferent distributions in lumbar
facets, anterior portion of lumbar intervertebral discs, and the
sacroiliac joints as 36%, 100%, and 97% respectively. These investigators
concluded that mechanosensitive afferents in the anterior
aspect of intervertebral discs and the sacroiliac joints are primarily
nociceptors, while mechanosensitive afferents in the lumbar facet
joints have both nociceptive and proprioceptive roles (Minaki et al.,
1999; Takebayashi et al., 1997; Yamashita et al., 1999). They suggested
that the lower distribution of proprioceptors in the sacroiliac
joints and intervertebral discs may reflect the lower mobility of
Activity dependent plasticity provides a mechanistic explanation
for how brief mechanical loads that characterize SM can produce
long-term changes in neurophysiology (Boal and Gillette,
2004; Sterling et al., 2010). It has been proposed that SM causes
coactivation of both low threshold (Ab/group II) and high-threshold
(Ad/group III and C/group IV) mechanosensitive afferents, suggesting
a ‘‘counter irritation’’ effect for SM that is similar to
modalities such as high intensity transcutaneous electrical nerve
stimulation (TENS), acupuncture, and vigorous deep massage (Boal
and Gillette, 2004).
A variety of plastic changes in spinal cord neurons have been
related to spinal pain (Larsson and Broman, 2008; Lu et al., 2007;
Merighi et al., 2004; Zeilhofer and Zeilhofer, 2008). These changes
include not only synaptic density, but also modifications in profile
symmetry and curvature and perforations of postsynaptic densities
(Bertoni-Freddari et al., 1996; Marrone and Petit, 2002). Moreover,
changes in the relative proportion and types of postsynaptic profiles
(e.g., dendritic spine, dendritic shaft, or soma) have been
noted (Calverley and Jones, 1990). Such changes were observed
recently in a small study with the External Link Model (ELM), supporting
the notion that chronic intervertebral hypomobility can
cause synaptic changes in the spinal cord (Bakkum et al., 2007).
Changes in sensory thresholds and reflex responses have been
reported in clinical studies exploring neuroplasticity associated
with joint dysfunction (Giesecke et al., 2004; Moss et al., 2007;
Sterling et al., 2010). Chronic low back pain subjects, when compared
with control subjects without pain, have lower pressurepain
detection thresholds at sites that are unrelated to the lumbar
spine (Giesbrecht and Battie, 2005). It has been suggested that this
finding may be related to development of central sensitization and
maladaptive pain processing involving widespread hypersensitivity.
Similarly, investigators examining chronic neck pain patients
with histories of whiplash injury concluded that deep tissue injury
produces generalized sensory threshold changes (Johansen et al.,
1999). Most recently, changes in thermal pain thresholds have
been associated with deep tissue injury (Bialosky et al., 2009;
Meeus and Nijs, 2007; Potvin et al., 2009).
Early animal experiments by Sato and Swenson (1984) and
DeBoer et al. (1988) demonstrated what appeared to be reflex
responses to transient vertebral misalignments in anesthetized
animals (Deboer et al., 1988; Sato and Swenson, 1984). Pickar
and McClain identified directional motion sensitivity in single fiber
group III and IV afferent units within the L5 dorsal root of the cat in
response to L5–L6 facet joint displacement (Pickar and Mclain,
1995). An extensive review of animal models used in the study
of subluxation and manipulation from 1964 to 2004 is provided
in Gatterman’s book, Foundations of Chiropractic-Subluxation
D’Attilio et al., a group of dental researchers, recently examined
the suggested relationship between dental occlusion and posture
(D’Attilio et al., 2005). A greater incidence of neck and trunk pain
is reported in patients with occlusal dysfunction and it is reported
that scoliosis patients have a substantial crossbite prevalence
(Kamper et al., 2010; Korbmacher et al., 2007; Visscher et al.,
2001). D’Attilio et al. examined whether an experimentally induced
crossbite in rats might alter spinal column alignment. They distributed
30 female Sprague Dawley rats (350 g) equally across two
study groups: an experimental group with a cross-bite induced by
building up the height of a single molar with a 0.5 mm composite
pad, and an untreated control group. After 1 week, experimental
group rats all had a cross-bite and, most strikingly, they also demonstrated
a change in spinal alignment that was similar to deformities
found in human idiopathic scoliosis (demonstrated in the rats
by full body X-ray). None of the control rats showed a change in
spinal alignment. They then built up the contralateral molar in
experimental group rats to restore occlusal balance. One week after
occlusion correction, experimental group rats all had normal bites
and straightened spinal alignment. These investigators attributed
the dynamic spine alignment response observed in experimentally
induced cross-bite rats to altered afferent input from the stomatognathic
apparatus into the upper cervical spinal cord.
Song et al., evaluated a course of instrument-assisted SM
(Activator, Phoenix, AZ) to reduce the severity and/or duration
of pain and hyperalgesia associated with experimentally induced,
localized spine inflammation in Sprague–Dawley rats (200–
250 g) (Song et al., 2006). These researchers injected 30 ll of an
inflammatory cocktail (bradykinin, serotonin, histamine, and prostaglandin)
into the left L5–L6 IVF of each rat to produce localized
IVF inflammation. They monitored hindpaw thermal and mechanical
thresholds, performed intracellular recordings of L5–L6 DRG
somata, and examined the DRG for signs of inflammatory tissue
reaction at the light microscopy level (vascular injection and
increased satellite cell count). A group of injection control rats
received an identical surgical prep procedure without the inflammatory
cocktail. A series of 10 instrument-assisted manipulations
were applied to the spinous processes of L4, L5, or L6 for 2 weeks
following the inflammatory cocktail injection (daily for the first
week and on alternate days for the second week). They reported
that L5 and L6 SM, but not L4 SM, reduced the severity and duration
of induced hyperalgesia and allodynia. Similarly, the electrophysiology
studies demonstrated that IVF inflammation
associated DRG hyperexcitability was significantly reduced by
SM. Lastly, the light microscopy studies showed vascular injection
(hyperemia) and satellitosis following the IVF inflammatory
cocktail injection, but these changes were significantly reduced
3–4 weeks after the SM. These investigators concluded that instrument-
assisted SM (Activator) can significantly reduce the severity
and duration of pain and hyperalgesia caused by lumbar IVF
inflammation. They commented that this may be attributed to improved
blood and nutrition supply to the DRG within the affected
IVF and noted that their study demonstrated SM effects that were
segmentally specific (SM of L5 and L6, but not L4, produced effects).
Lastly, they opined that SM, ‘‘. . . may ‘normalize’ articular
afferent input to the central nervous system with subsequent
recovery of muscle tone, joint mobility, and sympathetic activity.’’
3.3. Dentate ligament mediated cord distortion
This theory is especially interesting to chiropractors that limit
spinal manipulation to the upper cervical region (Eriksen, 2004).
With the publication of his book, The Subluxation Specific: The
Adjustment Specific B.J. Palmer asserted (Palmer, 1934):
No vertebral subluxation CAN exist below axis; therefore no
adjustment with any DIRECT INTENTION OR DESIGN could be
given below an axis, to get sick people well.
Emphasis by B.J. Palmer
B.J. Palmer ascribed the influence of subluxation to compression
of the spinal cord. For approximately 20 years he adamantly denied
the need to adjust below the axis. In later years he relented, admitting
some value to adjustments below the axis, but asserting that
these were ‘‘minor’’ subluxations. He maintained that only occiput/
atlas/axis subluxations constituted ‘‘major’’ subluxations.
Little has been published on the dentate ligament-cord distortion
theory. A paper by Grostic relates two mechanisms by which
the dentate ligaments may adversely influence the conduction of
neural impulses within the spinal cord (Grostic, 1988):
mechanical irritation via dentate ligament traction, and
occlusion and resultant local blood stasis and ischemia of the
upper cervical cord,
also produced by dentate ligament traction.
Grostic stated that the strength of the dentate ligaments in the
upper cervical region and the dynamics of cervical spine lengthening
on flexion contribute to the possibility of spinal cord distress
with upper cervical misalignments. A study by Jarzem et al. corroborates
the argument that cord distraction could produce a conduction
block (Jarzem et al., 1992). They reported decreased spinal
cord blood flow and concurrent interruption of somatosensory
evoked potentials after experimental cord distraction. A study by
Emery highlighted the mechanical strength and immobilizing
character of the upper cervical dentate ligaments (Emery, 1967).
He related numerous cases of perinatal necropsy that demonstrated
fatal kinking of the medulla–spinal cord junction in hydrocephalic
children because of the interaction of a freely movable
brainstem and a fixed upper cervical cord (fixed by strong dentate
Recently, several investigators have reported a connective tissue
bridge between the rectus capitus posterior minor (RCPm)
and the spinal dura in the region of the posterior atlanto-occipital
membrane (Hack et al., 1995; Humphreys et al., 2003; Nash et al.,
2005). The presence of this tissue bridge was unknown when Grostic
proposed the dentate ligament mediated cord distortion theory,
but it is certainly consistent with that mechanism. It has
been proposed that this connective tissue bridge has two important
physiological roles. It may prevent brain stem compression
that could occur as a result of dural infolding during cervical flexion
and extension and it may also stabilize the cranio-cervical
region (Nash et al., 2005). In addition, a pathophysiological role
has been proposed. It is thought that RCPm mediated tension on
the pain sensitive posterior cerebro-spinal dura may be a primary
mechanism for the etiology of cervicogenic headache (Alix and
In a randomized, controlled, clinical trial performed by Bakris
et al. at the Rush University Hypertension Center, the hypothesis
was tested that manual correction of a misaligned atlas vertebra
(C1) could normalize elevated systemic arterial blood pressure
(Bakris et al., 2007). The clinical rationale for the upper cervical
manipulation administered in this study follows directly from
the dentate-ligament-cord-distortion theory proposed by Grostic
(1988). Bakris et al. argued that if a misaligned C1 vertebra can indeed
produce relative ischemia of the brainstem circulation, this
may increase systemic blood pressure via well known brainstem
mechanisms (Akimura et al., 1995; Jannetta et al., 1985; Levy et
al., 2001). Moreover, they commented that blood pressure control
has not improved significantly in the US and that two or more antihypertensive
drugs are currently required to achieve blood pressure
control in more than 70% of hypertensive patients
(Chobanian et al., 2003; Hajjar et al., 2006). Consequently, Bakris
et al. were quite impressed when their study demonstrated that
restoration of atlas vertebra alignment via manual manipulation
was associated with marked, sustained reductions in blood pressure
similar to the use of two-drug combination therapy.
4. Subluxation as an indicator for spinal manipulation
The biomechanical features of subluxation have been identified
and foundational theories have been reviewed with discussion of
supportive evidence, arguments, and limitations. However, there
is still considerable uncertainty with regard to the diagnosis and
effective treatment of spine pain and disability. As noted above,
there is little correlation between degenerative changes observed
in imaging studies and patient neck and back pain complaints.
And, while patients and chiropractors frequently report significant,
even dramatic, improvement in neck and back pain complaints and
disabilities; large population-based clinical studies report only
small treatment effects; and basic science studies haven’t identified
clear causal mechanisms for the most common presentations of
spine pain and disability (Assendelft et al., 2003; Delitto, 2005;
Deyo, 2004; Kuijpers et al., 2011; Takahashi et al., 1990). Consequently,
there is a general appreciation that we still do not understand
the mechanisms underlying neck and back pain. It is
estimated that 85–90% of spine pain seen in clinical practice is diagnosed
as ‘‘idiopathic’’ or ‘‘non-specific’’ because its pathophysiology,
diagnosis, and treatment are not well-understood (Luo et al.,
2004; Airaksinen et al., 2006; Chou et al., 2007; Hooper et al., 2006).
Moreover, clinical investigators have come to believe that the
small effect size so commonly reported in population-based clinical
studies may be due largely to the heterogeneity of the study
populations (Kent et al., 2005, 2010). It has been suggested that
study populations contain subpopulations of responders, partial
responders, and non-responders to examined therapies (Fritz et
al., 2011; Kent et al., 2010). For any given study, the mean effect
size observed will be small when there is a nearly balanced mix
of responder and non-responder subpopulations in the study. Consequently,
clinical studies with small mean effect sizes may report
disparate results that are simply due to difference in the proportions
of responders, partial responders, and non-responders in heterogeneous
Further, with regard to any musculoskeletal derangement,
some, but not all patients will experience pain and disability. If
the derangement is a primary cause, a patient will respond to
treatment that corrects the specific derangement, unless other
important causal factors are present. The complex interaction between
multiple contributory causes in the etiology of disease is
known as a ‘‘web of causation.’’ If subluxation is actively maintaining
pain and disability in a subpopulation of study participants,
those individuals are likely to be responders to SM and report large
therapeutic effects. By contrast, if in another subpopulation of
study participants, the pain and disability is substantially maintained
by additional factors within the web of causation, those
individuals will report only modest relief (partial responders) or
no relief (non-responders). Within the web of causation, contributory
causes interact in complex ways to maintain each study participant’s
In a significant departure from the ‘‘one cause’’ perspective that
shaped early chiropractic philosophy (Peters, 2009), subluxation is
increasingly viewed as a contributory cause in a web of causation
(Hawk, 2006; Hofler, 2006; Phillips and Goodman, 2004). Wide
acceptance of the Vertebral Subluxation Complex (VSC) paradigm
among today’s chiropractic clinicians reflects this view. The VSC
is a theoretical construct identifying causal pathways that integrate
subluxation with diverse pathophysiological changes in
nerve, muscle, ligamentous, vascular and connective tissues (Seaman
and Faye, 2005). The VSC paradigm presents a holistic view
of subluxation with SM presented as a powerful therapeutic tool
in a broad clinical approach that includes nutrition, exercise, other
manual therapies, and psychosocial support.
The notion that meaningful treatment effects might be lost in
population-based studies is leading researchers to search for characteristics
that will identify likely responders to the various therapeutic
approaches administered for nonspecific neck and back
pain. Clinical prediction rules have been proposed to identify headache,
neck, and low back pain patients that are likely SM responders
(Childs et al., 2004; Fernandez-de-las-Penas et al., 2011;
Ssavedra-Hernandez et al., 2011). Interestingly, the clinical prediction
rules developed to date have shown no SM technique preference
(Cleland et al., 2006). In addition, a recent metanalysis
suggests that allowing clinicians to choose from a number of SM
techniques does not improve study outcomes (Kent et al., 2005).
These surprising observations call to question the assumption
stated at the beginning of this paper, ‘‘. . . it is reasonable to think
that patients responding to SM, a mechanically based therapy,
would have mechanical derangement of the spine as a critical causal
component.’’ Theoretical mechanisms and evidence supporting
this argument have been presented. However, a number of chiropractic
practitioners, educators, and researchers challenge this fundamental
assumption (Huijbregts, 2007; Keating et al., 2005).
Pickar et al. have demonstrated SM loading effects in cats without
targeting a predetermined mechanical derangement (Pickar et al.,
2007; Pickar and Kang, 2006). Chiradejnant et al. examined
whether clinician-selected mobilization techniques were more
effective in relieving low back pain than randomly-selected mobilization
techniques (Chiradejnant et al., 2003). They reported that
lumbar mobilization produced immediate low back pain relief,
but the choice of mobilization treatment had no effect.
In a related study, Haas et al. reported no benefit from clinically
determining target segments for SM (Haas et al., 2003). Neck pain
patients (n = 104) were randomly assigned to two groups. The
experimental study group received manipulation targeted to
individual cervical vertebrae according to end-play restriction
noted by the examining clinician. The control group received
manipulation determined by sham, computer-generated examination
findings; end-play examination was ignored and served as a
placebo assessment. Treatment was rendered on a single occasion
by a chiropractor. Outcomes were neck pain and stiffness assessed
before and after manipulation and at least 5 h following treatment.
The experimental and control groups both showed clinically
important improvement in neck pain and stiffness. However, there
were no clinically important or statistically significant differences
between the experimental and control groups in terms of pain or
stiffness outcomes. Findings were robust across patient, complaint,
and treatment characteristics. End-play assessment in and of itself
did not contribute to the same-day pain and stiffness relief observed
in neck pain patients receiving SM. The impact on a longer
course of treatment remains to be investigated. The researchers
commented, ‘‘These data suggest that pain modulation may not
be limited to mechanisms associated with manipulation of putative
5. Summary comments
The chiropractic basis for spinal manipulation has been presented
through consideration of its history, theoretical foundation,
and a diverse and rapidly developing multidisciplinary evidence
base. Clinical indications for SM have proven to be a perplexing
challenge for chiropractors, as it has for physical therapists and
osteopathic SM practitioners. The weight of evidence suggests that
SM is an effective therapeutic tool, but the informed ‘‘best application’’
of that tool is seriously wanting. Much more basic (mechanism-
based) and clinical research is needed.
Review of the current basic and clinical evidence highlights an
additional issue. Much of the evidence base, both basic and clinical,
is predicated upon short-term observations, but the experience of
the patient is clearly a long-term experience. With very few exceptions,
basic research studies examine exposure to risk factors or
therapeutic interventions that are present for only hours or, at best,
days. Similarly, clinical studies frequently examine outcomes after
only a single SM or a course of therapy that is much shorter than
that administered in clinical practice. There are unique challenges
associated with ‘‘chronic’’ research studies (Henderson et al.,
2008). Basic and clinical research study designs examining longterm
effects exact a high cost in time and money. The investment
risk is also greater, not just due to the increased time required to
conduct chronic studies, but also because greater time is needed
to evaluate and resolve problems that arise more frequently during
the course of these studies. Despite these greater costs and risks,
long-term basic and clinical studies are needed to more closely relate
to the patient’s long-term experience.
Nowhere is the immediate and practical relevance of this issue
more apparent than when considering the practice of ‘‘maintenance
care’’ (also known as ‘‘wellness care’’), ongoing care after the patient’s
main complaint is resolved (Christensen and National Board
of Chiropractic Examiners, 2010). While not unique to chiropractic,
SM maintenance care is commonly questioned by patients, 3rd
party payers, and the wider healthcare community. The chiropractic
perspective is that many individuals suffer from chronic health conditions
for which there is no ‘‘cure,’’ but these patients can be maintained
with minimal pain and disability through regular, periodic
SM treatment. It is estimated that 10–19% of patients will develop
chronic disabling neck or back pain (Bovim et al., 1994; Dionne et
al., 2011; Freburger et al., 2009). As noted previously, maintenance
care is not a concept unique to chiropractic. Many conditions (e.g.,
diabetes and hypertension) are controlled, but not cured, by ongoing
treatment, and most dental patients are on a maintenance care
program. SM maintenance care presents a health-services challenge
because it offers practitioners a stable revenue stream for a putative
benefit that is not easily accessed by patients and third-party payers.
Consequently, it is particularly important to evaluate the efficacy
of SM maintenance care programs with attention to critical
factors such as frequency and duration.
Two recent studies have examined chiropractic maintenance
care. Descarreax et al. Studied 30 patients with chronic non-specific
low back pain (chronic defined as P6 months duration) (Descarreaux
et al., 2004). Half were given 12 SM treatments in an intensive
1 month period and no treatment for a 9 month follow-up period.
The other half were given the same intensive 1 month period of
SM but, in the subsequent 9 months they received a maintenance
SM every 3 weeks. Pain and disability were monitored via a visual
analog pain score and a modified Oswestry questionnaire, respectively.
Both groups reported improved pain scores at the end of
the intensive SM period and maintained those scores over the subsequent
9 months. While both groups also reported improved Oswestry
disability scores at the end of the intensive treatment period,
only the group receiving maintenance care during the 9 month follow-
up period maintained that improvement. Patients not receiving
SM maintenance care reverted to pretreatment disability
levels over the follow-up period.
Most recently, a prospective, single blinded, placebo controlled
study was conducted to examine the long-term (10 months) effectiveness
of lumbar SM with and without SM maintenance care for
the treatment of chronic, nonspecific low back pain (Senna and
Machaly, 2011). These researchers randomly assigned 60 study
participants with chronic nonspecific low back pain (P6 months
duration), into 3 study groups of equal size: (1) Lumbar SM without
maintenance care received 12 SM treatments over a 1 month period
followed by no treatment for the succeeding 9 months, (2) Lumbar
SM with SM maintenance care also received 12 SM treatments over
a 1 month period followed by ‘‘maintenance SM’’ every 2 weeks for
the succeeding 9 months, and (3) Placebo Lumbar SM in which 12
sham SM treatments were administered over a 1 month period followed
by no treatment for a 9 month follow-up period. Pain and
disability scores, generic health status, and back-specific patient
satisfaction were measured at baseline and at 1, 4, 7, and 10 month
intervals. Study participants reported significantly reduced pain
and disability scores in both of the SM study groups compared to
the sham SM group at 1 month. However, only study participants
receiving SM followed by SM maintenance care showed improvement
in pain and disability scores at the 10 month evaluation. By
contrast, pain and disability scores were at pre-treatment levels
for study participants in the SM without maintenance care and
Sham SM groups at 10 months. These investigators concluded that
SM was effective as a treatment for chronic nonspecific low back
pain, but to obtain long-term benefits a course of SM maintenance
care may be required.
SM has been shown to be beneficial for painful conditions that
levy great personal and economic costs on the patient and society.
However, despite the considerable number and diversity of studies
identified here, little is known about the most fundamental aspects
of this therapy and it is clear that the most effective applications of
SM have not yet been realized. I have reviewed the basis for SM, its
indications, and theory from a chiropractic perspective. In addition
to research specifically focused on chiropractic, this perspective
was informed by studies from physical therapy, osteopathy, general
medicine, and surgery.
Dr. Henderson is an associate professor of research at the Palmer Center for Chiropractic Research, Florida campus. He developed the External Link Model (ELM) an experimental platform for examining the effects of intersegmental spine hypomobility. Dr. Henderson has used the ELM to study the biomechanical, histological, and neurophysiological consequences of intersegmental spine hypomobility. Currently, he employs the ELM to examine mechanisms by which spine manipulation is thought to produce clinically beneficial results. Dr. Henderson is a graduate of Western States Chiropractic College (DC, 1977) and the University of South Florida, College of Medicine (PhD, 1992).
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