The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: The Neurological Effect Part 3 of a 5 Part Series
The Mechanism of the Chiropractic
Spinal Adjustment/Manipulation:
Bio-Neuro-Mechanical Effect
Part 3 of a 5 Part Series
By: Mark Studin
William J. Owens
A report on the scientific literature
Citation: Studin M., Owens W., (2017) The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Bio-Neuro-Mechanical Component Part 3 of 5, American Chiropractor 39 (7), pgs. 30,32,34, 36, 38, 40-41
In part 1 of this series, we discussed the osseous mechanisms of the chiropractic spinal adjustment (CSA) and in part 2 we discussed the mechanical and neurological functions of connective tissue. It is in this connective tissue as well as in other neurological components located in the osseous structures of the spine that the primary effector structures of a CSA are to be found. To fully understand the bio-neuro-mechanical mechanism of the CSA, we must explore the mechanical aspect of the chiropractic adjustment, what effect it has on the neurological effector organs, how the spine and brain are inter-related and finally, how the muscles and ligaments (intervertebral discs) working in tandem effectuate homeostasis.
HISTORICAL REPORTING
Kent (1996) reported:
Dishman and Lantz developed and popularized the five component model of the “vertebral subluxation complex” attributed to Faye. However, the model was presented in a text by Flesia dated 1982, while the Faye notes bear a 1983 date.The original model has five components:
1. Spinal kinesiopathology
2. Neuropathology
3. Myopathology
4. Histopathology
5. Biochemical changes.
The “vertebral subluxation complex” model includes tissue specific manifestations described by Herfert which include:
1. Osseous component
2. Connective tissue involvement, including disc, other ligaments, fascia, and muscles
3.The neurological component, including nerve roots and spinal cord
4. Altered biomechanics
5. Advancing complications in the innervated tissues and/or the patient’s symptoms. This is sometimes termed the “end tissue phenomenon” of the vertebral subluxation complex.
Lantz has since revised and expanded the “vertebral sub- luxation complex” model to include nine components:
1. Kinesiology
2. Neurology
3. Myology
4. Connective tissue physiology
5. Angiology
6. Inflammatory response
7. Anatomy
8. Physiology
9. Biochemistry.
Lantz summarized his objectives in expanding the model: “The VSC allows for every aspect of chiropractic clinical management to be integrated into a single conceptual model, a sort of ‘unified field theory’ of chiropractic… (p.1)
However, like many theories, these concepts have proven close to accurate and this report of the literature, although not designed to prove or disprove the Vertebral Subluxation Complex, validated many of the previous “beliefs” based upon contemporary findings in the literature and personal clinical experience, which along with patient expectations, are the three key components to evidence-based medicine.
CONTEMPORARY FINDINGS
In Part 1, we discussed specific biomechanical references in modern literature.
Evans (2002) reported:
…on flexion of the lumbar spine, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with it. On attempted extension, the inferior articular process returns toward its neutral position, but instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying “lesion” under the capsule: a meniscoid entrapment…A large number of type III and type IV nerve fibers (nociceptors) have been observed within capsules of zygapophyseal joints. Pain occurs as distension of the joint capsule provides a sufficient stimulus for these nociceptors to depolarize. Muscle spasm would then occur to prevent impaction of the meniscoid. (p. 252-253)
This verifies that with a vertebrate out of position, there is a negative neurological sequella that causes a “cascade effect” bio-neuro-mechanically. Historically, this has been objectively identified and in chiropractic practices called a vertebral subluxation. This nomenclature has been accepted federally by the U.S. Department of Health and Human Services and by the Centers for Medicare and Medicaid Services as an identifiable lesion, for which the chiropractic profession has specific training in its diagnosis and management.
To further clarify the modern literature, Panjabi (2006) stated:
The spinal column has two functions: structural and transducer. The structural function provides stiffness to the spine. The transducer function provides the information needed to precisely characterize the spinal posture, vertebral motions, spinal loads etc. to the neuromuscular control unit via innumerable mechanoreceptors present in the spinal column ligaments, facet capsules and the disc annulus. These mechanical transducers provide information to theneuromuscular control unit which helps to generate muscular spinal stability via the spinal muscle system and neuromuscular control unit. (p. 669)
Panjabi (2006) reported:
1. Single trauma or cumulative microtrauma causes subfailure injury of the spinal ligaments and injury to the mechanoreceptors [and nociceptors] embedded in the ligaments.
2. When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors [and nociceptors] are corrupted.
3. Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
4. The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle.
5. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors [and nociceptors], further corrupting the muscle response pattern.
6. The corrupted muscle response pattern produces high stresses and strains in spinal components leading to further subfailure injury of the spinal ligaments, mechanoreceptors and muscles, and overload of facet joints.
7. The abnormal stresses and strains produce inflammation of spinal tissues, which have abundant supply of nociceptive sensors and neural structures. (p. 669-670)
This indicates that once there is a bio-neuro-mechanical lesion (aka vertebral subluxation), there is a “negative cascade” both structurally (biomechanically) and neurologically in the body’s attempt to create homeostasis. However, should the cause of the lesion not be “fixed,” the entire system will perpetually fail. Over time, due to the Piezoelectric effect and Wolff’s Law of remodeling, the skeletal structure is now permanently altered. Therefore, treatment goals then switch from curative to simply management and is a long-term process.
In part 2, we discussed subfailure,and will examine it again as explained by Solomnow (2009).
Solomonow (2009):
Inflammatory response in ligaments is initiated whenever the tissue is subjected to stresses which exceed its routine limits at a given time. For example, a sub-injury/failure load, well within the physiological limits of a ligament when applied to the ligament by an individual who does not do that type of physical activity routinely. (p. 143)
Jaumard, Welch and Winkelstein (2011) reported:
In the capsular ligament under stretch, the collagen fiber structure and the nerve endings embedded in that network and cells (fibroblasts, macrophages) are all distorted and activated. Accordingly, capsular deformations of certain magnitudes can trigger a wide range of neuronal and inflammatory responses…Although most of the proprioceptive and nociceptive afferents have a low-strain threshold (~10%) for activation, a few receptors have a high-strain threshold (42%) for signal generation via neural discharge. In addition, capsular strains greater than 47% activate nociceptors with pain signals transmitted directly to the central nervous system. Among both the low- and high-strain threshold neural receptors in the capsular ligament a few sustain their firing even after the stretching of the capsular ligament is released. This persistent afterdischarge evident for strains above 45% constitutes a peripheral sensitization that may lead to central sensitization with long-term effects in some cases. (p. 12)
The cascade effect works in 2 directions, one to create a bio-neuro-mechanically failed spinal system and one to correct a bio-neuro-mechanically failed system.
Pickar (2002) reported:
The mechanical force introduced into the during a spinal manipulation (CSA) may directly alter segmental biomechanics by releasing trapped meniscoids, releasing adhesions or by reducing distortion of the annulus fibrosis. (p. 359)
This fact verifies that there is an osseous-neurological component that exists with the nociceptors at the facet level.
Pickar (2002) also stated:
In addition, the mechanical thrust could either stimulate or silence nonnociceptive, mechanosensitive receptive nerve endings in paraspinal tissue, including skin, muscle, tendons, ligaments, facet joints and intervertebral disc. (p. 359)
CENTRAL NERVOUS SYSTEM MODULATION
When discussing central nervous system activity as a direct sequella to a CSA, we must divide our reporting into 2 components, reflexively at the area being adjusted and through higher cortical responses. When discussing local reflexive activity, we must also determine if it is critical to adjust the specific segment in question or if the adjustment will elicit neurological and end organ (muscle) responses to help create a compensatory action for the offending lesion.
Reed and Pickar (2015) reported in an animal study:
First, during clinically relevant spinal manipulative thrust durations (<=150 ms), unilateral intervertebral joint fixation significantly decreases paraspinal muscle spindle response compared with non-fixated conditions. Second and perhaps more importantly, this study shows that while L6 muscle spindle response decreases with L4 HVLA-SM, 60%-80% of an L6 HVLA-SM muscle spindle response is still elicited from an HVLA-SM delivered 2 segments away in both the absence and presence of intervertebral joint fixation. These findings may have clinical implications concerning specific (targeted) versus nonspecific (nontargeted) HVLA-SM. (p. E755-E756)
Reed and Pickar (2015) also reported:
The finding that nontarget HVLA-SM delivered 2 segments away elicited significantly less but yet a substantial percentage (60%–80%) of the neural response elicited during target HVLA-SM may have important clinical implications with regard to HVLA-SM thrust accuracy/specificity requirements. It may explain how target vs non-target site manual therapy interventions can show similar clinical efficacy. In a recent study using the same model as the current study, the increase in L6 muscle spindle response caused by an HVLA-SM is not different between 3 anatomical thrust contact sites (spinous process, lamina, and mammillary body) on the target L6 vertebra but is significantly less when the contact site is located 1 segment caudal at L7…The current study confirms that a nontarget HVLA-SM compared with a target HVLA-SM decreases spindle response but adds the caveat that a substantial percentage (60%–80%) of afferent response can be elicited from an HVLA-SM delivered 2 segments away irrespective of the absence or presence of intervertebral fixation. (p. E756)
Coronado, Gay, Bialosky, Carnaby, Bishop and George (2012) reported that:
Reductions in pain sensitivity, or hypoalgesia, following SMT [spinal manipulative therapy or the chiropractic adjustment] may be indicative of a mechanism related to the modulation of afferent input or central nervous system processing of pain…The authors theorized the observed effect related to modulation of pain primarily at the level of the spinal cord since 1.) these changes were seen within lumbar innervated areas and not cervical innervated areas and 2.) the findings were specific to a measure of pain sensitivity (temporal summation of pain), and not other measures of pain sensitivity, suggesting an effect related to attenuation of dorsal horn excitability and not a generalized change in pain sensitivity. (p. 752)
These findings indicate that a chiropractic spinal adjustment affects the central nervous system specifically at the interneuron level in the dorsal horn. This is part of the cascade effect of the CSA where we now have objectively identified the mechanism of the central nervous system stimulation and its effects.
Gay, Robinson, George, Perlstein and Bishop (2014)
…pain-free volunteers processed thermal stimuli applied to the hand before and after thoracic spinal manipulation (a form of MT [Manual Therapy]). What they found was, after thoracic manipulation, several brain regions demonstrated a reduction in peak BOLD [blood-oxygen-level–dependent] activity. Those regions included the cingulate, insular, motor, amygdala and somatosensory cortices, and the PAG [periaqueductal gray regions].
The purpose of this study was to investigate the changes in FC [functional changes] between brain regions that process and modulate the pain experience after MT [manual therapy]. The primary outcome was to measure the immediate change in FC across brain regions involved in processing and modulating the pain experience and identify if there were reductions in experimentally induced myalgia and changes in local and remote pressure pain sensitivity. (p. 615)
Therefore, a thoracic CSA adjustment produced direct and measurable effects on the central nervous system across multiple regions, specifically the cingular cortex, insular cortex, motor cortex, amygdala cortex, somatosensory cortex and periaqueductal gray matter. This could only occur if “higher centers,” also known as the central nervous system, were affected.
Gay, Robinson, George, Perlstein and Bishop (2014) went on to report:
Within the brain, the pain experience is subserved by an extended network of brain regions including the thalamus (THA), primary and secondary somatosensory, cingulate, and insular cortices. Collectively, these regions are referred to as thepain processing network(PPN) and encode the sensory discriminate and cognitive and emotional components of the pain experience. Perception of pain is dependent not merely on the neural activity within the PPN [pain processing network] but also on the flexible interactions of this network with other functional systems, including the descending pain modulatory system. (p. 617)
Daligadu, Haavik, Yielder, Baarbe, and Murphy (2013) reported that:
Numerous studies indicate that significant cortical plastic changes are present in various musculoskeletal pain syndromes. In particular, altered feed-forward postural adjustments have been demonstrated in a variety of musculoskeletal conditions including anterior knee pain, low back pain and idiopathic neck pain. Furthermore, alterations in trunk muscle recruitment patterns have been observed in patients with mechanical low back pain. (p. 527)
This concludes that there are observable changes in the function of the central nervous system seen in patients with musculoskeletal conditions and chronic pain. Chiropractors have observed this clinically and it demonstrates the necessity for chiropractic care for both short and long-term management of biomechanical spinal conditions.
CONCLUSION
Although there is significantly more research verifying what occurs with a CSA, the above outlines the basics of how the adjustment works both biomechanically and neurologically from the connective tissue and peripheral nerves to the central nervous system both at the cord level and higher cortical regions. The final question is one of public safety.
Based on their study on 6,669,603 subjects after the unqualified subjects had been removed, Whedon, Mackenzie, Phillips, and Lurie (2015) concluded, “No mechanism by which SM [spinal manipulation] induces injury into normal healthy tissues has been identified” (p. 265).
Part 4 will be the evidence of subluxation degeneration and the literature verifying the mechanisms. Part 5, the final part of our series, will be an in-depth contemporary comparative analysis of the chiropractic spinal adjustment vs. physical therapy joint mobilization.
References:
1. Kent, C. (1996). Models of vertebral subluxation: A review. Journal of Vertebral Subluxation Research, 1(1), 1-7.
2. Evans, D. W. (2002). Mechanisms and effects of spinal high-velocity, low-amplitude thrust manipulation: Previous theories. Journal of Manipulative and Physiological Therapeutics, 25(4), 251-262.
3. Department of Health and Human Services, Centers for Medicare and Medicaid Services. (2017). Medicare coverage for chiropractic services – Medical record documentation requirements for initial and subsequent visits. MLN Matters, Retrieved from https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNMattersArticles/downloads/SE1601.pdf
4. Panjabi, M. M. (2006). A hypothesis of chronic back pain: Ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.
5. Solomonow, M. (2009). Ligaments: A source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.
6. Jaumard, N. V., Welch, W. C., & Winkelstein, B. A. (2011). Spinal facet joint biomechanics and mechanotransduction in normal, injury and degenerative conditions.Journal of Biomechanical Engineering,133(7), 071010.
7. Pickar, J. G. (2002). Neurophysiological effects of spinal manipulation.Spine,2(5), 357-371.
8. Reed, W. R., & Pickar, J. G. (2015). Paraspinal muscle spindle response to intervertebral fixation and segmental thrust level during spinal manipulation in an animal model.Spine,40(13), E752-E759.
9. Coronado, R. A., Gay, C. W., Bialosky, J. E., Carnaby, G. D., Bishop, M. D., & George, S. Z. (2012). Changes in pain sensitivity following spinal manipulation: A systematic review and meta-analysis. Journal of Electromyography Kinesiology, 22(5), 752-767.
10. Gay, C. W., Robinson, M. E., George, S. Z., Perlstein, W. M., & Bishop, M. D. (2014). Immediate changes after manual therapy in resting-state functional connectivity as measured by functional magnetic resonance imaging in participants with induced low back pain.Journal of Manipulative and Physiological Therapeutics, 37(9), 614-627.
11. Daligadu, J., Haavik, H., Yielder, P. C., Baarbe, J., & Murphy, B. (2013). Alterations in coritcal and cerebellar motor processing in subclinical neck pain patients following spinal manipulation.Journal of Manipulative and Physiological Therapeutics, 36(8), 527-537.
12. Whedon, J. M., Mackenzie, T. A., Phillips, R. B., & Lurie, J. D. (2015). Risk of traumatic injury associated with chiropractic spinal manipulation in Medicare Part B beneficiaries aged 66-69 years. Spine, 40(4), 264-270.
The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Ligaments and the Bio-Neuro-Mechanical Component Part 2 of a 5 Part Series
The Mechanism of the Chiropractic
Spinal Adjustment/Manipulation:
Ligaments and the Bio-Neuro-Mechanical Component
Part 2 of a 5 Part Series
By: Mark Studin
William J. Owens
A report on the scientific literature
Citation: Studin M., Owens W., (2017) The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Ligaments and the Bio-Neuro-Mechanical Component, Part 2 of 5, American Chiropractor 39 (6), pgs. 22,24-26, 28-31
Introduction
When we consider the mechanism of the spinal adjustment/manipulation as discussed in part 1 of this series, for clarity for the chiropractic profession, it will be solely referred to as a chiropractic spinal adjustment (CSA) so as not to confuse chiropractic treatment with either physical therapy or osteopathy. In analyzing how the CSA works, we must go beyond the actual adjustment or thrust and look at the tissue and structures that “frame” the actions. Although there are osseous borders and boundaries, there is a significant network of connective tissue that plays a major role in the CSA. We will focus this discussion on the ligaments that both act as restraints to the human skeleton and also function as sensory organs, we will also examine the role of the muscles and tendons that interact with the ligaments. It is critical to realize that muscles act as active and amplified restraints in the spinal system.
The neurological innervations of the ligaments play a significant role in influencing the central nervous system, both reflexively and through brain pathways. Those innervations either support homeostasis in a balanced musculoskeletal environment or creates confusion in a system that has been impaired either post-traumatically or systemically. The human body does not discriminate the etiology of biomechanical failure, it only reacts to create a “low energy” or neutral state utilizing the lowest amount of energy to function. This balanced or “low energy state” is considered the most optimal function state as nervous system function is not compromised by aberrant sensory input, this is why a “low energy state” is considered the highest function state.
With understanding the full functional and resultant role of the ligaments and other connective tissues in either macro or repetitive micro traumas, bio-neuro-mechanical failure (something we have historically called vertebral subluxation) occurs. This is the basis for chiropractic care and explains why immediate (pain management), intermediate (corrective) and long-term (wellness or health maintenance) care are necessary to reintegrate the bio-neuro-mechanical system of the human body. Often, the best we can accomplish as practitioners is to support compensation secondary to tissue failure to slow down the resultant joint remodeling and neurological corruption/compromise.
Ligamentous Function
Solomonow (2009) wrote:
The functional complexity of ligaments is amplified when considering their inherent viscoelastic properties such as creep, tension–relaxation, hysteresis and time or frequency-dependent length–tension behavior. As joints go through their range of motion, with or without external load, the ligaments ensure that the bones associated with the joint travel in their prescribed anatomical tracks, keep full and even contact pressure of the articular surfaces, prevent separation of the bones from each other by increasing their tension, as may be necessary, and ensuring stable motion. Joint stability, therefore, is the general role of ligaments without which the joint may subluxate, cause damage to the capsule, cartilage, tendons, nearby nerves and blood vessels, discs (if considering spinal joints) and to the ligaments themselves. Such injury may debilitate the individual by preventing or limiting his/her use of the joint and the loss of function…Dysfunctional or ruptured ligaments, therefore, result in a complex- syndrome, various sensory–motor disorders and other long-term consequences, which impact the individual’s well-being, his athletic activities, employer, skilled work force pool and national medical expenses. (p. 137)
Ligaments are closely packed collagen fibers that are helical at rest in a crimp pattern. This crimp pattern allows the ligament to recruit other fibers when stressed to support the joint and helps prevent ligamentous failure or subfailure (tearing of the ligament). They are comprised of collagen and elastin which give them both tensile strength and elasticity with no two joints being alike in composition. Each joint has a specific biomechanical role and varies depending upon the needs of that joint.
Note. “Ligaments and tendons,” by I. Ziv, (n.d.), [PowerPoint slides]. Retrieved from https://wings.buffalo.edu/eng/mae/courses/417-517/Orthopaedic%20Biomechanics/ Lecture%203u.pdf
Solomonow (2008) continued:
As axial stretching of a ligament is applied, fibers or bundles with a small helical wave appearance straighten first and begin to offer resistance (increased stiffness) to stretch. As the ligament is further elongated, fibers or fiber bundles of progressively larger helical wave straighten and contribute to the overall stiffness. Once all the fibers are straightened, a sharp increase in stiffness is observed. (p. 137)
Solomonow (2008) later stated:
Over all, the mostly collagen (75%), elastin and other substances structure of ligaments is custom tailored by long evolutionary processes to provide various degrees of stiffness at various loads and at various ranges of motion of a joint, while optimally fitting the anatomy inside (inter-capsular) or outside (extra-capsular) a given joint. The various degrees of helical shape of the different fibers allows generation of a wide range of tensile forces by the fiber recruitment process, whereas the overall geometry of the ligament allows selective recruitment of bundles such as to extend function over a wide range of motion. The large content of water (70%) and the cross weave of the long fibers by short fibers provides the necessary lubrication for bundles to slide relative to each other, yet to remain bundled together and generate stiffness in the transverse directions.(p. 137)
Solomonow (2008):
Length–tension and recruitment: The general length–tension (or strain–stress) behavior of a ligament is non-linear…The initial [reports] demonstrate rather large strain for very small increase in load. Once all the waves in the collagen fibers of the ligament have been straightened out, and all of the fibers were recruited, additional increase in strain is accompanied with a fast increase in tension…
Creep: When a constant load is applied to a ligament, it first elongates to a given length. If left at the same constant load, it will continue to elongate over time in an exponential fashion up to a finite maximum…
Tension–relaxation:When ligaments are subjected to a stretch and hold over time (or constant elongation) the tension–relaxation phenomena is observed. The tension in the ligament increases immediately upon the elongation to a given value. As time elapses, the tension decreases exponentially to a finite minimum while the length does not change…
Strain rate: The tension developed in a ligament also depends on the rate of elongation or strain rate (Peterson, 1986). In general, slow rates of elongation are associated with the development of relatively low tension, whereas higher rates of elongation result in the development of high tension. Fast stretch of ligaments, such as in high-frequency repetitive motion or in sports activities are known to result in high incidents of ligamentous damage or rupture…Fast rates of stretch, therefore, may exceed the physiological loads that could be sustained by a ligament safely, yet it may still be well within the physiological length range. Development of high tension in the ligaments may result in rupture and permanent sensory–motor deficit to the joint in addition to deficit in its structural functions. (p. 137-139)
Author’s note: A fast strain rate within the physiological limit may also cause ligamentous damage as the ligament hasn’t had enough time to adapt (stretch) to its new tensile demand and this is called a “sub-failure.”
“This phenomenon is associated with repetitive motion when a series of stretch-release cycles are performed over time (Solomnow, 1008, p. 140).
Ligament Reaction to Trauma and Healing
Solomnow (2008) stated:
Ligament Inflammation: Inflammatory response in ligaments is initiated whenever the tissue is subjected to stresses which exceed its routine limits at a given time. For example, a sub-injury/failure load, well within the physiological limits of a ligament when applied to the ligament by an individual who does not do that type of physical activity routinely. The normal homeostatic metabolic, cellular, circulatory and mechanical limits are therefore exceeded by the load, triggering an inflammatory response…
Another case where acute inflammation is present is when physical activities presenting sudden overload/stretch cause a distinct damage to the tissue which is felt immediately. Such cases, as a sudden loss of balance, a fall, collision with another person, exposure to unexpected load, etc., may result in what is called a sprain injury or a partial rupture of the ligament. Acute inflammation sets in within several hours and may last several weeks and up to 12 months. The healing process, however, does not result in full recovery of the functional properties of the tissue. Mostly, only up to 70% of the ligaments original structural and functional characteristics are attained by healing post-injury (Woo et al. 1990)…
Chronic inflammation is an extension of an acute inflammation when the tissue is not allowed to rest, recover and heal. Repetitive exposure to physical activity and reloading of the ligament over prolonged periods without sufficient rest and recovery represent cumulative micro-trauma. The resulting chronic inflammation is associated with atrophy and degeneration of the collagen matrix leaving a permanently damaged, weak and non-functional ligament (Leadbenter, 1990). The dangerous aspect of a chronic inflammation is the fact that it builds up silently over many weeks, months or years (dependent on a presently unknown dose-duration levels of the stressors) and appears one day as a permanent disability associated with pain, limited motion, weakness and other disorders (Safran, 1985). Rest and recovery of as much as 2 years allows only partial resolution of the disability (Woo and Buckwalter, 1988). Full recovery was never reported. (p. 143-144)
Hauser et al. (2013) reported that once a ligament is overloaded in either a failure or subfailure, then the tissue fails which results in partial or complete tears known as a sprain. When this occurs, the body “attempts” to repair the damaged ligament, but cannot completely.
Hauser et al. (2013) wrote:
With time, the tissue matrix starts to resemble normal ligament tissue; however, critical differences in matrix structure and function persist. In fact, evidence suggests that the injured ligament structure is replaced with tissue that is grossly, histologically, biochemically, and biomechanically similar to scar tissue. (p. 6)
Hauser et al. (2013) also stated:
The persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics, depending on the functional demands placed on the tissue. Since remodeled ligament tissue is morphologically and biomechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joint and predisposing other soft tissues in and around the joint to further damage. (p. 7)
Hauser et al. (2013) further said:
In fact, studies of healing ligaments have consistently shown that certain ligaments do not heal independently following rupture, and those that do heal, do so with characteristically inferior compositional properties compared with normal tissue. It is not uncommon for more than one ligament to undergo injury during a single traumatic event. (p. 8)
Author’s note: Ligaments are made with fibroblasts which produce collagen and elastin, and model the ligament throughout puberty. Once puberty is over, the fibroblasts stop producing any ligamentous tissue and remain dormant. Upon injury, the fibroblast activates, but now can only produce collagen, leaving the joint stiffer and in a biomechanically compromised functional environment. The above comment verifies that in the literature.
Hauser et al. (2013) explained:
Osteoarthritis [OA] or joint degeneration is one of the most common consequences of ligament laxity. Traditionally, the pathophysiology of OA was thought to be due to aging and wear and tear on a joint, but more recent studies have shown that ligaments play a crucial role in the development of OA. OA begins when one or more ligaments become unstable or lax, and the bones begin to track improperly and put pressure on different areas, resulting in the rubbing of bone on cartilage. This causes the breakdown of cartilage and ultimately leads to deterioration, whereby the joint is reduced to bone on bone, a mechanical problem of the joint that leads to abnormality of the joint’s mechanics.
Hypermobility and ligament laxity have become clear risk factors for the prevalence of OA. The results of spinal ligament injury show that over time the inability of the ligaments to heal causes an increase in the degeneration of disc and facet joints, which eventually leads to osteochondral degeneration. (p. 9)
Ligaments as Sensory Organs
Spinal pain and the effects of the chiropractic spinal adjustment is both central and peripheral in etiology. According to Studin and Owens (2016), the CSA also affects the central nervous system with systemic sequelae verifying that chiropractic supports systemic changes and is not comprised solely of “back pain providers.” Although chiropractic is not limited to pain, chiropractors do treat back pain, inclusive of all spinal regions. Regarding pain, much of the pain generators originate in the ligaments.
Solomonow (2009) wrote:While ligaments are primarily known for mechanical support for joint stability, they have equally important sensory functions. Anatomical studies demonstrate that ligaments in the extremity joints and the spine are endowed with mechanoreceptors consisting of: Pacinian, Golgi, Ruffini and bare nerve endings. (Burgess and Clark, 1969; Freeman and Wyke, 1967a,b; Gardner, 1944; Guanche et al., 1995; Halata et al., 1985; Jackson et al., 1966; Mountcastle, 1974; Petrie et al., 1988, Schulz et al. 1984, Sjölander, 1989; Skoglund, 1956; Solomonow et al., 1996; Wyke, 1981; Yahia and Newman, 1991; Zimney and Wink, 1991). The presence of such afferents in the ligaments confirms that they contribute to proprioception and kinesthesia and may also have a distinct role in reflex activation or inhibition of muscular activities.(p. 144)
Dougherty (n.d.) reported:
Pacinian corpusclesare found in subcutaneous tissue beneath the dermis…and in the connective tissues of bone [ligaments and tendons], the body wall and body cavity. Therefore, they can be cutaneous, proprioceptive or visceral receptors, depending on their location…
When a force is applied to the tissue overlying the Pacinian corpuscle…its outer laminar cells, which contain fluid, are displaced and distort the axon terminal membrane. If the pressure is sustained on the corpuscle, the fluid is displaced, which dissipates the applied force on the axon terminal. Consequently, a sustained force on the Pacinian corpuscle is transformed into a transient force on its axon terminal. The Pacinian corpuscle 1° afferent axon response is rapidly adapting and action potentials are only generated when the force is first applied. (http://neuroscience.uth.tmc.edu/ s2/chapter02.html)
Dougherty (n.d.) stated:
TheRuffini corpusclesare found deep in the skin…as well as in joint ligaments and joint capsules and can function as cutaneous or proprioceptive receptors depending on their location. The Ruffini corpuscle…is cigar-shaped, encapsulated, and contains longitudinal strands of collagenous fibers that are continuous with the connective tissue of the skin or joint. Within the capsule, the 1° afferent fiber branches repeatedly and its branches are intertwined with the encapsulated collagenous fibers. (http://neuroscience.uth.tmc. edu/s2/chapter02.html) “Ruffini corpuscles in skin are considered to be skin stretch sensitive receptors of the discriminative touch system. They also work with the proprioceptors in joints and muscles to indicate the position and movement of body parts” (Dougherty, http://neuroscience.uth.tmc.edu/s2/chapter02.html).
Dougherty (n.d.) stated:
Golgi tendon organsare found in the tendons of striated extrafusal muscles near the muscle-tendon junction…Golgi tendon organs resemble Ruffini corpuscles. For example, they are encapsulated and contain intertwining collagen bundles, which are continuous with the muscle tendon, and fine branches of afferent fibers that weave between the collagen bundles…They are functionally “in series” with striated muscle. (http://neuroscience.uth.tmc.edu/s2/ chapter02.html)
“TheGolgi tendon organis a proprioceptor that monitors and signals muscle contraction against a force (muscle tension), whereas the muscle spindle is a proprioceptor that monitors and signals muscle stretch (muscle length)” (Dougherty, http://neuroscience.uth.tmc.edu/ s2/chapter02.html).
Dougherty (n.d.) stated:
…free nerve endings of 1° afferents are abundant in muscles, tendons, joints, and ligaments. These free nerve endings are considered to be the somatosensory receptors for pain resulting from muscle, tendon, joint, or ligament damage and are not considered to be part of the proprioceptive system. [These free nerve endings are called nociceptors.]
Solomonow (2009) commented:
The presence of such afferents in the ligaments confirms that they contribute to proprioception and kinesthesia and may also have a distinct role in reflex activation or inhibition of muscular activities…
Overall, the decrease or loss of function in a ligament due to rupture or damage does not only compromise its mechanical contributions to joint stability, but also sensory loss of proprioceptive and kinesthetic perception and fast reflexive activation of muscles and the forces they generate in order to enforce joint stability…
It was suggested, as far back as the turn of the last century, that a reflex may exist from sensory receptors in the ligaments to muscles that may directly or indirectly modify the load imposed on the ligament (Payr, 1900)…A clear demonstration of a reflex activation of muscles was finally provided in 1987 (Solomonow et al., 1987) and reconfirmed several times since then (beard et al., 1994; Dyhre-Poulsen and Krogsgard, 2000; Raunest et al., 1996; Johansson et al., 1989; Kim et al., 1995). It was further shown that such a ligamento-muscular reflex exists in most extremity joints (Freeman and Wyke, 1967b; Guanche et al., 1995, Knatt et al., 1995; Schaible and Schmidt, 1983; Schaible et al., 1986; Solomonow et al., 1996; Phillips et al., 1997; Solomonow and Lewis, 2002) and in the spine (Indahl et al., 1995, 1997; Stubbs et al., 1998; Solomonow et al., 1998). (p. 144).
“Ligamento-muscular reflexes, therefore, may be inhibitory or excitatory, as may be fit to preserve joint stability; inhibiting muscles that destabilize the joint or increased antagonist co-activation to stabilize the joint” (Solomonow, 2009, p. 145).
Spinal Stabilization and Destabilization
Panjabi (2006) reported:
1. Single trauma or cumulative microtrauma causes subfailure injury of the spinal ligaments and injury to the mechanoreceptors [and nociceptors] embedded in the ligaments.
2. When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors [and nociceptors] are corrupted.
3. Neuromuscular control unit has difficulty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
4. The muscle response pattern generated by the neuromuscular control unit is corrupted, affecting the spatial and temporal coordination and activation of each spinal muscle.
5. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors [and nociceptors], further corrupting the muscle response pattern. (p. 669)
The above stabilization-destabilization scenario is the foundation for why a CSA is clinically indicated for short, intermediate and long-term treatment (biomechanical stabilization) as clinically indicated. It also clearly outlines what the goal of the CSA is, to integrate the bio-neuro-mechanical system to bring the human body to utilize its lowest form of energy for homeostasis or as close to normal as tissue pathology allows.
This is part 2 of a 5-part series where part 1 covers the osseous mechanics of the chiropractic spinal adjustment. This part covered the ligamentous involvement from a supportive and neurological perspective. The topic of part 3 will be spinal biomechanics and their neurological components in addition to how the chiropractic spinal adjustment makes changes bio-neuro-mechanically. Part 4 will be an in-depth contemporary comparative analysis of the chiropractic spinal adjustment vs. physical therapy joint mobilization. The final part will be a concise overview of the chiropractic spinal adjustment.
References:
1. Solomonow, M. (2009). Ligaments: A source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.
2. Ziv, I. (n.d.). Ligaments and tendons [PowerPoint slides]. Retrieved from https://wings.buffalo.edu/eng/mae/courses/417-517/Orthopaedic%20Biomechanics/Lecture%203u.pdf
3. Hauser, R. A., Dolan, E. E., Phillips, H. J., Newlin, A. C., Moore, R. E., & Woldin, B. A. (2013). Ligament injury and healing: A review of current clinical diagnostics and therapeutics.The Open Rehabilitation Journal,6, 1-20.
4. Solomonow, M. (2006). Sensory–motor control of ligaments and associated neuromuscular disorders.Journal of Electromyography and Kinesiology,16(6), 549-567.
5. Studin M., & Owens W. (2016). Chiropractic spinal adjustments and the effects on the neuroendocrine system and the central nervous system connection. The American Chiropractor, 38(1), 46-51.
6. Dougherty, P. (n.d.). Chapter 2: Somatosensory systems. Neuroscience Online. Retrieved from http://neuroscience.uth.tmc.edu/s2/chapter02.html
7. Panjabi, M. M. (2006). A hypothesis of chronic back pain: Ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.
The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Osseous Mechanisms Part 1 of a 5 Part Series
The Mechanism of the Chiropractic
Spinal Adjustment/Manipulation:
Osseous Mechanisms
Part 1 of a 5 Part Series
By: Mark Studin
William J. Owens
Citation: Studin m., Owens W., (2017) The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Osseous Mechanisms, Part 1 of 5, American Chiropractor 39 (5), pgs. 30, 32, 34, 36-38
A report on the scientific literature
Introduction
There have been many reports in the literature on chiropractic care and its efficacy. However, the reporting is often “muddled” based upon interchangeable terminology utilized to describe what we do. The etiology of the verbiage being used has apparently been part of a movement to gain acceptance within the healthcare community, but this attempt for a change in view by the healthcare community has cost us. Currently, the scientific community has lumped together manipulation performed by physical therapists or osteopaths with chiropractic spinal adjustments because all three professions perform “hands on” manual therapy to the spine. For example, Martínez-Segura, De-la-LLave-Rincón, Ortega-Santiago, Cleland, and Fernández-de-Las-Peñas (2012) discussed how physical therapists commonly use manual therapy interventions directed at the cervical or thoracic spine, and the effectiveness of cervical and thoracic spine thrust manipulation for the management of patients with mechanical, insidious neck pain. Herein lies the root of the confusion when “manipulation” is utilized as a “one-size-fits-all” category of treatment as different professions have different training and procedures to deliver the manipulation, usually applying different treatment methods and realizing different results and goals.
In addition, as discussed by Sung, Kang, and Pickar (2004), the terms “mobilization,” “manipulation” and “adjustment” also are used interchangeably when describing manual therapy to the spine. Some manipulation and virtually all chiropractic adjusting “…involves a high velocity thrust of small amplitude performed at the limit of available movement. However, mobilization involves repetitive passive movement of varying amplitudes at low velocity” (Sung, Kang, & Picker, 2004, p. 115).
To offset confusion between chiropractic and any other profession that involves the performance of some type of manipulation, for the purpose of clarity, we will be referring to any type of spinal therapy performed by a chiropractor as a chiropractic spinal adjustment (CSA) and reserve manipulation for other professions who have not been trained in the delivery of CSA. Until now, the literature has not directly supported the mechanism of the CSA. However, it has supported each component and the supporting literature, herein, will define the neuro-biomechanical process of the CSA and resultant changes.
Components of the Adjustment or Thrust
Both human and animal studies have shown the tri-phasic process of the CSA and the time for the thrust duration of each phase. In addition, the timing at each phase has been shown to be integral in understanding the neurological effect of the CSA. The forces are broken into 3 phases. These are the pre-load force, which takes the tissue close to its paraphysiological limit, the peak force or thrust stage and the resolution stage.
Pickar and Bolton (2012) reported the following:
CSA, referred to in the literature as spinal manual therapy, “…in the cervical region has relatively little pre-load ranging from 0 to 39.5 N. In contrast, the average pre-load forces during [CSA] in the thoracic region (139 ± 46 N, ± SD) and sacroiliac region (mean 88 N ± 78 N) are substantially higher than in the cervical region and are potentially different from each other. From the beginning of the thrust to end of the resolution phase, [CSA] duration varies between 90 and 120 ms. (mean = 102 ms.). The time to peak force during the thrust phase ranges from 30 to 65 ms. (mean = 48 ms.). Peak applied forces range from 99 to 140 N (mean = 118 N, n = 6 treatments). In the same study with [CSA] directed at the thoracic (T4) region and applied to three different patients by the same practitioner, the mean (SD) time to peak force was 150 ± 77 ms. and mean peak force reached 399 ± 119 N. During the resolution phase, force returned to pre-[CSA] levels over durations up to two times longer than that of the thrust phase. When [CSA] was applied to the sacroiliac joint, mean applied peak forces reached 328 ± 78 N, with the thrust and resolution phases having similar durations (∼100ms.). The peak force during manipulation of the lumbar spine measured by Triano and Schultz (1997) tended to be higher than during the thoracic or sacroiliac manipulation measured by Herzog et al. (1994) and the force–time profiles resembled half-sine waves with the time to and from peak taking approximately 200 ms. Peak impulse forces during thoracic manipulation approximated the >400 N peak impulse force measured by Triano and Schultz (1997). (p. 786)
Note. “Spinal Manipulative Therapy and Somatosensory Activation,” by J. G. Pickar and P. S. Bolton, 2012, Journal of Electromyography and Kinesiology,22(5), 787. Copyright 2012 by Elsevier.
Pickar and Bolton (2012) reported that the physical characteristics of an CSA may vary based upon the technique being used and the individual practitioner. However, the above scenario is an illustration and guide to the time and force for of a CSA.
Zygapophysial (Z) joints
Cramer et al. (2002) explained the following:
One component of spinal dysfunction treated by chiropractors has been described as the development of adhesions in the zygapophysial (Z) joints after hypomobility. This hypomobility may be the result of injury, inactivity, or repetitive asymmetrical movements…one beneficial effect of spinal manipulation may be the “breaking up” of putative fibrous adhesions that develop in hypomobile or “fixed” Z joints. Spinal adjusting of the lumbar region is thought to separate or gap the articular surfaces of the Z joints. Theoretically, gapping breaks up adhesions, thus helping the motion segment reestablish a physiologic range of motion. (p. 2459)
Control subject [left] before the CSA and after [right] a CSA. The red arrows depict the increase in the Z-Joint
Note. “The Effects of Side-Posture Positioning and Spinal Adjusting on the Lumbar Z Joints: A Randomized Controlled Trial with Sixty-Four Subjects,” by G. D.Cramer, D. M. Gregerson, J. T. Knudsen, B. B. Hubbard, L. M. Ustas, & J. A., 2002, Spine,27(22), 2462. Copyright 2002 by Lippincott Williams & Wilkins.
Cramer et al. (2002) found the following:
…significant differences between several groups in this study, with the group that received chiropractic adjustments and remained in the side-posture position showing the greatest increase in gapping. This finding is consistent with the hypothesis that chiropractic adjusting gaps the Z joints…The Z joints were found gap during side-posture positioning, although not as much as during side-posture adjusting…The flexion that occurs during the side-posture position and side-posture spinal adjustment may allow for greater gapping during axial rotation and may account for the difference in results between the studies. However, because both the side-posture positioning group and the group that had side-posture adjusting followed by continued side-posture positioning received equal amounts of flexion, the thrust given during the chiropractic procedure had the effect of increasing the gapping of the Z joints. (p. 2464)
The average difference between the control subjects…and the subjects that received a chiropractic adjustment and remained in side-posture position was 1.33 mm…a difference of 0.71 mm was found between the side-posture group…and the group that received an adjustment and remained in the side-posture position…It will be recalled that the Z joints are very small [and this is a considerable gap in a joint as small as the Z joint]…Another important consideration is that the term “residual,” or “left-over” gapping, could be applied to the gapping measured in the adjustment group because it can be logically assumed that the Z joints gap a greater distance during the forceful loading of the manipulative procedure than recorded in this study. The tissues of the spine presumably bring the articular surfaces back toward the pre-adjustment (closed) position as the patient resumes a more typical side-posture position after the thrust of a manipulation. This “residual” gapping is what was seen during the 15- to 20-minute MRI scan taken immediately after the adjustment. (2464-2565)
What makes this significant is the residual time that occurs after the CSA. During this period, and the time that follows is the foundation for biomechanical changes in the adjacent discs and ancillary connective tissue attachments that will be discussed in the next article in the series. However, this is part of the foundation for bio-neuro-mechanical changes to the spine secondary to the CSA.
Meniscoid Entrapment
Evans (2002) reported the following:
…on flexion of the lumbar spine, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with it. On attempted extension, the inferior articular process returns toward its neutral position, but instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying “lesion” under the capsule: a meniscoid entrapment. A large number of type III and type IV nerve fibers (nociceptors) have been observed within capsules of zygapophyseal joints. Pain occurs as distension of the joint capsule provides a sufficient stimulus for these nociceptors to depolarize. Muscle spasm would then occur to prevent impaction of the meniscoid. The patient would tend to be more comfortable with the spine maintained in a flexed position, because this will disengage the meniscoid. Extension would therefore tend to be inhibited. This condition has also been termed a “joint lock” or “facet-lock” the latter of which indicates the involvement of the zygapophyseal joint.
The presence of fibro-adipose meniscoids in the cervical zygapophyseal joints suggests that a similar phenomenon might occur, but in the neck the precipitating movement would be excessive rotation. The clinical features of cervical meniscoid entrapment would be those of an acute torticollis in which attempted derotation would cause impaction and buckling of the entrapped meniscoid and painful capsular strain. Muscle spasm would then occur to prevent impaction of the meniscoid by keeping the neck in a rotated position. Under these circumstances the muscle spasm would not be the primary cause of torticollis but a secondary reaction to the entrapment of the meniscoid.
An HVLAT manipulation, involving gapping of the zygapophyseal joint reduces the impaction and opens the joint, so encouraging the meniscoid lo return to its normal anatomical position in the joint cavity. This ceases the distension of the joint capsule, thus reducing pain. (p. 252-253)
Evans (2002) also explained the following:
Zygapophyseal joint gapping induced during an HVLAT manipulation would further stretch the highly innervated joint capsule, leading to a “protective” reflex muscular contraction, as shown in electromyographic studies. The most important characteristic of a manipulative procedure that will provide joint gapping, before the induction of protective reflex muscular contraction, would be high velocity…the thrusting phase of an HVLAT manipulation required 91 ± 20 ms. to develop the peak force. If this period is compared with the time delay between the onset of the thrusting force and the onset of electromyographic activity, which ranges from 50 to 200 ms., we can see that a force of sufficient magnitude to gap the joint can be applied in a shorter time than that required for the initiation of a mechanoreceptor-mediated muscular reflex. Furthermore, once the muscle is activated (i.e. there is an electromyographic signal), it will take approximately another 40 to 100 ms until the onset of muscular force. It therefore seems unlikely that there are substantial muscular forces resisting the thrusting phase of HVLAT manipulation. Thus, HVLAT manipulation would again appear to be the treatment of choice for a meniscoid entrapment.
The cavitation event may not be a prerequisite for a “successful” HVLAT manipulation in the case of a meniscoid entrapment and may be an incidental side effect of high-velocity zygapophyseal joint gapping (which would be a prerequisite for success). Audible indication of successful joint gapping may, however, be regarded as desirable in itself as a clinical measure of “success.” A clinician’s perception of the occurrence of cavitation during an HVLAT manipulation has been shown to be very accurate and would therefore be a reliable measure of a ‘”successful” joint gapping. (p. 253-254)
Meniscoid entrapment. A) On flexion, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with It. B) On attempted extension, the inferior articular process returns upward to its neutral position, hut instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying “lesion” under the capsule. Pain occurs as a result of capsular tension, and extension is inhibited. C) CSA (Manipulation) of the joint involving flexion and gapping, reduces the impaction and opens the joint to encourage re-entry of the meniscoid into the joint space (D) Realignment of the joint.
Note. “Mechanisms and Effects of Spinal High-Velocity, Low-Amplitude Thrust Manipulation: Previous Theories,” by D. W. Evans, 2002, Journal of Manipulative and Physiological Therapeutics, 25(4), 253. Copyright 2002 by Elsevier.
This first part of a 5-part series covers the osseous mechanics of what the chiropractic spinal adjustment is comprised of. Part 2 will cover the ligamentous involvement from a supportive and neurological perspective. The topic of part 3 will be spinal biomechanics and its neurological components. Part 4 will be an in-depth contemporary comparative analysis of the chiropractic spinal adjustment vs. physical therapy joint mobilization. The final part will be a concise overview of the chiropractic spinal adjustment.
References:
1. Martínez-Segura, R., De-la-LLave-Rincón, A. I., Ortega-Santiago, R., Cleland J. A., Fernández-de-Las-Peñas, C. (2012). Immediate changes in widespread pressure pain sensitivity, neck pain, and cervical range of motion after cervical or thoracic thrust manipulation in patients with bilateral chronic mechanical neck pain: A randomized clinical trial. Journal of Orthopedics & Sports Physical Therapy, 42(9), 806-814.
2. Sung, P. S., Kang, Y. M., & Pickar, J. G. (2004). Effect of spinal manipulation duration on low threshold mechanoreceptors in lumbar paraspinal muscles: A preliminary report. Spine, 30(1), 115-122.
3. Pickar, J. G., & Bolton, P. S. (2012). Spinal manipulative therapy and somatosensory activation.Journal of Electromyography and Kinesiology,22(5), 785-794.
4. Cramer, G. D., Gregerson, D. M., Knudsen, J. T., Hubbard, B. B., Ustas, L. M., & Cantu, J. A. (2002). The effects of side-posture positioning and spinal adjusting on the lumbar Z joints: A randomized controlled trial with sixty-four subjects.Spine,27(22), 2459-2466.
5. Cramer, G. D., Henderson, C. N., Little, J. W. Daley, C., & Grieve, T.J. (2010). Zygapophyseal joint adhesions after induced hypombility. Journal of Manipulative and Physiological Therapeutics, 33(7), 508-518.
6. Evans, D. W. (2002). Mechanisms and effects of spinal high-velocity, low-amplitude thrust manipulation: Previous theories. Journal of Manipulative and Physiological Therapeutics, 25(4), 251-262.
7. Owens, Jr., E. F., Hosek, R. S., Sullivan, S. G. B., Russell, B. S., Mullin, L. E., & Dever, L. L. (2016). Establishing force and speed training targets for lumbar spine high-velocity, low-amplitude chiropractic adjustments. The Journal of Chiropractic Education, 30(1), 7-13.
8. Nougarou, F., Dugas, C., Deslauriers, C., Pagé, I., & Descarreaux, M. (2013). Physiological responses to spinal manipulation therapy: Investigation of the relationship between electromyographic responses and peak force.Journal of Manipulative and Physiological Therapeutics,36(9), 557-563.
9. Solomonow, M. (2009). Ligaments: A source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.
10. He, G., & Xinghua, Z. (2006). The numerical simulation of osteophyte formation on the edge of the vertebral body using quantitative bone remodeling theory. Joint Bone Spine, 73(1), 95-101.