news.gif (12017 bytes)Scientific Basis For Subluxation Sprain/Strain

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LibertyYour editor wrote these articles while a student at an accredited Chiropractic Medical School.  During those days, there were only two fully Accredited Chiropractic Schools.  The ACA gave permission to reproduce this research at Chiropractic Colleges.  It was through works like this concomitant with other talented Doctor's of Chiropractic, which helped the evolution of Chiropractic Medicine; today Chiropractic Colleges are accredited across this nation and the globe.


The Theory of Chiropractic Trauma, which had eluded scientists for centuries Part II (Published JACA 1981)


     After your author had written and published part one in this series, with a motivation of love for a profession, this soul had found a consistent set of variables within a consistent continuum relative to patient suffering and objective findings noted from son's of Doctor's of Chiropractic in my class as well as my developing recognition and subsequent investigation into the complaints, signs and symptoms of patients who present to Doctor's of Chiropractic and why they resolve with their care over far more radical cares offered by traditional medicine.  It was interesting that my initial theories, the "Somato-Neuro-Muscular and Viscero-Neuro-Muscular Pathway" and the Somato-Neuro-Muscular pathway did go on to explain the mechanism of pain and discomfort via direct trauma to the spine as well as how altered joint dynamics via spasm occured as a direct result of visceral irritation or disease. 

     Yet, during my research your author discovered that both anthropologists and Doctor's of Chiropractic had noted similar albeit uncorrelated findings.  My soon to be colleagues were reporting areas of compensatory restrictions in spinal motion or excesses in a compensatory area secondary to a primary injured spinal area.   For example,  a person with a functional scoliosis when strained, demonstrates these types of combinations of altered joint dynamics in their spines (e.g. their spine appears radiologically and through examination to be within normal limits and then when strained the spine present through radiological and clinical examination as a structural scoliosis which became a known false positive)

     Thus, it was now clear that your author needed to again investigate and report the forensic textbook sound mechanism of spinal injury whereby a secondary spinal reaction occurs subsequent to an overexertion injury to the spine.  And why.  This investigator did go on to discover the mechanism and report the findings which were excepted universally by science and medicine and have now stood the test of scientific and judicial review and time.  The paper was called the "Strain of Athleticism" published in May of 1981, in the Journal for the American Chiropractic Association-JACA.


     Health care providers from all generations have needed a therapy to aid the individual after he had exerted himself beyond his physical conditioning.  Hippocrates said, "Get knowledge of the spine, for this is the requisite for many diseases."1 Hippocrates wrote many books on health care, including, On Setting Joints By leverage and Manipulation and the Importance of Good Health.   Men of his time used their muscles at work: gathering food, building or fortifying dwellings and fighting beasts and other men.

     In 1895, D.D. Palmer rediscovered the knowledge that, when a vertebra is subluxated in rotation or a lateral flexion-rotation, the sign was of great benefit in making the final "total" diagnosis.

     Today's person is still likely to over-exert their muscles at work, in sports, or in situational activities, such as changing a flat tire on their car.  Because mankind will always utilize their muscles; possibly over-exert themselves and end up in their physician's office, it is important to re-examine "the Strain of Athleticism."

     The purpose of this article is to combine Hippocrates' and Palmer's early concepts with modern science and identify the mechanism of subluxations of the vertebral column, occurring as a direct result of muscular over-exertion, which has eluded scientists for centuries.


Physiological Relationships

Visceral Metabolites

     When the free end of a muscle is made to lift a weight, or to oppose a resistance held constant during contraction; the contraction is isotonic and the work done is the product of the distance shortened and the weight lifted by the muscle in overcoming the external resistance.  Under these isotonic conditions, the muscle cannot shorten until the force that it develops is greater than the load it must lift.  When the force of the muscle exceeds the load, the muscle begins to shorten.

     When a muscle contracts, as in isotonic exercise, large molecules of the resting organ break down into many small molecules, which pass into the tissue spaces.  These metabolites can remain in considerable concentrations in the tissue spaces for a long period and will slowly diffuse into the blood.  As the metabolites remaining in the tissue spaces are osmotically active, they attract fluid from the blood and retain it. Normally this facilitates a gradual diffusion of metabolites into the blood, owing to a difference of concentration.  However, during excessive muscular exertion, metabolites cannot be removed from the blood quickly enough.  This occurs because when a muscle contracts, it compresses the vessel in it if it develops more than 10% of its maximal tension.  When it develops more than 70% of its maximal tension, blood flow is completely stopped.3  Furthermore, tissue pressure exceeds pressure within small, thin-walled vessels and even within arteries, thus causing temporary occlusion.4  The increased energy skeletal muscle output for contraction engages the endothelium triggers as well as stimulation from the kidney's lead to Angiotensin II direct effect on these endothelial triggers which release endothelan-1 and prostanoids further causing vascular constrictions.  And combined with a concomitant fight/flight situation, the adrenal glands will release epinephrine and norepinephrine into the blood stream.  Both of these amines main effect on vascular beds is vasoconstriction (In low releases, epinephrine can cause vasodilatation) Thus the metabolites tend to accumulate during exercise and increase with each additional contraction.  In other words, local blood flow spurts and ceases with cyclic contraction and relaxation and these spurts of blood are not equal to the normal circulation, thus allowing toxic metabolites to accumulate.  During high-intensity static exercise, such as weight lifting, or a sudden trauma of equivalent overexertion, blood vessels are compressed by the skeletal muscle, thus increasing vascular resistance and decreasing blood flow (Opposite of dynamic, endurance exercise where there is a 20% increase in blood flow in exercising skeletal muscle due to vasodilators such as adenosine, carbon dioxide, and lactic acid which overcome the increased sympathetic outflow stimulation of alpha receptors which would otherwise cause the sympathetic (vasoconstriction) effect in skeletal muscle causing a "metabolic vasodilation of arterioles).  Hence, during muscular activity, (decrease in vascular resistance.) the weight of the muscle increases by 20% due to the increased amount of retained fluid and metabolites.  This swelling of the muscle may cause the muscle stiffness, which follows extreme exertion.5

Pain Metabolites

     During the first few minutes of maximal isotonic  contraction, or excessive exercise, anaerobic energy is sometimes needed until the acceleration of O2 debt mechanism in association with maximal utilization of the aerobic mechanism.6   The myoglobin-rich, capillary-rich, mitochondria-rich muscles of man offer the luxury of maximal utilization of aerobic energy mechanisms with a ready reserve anaerobic energy system able to yield energy when needed.  The energies released by anaerobic mechanisms due to lactic acidosis (increased anion-gap metabolic acidosis with tissue hypoxia/ anaerobic acidosis) are extremely important in maximal work, where they permit a man to expend energy far in excess of his capacity for carrying on oxidative metabolism.7  This process  is limited by the individual's tolerance for acidosis resulting from accumulation of lactic acid in the muscles, which is an end product of anaerobic glycolysis.8  One of the suggested causes of pain in ischemia is accumulation of large amounts of lactic acid in the tissues.9

     Potassium ions now are  considered important vasodilator metabolites, which have the task of dilating arterioles in the exercising muscle.  The increased blood flow is due to potassium ions' general effect to inhibit smooth muscle contraction.10   Potassium ions are also one of the suggested causes of pain in ischemia.11

     During muscular activity, sweat glands can be stimulated by the sympathetic system.  These sweat glands secrete a proteolytic enzyme called kalikreins into the tissue where it acts on alpha2-globulin (or A2) to split the polypeptide to lysyl-bradykinin when in tissue and to bradykininn when in plasma.  Ischemia also ruptures the tissue and the proteolytic enzyme is released.  Once formed, the bradykininn exists for only a matter of minutes because it is digested by the enzyme carboxypeptidase.12  The actions of kinins causes visceral smooth muscle contraction, relaxation of vascular smooth muscle, increased capillary permeability, lowers the threshold of pain in the area and causes severe pain.13

     Other metabolites also accumulate in the tissue spaces. Adenosine and Co2 for that matter cause vasodilation Increased hydrogen ions accumulate in muscles contracting in the absence of oxygen.14  And finally, Lewis originally hypothesized that sustained muscle contractions are painful because the muscle becomes ischemic, and a substance which stimulates pain endings accumulates (Factor P).15

    Histamine is an autacoid present at high levels in the lungs, skin, and the gastrointestinal tract and is released from  mast cells and basophiles by type 1 hypersensitivity reactions, drugs, venoms and trauma.  Through the activation of H1 receptors Histamine increases activation of peripheral nociceptive receptors and thus increase pain and pruritus.  Thus histamine alone can cause the classic symptoms of pain and pruritus.

     Thus, it is easy to envision that increased contraction of arterial blood vessels, ischemia, increased trapped noxious metabolites in the interstitial space (lactic acid, P Factor, bradykininn, potassium, hydrogen ions, histamine and metabolite products of muscle catabolism), increased tissue oncotic pressure, over-stimulation of nerve endings by the presence of metabolites, increased fluid in the interstitial space, temporary local soft tissue acidosis as a result of lactic acid, all yield muscle stiffness, muscular spasticity and pain as a result of muscular overexertion.

Neuronal Pathways

     When over-exertion has ended, yet a deep paravertebral muscle (e.g. unilateral rotator, multifides, etc) remains strained, stiff and spastic (primary muscle spasticity), the muscle may pull a vertebra into subluxation or a state of altered joint dynamics.  As the vertebra becomes subluxated, ligaments associated with it become stretched.  This stimulates the "Somato-Neuro-Muscular Pathway," which results in increased general ipsilateral paravertebral muscular spasticity and pain.16

     However, as the strained, stiff (primary spasticity) paravertebral muscle causes a subluxation (primary subluxation), the muscle also pulls on various muscle spindles (which detect muscle length) and golgi tendon organs (which detect muscle tension), as well as on neighboring joints.  The proprioceptors circuit impulses to the cerebellum via anterior and posterior spino-cerebellar tracts.17  The cerebellum is concerned with coordination of somatic motor activity, the regulation of muscle tone and mechanisms that influence and maintain equilibrium.18

     Fixating muscles which fix neighboring or even distant joints must be compensated by complex reciprocal innervation for coordinated control of the spinal equilibrium.  Thus, as the stiff, spastic muscle pulls the vertebrae into subluxation or a "state of altered joint dynamics", associated proprioceptors stimulate the cerebellum to send impulses from the dentate nucleus through the superior cerebellar peduncle to synapse in the contralateral thalamic nucleus.  From here the neuron travels to the motor cortex as the thalamocortical fibers.  In this manner, the influence of motor neuron activity in the cerebral cortex is maintained.19  Hence, impulses travel from the motor cortex via the corticospinal tract to anterior horns at spinal levels coordinated by the cerebellum and cerebral cortex.  From the anterior horns, lower motor neurons travel to associated paravertebral muscles.  This innervation increases muscle tonus (secondary muscular spasticity), which pulls neighboring and distant vertebrae into compensation subluxation (secondary subluxation).  These compensation subluxation may occur for many reasons.  One hypothesis is to allow some mobility for the biped as fighting the painful muscle spasticity and gravity.  A correlate is to maintain the eyes at near the horizontal.  Unfortunately, a distorted gait or some antalgic position may result.

     The cerebellum also activates the extra-pyramidal system via a circuit beginning in the deep cerebellar nuclei.  From these nuclei the neurons continue through the superior cerebellar peduncle to synapse in the centromedian nucleus of the thalamus.  The stimulus from the thalamus continues to travel via thalamostriate fibers to the basal ganglia.  The basal ganglia sends the impulse via the lenticular fasciculus, through the prerubral field to synapse with the red nucleus.  The red nucleus sends out two signals.  The first travels through the ventral tegmental decussation via the ruberospinal tract to synapse at motor centers at the level of the upper cervicals.  This provides precise muscle tone for stabilization of movements and maintenance of normal body orientation in space.20

     The second signal to leave the red nucleus travels through the substantia nigra to have an inhibitory effect on the reticular formation located in the midbrain tegmentum.  The effect will inhibit the reticulospinal and reticulobulbar tracts.21  These tracts synapse with motor nuclei.  In this manner smooth hypermyotomia is maintained and not that of multiple twitch-like actions.  However, the inhibition is not enough to inhibit the overworked muscles and balance the compensatory spasticity.

     It is now clear that progressive muscular over-exertion may cause increased contraction of arterial blood vessels, ischemia, metabolites (lactic acid, P Factor, bradykininn, potassium ions, hydrogen ions and metabolites formed by the breakdown of muscle) to accumulate in the tissue spaces, resulting in increased interstitial fluid colloid osmotic pressure, increased muscle fluid in the interstitial space, increased muscle stiffness, over-stimulation of nerve endings by the presence of trapped metabolites, temporary soft tissue acidosis resulting from lactic acid, pain, muscular spasticity, primary vertebral subluxations or areas of altered spinal joint dynamics, increased energy through the cerebellum, thalamic relay, cortical, pyramidal, extra-pyramidal and reticular systems, general hypermyotomia, neighboring or distant secondary areas of altered spinal joint dynamics (secondary subluxations), thus a multi-subluxated vertebral column.  This cyclic system describing subluxations resulting from over-exertion will be called the "Physio-Somato-Neuro-Somatic System."


    Hippocrates, D.D. Palmer and H.G. Wells all were men of great vision.  H.G. Wells wrote of men who would travel to the moon.  Almost a century later, man did walk on the moon.  Like Wells, both Hippocrates and Palmer wrote of concepts that were controversial in their time, but have become real experiences of people today. 

    The "Physio-Somato-Neuro-Somatic System" describes primary vertebral subluxations occurring as the result of over-exertion.  Furthermore, the system describes the occurrence of primary vertebral subluxations and their associated secondary compensatory subluxations which are the direct result of muscular strain and spasticity.  This system is just one more small step among the many giant steps left in communicating our chiropractic experience in the scientific language of the 1980's.  Of course the future may bring new language, but we, as professionals, must change, accept new corrections and bend as the wisdom of science bends in the currents of new knowledge.


1. Chiropractic Health Care, 2nd, Ed, The Foundation for Chiropractic Education and Research, 1977, P. 14

2. Samson Wright; Applied Physiology. 10th Ed, Oxford University Press, 1961, p. 19.

3. Ganong: Medical Physiology, 8th Ed, Lange Medical Publications, 1977, p. 471.

4. Vernon B. Mountcastle: Medical Physiology 13th Ed, Volume 1, 1974 p. 117.

5. Samson Wright; Applied Physiology. 10th Ed, Oxford University Press, 1961, p. 18.

6.  Vernon B. Mountcastle: Medical Physiology 13th Ed, Volume 1, 1974 pp 1279-1284

7.  Ibid: p. 1280

8.  Ibid:

9.   Guyton: 5th edition, W.B. Saunders Company 1976, pp 665

10. Ibid: p. 263

11.  Ganong: Medical Physiology, 8th Ed, Lange Medical Publications, 1977, p. 80.

12.  Guyton: 5th edition, W.B. Saunders Company 1977, p. 262.

13. i.  Best and Taylor; Physiological Basis of Medical Practice, 10th Ed, Williams & Wilkins Company, 1978, p. 3-216

    ii.  Vernon B. Mountcastle: Medical Physiology 13th Ed, Volume 1, 1974 pp 951-952.

    iii. Guyton: 5th edition, W.B. Saunders Company 1976, pp 664-665.

    iv. Samson Wright; Applied Physiology. 10th Ed, Oxford University Press, 1961, p.512

    v.  Orten and Neuhaus: Human Biochemistry, 9th Ed, C.V. Mosby Company, 1975, p. 765.

14.  Samson Wright; Applied Physiology. 10th Ed, Oxford University Press, 1961, p. 209

15.  Lewis, T.; Pain, The MacMillan Co., 1943, p, 99

16.  Scott D. Neff: "Neuroanatomy of Vertebral Subluxations, "The ACA Journal of Chiropractic, Volume 17, No 4, April 1980, p. s-55.

17.  Carpenter: Human Neuroanatomy, 7th edition, Williams and Williams Company, pp .249-252, Figures 10-11.

18.  Ibid:  pp 420 and 430

19.  Ibid:  p. 434

20.  Ibid pp 261-264; Figures 10-17, 384-386, 496-511 and 512-514.

21.  Ibid:  pp 393-397, 501-503


Ye shall know the truth, and the truth shall make you free.”John, viii, 32

For Part 1 the Neuroanatomy of Vertebral Subluxation hit this link


© & TM 1998 American Academy for Justice Through Science. All rights reserved.

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