Chiropractic & Central Afferent Inhibition:

A Chiropractic Care Path & Mechanism for Chronic Pain, Tremors, Spatial and Inhibitory Distortion

 

By Mark Studin

William J. Owens

Michael Barone

A report on the scientific literature 

 

Although it is unusual in the literature to place a disclaimer in the beginning of an article, we want to ensure that our reporting is not inflammatory since the foundation of this article was written with the following limitation in our primary literary source, Haavik, Niazi, Holt and Murphy (2017) reported:

 

This study was not designed to test the efficacy of chiropractic care for treating chronic pain; therefore, conclusions about efficacy cannot be drawn from our findings. The study did not include randomization with an adequate control group, thus limiting the interpretations that can be made about the changes in pain observed in the trial. Causation cannot be claimed. (pg. 135)

 

Although Haavik, et al. reported limitations in their study, the results cannot be overlooked or minimized, particularly when those results match what doctors working within a “Best Practice Model” (the patient and doctor feedback component) have been reporting for decades. Additionally, in the clinical setting, this information provides direction to practitioners searching for answers although the mechanisms are not yet fully understood. Results often don’t mandate detailed knowledge of the mechanism and that is the primary reason why both “evidenced based” and “best practice” models must be embraced and combined (pure literature results with doctor and patient feedback or experiences) as a matter of public health.

 

When we consider central afferent neurological input, the inability to inhibit those signals leads to sensorimotor disturbances that are found in the chronicity of many chronic pain conditions, essential tremors, dystonia and other central spatial and temporal mismatches. In addition, we must consider to the long-term negative sequalae of those conditions, such as brain shrinkage.

 

Baliki, Geha, Apkarian and Chialvo (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).

 

Essential Tremors which, according to Wikipedia

 

Essential tremor (ET, also referred to as benign tremor, familial tremor, or idiopathic tremor) is the most common movement disorder; its cause is unknown. It typically involves a tremor of the arms, hands or fingers but sometimes involving the head, vocal cords or other body parts during voluntary movements such as eating and writing.[1] It is distinct from Parkinson's disease—and often misdiagnosed as such—although some individuals have both conditions. Essential tremor is commonly described as an action tremor (i.e., it intensifies when one tries to use the affected muscles) or postural tremor (i.e., present with sustained muscle tone) rather than a resting tremor, such as is seen in Parkinson’s, which is usually not included among its symptoms. (https://en.wikipedia.org/wiki/Essential_tremor)

 

Restuccia, Valeriani, Barba, Le Pera, Bentivoglio, Albanese and Tonali (2003) reported:

 

...our present data seem to indicate that somatomotor cortical areas play an important role in generating ET. This finding can be important in the future understanding of its pathophysiologic mechanisms, as well as in its management. (pg. 127)

 

This study suggests that somatosensory cortical areas plays an important role, therefore the afferents “feeding” that region is critical in normalizing function of the cortex a that region. Another negative sequela of aberrant input.

When we consider one potential etiology of maladaptive plastic changes in the brain that can cause chronic pain, essential tremors, brain shrinkage and a host of other maladies, regulatory control of the impulses must be considered and interfered with. The lack of gating (inhibition) will lead to an overflow of impulses and crate a negative cascade that can lead to chronic and often permanent changes. Haavik, Niazi, Holt and Murphy (2017) reported:

 

Thus, distorted sensory information is thought to disturb SMI (sensorimotor integration) and impair accurate motor control. In normal circumstances, 2 inputs that engage the sensory system have a reciprocally inhibitory action that gates the total amount of signal at all central levels, spatially and temporally limiting the amount of input engaging the CNS. This is thought to prevent sensory “overflow.” The defective gating may cause an input-output mismatch in specific motor programs, and such mismatches in motor programs may in themselves lead to production of distorted sensory information and issue of less than ideal motor commands. In this way, the chronicity of the problem can be maintained via a self-perpetuating mechanism. The reduced frontal N30 SEP (somatosensory evoked potential) peak ratio observed in the current study after 12 weeks of chiropractic care may reflect a normalization of pain-induced central maladaptive plastic changes and may reflect one mechanism for the improvement of functional ability reported following chiropractic adjustment or manipulation. (pg. 134)

 

The N30 ratio change represented on average a 37.4% decrease following the 12 weeks of chiropractic care. The N30 MU (median-ulnar) amplitude changes following chiropractic care represented an 18.0% decrease in amplitude compared with baseline (pg. 131) Alongside this change in the N30 SEP ratio, the subjects reported a decrease in both current pain and average pain over the last week. A control period of 2 weeks of no intervention resulted in no significant changes in any SEP peak ratio. (pg. 134)

 

When considering care paths for this population of patients, the following was reported by Haavik, Niazi, Holt and Murphy (2017) reported:

 

The 2-week control period, during which no intervention was applied, was followed by a 12-week chiropractic care intervention. During the 12 weeks of chiropractic care, the chiropractor assessed and treated the subject as she would any other chronic pain patient. The participating chiropractor (H.H., with 7 years clinical experience) assessed the spine for segmental dysfunction using tenderness on palpation and passive intervertebral and global motion of the spine. Other treatments included as part of chiropractic care were exercises, peripheral joint adjustments/manipulations, soft tissue therapy, and pain education if deemed by the chiropractor to be appropriate based on history and examination. The chiropractic adjustment/manipulation was the delivery of a high-velocity, low-amplitude thrust to dysfunctional spinal segments. (pgs. 129-130)

 

The changes observed conclude (with the aforementioned disclaimer that more research is needed) that chiropractic is a verifiable treatment option. Haavik, Niazi, Holt and Murphy (2017) continued:

 

The changes observed in dual SEP ratios after several weeks of chiropractic care in a chronic pain population suggest that this treatment option may improve gating of peripheral afferent input to the brain, thus improving impaired SMI in cortical motor areas and improving processing of motor programs. Impaired SMI and defective motor programming is known to be present in various chronic pain populations and is implicated in the clinical symptomatology. We know from the literature that in normal circumstances, afferent input to the motor system leads to finely tuned activation of neural elements and ultimately results in the correct execution of movement. Multiple experimental and clinical studies have confirmed the importance of sensory feedback to the motor system. Thus, distorted sensory information is thought to disturb SMI and impair accurate motor control. In normal circumstances, 2 inputs that engage the sensory system have a reciprocally inhibitory action that gates the total amount of signal at all central levels, spatially and temporally limiting the amount of input engaging the CNS. This is thought to prevent sensory “overflow.” The defective gating may cause an input-output mismatch in specific motor programs, and such mismatches in motor programs may in themselves lead to production of distorted sensory information and issue of less than ideal motor commands. In this way, the chronicity of the problem can be maintained via a self-perpetuating mechanism. The reduced frontal N30 SEP peak ratio observed in the current study after 12 weeks of chiropractic care may reflect a normalization of pain-induced central maladaptive plastic changes and may reflect one mechanism for the improvement of functional ability reported following chiropractic adjustment or manipulation. (pgs. 134-135)

 

Haavik, Niazi, Holt and Murphy (2017) concluded:

 

After the 12 weeks of chiropractic care, when he was also feeling better symptomatically, this was reversed, and all of his MU traces for all SEP peak complexes were smaller in amplitude than his M + U trace, indicating a greater level of central reciprocal inhibition was occurring… Thus, if sensory “overflow” occurs, then incomplete processing of this incoming signal may occur in the brain, resulting in its perceiving not only excessive, but also spatially distorted information. (pg. 135)

 

The N9 SEP peak (the “N” is a location for electrodes) reflects the afferent signal over the brachial plexus before it enters the CNS, and thus can be used to ensure that the incoming signal is consistent before and after an intervention. Furthermore, these experiments demonstrated that the subjects' N30 SEP peak ratios decreased significantly after a single chiropractic manipulation of the cervical spine. As the N30 SEP peak is thought to reflect early cortical SMI, the authors argued that their results suggest that the subject's SMI networks' ability to suppress the dual input after the adjustment was increased. The N30 SEP peak ratios remained decreased even after repeating the 20-minute repetitive thumb abduction task. This suggested that the treatment effects appear to have altered the way in which each subject's CNS responded to the repetitive thumb typing task.

 

When considering treating chronic pain, dystonia, essential tremor or any other type of patient where there are spatial (distorted or excessive afferent) input issues, the above care path (treatment plan) should be considered. By not completed a complete treatment protocol might expose your patient to a chronic issue that may become permanent if the maladaptive cortical changes persist over time. Since there are no timetables for how long a patient can withstand for the issue to become permanent and there is an indexed peer reviewed suggestion of correction, that must be adhered as a minimum until further evidence suggests otherwise. In addition, no two patients are alike and the treatment plan should be guided with a full clinical reevaluation and consider performing that examination every 30 days of active care considering all facets, both history and clinical.

 

 

References:

  1. Haavik, H., Niazi, I. K., Holt, K., & Murphy, B. (2017). Effects of 12 Weeks of Chiropractic Care on Central Integration of Dual Somatosensory Input in Chronic Pain Patients: A Preliminary Study. Journal of manipulative and physiological therapeutics40(3), 127-138.
  2. Restuccia, D., Valeriani, M., Barba, C., Le Pera, D., Bentivoglio, A., Albanese, A. & Tonali, P. (2003). Abnormal gating of somatosensory inputs in essential tremor. Clinical neurophysiology114(1), 120-129.
  3. 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
  4. Essential Tremor (2017) retrieved from: https://en.wikipedia.org/wiki/Essential_tremor

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Published in Neck Problems

Chronic Pain and Chiropractic:

A 12-Week Solution & Necessity for Care

 

By Mark Studin

William J. Owens

A report on the scientific literature and commentary 

 

 

How long should a patient be under chiropractic care? This has been the struggle for many in the insurance industry, the legal community, licensure boards and a “hot topic” politically. There are the CCGPP [Council on Chiropractic Guidelines and Practice Parameters], the Croft Guidelines, Best Practice for Chiropractic Care for Older Adults, Best Practices Recommendations for Chiropractic Care for Infants, Children and Adolescents, Chiropractic Practice Guidelines: Chiropractic Care for Low Back Pain. These are just some of the chiropractic industry’s guidelines, then you must consider the insurance industry’s care paths where most are hidden behind statements like “medical necessity” and “eligible charges.” Those are “buzz phrases” indicating they have a guideline, but most will neither publish or make them available to the providers, their insured or the public claiming proprietary information giving them a legal basis for the secrecy.

 

 

Aetna, as an example lists specifics for care and then goes further to limit a significant number of techniques, procedures and diagnostics claiming they are “experimental.” Although Medicare considers chiropractic a covered service they limit treatment arbitrarily according based upon significant feedback from many in the profession.  Workers Compensation Boards have guidelines that are either legislated or created based upon a case law judge’s opinion which include arguments from the defense to support limiting care.  At best, that is an arbitrary process based upon rhetoric or legislation that is too often ignorant of the scientific literature resulting in serious imposed limits in scope of treatment as we see in California, New York and many other states.

 

 

Although the guideline landscape is expansive, these authors choose to rely on a hybrid of both “Best Practice” and “Evidenced Based” method in the development of treatment plans. Both have a strong place in clinical practice, academic settings, the courts and third-party reimbursement systems.

 

Best Practice is defined as “a method or technique that has consistently shown results superior to those achieved with other means, and that is used as a benchmark. In addition, a best practice can evolve to become better as improvements are discovered. Best practice is considered by some as a businessbuzzword, used to describe the process of developing and following a standard way of doing things that multiple organizations can use" (Best Practice, http://en.wikipedia.org/ wiki/Best practice).

 

These are certain procedures in healthcare that are taught in schools, internships and residencies and are considered the “standard” by which care is expected to follow. These practices are based on clinical experience and rely heavily on time-tested approaches, that is how a profession evolves and grows.  Surprisingly, most of the best medical practice care paths are not published in the peer-reviewed indexed literature. This is due to many factors, but the most obvious are applications of financial resources and grants to “new” discoveries and the simple fact that the clinical arena is well positioned to monitor and adjust these practices in a timely manner allowing practitioners to keep pace with the literature that follows. In recent times, although it has been talked about for decades, there is another parameter that exists and although focuses on best practices, there is a strong reliance on published studies, aka “evidence”, as the main driver of whether a procedure is approved and reimbursed. This is extremely problematic to healthcare outcomes.

Evidence-based practice(EBP) is an interdisciplinary approach to clinical practice that has been gaining ground following its formal introduction in 1992. It started inmedicineasevidence-based medicine (EBM) and spread to other fields such as dentistry, nursing, psychology,

education, library and information science and other fields. Its basic principles are that all practical decisions made should be based on three important criteria.  First, they must be based on the practicing provider’s clinical experience, secondly, they should be based on published research studies and thirdly should consider the patients expectations.

 

"Evidence-based behavioral practice(EBBP) entails making decisions about how to promote health or provide care by integrating the best available evidence with practitioner expertise and other resources, and with the characteristics, state, needs, values and preferences of those who will be affected. This is done in a manner that is compatible with the environmental and organizational context. Evidence is comprised of research findings derived from the systematic collection of data through observation and experiment and the formulation of questions and testing of hypotheses" (Evidence-Based Practice, http://en.wikipedia.org/wiki/Evidence-based_practice).

 

This highly-debated topic of evidence-based vs. best practice has valid issues on each side, but putting them together as a hybrid would allow them to thrive in both a healthcare delivery and reimbursement system; therefore, all sides would win. This would allow advances in healthcare to save more lives, increase the quality of life and at the same time, offer enough safeguards to prevent abuse to payors. A one-sided approach would tip the scales to favor either the provider/patients or the payors which, in the end, results in distrust and conflict.

Evidence-based medicine proponents argue that it would eliminate waste and reduce costs while providing patients with the most up-to-date care available. Those against this concept argue that reliance on evidence-based care would eliminate many procedures that fall under the best medical practice parameters and remove the clinical decision making and professional experience from the equation. They feel what would be left is denial of good therapies and the stifling of innovation since the process of establishing a research study, following its participants and publishing those findings can take many years not to mention poor study design or research bias can have both a profound effect on the evidence provided and severely delay the final publication. This delay would eventually cost either lives or severely diminish the quality of life for those who could have been helped during the research and publication processes.

Haavik, Niazi, Holt and Murphy (2017) reported:

 

Post hoc tests using the Bonferroni correction revealed significant mean differences in N30 MU amp (P = .049) and N30 MU to M + U ratio data (P = .001) during the chiropractic intervention, but no significant changes were observed during the control period (P = .1 for N30 MU amp and P = .3 for N30 MU to M + U ratio data). The effect size for the change in N30 MU amp was 0.61, and for the N30 MU to M + U ratio it was 0.66. The N30 ratio change represented on average a 37.4% decrease following the 12 weeks of chiropractic care. The N30 MU amplitude changes following chiropractic care represented an 18.0% decrease in amplitude compared with baseline. (Pg 131)

 

These results were based upon a limited study, but validates that a chiropractic spinal adjustment modulated aberrant afferent input by 37.4% in median and ulnar nerve rations and 18% in median and ulnar nerve amplitudes.

 

The authors went on to report:

 

The purpose of this preliminary study was to assess whether the dual SEP technique is sensitive enough to measure changes in cortical intrinsic inhibitory interactions in patients with chronic neck pain after a 12-week period of chiropractic care and, if so, whether any such changes related to changes in symptomatology. (pg. 128)

 

This was tested to determine if inhibitory innervation was affected specifically by a chiropractic spinal adjustment and the outcomes conclusively, against a 2-week control period of the same test subjects confirmed these results.

Haavik, Niazi, Holt and Murphy (2017) went on to describe the 12 weeks of chiropractic care that realized these results:

 

The chiropractic care plan was pragmatic and generally consisted of 2 to 3 visits per week for the first 2 to 3 weeks. Frequency was reduced based on clinical findings and patient symptomatology. By the end of the 12-week period, participants were seen once or twice a week. No requirements were placed on the treating chiropractor, other than including chiropractic adjustment or manipulation during treatment; thus, the care plan was designed in conjunction with patient preferences and was based on the patients’ history, symptoms, wishes, and time availability as well as the clinician’s clinical experience and knowledge. (pg. 130)

 

Although the length of care in this study does not render a specific guideline, it does validate that it takes time to realize changes in the mechanics of the spine and the human nervous system.  The results are consistent with the “Best Practice Model” and the authors 57 years of combined experience and results. Twelve weeks of care is a conservative and reasonable time frame since we are observing and considering that cerebral neuroplastic changes are a direct and verifiable result of a chiropractic spinal adjustment. Less than 12 weeks of chiropractic spinal adjusting has not been evidenced to make these reported changes, therefore we must consider this threshold for care.Concurrently, what we see is that less treatment time does not allow the connective tissue to help the spine as one contiguous organ system to remodel to a homeostatic state (a conversation for a different paper).

 

Chiropractic care for chronic pain patients requires a both a combination of Best Practice and Evidenced Based models as the literature is now verifying that a chiropractic spinal adjustment is an effective care path and 12 weeks is a minimum to see neuroplastic changes.  Clinically speaking however, to confirm the optimum care path for this particular population of patients, continuation of care should be based on re-evaluations every 30-days and should continue as clinical sign and symptoms persist and there is evidence that the patient is benefiting both in the short and long term.   Additionally, no significant improvement over the first 12 weeks should be considered acceptable as neuroplastic changes are a process. Although these authors have rarely personally experienced a lack of significant neuro-biomechanical changes over that time period, it is a clinical decision that must be derived by the treating provider in a “Best Practice Model” and not a 3rd party.

 

References:

  1. Aetna Chiropractic Services (2017) Retrieved from: http://www.aetna.com/cpb/medical/data/100_199/0107.html
  2. https://www.medicare.gov/coverage/chiropractic-services.html
  3. Best Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, from http://en.wikipedia.org/wiki/Best_practice
  4. Evidence-Based Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, from http://en.wikipedia.org/wiki/Evidence-based_practice
  5. Sackett, D. L., Rosenberg, W. M., Gray, J. A., Haynes, R. B., & Richardson, W. S. (1996) Evidence based medicine: What it is and what it isn't. British Medical Journal, 312(7023), 71-72.
  6. Haavik, H., Niazi, I. K., Holt, K., & Murphy, B. (2017). Effects of 12 Weeks of Chiropractic Care on Central Integration of Dual Somatosensory Input in Chronic Pain Patients: A Preliminary Study. Journal of manipulative and physiological therapeutics40(3), 127-138.

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Published in Neck Problems

The Mechanism of the Chiropractic

Spinal Adjustment/Manipulation:

Subluxation Degeneration

 

Effect of Sagittal Alignment on Kinematic Changes and Degree of Disc Degeneration in the Lumbar Spine

 

Part 4 of a 5 Part Series

 

William J Owens Jr   

Mark E. Studin  

 

A report on the scientific literature

 

More and more evidence is coming forward demonstrating both spinal stability and biomechanical balance as an important aspect of spine care.  The good news is this is well within chiropractic’s scope, however many doctors of chiropractic are missing the education to accurately evaluate and objectify these types of biomechanical lesions.  Our profession has spent most the last 122 years focused on TREATING these biomechanical lesions (Vertebral Subluxation, Joint Fixation, etc.) with little regard to the “assessment” component.  The reason that is a critical statement, is that too often we treat compensation vs. the unstable joint. 

 

Our founding doctors had used very specific techniques to analyze the spine from a functional perspective and most of our contemporary treatment techniques came out of these analysis, which are the basis for many of our most common techniques taught in today’s chiropractic academia.  It seems in hindsight, that the major discussions of the time [early chiropractic] were about “identification” of the lesion to adjust, then evolved into the best WAY to deliver the adjustment.  

Our roots and subsequently the true value and expertise of the doctor of chiropractic is in the assessment with treatment far secondary to an accurate diagnosis  The medical community that both the authors and the doctors we teach no longer confuse our delivering of chiropractic care with a physical therapy manipulation or mobilization.  The reason, our focus is on the diagnosis, prognosis and treatment plan BEFORE we render our treatment. 

With medical specialists who understand spine, our conversation centers on spinal biomechanics and how a specific chiropractic spinal adjustment will restore sagittal/coronal alignment and coupled motion balance the spine.  We discuss spinal biomechanics and have the literature and credentials to validate our diagnosis, prognosis and treatment plan.  Chiropractic has been the leader in this treatment for over a century, but since we had chosen to stay outside of the mainstream healthcare system we had no platform to take a leadership position or be heard. 

Medicine at both the academic and clinical levels are embracing chiropractic as the primary solution to mechanical spine issues (no fracture, tumor or infection) because as one primary care provider shared with us “traditional medical therapies inclusive of physical therapy has no basis in reality in how to treat these patients, which has led us in part, to the opiate crisis.” Part of the validation of what chiropractic offers in a biomechanical paradigm comes from surgical journals in the medical community. 

  Keorochana et al, (2011) published in Spine and out of UCLA, titled “To determine the effects of total sagittal lordosis on spinal kinematics and degree of disc degeneration in the lumbar spine. An analysis using positional MRI.”  Remember that this article was 8 years ago and as a concept has evolved considerably since it was first discussed in the late 1990s.  This is the clinical component of what Panjabi had successfully described and reproduced in the laboratory. It is now starting to become mainstream in clinical practice. 

Many people ask why would surgeons care about the biomechanics of the spine when they are looking simply for an anatomical lesion to stabilize [fracture, tumor, infection, cord compression]?  The authors answer this question by stating “It has also been a topic of great interest in the management of lumbar degenerative pathologies, especially when focusing on the role it may play in accelerating adjacent degeneration after spinal fusionand non-fusion procedures such as dynamic stabilization and total disc replacement.”  [pg. 893] 

They continue by stating “Alterations in the stress distribution may ultimately influence the occurrence of spinal degeneration. Moreover, changes in sagittal morphology may alter the mechanics of the lumbar spine, affecting mobility. Nevertheless, the relationships of sagittal alignment on lumbar degeneration and segmental motion have not been fully defined.” [pg. 893] This is precisely what our founding fathers called “Subluxation and Subluxation Degeneration!” 

Regarding the type and number of patients in the study, the authors reported the following, “pMRIs [positional MRI] of the lumbar spine were obtained for 430 consecutive patients (241 males and 189 females) from February 2007 to February 2008. All patients were referred for pMRI [positional MRI – which included compression in both flexion and extension with a particular focus on segmentation translation and angular motions] due to complaints of low back pain with or without leg pain.” [pg. 894] This is the part where they looked for hypermobility. 

In the first step in the analysis, the authors reviewed data regarding the global sagittal curvature as well as the individual angular segmental contributions to the curvature.  The next step involved the classification of the severity of lumbar disc degeneration using the Pfirrmann classification system. [See Appendix A if you are not familiar]. This is where they looked for segmental degeneration.  The patients were then classified based on the lordosis angle [T12-S1]. The groups were as follows: 

Group A – Straight Spine or Kyphosis – [lordosis angle <20°]  

Group B – Normal Lordosis – [lordosis angle 20° to < 50°]  

Group C – Hyperlordosis – [lordosis angle >50°] 

There is a structural categorization [lordosis] and a degenerative categorization [Pfirrmann] in this paper and the authors sought to see if there was a predictable relationship.

 

The results of this study were interesting and validated much of what the chiropractic profession has discussed relating to segmental “compensation” in the spine.  Meaning, when one segment is hypomobile, adjacent segments will increase motility to compensate.  The authors stated, “The sagittal lumbar spine curvature has been established as an important parameter when evaluating intervertebral disc loads and stresses in both clinical and cadaveric biomechanical investigations.” [pg. 896] They continue by stating “In vitro [in the laboratory or outside of the living organism] biomechanical tests do not take into account the influence of ligaments and musculature, and may not adequately address the complex biomechanics of the spine.” [pg. 896] 

When it comes to spinal balance and distribution of loads in the spine, the authors reported “Our results may indicate that the border segments of lordosis, especially in the upper lumbar spine (L1–L2, L2–L3, and L3–L4), have greater motion in straight or kyphotic spines, and less segmental motion in hyperlordotic patients.” [pg. 896] 

They continued by stating, A greater degree of rigidity is found at the apical portion of straight or kyphotic spines, and more mobility is seen at the apical portion of hyperlordotic spines.” [pg. 897]  Therefore, in both cases we see that changes in the sagittal configuration of the human spine has consequences for the individual segments involved. 

This raises the question, “how does this related to accelerated degeneration of the motion segments involved?” [Subluxation Degeneration] The authors reported, “Regarding the relationship between the degree of disc degeneration and posture, subjects with straight or kyphotic spines tended to have a greater degree of disc degeneration at border segments, with statistical significance in the lower spine (L5–S1). On the other hand, hyperlordotic spines had a significantly greater degree of disc degeneration at the apex and upper spine (L4–L5 and L1–L2). The severity of disc degeneration tended to increase with increased mobility at the segments predisposed to greater degeneration (border segments of straight or kyphotic spines and apical segments of hyperlordotic spines).” [pg. 897] 

The scientific literature and medicine is now validating (proving) what chiropractic has championed for 122+ years, that the human spine is a living neurobiomechanical entity, which responds to the changes in the external environment and compensates perpetually seeking a homeostatic equilibrium.  We can now have verification that changes or compensation within the spinal system as a result of a bio-neuro-mechanical lesion (vertebral subluxation) results in degeneration (subluxation degeneration) of individual motion segments. 

In conclusion, the authors state… 

“Changes in sagittal alignment may lead to kinematic changes and influence load bearing and the distribution of disc degeneration at each level.” [pg. 897] 

“Sagittal alignment may alter spinal load and mobility, possibly influencing segmental degeneration.” [pg. 897] 

“Motion and the segmental contribution to the total mobility tended to be lower at the border of lordosis, especially at the upper segments, and higher at the apex of lordosis in more lordotic spines, whereas the opposite was seen in straight or kyphotic spines.”  [pg. 897]

 

Although medicine is addressing this at the surgical level, as a profession they realize they have no conservative solutions, which has “opened the door” for the credentialed doctor of chiropractic to be in a leadership role in both teaching medicine about the role of the chiropractor as the primary spine care provider and the central focus of the care path for mechanical spine issues. 

When communicating with patients and medical professionals it is critically important to educate them on what “current research” is showing and why it is important that this chiropractic approach to spine care is the future of spine care in the United States. 

 

REFERENCE: 

1. Keorochana, G., Taghavi, C. E., Lee, K. B., Yoo, J. H., Liao, J. C., Fei, Z., & Wang, J. C. (2011). Effect of sagittal alignment on kinematic changes and degree of disc degeneration in the lumbar spine: an analysis using positional MRI. Spine36(11), 893-898. 

2. Teichtahl, A. J., Urquhart, D. M., Wang, Y., Wluka, A. E., Heritier, S. & Cicuttini, F. M. (2015). A dose-response relationship between severity of disc degeneration and intervertebral disc height in the lumbosacral spine. Arthritis Research & Therapy, 17(297). Retrieved from https://openi.nlm.nih.gov/detailedresult.php?img=PMC4619538_13075_2015_820_Fig1_HTML&req=4 

3. Teraguchi, M., Yoshimura, N., Hashizume, H., Muraki,S., Yamada, H.,Minamide, A., Oka, H., Ishimoto, Y., Nagata, K. Kagotani, R., Takiguchi, N., Akune, T., Kawaguchi,  H., Nakamura, K., & Yoshida, M. (2014). Prevalence and distribution of intervertebral disc degeneration over the entire spine in a population-based cohort: the Wakayama Spine Study. Osteoarthritis and Cartilage, 22(1). Retrieved from http://www.sciencedirect.com/science/article/pii/S1063458413010029 

4. Puertas, E.B., Yamashita, H., Manoel de Oliveira, V., & Satiro de Souza, P. (2009). Classification of intervertebral disc degeneration by magnetic resonance. Acta Ortopédica Brasileira, 17(1). Retrieved from http://www.scielo.br/scielo.php?pid=S1413-78522009000100009&script=sci_arttext&tlng=en

 

 

 

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Published in Neck Problems

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

A Chiropractic Adjustment Has a Direct Effect of the Pre-Frontal Cortex of the Brain

 

Verifying a positive effect of the chiropractic spinal adjustment on reflexes, memory, coordination and decision making

 

By: Mark Studin

William J. Owens

 

A report on the scientific literature

For most of the 20th century, based upon results in individual chiropractic offices, the profession’s success was founded on a patient-based model. This model drove utilization at predominantly a “grass roots” level and over the last 10-20 years, research has started to give reasons to why patients not only get out of pain, but executive functions such as decision making, anxiety, managing tasks and being able to focus at a higher level are improving. It is these types of results that have driven many patients to appreciate chiropractic as a “miracle cure” while others, mostly from organized medicine and insurers, who in the past have considered it an "invalid claim” because of the lack of credible evidence despite mounting feedback from patients over the last century. Factually, their arguments had merit on many issues in the past, but as research has been published through the years, those arguments are outdated and incorrect.

"Evidence-based behavioral practice (EBBP) entails making decisions about how to promote health or provide care by integrating the best available evidence with practitioner expertise and other resources, and with the characteristics, state, needs, values and preferences of those who will be affected. This is done in a manner that is compatible with the environmental and organizational context. Evidence is comprised of research findings derived from the systematic collection of data through observation and experiment and the formulation of questions and testing of hypotheses" (Evidence-Based Practice, http://en.wikipedia.org/wiki/Evidence-based_practice).

When considering a purely “evidenced-based” approach, it often precludes advances through a doctor’s immediate experiences in “breakthroughs” that has historically saved lives and then set up the research to render the evidence of what doctors have found on an “experiential level.” This is formally termed best medical practice.

“Abest practice is a method or technique that has consistently shown results superior to those achieved with other means and that is used as a benchmark. In addition, a "best" practice can evolve to become better as improvements are discovered. Best practice is considered by some as a business buzzword, used to describe the process of developing and following a standard way of doing things that multiple organizations can use" (Best Practice, http://en.wikipedia.org/ wiki/Best_practice).

Sackett, Rosenberg, Gray, Haynes and Richardson (1996) stated, 

 “Criticism has ranged from evidence based medicine being old hat to it being a dangerous innovation, perpetrated by the arrogant to serve cost cutters and suppress clinical freedom (p. 71)."  They go on to comment “Good doctors use both individual clinical expertise and the best available external evidence, and neither alone is enough. Without clinical expertise, practice risks becoming tyrannized by evidence, for even excellent external evidence may be inapplicable to or inappropriate for an individual patient. Without current best evidence, practice risks becoming rapidly out of date, to the detriment of patients" (Sackett et al, 1996, p. 72).  The point is that the provider plays a huge role and ultimately is the check and balance of this process. Without the provider, the payor becomes the determining factor in the delivery of healthcare by "tying the doctor's hands" with the limitation of evidence. 

They further stated:

“External clinical evidence can inform, but can never replace, individual clinical expertise, and it is this expertise that decides whether the external evidence applies to the individual patient at all and, if so, how it should be integrated into a clinical decision" (Sackett et al, 1996, p. 73).  Lastly, they state, “Evidence based medicine is not restricted to randomized trials and meta-analyses. It involves tracking down the best external evidence with which to answer our clinical questions" (Sackett et al, 1996, p. 73). This is often a process that takes years, preventing the final papers from being published in a timely enough fashion to meet the ever-changing advancement of medicine and the technologies that support the current needs of the patients.  

When considering executive function at the central (brain) level, based upon contemporary literature, we can now go beyond the “best medical practice” model of purely patient feedback and as Sackett et. Al. suggested, add the evidence as verification. In order to better understand how chiropractic plays a role in executive function, we must start at neural plasticity. According to Leung et. Al (2015) Neural plasticity refers to the capacity of our brain to change in response to internal demand and/or external experience. Burgeoning research has corroborated that the neural plastic changes induced in our brains and behaviors are specific to the experiences. [pg. 1] 

Neuroplasticity, also known as brain plasticity or neural plasticity, is an umbrella term that describes lasting change to the brain throughout an individual's life course. The term gained prominence in the latter half of the 20th century, when new research showed that many aspects of the brain can be altered (or are "plastic”) even into adulthood. (https://en.wikipedia.org/wiki/Neuroplasticity) 

This article focuses on the actions and effects of neuroplasticity on the pre-frontal cortex of the brain. According to Lelic et. Al (2016) 

The prefrontal cortex is known to play a vital role in SMI and is also responsible for a number of other functions. The prefrontal cortex is known to be a key structure responsible for the performance of what is known as “executive functions.” Executive function is the mechanism by which the brain integrates and coordinates the operations of multiple neural systems to solve problems and achieve goals based on the ever-changing environment around us. Executive function is considered to be a product of the coordinated operation of various neural systems and is essential for achieving any particular goal. The prefrontal cortex is believed to be the main brain structure responsible for enabling this coordination and control. It requires planning a sequence of subtasks to accomplish a goal, focusing attention on relevant information as well as inhibiting irrelevant distractors, being able to switch attention between tasks monitoring memory, initiation of activity, and responding to stimuli. [pg. 7] 

Lelic et. Al.’s study resulted in two major findings. Firstly, the study reproduced previous findings of somatosensory evoked potential (SEPs) studies that have shown that chiropractic spinal adjusting of dysfunctional spinal segments alters early sensorimotor integration (SMI) of input from the upper limb. The second major finding of this study was that we were able to show, using dipole source localization, that this change in SMI that occurs after spinal manipulation predominantly happens in the prefrontal cortex. The SEP peak showed multiple neural generators including primary sensory cortex, basal ganglia, thalamus, premotor areas, and primary motor cortex. The frontal N30 peak is therefore thought to reflect early SMI.

The current study adds to previous work by not only confirming that spinal manipulation [chiropractic spinal adjustment] of dysfunctional joints decreases the N30 SEP peak amplitude but also demonstrating that this decrease occurs predominantly in one of the known neural generators of N30, that is, the prefrontal cortex. This suggests that, at least in part, the mechanisms by which spinal manipulation improves performance are due to a change in function at the prefrontal cortex.

Lelic et. Al (2016) continued,

The prefrontal cortex is known to play a vital role in SMI and is also responsible for a number of other functions. The prefrontal cortex is known to be a key structure responsible for the performance of what is known as “executive functions.” Executive function is considered to be a product of the coordinated operation of various neural systems and is essential for achieving any particular goal. The prefrontal cortex is believed to be the main brain structure responsible for enabling this coordination and control. It requires planning a sequence of subtasks to accomplish a goal, focusing attention on relevant information as well as inhibiting irrelevant distractors, being able to switch attention between tasks, monitoring memory, initiation of activity, and responding to stimuli. A change in prefrontal activity following chiropractic care may therefore explain and/or link some of the varied improvements in neural function previously observed in the literature, such as improved joint position sense error, reaction time, cortical processing, cortical sensorimotor integration, reflex excitability, motor control, and lower limb muscle strength.

To accomplish the coordinated operations of multiple neural systems and structures, the prefrontal cortex must monitor the activities in other cortical and subcortical structures and control and integrate their operations by sending command signals in a so-called “top-down” manner. This is a complex operation, and the importance of this monitoring, integration, and coordination is highlighted in studies where damage to the prefrontal cortex has been shown to impair the ability to create new and adaptive action programs or choose the best among several equally probable alternatives, despite such individuals displaying normal IQs in most psychological tests, having normal long-term memory functions, and exhibiting normal perceptual, motor, and language skills

 To accomplish the coordinated operations of multiple neural systems and structures, the prefrontal cortex must monitor the activities in other cortical and subcortical structures and control and integrate their operations by sending command signals in a so-called “top-down” manner. This is a complex operation, and the importance of this monitoring, integration, and coordination is highlighted in studies where damage to the prefrontal cortex has been shown to impair the ability to create new and adaptive action programs or choose the best among several equally probable alternatives, despite such individuals displaying normal IQs in most psychological tests, having normal long-term memory functions, and exhibiting normal perceptual, motor, and language skills [43].The change in prefrontal cortex as seen in this study therefore suggests that the altered input from dysfunctional joints that leads to altered processing of somatosensory inputs can influence processing of somatosensory information by the prefrontal cortex.

Chiropractic care, by treating the joint dysfunction, appears to change processing by the prefrontal cortex. This suggests that chiropractic care may as well have benefits that exceed simply reducing pain or improving muscle function and may explain some claims regarding this made by chiropractors.

Although the change in N30 due to chiropractic treatment is an important finding, it is not clear how long this finding lasts. To date, some of the authors of this study have shown that the N30 changes on average are present for at least 20–30 minutes after spinal manipulation. For some subjects, the changes were still evident at 30 minutes after spinal manipulation and we have not yet followed up for longer than 30 minutes, due to the length of the study as is.

The literature has clearly suggested that a chiropractic spinal adjustment has a clear and reproducible effect on brain physiology and function and is consistent with reports from Reed, Pickjar, Sozio and Long (2014) and Gay, Robinson, George, Peristen and Bishop (2014) on a chiropractic spinal adjustment effecting brain function. These results, in addition to chiropractic patient’s feedback since 1895, have combined both “best practice” and evidenced based” models and start to explain through science, why people are experiencing so much more than their beck or neck pain resolving.

References:

  1. Best Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, fromhttp://en.wikipedia.org/wiki/Best_practice
  2. Evidence-Based Practice. (n.d.). In Wikipedia. Retrieved January 3, 2012, fromhttp://en.wikipedia.org/wiki/Evidence-based_practice
  3. Leung, N. T., Tam, H. M., Chu, L. W., Kwok, T. C., Chan, F., Lam, L. C., ... & Lee, T. (2015). Neural plastic effects of cognitive training on aging brain.Neural plasticity,2015.
  4. Neuroplasticity (2017), Retrieved from: https://en.wikipedia.org/wiki/Neuroplasticity
  5. Lelic, D., Niazi, I. K., Holt, K., Jochumsen, M., Dremstrup, K., Yielder, P., ... & Haavik, H. (2016). Manipulation of dysfunctional spinal joints affects sensorimotor integration in the prefrontal cortex: A brain source localization study.Neural plasticity,2016
  6. Reed, W. R., Pickar, J. G., Sozio, R. S., & Long, C. R. (2014). Effect of spinal manipulation thrust magnitude on trunk mechanical activation thresholds of lateral thalamic neurons.Journal of Manipulative and Physiological Therapeutics, 37(5), 277-286.
  7. 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..

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Published in Low Back Problems

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 Education30(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.

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Published in Neck Problems

Efficacy of Chiropractic Care on Cervical Herniated Discs with Degenerative Changes in the Spine

 

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

William J. Owens DC, DAAMLP

A report on the scientific literature

 

INTRODUCTION

When studying chiropractic care in relationship to herniated discs and degeneration, we must first look carefully at each component to ensure that we are consistent with language to ensure a better understanding. 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 has 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. 

HERNIATED DISCS

 

When considering disc issues, Fardone et. Al (2014) defined the nomenclature that has been widely accepted both in academia and clinically and should be adhered to, to ensure that reporting and visualizing pathology is consistent with the morphology visualized. In the past, this has been a significant issue as many have called a bulge a protrusion, a prolapse or herniation. In today’s literature Fardone’s document has resolved much of those problems.

 

Herniated Disc: “Herniated disc is the best general term to denote displacement of disc material. The term is appropriate to denote the general diagnostic category when referring to a specific disc and to be inclusive of various types of displacements when speaking of groups of discs. The term includes discs that may properly be characterized by more specific terms, such as ‘‘protruded disc’’ or ‘‘extruded disc.’’ The term ‘‘herniated disc,’’ as defined in this work, refers to localized displacement of nucleus, cartilage, fragmented apophyseal bone, or fragmented annular tissue beyond the intervertebral disc space. ‘‘Localized’’ is defined as less than 25% of the disc circumference. The disc space is defined, craniad and caudad, by the vertebral body end plates and, peripherally, by the edges of the vertebral ring apophyses, exclusive of the osteophyte formation. This definition was deemed more practical, especially for the interpretation of imaging studies, than a pathologic definition requiring identification of disc material forced out of normal position through an annular defect.” (page E1454)

 

SPINAL DEGENERATION

 

Spinal degenerating is typically associated with vertebral body endplate changes, or degeneration of the bones of the spine and it starts at the edges. These changes were classified by Michael Modic MD, Neuroradiologist in 1988 and were classified into 3 categories:

Viroslav (2016) reported:

On histopathologic section, type 1 changes are associated with fissuring of the endplates and infiltration of vascularized fibrous tissue. Increased osteoclasts, osteoblasts, and reactive woven bone are also found, indicating that type 1 changes are due to an inflammatory-type response. Type 2 changes occur due to conversion of red marrow to fatty marrow, and type 3 changes represent subchondral sclerosis…. later studies have shown that endplate changes can fluctuate between types, and some changes can regress completely. Mixed Modic endplate changes are commonly seen, and support the contention that all of the changes are manifestations of the same process at different stages. Modic changes can also regress following lumbar fusion. (http://radsource.us/vertebral-endplate-changes/)

 

In short, Modic changes are stages reflective of the process the vertebrate undergoes in degeneration. First there is inflammation, then the marrow changes to fat preventing nutrients to feed the bone, followed by sclerotic or degeneration of bone. In the context of this article, how are spinal herniations responding to chiropractic care in lieu of inherent degenerative changes.

 

CHIROPRACTIC CARE

Kressig et. Al (2016) reported:

Although patients who were Modic positive had higher baseline NDI (Neck Disability Index) scores, the proportion of these patients improved was higher for all time points up to 6 months. Pg. 565

The results of the present study on patients with CDH (Cervical Disc Herniation), which indicate better treatment outcomes for patients with CDH with MCs (Modic Changes), are generally consistent with those reported for patients with LDH (lumbar disc herniation), other than the fact that the patients with CDH and MC reported no relapses…It is also important to mention that none of the patients in the present study reported worsening of their condition. Cervical HVLA manipulation (chiropractic spinal adjustment) has been controversial, with suggestions that it can lead to vertebral artery dissection and stroke. However, in 2007, a prospective national survey by Thiel et al studied almost 20 000 patients who were treated with cervical HVLA manipulation or mechanically assisted thrust. There were no reports of serious adverse events, which were defined as symptoms with immediate onset after treatment and with persistent or significant disability. Pg. 572

 

CONCLUSION

 

This report on the literature verifies that chiropractic care renders significant improvement in patients with cervical disc herniation in the presence of inflammation and/or degenerative changes using an accepted disability index in a verifiable scenario. This, in conjunction with other numerous report on the efficacy of chiropractic successfully treating patients with herniated discs offers solutions to an injured public.

 

Links to other articles:

 

Chiropractic Outcome Studies on Treatment of Fragmented/Sequestered and Extruded Herniated Discs and Radicular Pain

 

Spinal Fusion vs. Chiropractic for Mechanical Spine Pain

 

Cervical Disc Herniation with Radiculopathy (Arm Pain): Chiropractic Care vs. Injection Therapy

 

Disc Herniations and Low Back Pain Post Chiropractic Care

 

References:

  1. Kressig, M., Peterson, C. K., McChurch, K., Schmid, C., Leemann, S., Anklin, B., & Humphreys, B. K. (2016). Relationship of Modic Changes, Disk Herniation Morphology, and Axial Location to Outcomes in Symptomatic Cervical Disk Herniation Patients Treated With High-Velocity, Low-Amplitude Spinal Manipulation: A Prospective Study.Journal of manipulative and physiological therapeutics,39(8), 565-575.
  2. 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.
  1. 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.
  2. Viroslav A. (2016) Vertebral Endplate Changes, Retrieved from: http://radsource.us/vertebral-endplate-changes/
  1. Fardon, D. F., Williams, A. L., Dohring, E. J., Murtagh, F. R., Gabriel Rothman, S. L., & Sze, G. K. (2014). Lumbar disc nomenclature: Version 2.0. Recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 39(24), E1448-E1465.

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Published in Neck Problems

Chiropractic Care for Neck and Low Back Pain: Evidenced Based Outcomes

 

98.5% of chiropractic patients had their expectations exceeded

 

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

William J. Owens DC, DAAMLP

A report on the scientific literature

 

As the scientific, academic and reimbursement establishments further entrench in an evidenced based model, it is critical to both examine and utilize studies when treating mechanical spine patients with chiropractic care. Although there are many sects in the chiropractic profession who shun the title “mechanical spine pain,” it is universally accepted term interprofessionally for any etiology of spine pain exclusive of tumor, fracture or infection. This definition fits every licensure board’s scope of practice for chiropractic where chiropractic is licensed. 

 

In the United Kingdom, Field and Newell (2016) reported that back pain accounts for 4.8% of all social benefit claims with overall costs reaching $7 billion pounds or $9.35 billion US dollars. Boyles (2016) reported that “Researchers from the University of Washington, Seattle, found that the nation's dramatic rise in expenditures for the diagnosis and treatment of back and neck problems has not led to expected improvements in patient health. Their study appears in the Feb. 13 issue ofThe Journal of the American Medical Association. After adjustment for inflation, total estimated medical costs associated with back and neck pain increased by 65% between 1997 and 2005, to about $86 billion a year… Yet during the same period, patients reported more disability from back and neck pain, including moredepressionand physical limitations.

 

“We did not observe improvements in health outcomes commensurate with the increasing costs over time," lead researcher Brook I. Martin, MPH, and colleagues wrote. "Spine problems may offer opportunities to reduce expenditures without associated worsening of clinical outcomes." (http://www.webmd.com/back-pain/news/20080212/86-billion-spent-on-back-neck-pain)

 

Although it has been widely reported that expenditures a decade later has far exceeded the 2005 figure, the opioid epidemic, in part from musculoskeletal etiology is another example WebMD’s reporting on the American Medical Association’s finding of increased disability from neck and back pain inclusive of depression and physical limitations. The variable therefore is not predicated on financial expenditures, but treatment paradigms that work and have been verified in an evidenced based environment. 

 

Clinicians should always be striving to offer the best care at the lowest cost available. Carriers should always strive to fulfill their contractual obligation of providing necessary care delivered in a usual and customary manner while preventing overutilization through built-in safeguards. With doctors managing their patient’s conditions, there are two major parameters that are utilized, best medical practice also known as “experience” and evidence-based practice or that which has only been concluded in the medical literature. Both have a strong place in the healthcare delivery and reimbursement systems.  

"A best practiceis a method or technique that has consistently shown results superior to those achieved with other means, and that is used as a benchmark. In addition, a "best" practice can evolve to become better as improvements are discovered. These are procedures in healthcare that are taught in schools, internships and residencies and are considered the “standard” by which procedures are followed. These practices are based on clinical experience and rely heavily on time-tested approaches. Surprisingly, most of the best medical practice care paths are not published in the peer-reviewed indexed literature. This is due to many factors, but the most obvious are applications of financial resources to “new” discoveries and the simple fact that the clinical arena is adequate to monitor and adjust these practices in a timely manner for practice to keep up with the literature that follows. 

 

Evidence-based practice(EBP) is an interdisciplinary approach to clinical practice that has gained ground following its formal introduction in 1992. It started inmedicineasevidence-based medicine (EBM) and spread to other fields such as dentistry, nursing, psychology,

education, library and information science and other fields. Its basic principles are that all practical decisions made should 1) be based on research studies and 2) that these research studies are selected and interpreted according to some specific norms characteristic for EBP. Typically, such norms disregardtheoretical studiesandqualitative studiesand considerquantitative studiesaccording to a narrow set of criteria of what counts as evidence.

 

 

"Evidence-based behavioral practice(EBBP) entails making decisions about how to promote health or provide care by integrating the best available evidence with practitioner expertise and other resources, and with the characteristics, state, needs, values and preferences of those who will be affected. This is done in a manner that is compatible with the environmental and organizational context. Evidence is comprised of research findings derived from the systematic collection of data through observation and experiment and the formulation of questions and testing of hypotheses" (Evidence-Based Practice, http://en.wikipedia.org/wiki/Evidence-based_practice).

 

This highly-debated topic of evidence-based vs. best practice has valid issues on each side, but putting them together as a hybrid would allow them to thrive in both a healthcare delivery and reimbursement system; all sides would win. This would allow advances in healthcare to save more lives, increase the quality of life and at the same time, offer enough safeguards to prevent abuse to payors. A one-sided approach would tip the scales to either the provider/patients or the payors.

Fields and Newell (2016) studied 2 groups of patients, those treated in private practices and the second in the United Kingdom’s funded National Health Service clinics. For this report, I will focus on the Government funded National Health Service statistics. The evidence sought was the satisfaction of patients with both neck and low back pain who underwent chiropractic care and in this report it satisfies both paradigms of “Best Practice and Evidenced Based Practice” models. They reported that 98.5% of neck and low back pain “patients were more likely to have had their expectations exceeded” (pg. 57) under chiropractic care.

 

 

In a healthcare environment, where overspending is both not the solution and problematic by creating iatrogenic issues in the form of opioid addiction and unresolved biomechanical failures leading to premature long-term musculoskeletal degenerative Fields and Newell have simply asked the patients, have your needs been met or exceeded. Not to diminish studies on the why or how come, patient satisfaction in an evidenced based outcome study that verifies it works with a drug-free option.

 

 

As with many of our articles from here forward, I would like to leave you with a last and seemingly unrelated statement.  I felt it was important to add this at the end since many of our critics negatively portray the safety of chiropractic care.  This statement shall put that to rest leaving only personal biases left standing. Whedon, Mackenzie, Phillips, and Lurie (2015) based their study on 6,669,603 subjects and after the unqualified subjects had been removed from the study, the total patient number accounted for 24,068,808 office visits. They concluded, “No mechanism by which SM [spinal manipulation] induces injury into normal healthy tissues has been identified”(Whedon et al., 2015, p. 5). This study supersedes all the rhetoric about chiropractic and stroke and renders an outcome assessment to help guide the triage pattern of mechanical spine patients.

 

References:

  1. Field J., Newell D. (2016) Clinical Outcomes In a Large Cohort of Musculoskeletal Patients Undergoing Chiropractic Care In the United Kingdom: A Comparison of Self and National Health Service Referral Routes, Journal of Manipulative and Physiological Therapeutics, 39(1), pgs. 54-62
  2. Boyles S., $86 Billion Spent on Back, Neck Pain, WebMD (2016) Retrieved from: http://www.webmd.com/back-pain/news/20080212/86-billion-spent-on-back-neck-pain
  3. Best Practice. (2016). In Wikipedia. Retrieved from http://en.wikipedia.org/wiki/Best_practice
  4. Evidence-Based Practice. (2016). In Wikipedia. Retrieved from http://en.wikipedia.org/wiki/Evidence-based_practice
  5. 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

Chiropractic’s Mechanism in Pain Modulation and the Connection to Systemic Diseases

 

A Literature Review and Synthesis on the Possible Effects of Chiropractic on Cancers, Systemic Diseases, Mental and Social Disorders and Sexual Behavior

A report on the scientific literature 


 

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

 William J. Owens DC, DAAMLP

 -----

Citation: Studin M., Owens W. (2016) Chiropractic’s Mechanism in Pain Modulation and the Connection to Systemic Disease, Dynamic Chiropractor 34(3) 26-33

 

Chiropractors for over a century have been called “quacks” and “charlatans” for reporting what they have observed in their patients as a result of their care. The maladies that chiropractors have witnessed the disappearance of include cancers, eczema, infertility, high blood pressure, diabetes, arthritis, emotional disturbances and many more. Historically, this has brought the “ire” of organized medicine and other splinter groups to attack the chiropractic profession with the mantra of “there is no scientific evidence” to support these allegations. One author of this paper, Dr Studin, has spent 35 years experiencing this phenomenon where patients reported the aforementioned maladies and a long list of other diseases which “miraculously” disappeared with treatment.

 

 

To be clear, this wasn’t an isolated instance, but rather year after year that and in meetings with other chiropractor’s similar stories were heard.  However, sharing these findings amongst chiropractors was much easier than sharing it with the healthcare community because of the persecution against chiropractors and the outcry of “quackery.” In fact, many of the chiropractic practitioners who witnessed these results felt the best way to approach this was to only discuss this with patients.  They purposefully avoided any other healthcare providers in these conversations because there was no scientific evidence to back up the repeated observations.

 

 

To the medical community, these were religious type beliefs and we, as chiropractors, were proselytizing our religion of chiropractic on patients and the community. Based on the lack of published evidence, their allegations against us was not without merit albeit misguided and fueled in part by economics. However, medicine saw beliefs based upon observations on the chiropractic side and medicine required published evidence for verification no matter the claims and testimonials from an ever-increasing segment of the public. Today, the benefits of chiropractic care have remained constant with the same stream of patients getting well. However, the evidence has now started to support these findings and the chiropractic profession has gone beyond proselytizing our beliefs to being able to cite specific research that supports and justifies chiropractic care as part of mainstream healthcare. We can now share our results, which are consistent with the scientific literature that often has been discovered or proven beyond the chiropractic profession.

 

 

NOTE: Although the following evidence verifies what our profession has been witnessing over the last decade, please understand that the research is just beginning to show evidence and much more is needed to bring our profession to where it needs to be. As a result, every practitioner and every chiropractic academic institution needs to both support and be involved in research. Our professional institutions and their research departments MUST take an active and serious role in producing and publishing research. Otherwise, it will come from another source such as osteopathy or physical therapy and prevent chiropractic from taking it’s unique place in healthcare.

 

Chiropractic Adjustment and Central Nervous System Changes

 

We have held for quite some time that studying how the adjustment works for the treatment of pain is the first step in truly understanding how the chiropractic adjustment affects systemic diseases. It has been shown that the chiropractic adjustment has a direct effect on many regions in the brain where pain mediation arises. As evidence, Reed, Pickar, Sozio, and Long (2014) reported:

…forms of manual therapy have been clinically shown to increase mechanical pressure pain thresholds (i.e., decrease pain sensitivity) in both symptomatic and asymptomatic subjects.Cervical spinal manipulation has been shown to result in unilateral as well as bilateral mechanical hypoalgesia [reduction in pain]. Compared with no manual therapy, oscillatory spinal manual therapy at T12 and L4 produced significantly higher paraspinal pain thresholds at T6, L1, and L3 in individuals with rheumatoid arthritis. The immediate and widespread hypoalgesia associated with manual therapy treatments has been attributed to alterations in peripheral and/or central pain processing including activation of descending pain inhibitory systems.

Increasing evidence from animal models suggests that manual therapy activates the central nervous system and, in so doing, affects areas well beyond those being treated. (p. 277)

 

 

Reed et al. (2014) continued stating, “Several clinical studies indicate that spinal manipulation [chiropractic spinal adjustment] alters central processing of mechanical stimuli evidenced by increased pressure pain thresholds and decreased pain sensitivity in asymptomatic and symptomatic subjects following manipulation” (p. 282).

 

In another paper, Gay, Robinson, George, Perlstein, and Bishop (2014) reported, “With the evidence supporting efficacy of MT [manual therapy or chiropractic spinal adjustments] to reduce pain intensity and pain sensitivity, it is reasonable to assume that the underlying therapeutic effect of MT is likely to include a higher cortical component” (p. 615).   The authors continued by stating, “…pain-free volunteers processed thermal stimuli applied to the hand before and after thoracic spinal manipulation (a form of MT).  What they found was that 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]” (Gay et al., 2014, p. 615).

 

The above two studies are only a small part of a growing body of evidence showing that the chiropractic spinal adjustment directly affects the functioning of the central nervous system and is the core of pain modulation with chiropractic care and the foundation to the next level, as outlined below. 

 

The Effect of the Chiropractic Adjustment on Neuropeptides (Neurotensin-Oxytocin-Cortisol)

NOOC Axis = Neurotensin-Orexin-Oxytocin-Cortisol

Regarding neuropeptides, Burbach (2011) reports:

We know neuropeptides now for over 40 years as chemical signals in the brain. The discovery of neuropeptides is founded on groundbreaking research in physiology, endocrinology, and biochemistry during the last century and has been built on three seminal notions: (1) peptide hormones are chemical signals in the endocrine system; (2) neurosecretion of peptides is a general principle in the nervous system; and (3) the nervous system is responsive to peptide signals. These historical lines have contributed to how neuropeptides can be defined today: “Neuropeptides are small proteinaceous substances produced and released by neurons through the regulated secretory route and acting on neural substrates.” Thus, neuropeptides are the most diverse class of signaling molecules in the brain engaged in many physiological functions. (p. 1)

 

 

Simply put, neuropeptides are the transmitters that allow the brain to communicate within itself and with the rest of the body’s functions. The increase or decrease of these neuropeptides/neurotransmitters alters human physiology (function) and any action upon the body that affects the neurotransmitters can either help normalize function or conversely destroy functioning with the human body.  This is the foundation of homeostasis and, therefore, if we can affect the function of neurotransmitters, then it is safe to say we can have a level of influence on homeostasis.  This obviously ties into our founder’s observations and the beginning of chiropractic! 

 

 

In an additional paper, Plaza-Manzano et al. (2014) wrote, “Several neuropeptides, such as neurotensin, oxytocin, or orexin A have been associated with hypoalgesia and pain modulation, and it is well known that cortisol plays an analgesic role related to stress responses. Recent theories have also suggested that chronic pain could be partly maintained by maladaptive physiological responses of the organism facing a recurrent stressor, a situation related to high cortisol levels” (p. 231). The authors continued by stating, “To make better therapeutic decisions, professionals would profit from knowing whether one type of SM (adjustment) is better than others in terms of antinociceptive (authors comment: antinociceptive = pain inhibition) effects (neurotensin, orexin A, oxytocin, and cortisol). Taking these data into account, our purpose was to determine whether cervical and thoracic manipulation would induce differences in neuropeptide production or have a similar biochemical response (Plaza-Manzano et al., 2014, p. 232).

 

 

Plaza-Manzano et al. (2014) went on to say “…within-group comparisons in cervical and thoracic manipulation groups showed a significant increase in neurotensin levels immediately post-intervention compared with pre-intervention levels… At the descriptive level, an important decrease in orexin A concentration was detected after the intervention in the thoracic SM (spinal manipulation) group in comparison with the control group… the cervical SM group showed increased oxytocin values when compared with the thoracic SM group immediately post-intervention (Plaza-Manzano et al., 2014, p. 234). At 2 hours after the intervention, an increase was found only in the cervical SM group when compared with pre-intervention levels… the cervical SM group showed a significant increase in cortisol plasma concentration immediately post-intervention compared with baseline values” (Plaza-Manzano et al. 2014, p. 235). 

 

 

Neurotensin

Orexin

Oxytocin

Cortisol

Cervical Adjustment

Increased levels

Not reported

Increased levels

Increased levels

Thoracic Adjustment

Increased levels

Increased levels

No Change

Significant Decrease at

2 hours

 

 

Regarding pain Plaza-Manzano et al. (2014) stated:

It is well established that neurotensin affects the activity of oxytocin-positive cells in the supraoptic nucleus. Oxytocin is a nonapeptide that plays a major neuroendocrine role, modulating several physiological functions in mammals, like somatosensory transmission, nociception, and pain. Oxytocin is synthesized and secreted by a subpopulation of the paraventricular and supraoptic nuclei of the hypothalamus. In fact, several studies now support the idea that oxytocin exerts a potent antinociceptive control after its release in the spinal cord from hypothalamo-hypophysal descending projections (from the brain) … In studies involving human subjects, pain relief was reported in central neurogenic pain and in low back pain after the intracerebroventricular and intrathecal administration of oxytocin (aka pharmaceutical intervention). No previous study has evaluated whether SM has an effect on oxytocin plasmatic concentration. Our results suggest that the increase of the plasmatic concentration of oxytocin following an SM could be partly responsible for the analgesic effect linked to manual therapy techniques due to the activation of descending pain-inhibitory pathways. Orexins are known to be a hypothalamic peptide critical for feeding and normal wakefulness...Orexinergic projections were identified in periaqueductal gray matter, the rostral ventral medulla, the dorsal horn, and the dorsal root ganglion. Emerging evidence shows that the central nervous system administration (intracranial ventricle or intrathecal injection) of orexin A can suppress mechanical allodynia and thermal hypersensitivity in multiple pain models, suggesting the regulation of nociceptive processing via spinal and supraspinal mechanisms. In addition, orexins showed antinociceptive effects on models of pain, such as neuropathic pain, carrageenan test, and postoperative pain… Cortisol is therefore one of the biochemical factors delivered in stress situations that acts to decrease local edema and pain by blocking early stages of inflammation. In addition, it is also believed that high cortisol levels promote wound healing by stimulating gluconeogenesis. The response to stress is triggered by the stimulation of the hypothalamus-pituitary-adrenal axis. It has been proven that a subject’s level of stress can be correlated with secreted cortisol levels. (p. 236) 

 

 

The above study explains the neurochemical mechanism through which pain in mediated via the chiropractic spinal adjustment. Many of the pharmacological and nutraceutical interventions also target these systems through a variety of measures, some with significant negative side-effects.  Next, let’s examine what control these neuropeptides have in the human body beyond pain control. This will begin to explain the systemic connection with the chiropractic adjustment.

 

Systemic Effect of the Chiropractic Adjustment by Increasing of the NOC Axis

 

According to St-Gelais, Jomphe and Trudeau (2006), “…we focus our attention on the roles of NT [neurotensin] in the CNS. However, it is important to point out that this peptide is also highly expressed peripherally where it acts as a modulator of the gastrointestinal and cardiovascular systems” (p. 230). These authors discussed the role of antipsychotic drugs in cases of schizophrenia and how it was used to elevate the neurotensin level.  They found it would promote partial recovery while an additional study revealed that unmediated patients displayed a lowering of neurotensin.

 

An increase in neurotensin acts as a psychostimulant. A study conducted over the course of 25 years on individuals with drug abuse issues showed that increasing neurotensin levels decreased effects of psychostimulants such as amphetamines and cocaine. This study on drug addiction, according to St-Gelais et al. (2006), was conducted on animals, but there are many in chiropractic who have reported on a case-by-case basis that integrating chiropractic has helped many with drug abuse issues. Perhaps what this article suggests can help find more answers.

 

 

St-Gelais et al. (2006) also found a strong connection with a decrease in neurotensin in the following:

 

  1. Schizophrenia
  2. Gastrointestinal function
  3. Cardiac function
  4. Parkinson’s disease
  5. Elevated blood pressure
  6. Eating disorders
  7. Cancer of the
    1. Colon
    2. Lungs
    3. Ovaries
    4. Pancreas
    5. Prostate
    6. Bones
    7. Brain
  8. Alzheimer’s
  9. Stroke (ischemic deaths)
  10. Inflammation

 

Although the literature has not yet conclusively shown that any one of the central nervous system conditions are causally involved with the reduction of neurotensin, the literature strongly suggest that it plays a significant role. There is definitely a common denominator in neurotensin levels and these seemingly uncorrelated conditions.

 

Orexins, also known as hypocretins, according to Ebrahim, Howard, Kopelman, Sharief and Williams (2002) have an important role in sleep and (mental) arousal states. They state, “The hypocretins are thought to act primarily as excitatory neurotransmitters…suggesting a role for the hypocretins in various central nervous functions related to noradrenergic innervation, including vigilance, attention, learning, and memory. Their actions on serotonin, histamine, acetylcholine and dopamine neurotransmission is also thought to be excitatory and a facilitatory role on gamma-aminobutyric acid (GABA) and glutamate-mediated neurotransmission is suggested” (p. 227).

 

Ebrahim et al. (2002) continued:

Apart from their primary role in the control of sleep and arousal, the hypocretins have been implicated in multiple functions including feeding and energy regulation, neuroendocrine regulation, gastrointestinal and cardiovascular system control, the regulation of water balance, and the modulation of pain. A role in behaviour is also postulated. The cell bodies responsible for hypocretin synthesis are localized to the tuberal part of the hypothalamus, the so-called feeding centre...[which] has led to the suggestion that the hypocretins are mediators of energy metabolism. The neuroendocrine effects of the hypocretins include a lowering of plasma prolactin and growth hormone and an increase in the levels of corticotropin and cortisol, insulin and luteinizing hormone. Central administration of the hypocretins increases water consumption, stimulates gastric acid secretion and increases gut motility. The hypocretins increase mean arterial blood pressure and heart rate. The localization of long descending axonal projections containing hypocretin at all levels of the spinal cord suggests a role in the modulation of sensation and pain. Strong innervation of the caudal region of the sacral cord suggests a role in the regulation of both sympathetic and parasympathetic functions. (p. 227-228)

 

According to Lee, Macbeth, Pagani and Young (2009), oxytocin is a product of the hypothalamus and pituitary and according to Plaza-Manzano et al. (2014) it has been linked to the endogenous synthesis of opioids, thereby adding further explanation to the antinociceptive effects in the reduction of pain centrally. This partially explains the pain mechanism of the chiropractic adjustment.

 

 

For non-pain actions of oxytocin, beyond the actions of uterine contractions and lactation (You remember that board question, right?), Lee et al. (2009) reported that oxytocin is integral in:

 

  1. Social memory
  2. Social bonding
  3. Parental behavior
  4. Human behavior
  5. Sexual behavior
  6. Social behaviors (i.e. aggression)
  7. Learning
  8. Memory (overall)
  9. Anxiety
  10. Eating behavior
  11. Sugar metabolism

 

Willenberg et al. (2000) reported, “Corticotropin-releasing hormone (CRH) and its receptors are widely expressed in the brain and peripheral tissues. This hormone is the principal regulator of the hypothalamic-pituitary-adrenal (HPA) axis and exerts its effects via two main receptor subtypes, type 1 (CRH-R1) and 2 (CRH-R2). CRH also activates both the adrenomedullary and systemic sympathetic system limbs and an intraadrenal CRH/ACTH/cortisol system…” (p. 137).

 

According to Smith and Vale (2006) “The principal effectors of the stress response are localized in the paraventricular nucleus (PVN) of the hypothalamus, the anterior lobe of the pituitary gland, and the adrenal gland. This collection of structures is commonly referred to as the hypothalamic-pituitary-adrenal (HPA) axis...In addition to the HPA axis, several other structures play important roles in the regulation of adaptive responses to stress. These include brain stem noradrenergic neurons, sympathetic adrenomedullary circuits, and parasympathetic systems” (pgs. 383-384) 

 

 

Smith and Vale (2006) also reported the following function of the HPA axis that has a direct control by corticotropin-releasing hormones:

  1. Autonomic nervous system function
  2. Learning
  3. Memory
  4. Feeding
  5. Reproduction related behaviors
  6. Metabolic changes
  7. Cardiovascular regulation
  8. Immune system

In addition, Willenberg et al. (2000) added the following”

  1. Mental disorders
  2. Depression
  3. Schizophrenia

 

Conclusion

 

For over a century, chiropractic patients have been reporting the “miracles” of the results rendered in chiropractic offices worldwide and yet chiropractors have been persecuted and often vilified by the medical profession due to the lack of scientific evidence. Although this is a very broad perspective of the potential of the chiropractic care, it is now virtually impossible to ignore the fact that the chiropractic adjustment affects changes in neuropeptides in blood sample post-adjustment. These blood markers verify that changes are made in the human body and these changes have far reaching effects on both wellness and disease care. Medicine has been attempting to reproduce these effects via pharmaceutical intervention and a part of the solution now has to be chiropractic care based upon the evidence reported. 

This is just the beginning, as more evidence is needed to verify the full effects of the chiropractic spinal adjustment. We have a lot of work to do, but the scientific foundation of what chiropractors have observed since our beginning is getting stronger every month as more research is published.  

We would like to leave you with a last and seemingly unrelated statement.  We felt it was important to add this at the end since many of our critics negatively portray the safety of chiropractic care.  This statement shall put that to rest leaving only personal biases left standing. Whedon, Mackenzie, Phillips, and Lurie(2015) based their study on 6,669,603 subjects and after the unqualified subjects had been removed from the study, the total patient number accounted for 24,068,808 office visits. They concluded, “No mechanism by which SM [spinal manipulation] induces injury into normal healthy tissues has been identified”(Whedon et al., 2015, p. 5). This study supersedes all the rhetoric about chiropractic and stroke and renders an outcome assessment to help guide the triage pattern of mechanical spine patients.

References:

1. Reed, W. R., Pickar, J. G., Sozio, R. S., & Long, C. R. (2014). Effect of spinal manipulation thrust magnitude on trunk mechanical activation thresholds of lateral thalamic neurons.Journal of Manipulative and Physiological Therapeutics, 37(5), 277-286.

2. 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.

3. Burbach, J. P. (2011). What are neuropeptides? In J. Walker (Ed.),Methods in molecular biology (pp. 1-36). Clifton, New Jersey: Humana Press.

4. Plaza-Manzano, G., Molina-Ortega, F., Lomas-Vega, R., Martinez-Amat, A., Achalandabaso, A., & Hita-Contreras, F. (2014). Changes in biochemical markers of pain perception and stress response after spinal manipulation.Journal of Orthopedic and Sports Physical Therapy, 44(4), 231-239.

5. St-Gelais, F., Jomphe C., & Trudeau, L. (2006). The role of neurotensin in central nervous system pathophysiology: What is the evidence?Journal of Psychiatry & Neuroscience,31(4) 229-245.

6. Ebrahim, I. O., Howard, R. S., Kopelman, M. D., Sharief, M. K., & Williams, A. J. (2002). The hypocretin/orexin system.Journal of the Royal Society of Medicine,95(5), 227-230.

7. Lee, H. J., Macbeth, A. H., Pagani, J. H., & Young, W. S. (2009). Oxytocin: The great facilitator of life.Progressive Neurobiology, 88(2), 127-151.

8. Willenberg, H. S., Bornstein, S. R., Hiroi, N., Path, G., Goretzki, P. E., Scherbaum, W. A., & Chorusos, G. (2000). Effects of a novel corticotropin-releasing-hormone receptor type I antagonist on human adrenal function.Molecular Psychiatry, 5(2), 137-141.

9. Smith, S. M., & Vale, W. W. (2006). The role of hypothalamic-pituitary-adrenal axis neuroendocrine response to stress.Dialogue in Clinical Neuroscience, 8(4), 383-395.

10. 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.

Dr. Mark Studin is an Adjunct Associate Professor of Chiropractic at the University of Bridgeport College of Chiropractic, an Adjunct Professor of Clinical Sciences at Texas Chiropractic College and a clinical presenter for the State of New York at Buffalo, School of Medicine and Biomedical Sciences for post-doctoral education, teaching MRI spine interpretation, spinal biomechanical engineering and triaging trauma cases. He is also the president of the Academy of Chiropractic teaching doctors of chiropractic how to interface with the medical and legal communities (www.DoctorsPIProgram.com), teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally and studies trends in healthcare on a national scale (www.TeachDoctors.com). He can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. or at 631-786-4253.

 

 

Dr. Bill Owens is presently in private practice in Buffalo and Rochester NY and generates the majority of his new patient referrals directly from the primary care medical community.  He is an Associate Adjunct Professor at the State University of New York at Buffalo School of Medicine and Biomedical Sciences as well as the University of Bridgeport, College of Chiropractic and an Adjunct Professor of Clinical Sciences at Texas Chiropractic College.  He also works directly with doctors of chiropractic to help them build relationships with medical providers in their community. He can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. or www.mdreferralprogram.com or 716-228-3847  

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