The Basis for Spinal Manipulation:
Chiropractic Perspective of
Indications and Theory

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:

FROM:   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.

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.

      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.

      Intervertebral hyper-mobility

Figure 1

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 Gatterman, 2005).

      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 of injury.

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., 2011).

      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 misalignment.

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.

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):

  1. 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).

  2. 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.

  3. 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”.

      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:

  1. It [subluxation] must be out of relationship to its correspondents above and below.

  2. There must be an occlusion of a foramin sic or spinal canal.

  3. There must exist a pressure or tension upon spinal nerves or spinal cord.

  4. There must be present an interference to transmission of mental impulse supply.

  5. Resistance of that transmission is always present.

  6. 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.

Figure 2

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.

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 appendicular joints.

      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 health outcomes.

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 these joints.

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 (Henderson, 2005a).

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.’’

      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):

(1) Direct mechanical irritation via dentate ligament traction, and

(2) Venous 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 ligament attachments).

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 Bates, 1999).

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.

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 study populations.

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 complaint.

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 motion restrictions.’’

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).


Abbott JH, Flynn TW, Fritz JM, Hing WA, Reid D, Whitman JM.
Manual physical assessment of spinal segmental motion: intent and validity.
Man Ther 2009;14(1):36–44.

Airaksinen O, Brox J, Cedraschi C, Hildebrandt J, Klaber-Moffett J, Kovacs F, et al.
European Guidelines for the Management of Chronic Nonspecific Low Back Pain
European Spine Journal 2006 (Mar);   15 Suppl 2:  S192–300

Akimura T, Furutani Y, Jimi Y, Saito K, Kashiwagi S, Kato S, et al.
Essential hypertension and neurovascular compression at the ventrolateral medulla oblongata: MR evaluation.
AJNR Am J Neuroradiol 1995;16(2):401–5.

Alix ME, Bates DK.
A Proposed Etiology of Cervicogenic Headache: The Neurophysiologic Basis and Anatomic
Relationship Between the Dura Mater and the Rectus Posterior Capitis Minor Muscle

J Manipulative Physiol Ther 1999 (Oct); 22 (8): 534–539

Alyas F, Connell D, Saifuddin A.
Upright positional MRI of the lumbar spine.
Clin Radiol 2008;63(9):1035–48.

Assendelft WJJ, Morton SC, Yu EI, Suttorp MJ, Shekelle PG.
Spinal manipulative therapy for low back pain – A meta-analysis of effectiveness relative to other therapies.
Ann Intern Med 2003;138(11):871–81.

Bakkum, B.W., Henderson, C.N., Hong, S.P., and Cramer, G.D.
Preliminary Morphological Evidence That Vertebral Hypomobility Induces Synaptic Plasticity
in the Spinal Cord

J Manipulative Physiol Ther. 2007 (Jun); 30 (5): 336–342

Bakris G., Dickholtz M., Meyer P.
Atlas Vertebra Realignment and Achievement of Arterial Pressure Goal in Hypertensive Patients:
A Pilot Study

Journal of Human Hypertension 2007 (May); 21 (5): 347–352

Benjamin M.
The fascia of the limbs and back – a review.
J Anat 2009;214(1):1–18.

Bertoni-Freddari C, Fattoretti P, Paoloni R, Caselli U, Galeazzi L, Meier-Ruge W.
Synaptic structural dynamics and aging.
Gerontology 1996;42(3):170–80.

Bialosky JE, Bishop MD, Robinson ME, Zeppieri Jr G, George SZ.
Spinal manipulative therapy has an immediate effect on thermal pain sensitivity in people with low back pain: a randomized controlled trial.
Phys Ther 2009;89(12):1292–303.

Billis EV, Foster NE, Wright CC.
Reproducibility and repeatability: errors of three groups of physiotherapists in locating spinal levels by palpation.
Man Ther 2003;8(4):223–32.

Boal RW, Gillette RG.
Central neuronal plasticity, low back pain and spinal manipulative therapy.
J Manipulative Physiol Ther 2004;27(5):314–26.

Boden SD, McCowin PR, Davis DO, Dina TS, Mark AS, Wiesel S.
Abnormal magneticresonance scans of the cervical spine in asymptomatic subjects. A prospective investigation.
J Bone Joint Surg Am 1990;72(8):1178–84.

Borenstein DG, O’Mara Jr JW, Boden SD, Lauerman WC, Jacobson A, Platenberg C, et al.
The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects: a seven-year follow-up study.
J Bone Joint Surg Am 2001;83-A(9):1306–11.

Bovim G, Schrader H, Sand T.
Neck pain in the general population.
Spine 1994;19(12):1307–9.

Busscher I, van Dieen JH, Kingma I, van der Veen AJ, Verkerke GJ, Veldhuizen AG.
Biomechanical characteristics of different regions of the human spine: an in vitro study on multilevel spinal segments.
Spine (Phila Pa 1976) 2009;34(26):2858–64.

Cakir B, Carazzo C, Schmidt R, Mattes T, Reichel H, Kafer W.
Adjacent segment mobility after rigid and semirigid instrumentation of the lumbar spine.
Spine (Phila Pa 1976) 2009;34(12):1287–91.

Calverley RK, Jones DG.
Contributions of dendritic spines and perforated synapses to synaptic plasticity.
Brain Res Brain Res Rev 1990;15(3):215–49.

Childs JD, Fritz JM, Flynn TW, Irrgang JJ, Johnson KK, Majkowski GR, et al.
A Clinical Prediction Rule To Identify Patients With Low Back Pain Most Likely To Benefit
from Spinal Manipulation: A Validation Study

Annals of Internal Medicine 2004 (Dec 21); 141 (12): 920–928

Chiradejnant A, Maher CG, Latimer J, Stepkovitch N.
Efficacy of ‘‘therapist-selected’’ versus ‘‘randomly selected’’ mobilisation techniques for the treatment of low back pain: a randomised controlled trial.
Aust J Physiother 2003;49(4):233–41.

Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo Jr JL, et al.
Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
Hypertension 2003;42(6):1206–52.

Cholewicki J, Crisco III JJ, Oxland TR, Yamamoto I, Panjabi MM.
Effects of posture and structure on three-dimensional coupled rotations in the lumbar spine. A biomechanical analysis.
Spine 1996;21(21):2421–8.

Chou R, Qaseem A, Snow V, Casey D, Cross JT Jr., Shekelle P, Owens DK:
Diagnosis and Treatment of Low Back Pain: A Joint Clinical Practice Guideline
from the American College of Physicians and the American Pain Society

Annals of Internal Medicine 2007 (Oct 2); 147 (7): 478–491

Christensen MG,
Practic Analysis of Chiropractic: 2010
A project report, survey analysis, and summary of the practice
of chiropractic within the United States.
National Board of Chiropractic Examiners.
Greeley, CO: National Board of Chiropractic Examiners

Cleland JA, Fritz JM, Kulig K, Davenport TE, Eberhart S, Magel J, et al.
Comparison of the effectiveness of three manual physical therapy techniques in a subgroup of patients with low back pain who satisfy a clinical prediction rule: a randomized clinical trial.
Spine (Phila Pa 1976) 2009;34(25):2720–9.

Cleland JA, Fritz JM, Whitman JM, Childs JD, Palmer JA.
The use of a lumbar spine manipulation technique by physical therapists in patients who satisfy a clinical prediction rule: a case series.
J Orthop Sports Phys Ther 2006;36(4):209–14.

Cramer GD, Darby SA.
Basic and clinical anatomy of the spine, spinal cord, and ANS.
2nd ed. St. Louis: Elsevier Mosby; 2005.

Cramer G.D., Fournier J.T., Henderson C.N., Wolcott C.C.
Degenerative Changes Following Spinal Fixation in a Small Animal Model
J Manipulative Physiol Ther 2004 (Mar); 27 (3): 141–154

D’Attilio M, Filippi MR, Femminella B, Festa F, Tecco S.
The influence of an experimentally-induced malocclusion on vertebral alignment in rats: a controlled pilot study.
Cranio 2005;23(2):119–29.

Deboer KF, Schutz M, McKnight ME.
Acute effects of spinal manipulation on gastrointestinal myoelectric activity in conscious rabbits.
Manual Med 1988;3:85–94.

Delitto A.
Research in low back pain: time to stop seeking the elusive ‘‘magic bullet’’.
Phys Ther 2005;85(3):206–8.

Descarreaux M, Blouin JS, Drolet M, Papadimitriou S, Teasdale N:
Efficacy of Preventive Spinal Manipulation for Chronic Low-Back Pain and Related Disabilities:
A Preliminary Study

J Manipulative Physiol Ther 2004 (Oct); 27 (8): 509–514

DeStefano LA, Greenman P.
Greenman’s principles of manual medicine. 4th ed.
Philadelphia: Wollters Kluwer/Lippincott Williams & Wilkins Health; 2011.

Deyo RA.
Treatments for back pain: can we get past trivial effects?
Ann Intern Med 2004;141(12):957–8.

Dionne CE, Le SN, Franche RL, Dorval M, Bombardier C, Deyo RA.
Five questions predicted long-term, severe, back-related functional limitations: evidence from three large prospective studies.
J Clin Epidemiol 2011;64(1):54–66.

Emery JL.
Kinking of the medulla in children with acute cerebral oedema and hydrocephalus and its relationship to the dentate ligaments.
J Neurol Neurosurg Psychiatry 1967;30(3):267–75.

Enebo BA, Gatterman MI.
Kinesiology: an essential approach toward understanding the chiropractic subluxation.
In: Gatterman MI, editor. Foundations of chiropractic: subluxation. 2nd ed.
St. Louis:Mosby Yearbook Inc.; 2005. p. 245–82.

Eriksen K.
Upper cervical subluxation complex. A review of the chiropractic and medical literature. 1st ed.
Philadelphia: Lippincott Williams & Wilkins; 2004.

Fernandez-de-las-Penas C.
Interaction between trigger points and joint hypomobility: a clinical perspective.
J Man Manip Ther 2009;17(2):74–7.

Fernandez-de-las-Penas C, Cleland JA, Palomeque-del-Cerro L, Caminero AB, Guillem-Mesado A, Jimenez-Garcia R.
Development of a clinical prediction rule for identifying women with tension-type headache who are likely to achieve short-term success with joint mobilization and muscle trigger point therapy.
Headache 2011;51(2):246–61.

Freburger JK, Holmes GM, Agans RP, Jackman AM, Darter JD, Wallace AS, et al.
The rising prevalence of chronic low back pain.
Arch Intern Med 2009;169(3):251–8.

French SD, Green S, Forbes A.
Reliability of chiropractic methods commonly used to detect manipulable lesions in patients with chronic low-back pain.
J Manipulative Physiol Ther 2000;23(4):231–8.

Fritz JM, Koppenhaver SL, Kawchuk GN, Teyhen DS, Hebert JJ, Childs JD.
Preliminary investigation of the mechanisms underlying the effects of manipulation: exploration of a multi-variate model including spinal stiffness, multifidus recruitment, and clinical findings.
Spine (Phila Pa 1976) 2011.

Fritz JM, Whitman JM, Childs JD.
Lumbar spine segmental mobility assessment: an examination of validity for determining intervention strategies in patients with low back pain.
Arch Phys Med Rehabil 2005;86(9):1745–52.

Fryer G, Morse CM, Johnson JC.
Spinal and sacroiliac assessment and treatment techniques used by osteopathic physicians in the United States.
Osteopath Med Prim Care 2009;3:4.

Frymoyer JW, Wiesel SW.
The adult and pediatric spine. 3rd
ed. Philadelphia: Lippincott Williams & Wilkins; 2004.

Genevay S, Atlas SJ.
Lumbar spinal stenosis.
Best Pract Res Clin Rheumatol 2010;24(2):253–65.

Giesbrecht RJ, Battie MC.
A comparison of pressure pain detection thresholds in people with chronic low back pain and volunteers without pain.
Phys Ther 2005;85(10):1085–92.

Giesecke T, Gracely RH, Grant MA, Nachemson A, Petzke F, Williams DA, et al.
Evidence of augmented central pain processing in idiopathic chronic low back pain.
Arthritis Rheum 2004;50(2):613–23.

Giles, LGF.
Mechanisms of Neurovascular Compression Within the Spinal and Intervertebral Canals
Plenary paper for the 1999 World Chiropractic Congress.
J Manipulative Physiol Ther. 2000 (Feb); 23 (2): 107–111

Gore DR, Sepic SB, Gardner GM.
Roentgenographic findings of the cervical spine in asymptomatic people.
Spine 1986;11(6):521–4.

Grostic JD.
Dentate ligament-cord distortion hypothesis.
Chiropr Res J 1988;1(1):47–55.

Gu X, Yang L, Wang S, Sung B, Lim G, Mao J, et al.
A rat model of radicular pain induced by chronic compression of lumbar dorsal root ganglion with SURGIFLO.
Anesthesiology 2008;108(1):113–21.

Haas M, Groupp E, Panzer D, Partna L, Lumsden S, Aickin M.
Efficacy of cervical endplay assessment as an indicator for spinal manipulation.
Spine 2003;28(11):1091–6.

Haas M, Taylor JA, Gillette RG.
The routine use of radiographic spinal displacement analysis: a dissent.
J Manipulative Physiol Ther 1999;22(4):254–9.

Haavik-Taylor H, Murphy B.
The Effects of Spinal Manipulation on Central Integration of Dual Somatosensory Input
Observed After Motor Training: A Crossover Study

J Manipulative Physiol Ther. 2010 (May); 33 (4): 261–272

Hack GD, Koritzer RT, Robinson WL, Hallgren RC, Greenman PE.
Anatomic relation between the rectus capitis posterior minor muscle and the dura mater.
Spine (Phila Pa 1976) 1995;20(23):2484–6.

Hajjar I, Kotchen JM, Kotchen TA.
Hypertension: trends in prevalence, incidence, and control.
Annu Rev Public Health 2006;27:465–90.

Haneline MT, Young M.
A review of intraexaminer and interexaminer reliability of static spinal palpation: a literature synthesis.
J Manipulative Physiol Ther 2009;32(5):379–86.

Hansson T, Suzuki N, Hebelka H, Gaulitz A.
The narrowing of the lumbar spinal canal during loaded MRI: the effects of the disc and ligamentum flavum.
Eur Spine J 2009;18(5):679–86.

Harlick JC, Milosavljevic S, Milburn PD.
Palpation identification of spinous processes in the lumbar spine.
Man Ther 2007;12(1):56–62.

Hasegawa T, An HS, Haughton VM, Nowicki BH.
Lumbar foraminal stenosis: critical heights of the intervertebral discs and foramina. A cryomicrotome study in cadavera.
J Bone Joint Surg Am 1995;77(1):32–8.

Hawk C.
Is it time to adjust our thinking about subluxation?
J Am Chiro Assoc 2006;20–2.

Henderson CNR.
Animal models in the study of subluxation and manipulation: 1964–2004.
In: Gatterman MI, editor. Foundations of chiropractic: subluxation. 2nd ed.
St. Louis: Mosby Yearbook Inc.; 2005a. p. 47–103.

Henderson CNR.
Three neurophysiologic theories on the chiropractic subluxation.
In: Gatterman MI, editor. Foundations of chiropractic: subluxation. 2nd ed.
St. Louis: Elsevier Mosby; 2005b. p. 296–303.

Henderson, C. N., Cramer, G. D., Zhang, Q., DeVocht, J. W.,
Sozio, R. S., & Fournier, J. T.
Introducing the External Link Model for Studying Spine Fixation and Misalignment:
Current Procedures, Costs, and Failure Rates

J Manipulative Physiol Ther 2009 (May); 32 (4): 294–302

Hengeveld E, Banks K, Maitland GD.
Maitland’s peripheral manipulation. 4th ed.
Edinburgh: Elsevier/Butterworth Heinemann; 2005.

Hicks GE, Fritz JM, Delitto A, McGill SM.
Preliminary development of a clinical prediction rule for determining which patients with low back pain will respond to a stabilization exercise program.
Arch Phys Med Rehabil 2005;86(9):1753–62.

Hitselberger WE, Witten RM.
Abnormal myelograms in asymptomatic patients.
J Neurosurg 1968;28(3):204–6.

Hofler M.
Getting causal considerations back on the right track.
Emerg Themes Epidemiol 2006;3:8.

Holm S, Indahl A, Solomonow M.
Sensorimotor control of the spine.
J Electromyogr Kinesiol 2002;12(3):219–34.

Holmgren U, Waling K.
Inter-examiner reliability of four static palpation tests used for assessing pelvic dysfunction.
Man Ther 2008;13(1):50–6.

Holt EP.
The question of lumbar discography.
J Bone Joint Surg Am 1968;50(4):720–6.

Hooper PD, Morris CE, Cassidy JD, Grunnet-Nilsson N.
Nonspecific low back pain and chronic low back syndrome.
In: Morris CE, editor. Low back syndromes. New York:
McGraw-Hill; 2006. p. 287–302.

Howe JF, Loeser JD, Calvin WH.
Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression.
Pain 1977;3:25–41.

Huijbregts P.
Clinical prediction rules: time to sacrifice the holy cow of specificity?
J Man Manipulative Ther 2007;15(1):5–8.

Humphreys BK, Kenin S, Hubbard BB, Cramer GD.
Investigation of connective tissue attachments to the cervical spinal dura mater.
Clin Anat 2003;16(2):152–9.

Inufusa A, An HS, Lim TH, Hasegawa T, Haughton VM, Nowicki BH.
Anatomic changes of the spinal canal and intervertebral foramen associated with flexionextension movement.
Spine (Phila Pa 1976) 1996;21(21):2412–20.

Jannetta PJ, Segal R, Wolfson Jr SK.
Neurogenic hypertension: etiology and surgical treatment. I. Observations in 53 patients.
Ann Surg 1985;201(3):391–8.

Jarzem PF, Quance DR, Doyle DJ, Begin LR, Kostuik JP.
Spinal cord tissue pressure during spinal cord distraction in dogs.
Spine (Phila Pa 1976) 1992;17(Suppl. 8):S227–34.

Johansen MK, Graven-Nielsen T, Olesen AS, Arendt-Nielsen L.
Generalised muscular hyperalgesia in chronic whiplash syndrome.
Pain 1999;83:229–34.

Kamper SJ, Maher CG, Herbert RD, Hancock MJ, Hush JM, Smeets RJ.
How little pain and disability do patients with low back pain have to experience to feel that they have recovered?
Eur Spine J 2010;19(9):1495–501.

Kang YM, Choi WS, Pickar JG.
Electrophysiologic evidence for an intersegmental reflex pathway between lumbar paraspinal tissues.
Spine 2002;27(3): E56–63.

J Keating, K Charton, J Grod, S Perle, D Sikorski, J Winterstein
Subluxation: Dogma or Science?
Chiropractic & Osteopathy 2005 (Aug 10); 13: 17

Kent P, Keating JL, Leboeuf-Yde C.
Research methods for subgrouping low back pain.
BMC Med Res Methodol 2010;10:62.

Kent P, Marks D, Pearson W, Keating J.
Does clinician treatment choice improve the outcomes of manual therapy for nonspecific low back pain? A metaanalysis.
J Manipulative Physiol Ther 2005;28(5):312–22.

Korbmacher H, Koch L, Eggers-Stroeder G, Kahl-Nieke B.
Associations between orthopaedic disturbances and unilateral crossbite in children with asymmetry of the upper cervical spine.
Eur J Orthod 2007;29(1):100–4.

Kuijpers T, van Middelkoop M, Rubinstein SM, Ostelo R, Verhagen A, Koes BW, et al.
A systematic review on the effectiveness of pharmacological interventions for chronic non-specific low-back pain.
Eur Spine J 2011;20(1):40–50.

Langevin H.M., Sherman K.J.
Pathophysiological Model for Chronic Low Back Pain Integrating Connective Tissue
and Nervous System Mechanisms

Medical Hypotheses 2007 (Jan);   68 (1):   74–80

Larsson M, Broman J.
Translocation of GluR1-containing AMPA receptors to a spinal nociceptive synapse during acute noxious stimulation.
J Neurosci 2008;28(28):7084–90.

Latremoliere A, Woolf CJ.
Central sensitization: a generator of pain hypersensitivity by central neural plasticity.
J Pain 2009;10(9):895–926.

Le B, Davidson B, Solomonow D, Zhou BH, Lu Y, Patel V, et al.
Neuromuscular control of lumbar instability following static work of various loads.
Muscle Nerve 2009;39(1):71–82.

Leach RA.
The chiropractic theories: a textbook of scientific research. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2004.

Legaspi O, Edmond SL.
Does the evidence support the existence of lumbar spine coupled motion? A critical review of the literature.
J Orthop Sports Phys Ther 2007;37(4):169–78.

Levy EI, Scarrow AM, Jannetta PJ.
Microvascular decompression in the treatment of hypertension: review and update.
Surg Neurol 2001;55(1):2–10.

Lewit K.
Manipulative therapy: musculoskeletal medicine.
Edinburgh: Churchill Livingstone/Elsevier; 2010.

Lu VB, Ballanyi K, Colmers WF, Smith PA.
Neuron type-specific effects of brainderived neurotrophic factor in rat superficial dorsal horn and their relevance to ‘central sensitization’.
J Physiol 2007;584(Pt 2):543–63.

Lund T, Nydegger T, Schlenzka D, Oxland TR.
Three-dimensional motion patterns during active bending in patients with chronic low back pain.
Spine (Phila Pa 1976) 2002;27(17):1865–74.

Lundberg G, Gerdle B.
Correlations between joint and spinal mobility, spinal sagittal configuration, segmental mobility, segmental pain, symptoms and disabilities in female homecare personnel.
Scand J Rehabil Med 2000;32(3):124–33.

Marrone DF, Petit TL.
The role of synaptic morphology in neural plasticity: structural interactions underlying synaptic power.
Brain Res Brain Res Rev 2002;38(3):291–308.

Meeus M, Nijs J.
Central sensitization: a biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome.
Clin Rheumatol 2007;26(4):465–73.

Merighi A, Carmignoto G, Gobbo S, Lossi L, Salio C, Vergnano AM, et al.
Neurotrophins in spinal cord nociceptive pathways.
Prog Brain Res 2004;146:291–321.

Minaki Y, Yamashita T, Ishii S.
An electrophysiological study on the mechanoreceptors in the lumbar spine and adjacent tissues.
Neuro- Orthopedics 1996;20:23–35.

Minaki Y, Yamashita T, Takebayashi T, Ishii S.
Mechanosensitive afferent units in the shoulder and adjacent tissues.
Clin Orthop Relat Res 1999;369:349–56.

Morishita Y, Hida S, Naito M, Arimizu J, Matsushima U, Nakamura A.
Measurement of the local pressure of the intervertebral foramen and the electrophysiologic values of the spinal nerve roots in the vertebral foramen.
Spine (Phila Pa 1976) 2006;31(26):3076–80.

Moss P, Sluka K, Wright A.
The initial effects of knee joint mobilization on osteoarthritic hyperalgesia.
Man Ther 2007;12(2):109–18.

Nash L, Nicholson H, Lee AS, Johnson GM, Zhang M.
Configuration of the connective tissue in the posterior atlanto-occipital interspace. A sheet plastination and confocal microscopy study.
Spine 2005;30(12):1359–66.

Norlander S, Nordgren B.
Clinical symptoms related to musculoskeletal neckshoulder pain and mobility in the cervico-thoracic spine.
Scand J Rehabil Med 1998;30(4):243–51.

Palmer BJ.
The hour has arrived.
Davenport: Palmer School of Chiropractic; 1931.

Palmer BJ.
The subluxation specific - the adjustment specific.
Davenport: Palmer School of Chiropractic; 1934.

Palmer DD, Palmer BJ.
The science of chiropractic: principles and adjustments. 1st ed.
Davenport: Palmer School of Chiropractic; 1906.

Panjabi M, Henderson G, Abjornson C, Yue J.
Multidirectional testing of one- and two-level ProDisc-L versus simulated fusions.
Spine (Phila Pa 1976) 2007;32(12):1311–9.

Panjabi MM.
Clinical spinal instability and low back pain.
J Electromyogr Kinesiol 2003;13(4):371–9.

Panjabi MM, Crisco JJ, Vasavada A, Oda T, Cholewicki J, Nibu K, et al.
Mechanical properties of the human cervical spine as shown by three-dimensional load– displacement curves.
Spine (Phila Pa 1976) 2001;26(24):2692–700.

Peters RE.
Subluxation – Historical Perspectives
Chiropractic Journal of Australia 2009 (Dec);   39 (4):   151–164

Peterson CK, Gatterman MI.
The nonmanipulable subluxation. In: Gatterman MI, editor. Foundations of chiropractic: subluxation. 2nd ed.
St. Louis: Mosby Yearbook Inc.; 2005. p. 168–90.

Phillips CV, Goodman KJ.
The missed lessons of Sir Austin Bradford Hill.
Epidemiol Perspect Innov 2004;1(1):3.

Pickar JG, Kang YM.
Paraspinal muscle spindle responses to the duration of a spinal manipulation under force control.
J Manipulative Physiol Ther 2006;29(1):22–31.

Pickar JG, Mclain RF.
Responses of mechanosensitive afferents to manipulation of the lumbar facet in the cat.
Spine 1995;20(22):2379–85.

Pickar JG, Sung PS, Kang YM, Ge W.
Response of lumbar paraspinal muscles spindles is greater to spinal manipulative loading compared with slower loading under length control.
Spine J 2007;7(5):583–95.

Potvin S, Larouche A, Normand E, de Souza JB, Gaumond I, Grignon S, et al.
DRD3 Ser9Gly polymorphism is related to thermal pain perception and modulation in chronic widespread pain patients and healthy controls.
J Pain 2009;10(9):969–75.

Preuss R, Fung J.
Can acute low back pain result from segmental spinal buckling during sub-maximal activities? A review of the current literature.
Manual Therapy 2005;10:14–20.

Puentedura EJ, Landers MR, Cleland JA, Mintken PE, Huijbregts P, Fernandez-de-las- Penas C.
Thoracic spine thrust manipulation versus cervical spine thrust manipulation in patients with acute neck pain: a randomized clinical trial.
J Orthop Sports Phys Ther 2011;41(4):208–20.

Raney NH, Petersen EJ, Smith TA,CowanJE, Rendeiro DG, Deyle GD, et al.
Development of a clinical prediction rule to identify patients with neck pain likely to benefit from cervical traction and exercise.
Eur Spine J 2009;18(3):382–91.

Sakamoto N, Yamashita T, Takebayashi T, Sekine M, Ishii S.
An electrophysiologic study of mechanoreceptors in the sacroiliac joint and adjacent tissues.
Spine (Phila Pa 1976) 2001;26(20):E468–71.

Sato A, Swenson RS.
Sympathetic nervous system response to mechanical stress of the spinal column in rats.
J Manipulative Physiol Ther 1984;7(3):141–7.

Schaible HG, Richter F, Ebersberger A, Boettger MK, Vanegas H, Natura G, et al.
Joint pain.
Exp Brain Res 2009;196(1):153–62.

Seaman DR, Faye LJ.
The vertebral subluxation complex.
In: Gatterman MI, editor. Foundations of chiropractic: subluxation. 2nd ed.
St. Louis: Elsevier Mosby; 2005. p. 195–226.

Seaman DR, Winterstein JF.
Dysafferentation: A Novel Term to Describe the Neuropathophysiological Effects
of Joint Complex Dysfunction. A Look at Likely Mechanisms of Symptom Generation

J Manipulative Physiol Ther 1998 (May); 21 (4): 267-280

Senna M.K., Machaly S.A.
Does Maintained Spinal Manipulation Therapy for Chronic Non-specific Low Back Pain
Result in Better Long Term Outcome?

Spine (Phila Pa 1976) 2011 (Aug 15); 36 (18): 1427–1437

Shono Y, Kaneda K, Abumi K, McAfee PC, Cunningham BW.
Stability of posterior spinal instrumentation and its effects on adjacent motion segments in the lumbosacral spine.
Spine (Phila Pa 1976) 1998;23(14):1550–8.

Sluka KA.
Stimulation of deep somatic tissue with capsaicin produces long-lasting mechanical allodynia and heat hypoalgesia that depends on early activation of the cAMP pathway.
J Neurosci 2002;22(13):5687–93.

Smit TH, van Tunen MS, van der Veen AJ, Kingma I, van Dieen JH.
Quantifying intervertebral disc mechanics: a new definition of the neutral zone.
BMC Musculoskelet Disord 2011;12:38.

Smith OG, Langworthy SM, Paxson MC.
Modernized chiropractic. 1st ed.
Cedar Rapids: Laurance Press; 1906.

Snider KT, Snider EJ, Degenhardt BF, Johnson JC, Kribs JW.
Palpatory accuracy of lumbar spinous processes using multiple bony landmarks.
J Manipulative Physiol Ther 2011;34(5):306–13.

Song XJ, Gan Q, Cao JL, Wang ZB, Rupert RL.
Spinal manipulation reduces pain and hyperalgesia after lumbar intervertebral foramen inflammation in the rat.
J Manipulative Physiol Ther 2006;29(1):5–13.

Song XJ, Hu SJ, Greenquist KW, Zhang JM, LaMotte RH.
Mechanical and thermal hyperalgesia and ectopic neuronal discharge after chronic compression of dorsal root ganglia.
J Neurophysiol 1999;82(6):3347–58.

Ssavedra-Hernandez M, Castro-Sanchez AM, Fernandez-de-las-Penas C, Cleland JA, Ortega-Santiago R, Arroyo-Morales M.
Predictors for identifying patients with mechanical neck pain who are likely to achieve short-term success with manipulative interventions directed at the cervical and thoracic spine.
J Manipulative Physiol Ther 2011;34(3):144–52.

Steffen T, Rubin RK, Baramki HG, Antoniou J, Marchesi D, Aebi M.
A new technique for measuring lumbar segmental motion in vivo. Method, accuracy, and preliminary results.
Spine (Phila Pa 1976) 1997;22(2):156–66.

Sterling M, Pedler A, Chan C, Puglisi M, Vuvan V, Vicenzino B.
Cervical lateral glide increases nociceptive flexion reflex threshold but not pressure or thermal pain thresholds in chronic whiplash associated disorders: a pilot randomised controlled trial.
Man Ther 2010;15(2):149–53.

Stovall BA, Kumar S.
Anatomical landmark asymmetry assessment in the lumbar spine and pelvis: a review of reliability.
PM R 2010;2(1):48–56.

Stubbs M, Harris M, Solomonow M, Zhou B, Lu Y, Baratta RV.
Ligamento-muscular protective reflex in the lumbar spine of the feline.
J Electromyogr Kinesiol 1998;8(4):197–204.

Takahashi O, Shiosaka S, Traub RJ, Ruda MA.
Ultrastructural demonstration of synaptic connections between calcitonin gene-related peptide immunoreactive axons and Dynorphin A(1–8) immunoreactive dorsal horn neurons in a rat model of peripheral inflammation and hyperalgesia.
Peptides 1990;11(6):1233–7.

Takebayashi T, Yamashita T, Minaki Y, Ishii S.
Mechanosensitive afferent units in the lateral ligament of the ankle.
J Bone Joint Surg Br 1997;79(3):490–3.

Thompson RE, Pearcy MJ, Downing KJ, Manthey BA, Parkinson IH, Fazzalari NL.
Disc lesions and the mechanics of the intervertebral joint complex.
Spine 2000;25(23):3026–35.

Triano J.
The theoretical basis for spinal manipulation.
In: Haldeman S, Budgell B, editors. Principles and practice of chiropractic. 3rd ed.
New York: McGraw-Hill; 2005. p. 361–81.

van Trijffel E, Oostendorp RA, Lindeboom R, Bossuyt PM, Lucas C.
Perceptions and use of passive intervertebral motion assessment of the spine: a survey among physiotherapists specializing in manual therapy.
Man Ther 2009;14(3):243–51.

van Trijffel E, Plochg T, van Hartingsveld F, Lucas C, Oostendorp RA.
The role and position of passive intervertebral motion assessment within clinical reasoning and decision-making in manual physical therapy: a qualitative interview study.
J Man Manip Ther 2010;18(2):111–8.

van Tulder MW, Assendelft WJ, Koes BW, Bouter LM.
Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies.
Spine (Phila Pa 1976) 1997;22(4):427–34.

Visscher CM, Lobbezoo F, De BW, van der Zaag J, Naeije M.
Prevalence of cervical spinal pain in craniomandibular pain patients.
Eur J Oral Sci 2001;109(2):76–80.

Wall PD, Devor M.
Sensory afferent impulses originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats.
Pain 1983;17:321–39.

Walsh TR, Weinstein JN, Spratt KF, Lehmann TR, Aprill C, Sayre H.
Lumbar discography in normal subjects. A controlled, prospective study.
JBS 1990;72(7):1081–8.

White AA, Panjabi MM.
Clinical biomechanics of the spine. 2nd ed.
Philadelphia: J.B. Lippincott Company; 1990.

Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N.
A study of computerassisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients.
Spine 1984;9(6):549–51.

Winkelstein BA, DeLeo JA.
Mechanical thresholds for initiation and persistence of pain following nerve root injury: mechanical and chemical contributions at injury.
J Biomech Eng 2004;126(2):258–63.

Witt I, Vestergaard A, Rosenklint A.
A comparative analysis of X-ray findings of the lumbar spine in patients with and without lumbar pain.
Spine 1984;9(3):298–300.

Wolpaw JR, Tennissen AM.
Activity-dependent spinal cord plasticity in health and disease.
Annu Rev Neurosci 2001;24:807–43.

Woolf CJ, Wall PD.
Relative effectiveness of C primary afferent fibers of different origins in evoking a prolonged facilitation of the flexor reflex in the rat.
J Neurosci 1986;6(5):1433–42.

Yahia L, Rhalmi S, Newman N, Isler M.
Sensory innervation of human thoracolumbar fascia. An immunohistochemical study.
Acta Orthop Scand 1992;63(2):195–7.

Yamashita T.
Mechanosensitive afferent units in the lumbar facet joint.
J Bone Joint Surg 1990;72-a(6):865–70.

Yamashita T, Minaki Y, Oota I, Yokogushi K, Ishii S.
Mechanosensitive afferent units in the lumbar intervertebral disc and adjacent muscle.
Spine (Phila Pa 1976) 1993;18(15):2252–6.

Yamashita T, Minaki Y, Takebayashi T, Sakamoto N, Ishii S.
Neural response of mechanoreceptors to acute inflammation in the rotator cuff of the shoulder joint in rabbits.
Acta Orthop Scand 1999;70(2):137–40.

Zeilhofer HU, Zeilhofer UB.
Spinal dis-inhibition in inflammatory pain.
Neurosci Lett 2008;437(3):170–4.

Zito G, Jull G, Story I.
Clinical tests of musculoskeletal dysfunction in the diagnosis of cervicogenic headache.
Man Ther 2006;11(2):118–29.


Since 11-04-2012

                  © 1995–2024 ~ The Chiropractic Resource Organization ~ All Rights Reserved