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 Research1(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.

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Published in Neck Problems

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.

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Published in Neck Problems

Chiropractic, Chronic Back Pain and Brain Shrinkage:

 

A better understanding of Alzheimer’s, Dementia, Schizophrenia, Depression and Cognitive Disorders and Chiropractic’s Role

 

A Review of the Mechanisms

 

A report on the scientific literature 


By: Mark Studin DC, FASBE(C), DAAPM, DAAMLP

William J. Owens DC, DAAMLP

Frank Zolli DC, EdD

 

 

Reference: Studin M., Owens W., Zolli F., (2015) Chiropractic, Chronic Back Pain and Brain Shrinkage:A better understanding of Alzheimer’s, Dementia, Schizophrenia, Depression and Cognitive Disorders and Chiropractic’s Role, A Literature Review of the Mechanisms, The American Chiropractor, 37(10) 36-38, 4042, 44-45

 

Since its inception in 1895, Chiropractic has been focused on the spine and its role in the total health and function of the human body.  Throughout its history, the profession has moved from a “bone on nerve” model to a “biomechanical/functional” model however as we evolve (through scientific findings) in our understanding of the true nature of the chiropractic principles, we now conclusively know that chiropractic results are based on the central nervous system and the detrimental role of spinal dysfuntion in the maintenance of homeostasis and “dis-ease” in the human body.  This article bridges the gap between the foundational chiropractic principles taught by the Palmers and their predecessors and today’s breakthrough findings and the correlation between unchecked spinal dysfunction AKA chronic spine pain and its effect on the brain. 

 

 

Peterson ET. AL. (2012) reported, “The … prevalence of low back pain is stated to be between 15% and 30%, the 1-year period prevalence between 15% and 45%, and a life-time prevalence of 50% to 80%” (pg. 525). While acute pain is a normal short-lived unpleasant sensation triggered in the nervous system to alert you to possible injury with a reflexive desire to avoid additional injury, chronic pain is different. Chronic pain persists and fundamentally changes the patient’s interaction with their environment. In chronic pain it is well documented that aberrant signals keep firing in the nervous system for weeks, months, even years.1 Baliki Et. AL. (2008) stated “Pain is considered chronic when it lasts longer than 6 months after the healing of the original injury. Chronic pain patients suffer from more than pain, they experience depression, anxiety, sleep disturbances and decision making abnormalities that also significantly diminish their quality of life” (pg. 1398). Chronic pain patients also have shown to have changes in brain function in sufferers with Alzheimer’ disease, depression, schizophrenia and attention deficit hyperactivity disorder giving further insight into disease states. In addition, chronic pain has a cause and effect on the morphology of the spinal cord and the brain in particular resulting in a process termed “linear shrinkage”, which has been suggested to cause ancillary negative neurological sequella.  

 

Apkarian Et. Al. (2004) reported that “Ten percent of adults suffer from severe chronic pain. Back problems constitute 25% of all disabling occupational injuries and are the fifth most common reason for visits to the clinic; in 85% of such conditions, no definitive diagnosis can be made.” (pg. 10410) Apkarian Et. AL. (2011) reported “Clinically, the most relevant conditions in which human brain imaging can have a substantial impact are chronic conditions, as they remain most poorly understood and minimally treatable by existing (author’s note: medical) therapies” (pg. S53). So in essence what these authors are stating is although many people suffer from chronic spine pain, very few of them are actually diagnosed with a “medical condition” AKA an “anatomical” lesion.  The chiropractic profession has long professed the lesion is actually functional and based on aberrant spinal biomechanics [Subluxation]. 

 

 

When we look at the human population on a larger scale and from a medical perspective, we see there is a deficit in spinal care paths with resultant negative sequella of chronic back pain.  Alkarian’s conclusion was querying allopathic doctors who have little to no training or experience in treating mechanical back pain, AKA spinal dysfunction of biomechanical origin, AKA chiropractic subluxation complex.  Raissi ET. Al. (2005) reported regarding medical providers, “(92.2%) believed that musculoskeletal education had not been sufficient in general practitioner training courses. Of the respondents, 56.8% had visited at least one disabled patient during the previous month, while 11% had visited more than 10 in the same period, but 84.3% had not studied disabilities. Musculoskeletal physical examination was the most needed educational field cited by general practitioners” (pg. 167).

 

Day Et. Al. (2007) reported that only 26% of fourth year Harvard medical students had a cognitive mastery of physical medicine (pg. 452). Schmale (2005) reported “Incoming interns at the University of Pennsylvania took an exam of musculoskeletal aptitude and competence, which was validated by a survey of more than 100 orthopaedic program chairpersons across the country. Eighty-two percent of students tested failed to show basic competency. Perhaps the poor knowledge base resulted from inadequate and disproportionately low numbers of hours devoted to musculoskeletal medicine education during the undergraduate medical school years. Less than 1⁄2 of 122 US medical schools require a preclinical course in musculoskeletal medicine, less than 1⁄4 require a clinical course, and nearly 1⁄2 have no required preclinical or clinical course. In Canadian medical schools, just more than 2% of curricular time is spent on musculoskeletal medicine, despite the fact that approximately 20% of primary care practice is devoted to the care of patients with musculoskeletal problems. Various authors have described shortcomings in medical student training in fracture care, arthritis and rheumatology, and basic physical examination of the musculoskeletal system (pg. 251).  

 

With continued evidence of lack of musculoskeletal medicine and a subsequent deficiency of training in spine care, particularly of biomechanical [Subluxation] orientation, the question becomes which profession has the educational basis, training and clinical competence to manage these cases?  Let’s take a closer look at chiropractic education as a comparison. 

 

Fundamental to the training of doctors of chiropractic according to the American Chiropractic Association is 4,820 hours (compared to 3,398 for physical therapy and 4,670 to medicine) and receive a thorough knowledge of anatomy and physiology. As a result, all accredited doctor of chiropractic degree programs focus a significant amount of time in their curricula on these basic science courses. So important to practice are these courses that the Council on Chiropractic Education, the federally recognized accrediting agency for chiropractic education requires a curriculum which enables students to be “proficient in neuromusculoskeletal evaluation, treatment and management.” In addition to multiple courses in anatomy and physiology, the typical curriculum in chiropractic education includes physical diagnosis, spinal analysis, biomechanics, orthopedics and neurology. As a result students are afforded the opportunity to practice utilizing this basic science information for many hours prior to beginning clinical services in their internship.

 

To qualify for licensure, graduates of chiropractic programs must pass a series of examinations administered by the National Board of Chiropractic Examiners (NBCE). Part one of this series consists of six subjects, general anatomy, spinal anatomy, physiology, chemistry, pathology and microbiology. It is therefore mandatory for a chiropractor to know the structure and function of the human body as the study of neuromuscular and biomechanics is weaved throughout the fabric of chiropractic education. As a result, the doctor of chiropractic is expert in the same musculoskeletal genre that medical doctors are poorly trained in their doctoral education as referenced above.

 

Now that we have a general idea of why current musculoskeletal and spine care paths are failing, let’s examine what the negative effects are with a focus on what happens to the central nervous system when a patient is suffering from chronic pain.  The following paragraphs describe what happens to the brain as a result of chronic pain and then offers solutions based upon evidenced based studies.

 

Chronic Pain Affecting Brain Activity at Rest

 

Baliki ET. Al (2008) reported “Recent studies have demonstrated that chronic pain harms cortical areas unrelated to pain, long-term pain alters the functional connectivity of cortical regions known to be active at rest, i.e., the components of the “default mode network” (DMN). This DMN is marked by balanced positive and negative correlations between activity in component brain regions. In several disorders, however this balance is disrupted. Studying with fMRI [functional MRI] a group of chronic back pain patients and healthy controls while executing a simple visual attention task, we discovered that chronic back pain patients, despite performing the task equally well as controls, displayed reduced deactivation in several key default mode network regions. These findings demonstrate that chronic pain has a widespread impact on overall brain function, and suggest that disruptions of the default mode network may underlie the cognitive and behavioral impairments accompanying chronic pain.” (pg. 1398)

 

“The existence of a resting state in which the brain remained active in an organized manner, is called the ‘default mode of brain function. The regions exhibiting a decrease in activity during task performance are the component members of the “default-mode network” (DMN), which in concerted action maintain the brain resting state. Recent studies have already demonstrated that the brain default mode network is disrupted in autism, Alzheimer’ disease, depression, schizophrenia and attention deficit hyperactivity disorder, suggesting that the study of brain resting activity can be useful to understand disease states as well as potentially provide diagnostic information.”  (pg. 1398)  This is important since for the first time we are starting to see a published correlation between spinal function, chronic pain and central nervous system changes.  This is what our founders have observed yet were unable to prove.

 

“Thus, the alterations in the patient’s brain at ‘rest’ can result in a different default mode network organization. In turn, potential changes in the default-mode network activity could be related to symptoms (other than pain) commonly exhibited by chronic pain patients, including depression and anxiety, sleep disturbances, and decision-making abnormalities, which also significantly diminish their quality of life… chronic pain patients display a dramatic alteration in several key default-mode network regions, suggesting that chronic pain has a widespread impact on overall brain function” (pg. 1398).  This information is pointing to the fact that a doctor of chiropractic should be involved in the triage and treatment of these patients and part of a long term spinal care program. 

 

Baliki ET. Al (2008) continued “Consistent with extensive earlier work examining visuospatial attention tasks, dominant activations were located in posterior parietal and lateral prefrontal cortices, whereas deactivations occurred mainly within Pre-Frontal Cortex and Posterior Cingulate/Cuneate Cortexes. Although activations in chronic back pain patients’ and controls’ brains were similar, chronic back pain patients exhibited significantly less deactivations than healthy subjects in Pre-Frontal Cortex, amygdala, and Posterior Cingulate/Cuneate Cortexes.  The focus was on identifying differences in the way chronic back pain patients’ brains process information not related to pain. This is the first study demonstrating that chronic back pain patients exhibit severe alterations in the functional connectivity between brain regions implicated in the default mode network. It seems that enduring pain for a long time affects brain function in response to even minimally demanding attention tasks completely unrelated to pain. Furthermore, the fact that the observed task performance, compared with healthy subjects, is unaffected, whereas the brain activity is dramatically different, raises the question of how other behaviors are impaired by the altered brain activity” (pg. 1399).

 

“However, the disruption of functional connectivity observed here with increased chronic back pain duration may be related to the earlier observation of brain atrophy increasing with pain duration also in chronic back pain patients. Patient’s exhibit increased pre-frontal cortex activity in relation to spontaneous pain, in addition to dorsolateral prefrontal cortex atrophy. Therefore, the decreased deactivations described here may be related to the dorsolateral pre-frontal cortex /pre-frontal cortex mutual inhibitory interactions perturbed with time. If that is the case, it will support the idea of a plastic, time-dependent, reorganization of the brain as patients continue to suffer from chronic back pain.

 

Mechanistically, the early stages of this cortical reorganization may be driven by peripheral and spinal cord events, such as those that have been documented in animal models of chronic pain, whereas later events may be related to coping strategies necessary for living with unrelenting pain. It is important to recognize that transient but repetitive functional alterations can lead to more permanent changes. Accordingly, long term interference with normal activity may eventually initiate plastic changes that could alter irreversibly the stability and subsequently the conformation of the resting state networks” (pg. 1401).

 

 

Brain Region

Function

Cingulate Cortex

Emotions, learning, motivation, memory

Insular Cortex

Consciousness, homeostasis, perception, motor control, self-awareness, cognitive function

Motor Cortex

Voluntary movements

Amygdala Cortex

Memory, decision making, emotional reactions

Somatosensory Cortex

Proprio and mechano-reception, touch, temperature, pain of the skin, epithelial, skeletal muscle, bones, joints, internal organs and cardiovascular systems

Periaqueductal Gray

Ascending and descending spinothalamtic tracts carrying pain and temperature fibers

 

 

 

 

 

 

 

 

 

 

 

 

THALAMUS

 

 

 

Chronic Pain Causing Brain “Shrinkage”

 

Apkarian ET. Al (2004) reported “Chronic back pain patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Patients with chronic back pain showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10-20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3loss of gray matter for every year of chronic pain. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic chronic back pain. Our results imply that chronic back pain is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.

 

It is assumed that the cerebral cortex passively reflects spinal changes and reverts to its normal state after cessation of chronic pain. Our studies show that chronic back pain (sustained for >6 months) is accompanied by abnormal brain chemistry, mainly a reduction in theN-acetyl-aspartate-creatine ratio in the prefrontal cortex, implying neuronal loss or dysfunction in this region and reduced cognitive abilities on a task that implies abnormal prefrontal processing” (pg. 10410).

 

Apkarian ET. Al (2004) continued “At the whole-brain level, this reduction is related to pain duration, regionally depends on multiple pain-related characteristics, and is more severe in the neuropathic subtype. Therefore, these data present strong evidence that the pathophysiology of chronic pain includes cortical processes, and the observed changes likely constitute the physical substrate of the cognitive and behavioral properties of chronic pain” (pg. 10411).

 

“Thus, regional gray matter changes are strongly and specifically related to pain characteristics, and this pattern is opposite for neuropathic compared with non-neuropathic types. This dissociation is consistent with extensive clinical data showing that neuropathic pain conditions are more debilitating and have a stronger negative affect, which may be directly attributable to the larger decrease in gray matter density that we observe in the dorso-lateral pre-frontal cortex (DLPFC) of neuropathic chronic back pain patients.  Moreover, only 18% of whole-brain gray matter variance could be explained by pain duration. Therefore, a large portion of the whole-brain atrophy in chronic back pain cannot be accounted for by the measured pain characteristics, implying that there may be genetic and experiential predispositions contributing to the observed atrophy. In the DLPFC, a larger proportion of the variance could be explained by pain characteristics (40% for neuropathic chronic back pain; 80%for non- neuropathic chronic back pain), implying a tighter relationship between regional brain atrophy and perceived pain. Therefore, we suggest that the pattern of brain atrophy is directly related to the perceptual and behavioral properties of neuropathic chronic back pain.”

 

The observed regional pattern of atrophy is distinct from that seen in chronic depression or anxiety and shows a minimal relationship with anxiety and depression traits. Thus, it seems to be specific to chronic pain, especially because the regions showing atrophy, the thalamus and DLPFC, participate in pain perception. The DLPFC is activated in acute pain, with responses that do not code stimulus intensity. Recent evidence suggests that the DLPFC exerts “top-down” inhibition on orbitofrontal activity, limiting the magnitude of perceived pain. Thus, DLPFC atrophy may lead to a disruption of its control over orbitofrontal activity, which in turn is critical in the perception of negative affect in general and particularly in pain states. Thalamic atrophy in chronic back pain is important, because it is a major source of nociceptive inputs to the cortex and damage to this region may be a reason for the generalized sensory abnormalities commonly associated with chronic pain” (pg. 10413).

 

“The dorsal anterior cingulate is shown to be specifically involved in pain affect in normal subjects and exhibits decreased nociceptive signaling in various chronic pain states, which may again be caused by thalamic atrophy because the anterior thalamus is a primary input to the anterior cingulate. Therefore, we suggest that regional atrophy dictates the brain activity observed in chronic pain, and it may explain the transition from acute to chronic pain by shifting brain activity related to pain affect away from the anterior cingulate to orbitofrontal cortex.”

 

“It is possible that some of the observed decreased gray matter reflects tissue shrinkage [changes in extracellular space and microvascular volume may cause tissue shrinkage without substantially impacting neuronal properties], implying that proper treatment would reverse this portion of the decreased brain gray matter. The atrophy may be also attributable to more irreversible processes, such as neurodegeneration, which we favor because the main brain region involved (the DLPFC) also exhibits decreasedN-acetyl-aspartate, and decreasedN-acetyl-aspartate has been observed in most neurodegenerative conditions. Recent evidence also suggests that after nerve injury, some components of pain behavior are a consequence of hyperactivity of spinal cord microglia, and a histological study has shown a reduction in glial numbers in the cortex in major depressive disorder and bipolar disorder” (pg. 10414).

This article suggests that there is a reversible component in brain atrophy with the resolution of the chronic back pain, with strong evidence that there are some tissue structures that will be permanently damaged should the chronic pain go beyond the defined 6 months.  Clearly there are many different professions that handle the anatomical components of spine pain such as fracture, infection, disc herniation or tumor.  There is only one profession that has the education and training to treat the aberrant spinal biomechanics; chiropractic.  Since chiropractors are trained in treating/managing/triaging the anatomical lesions while also being the best suited to treat the biomechanical component, the evidence verifies that  the first contact for spine pain be a doctor of chiropractic who is also trained in differential diagnosis of underlying pathology. .

 

Brain Regions Effected

 

Apkarian ET. AL (2011) reported “The surprise was that the brain region best reflecting high magnitude of back pain was localized to the medial prefrontal cortex, extending into anterior cingulate cortex, a region not anticipated by acute pain studies. Additionally, brain areas observed for acute pain, like portions of the insula and mid- anterior cingulate cortex were only active transiently and only when the back pain magnitude was on the increase. These results are exciting because, for the first time, we are able to observe brain activity reflecting the subjective perception of the pain that chronic back pain patients come to the clinic to complain. We interpret the transient activity as a nociceptive signal from the periphery, which then is converted into a sustained emotional suffering signal in medial prefrontal cortex (pg. S54).

 

“Thus we can assert that, at least in this group of chronic pain patients, different brain areas encode the perceived magnitude for distinct types of pain. The prevalent expectation for brain activity in chronic pain is a sustained or enhanced activation of the brain areas already identified for acute pain. This view is partly implied by the chronic pain definition and by notions of specificity theory or labeled line theory of pain (where supraspinal organization and representation of pain is assumed to be through fixed and immutable routes). This is exactly what we donotsee. Instead these results imply that functional anatomy or physiology or some combination of both have changed in the brain of chronic back pain patients. It is also important to remember that the close relationships between fundamental properties of back pain and activity in medial prefrontal cortex and insula are correlational, and that both medial prefrontal cortex and insula respond to a long list of cognitive and emotional states (pg. S55). The morphological studies show that the brain structure undergoes changes at multiple spatial and temporal scales, which are for the most part specific to the type of chronic pain studied. That some of these changes are reversible by cessation of chronic pain speaks to the specificity of the processes and also demonstrate that chronic pain may in fact by used as a unique tool with which the dynamics of brain plasticity can be studied at multiple spatial and temporal scales” (pg. S56).

 

Chiropractic as a Solution for Chronic Back Pain

 

 

Peterson ET. AL. (2012) reported “investigate outcomes and prognostic factors in patients with acute or chronic low back pain (LBP) undergoing chiropractic treatment. In chronic LBP, recent studies indicate that significant improvement is often fairly rapid, usually by the fourth visit, and that patients initially receiving treatment 3 to 4 times a week have better outcomes. Patients with chronic and acute back pain both reported good outcomes, and most patients with radiculopathy (neurogenic) also improved” (pg. 525). “At 3 months, 69% of patients with chronic pain stated that they were either much better or better. This is unlikely to be due to the natural history of LBP because these patients have already passed the period when natural history occurs “(pg. 531).  A study by Tamcan et al (2010) was the only population based study of the so called “natural history” of lower back pain and the authors found the “natural history” of chronic lower back pain was not ending in resolution of symptoms but instead they documented patients moving “in and out” of a level of pain they could tolerate.   Based on the only population-based study of chronic lower back pain, the idea that the “natural history” of lower back pain ends with resolution of symptoms is a complete myth and one that is perpetuated by our present healthcare system.

 

 

Lawrence ET. AL (2008) reported “Existing research evidence regarding the usefulness of spinal adjusting… indicates the following, as much or more evidence exists for the use of SMT [spinal manipulation] to reduce symptoms and improve function in patients with chronic LBP as for use in acute and subacute LBP. The manual therapy group showed significantly greater improvements than did the exercise group for all outcomes. Results were consistent for both the short-term and the long-term” (pg. 670).

 

 

Dunn ET. AL. (2011) reported “The clinical outcomes achieved for this sample should be considered within the context of this veteran patient base, which is typically represented by older, white males with multiple comorbidities. A high percentage of overall service-connected disability was noted, with only a small percentage associated with the low back region. Considerable psychological comorbidity was found, with a high prevalence of PTSD (post-traumatic stress disorder) and depression diagnoses. PTSD and chronic pain tend to co-occur and may interact in a way that can negatively affect either disorder. A previous retrospective study of chiropractic management for neck and back pain demonstrated less improvement among those with PTSD. These points are significant because severe comorbidities and psychosocial factors lessen the likelihood of obtaining positive outcomes with conservative measures, including [chiropractic adjustments], for chronic low back pain. Mean percentages of clinical improvement exceeded the minimum clinically important difference, despite the levels of service-connected disability and comorbidity among this sample of veteran patients” (pg. 930). They went on to conclude that in spite of significant comorbidities that historically compromise positive results, 60.2% of patients met or exceeded the minimum clinically important difference for improvement (pg. 927).

 

Conclusion

 

Chronic pain as defined by that which has last for 6 months or longer which causes significant brain aberration in both morphology (size) and function.  The  literature suggests that this could be the precursor for many diseases as sequella of the human body’s natural reaction to prolonged pain.   Chronic back pain is one of the leading causes of chronic pain and medicine has little to no training or solutions as reported in the literature. Conversely, chiropractic has significant training and has been proven in “blinded” studies to have significant positive outcomes even in significantly adverse condition to help resolve chronic pain. As a result, the negative sequella on the brain of chronic pain, including shrinkage of the brain can be reversed through chiropractic care as the evidence has verified that once the chronic pain has resolved, the brain has the ability to return to its normal size and regain much function.

 

 

Although this evidence is strong, more research is needed and this further sets the foundation for understanding how chiropractic directly effects diseases in the human body. In addition, this also takes the chiropractic profession to the next level of understanding how and why a chiropractic adjustment works.  

 

 

References:

  1. National Institute of Neurological Disorders and Stroke, NINDS Chronic Pain Information Page (July 2015), retrieved from: http://www.ninds.nih.gov/disorders/chronic_pain/chronic_pain.htm
  2. Baliki N., Geha P., Apkarian A., Chialvo D., (2008) Beyond Feeling: Chronic Pain Hurts the Brain, disrupting the Default-Mode Network Dynamics, Journal of Neurosciences 28(6) 1398-1403
  3. Apkarian V., Sosa Y., Sonty S., Levy R., Harden N., Parrish T., Gitelman D., (2004) Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density, The Journal of Neuroscience, 24(46) 10410-10415
  4. Apkarian A., Hashmi J., Baliki M., (2011) Pain and the brain: Specificity and plasticity of the brain in clinical chronic pain, Pain 152, S49-S54
  5. Raissi G., Mansoon K., Madani P., Rayegani S., (2006) Survey of General Practitioners’ attitudes Toward Physical Medicine and Rehabilitation, International Journal of Rehabilitation Research 26: 167-170
  6. Day C., Yeh A., Franko O., Ramirez M., Krupat E. (2007) Musculoskeletal Medicine: An Assessment of the Attitudes of Medical Students at Harvard Medical School, Academic Medicine 82: 452-457
  7. Schmale G. (2005) More Evidence of Educational Inadequacies in Musculoskeletal Medicine 437, 251-259
  8. Peterson C., Bolton J., Humphreys K., (2012) Predictors of Improvement in Patients With Acute and Chronic Low Back Pain Undergoing Chiropractic Treatment, Journal of Manipulative and Physiological Therapeutics, 35(7) 525-533
  9. Lawrence, D., Meeker W., Branson R., Bronford G., Cates J., Haas M., Haneline M., Micozzi M., Updyke W., Mootz R., Triano J., Hawk C., (2008) chiropractic management of low back pain and low back-related leg complaints: a literature synthesis, Journal of Manipulative and Physiological Therapeutics, 31(9) 659-674
  10. Dunn A., Green B., Formolo L., Chicoine D. (2011) Retrospective case series of clinical outcomes associated with chiropractic management for veterans with low back pain, Journal of Rehabilitation Research & Development, 48(8) 927-934
  11. Tamcan, O., Mannion, A. F., Eisenring, C., Horisberger, B., Elfering, A., & Müller, U. (2010). The course of chronic and recurrent low back pain in the general population. Pain, 150(3), 451-457.

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