The Definition of Subluxation

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

The definition of subluxation, as adopted by the American Chiropractic Association
and the Association of Chiropractic Colleges is:

“A subluxation is a complex of functional and/or structural and/or pathological articular changes that compromise neural integrity, and may influence organ system function and general health.”

The subluxation has just recently been re-defined by the Rubicon Group and states:

“We currently define a chiropractic subluxation as a self-perpetuating, central segmental motor control problem that involves a joint, such as a vertebral motion segment, that is not moving appropriately, resulting in ongoing maladaptive neural plastic changes that interfere with the central nervous system’s ability to self-regulate, self-organize, adapt, repair and heal.”

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The classical definitions of subluxation are listed below:

The 5 Component “Vertebral Subluxation Complex” Model   [3, 4, 7, 8]

According to Kent: [1] Dishman [2] and Lantz [3, 4] developed and popularized the five
component model of the “vertebral subluxation complex” attributed to Faye. [5]

However, the model was presented in a text by Flesia [6] dated 1982, while the Faye's
notes bear a 1983 date.


The original model has five components:

1. Kinesiopathology – spinal pathomechanics, including alignment and motion irregularities, involving:

   • Hypomobility, segmental blockade, fixation:   Abnormal restriction of joint motion, OR
     

   • Hypermobility:   Abnormal increase in joint motion.
     

   • Compensation reaction:   Long term hypomobility causes the joint above the hypomobile area and occasionally the joint below to become hypermobile.
     

   • Loss of joint play:   The loss of normal vertical "joint slack/play" so that the joint becomes hypomobile on the vertical plane.
     

   • Loss of central axis of motion:   The loss of normal "Joint Slack/play" so that the joint becomes hypomobile on the rotational joint plane.
     

   • Positional dyskinesia, dynamic misalignment:   Joint misalignment throughout the entire range of motion of the involved joint.

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2. Neuropathophysiology, Neuropathology – compressed or facilitated nerve tissue, involving:

   • Compressive lesion, the pinched nerve, neurological hypoactivity:   The literature indicates that of the neurological damage induced by spinal kinesiopathologic changes, about 10–15% results in a compressive profile.
     

   • Facilitative lesion, the facilitative segment, neurological irritation, neurological hyperactivity:   The literature indicates that, of the neurological damage induced by spinal kinesiopathologic changes, about 85–90% results in a facilitated profile.
     

   • Articular neuropathy,   the hyaline cartilage pads in the diarthrodial spinal joints as well as the local articular ligamentous support tissue are seriously stressed during an acute episode of the vertebral subluxation complex and more so in long term uncorrected vertebral subluxation complex episodes. This causes, in addition to the histopathologically induced pathoanatomical changes due to long term uncorrected vertebral subluxation complex, significant damage to the balance and proprioceptive nerve endings (the Type I Mechano receptors, Type II & III Articular Receptors and Type IV Nociceptive 'Pain' Receptors) in the articular surfaces and the capsular ligaments so that "Noxious" nerve impulses are fired off afferently back to the spinal balance center in the cerebellum, the proprioceptor center in the cerebral cortex and in the Limbic 'joint pain' regions of the cerebral cortex. Surprisingly, the spinal cord stores facilitated data also, causing reflexogenic activity from the involved joint.

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3. Myopathology – muscle spasm, muscle weakness/ atrophy involving:

   There are parallel changes in the organ depots, of course. However, this is dealt with broadly under component #5. Myopathology is listed as a separate major component of the vertebral subluxation complex simply because myopathology is more readily testable and recognizable at the office level than are organ depot changes. The myopathological phenomenon associated with the vertebral subluxation complex are identical with myopathology induced by nerve damage due to other causes than spinal kinesiopathology. These changes can be referenced in many text books dealing with basic clinical pathology, clinical neuropathology and sports injuries.
   
   A.   From the compressive lesion:
   

   1. Neurological hypoactivity
      

   2. Hypotonus
      

   3. Atrophy
      

   4. Fibrosis (To varying degrees). The current literature points out that fibrosis in muscle tissue begins within one week of the original injury and becomes permanent within a few weeks. Krusen's Handbook of Physical Medicine and Rehabilitation, 1982, edited by Kottke, Stillwell, and Lehman. ISBN 07216-5501-7, chapter 18, pg. 391," Adhesion Formation." Experimental Models of Osteoarthritis: The Role of Immobilization, T. Videman, Clinical Biomechanics, 2:223–229, 1987, and the various papers by Videman there referenced. Managing Low Back Pain, 1st Ed. 1983, 2nd Ed. 1988; edited by W. H. Kirkaldy-Willis. 1st Ed. ISBN 0-443-08189-1 2nd Ed. ISBN 0-443-085358 Patholgenesis of Low Back Pain: Clinical Applications by Kirkaldy-Willis, MD, "Pathophysiology: Overview, Myofascial Cycle." These reports explain the progressive nature of fibrotic muscle degeneration, therefore leading to permanent spinal biomechanical aberrant function. Since, fibrosis begins within the first week after injury, and becomes irreversible shortly after that the basis for appropriate intervention within the three types of chiropractic care must be rethought.

   
   B.   From the facilitative lesion:

   1. Neurological hyperactivity
      

   2. Hypertonus
      

   3. Spasm
      

   4. Fibrosis (see above)

   
   C. From articular neuropathy

   1. "Erroneous" adaptation responses
      

   2. Adaptive spasm and weakness
      

   3. Resulting fibrous tissue (see above)

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4. Histopathology – inflammation, edema and swelling of tissue, usually local to the traumatized area, involving:

   Basically, histopathology is to be considered as the entire range of the inflammatory process. Uncorrected, this leads to fibrotic degeneration. In some cases this degenerative process leads to calcific salt deposition within the fibrous lattice. The literature presents three phases of fibrotic/ calcific ligamentous degeneration.

Phase 1 –   The original sprain.

Phase 2 –   The beginnings of fibrosis.

Phase 3 –   Complete fibrosis. Complete fibroses and the beginnings of fibrosis are not reversible, leading to permanent spinal biomechanical impairment. Bone degeneration is considered under component #5.

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5. Pathophysiology, Pathology, Biochemical Changes – pathophysiologic and pathoanatomical changes due to the previous four components usually seen locally as degeneration, fibrous tissue and/or erosion local and peripherally as a loss of global homeostasis.

A.   Local to the spine:


1. Bone degeneration-   Bone and soft tissue degeneration is an inevitable consequence of uncorrected spinal trauma (micro or macro) and to a degree, a result of a shifting postural alignment to gravity.
   

2. Bone regeneration-   A normal physiologic phenomenon. Bone regeneration alters architectural outlines of bone when the involved bone tissue becomes chronically out of alignment with gravity. This can be seen on spinal x-rays and is usually confused with the spinal degenerative process.

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Lantz   [5] has since revised and expanded the “vertebral subluxation complex” model
to include nine components:

The 9 Component Vertebral Subluxation Complex Model

1. Kinesiology
   
2. Neurology
   
3. Myology
   
4. Connective Tissue Physiology
   
5. Angiology
   
6. Inflammatory Response
   
7. Anatomy
   
8. Physiology
   
9. Biochemistry

He summarizes his objectives for expanding the model:   [5]

“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... Each component can, in turn, be described in terms of precise details of anatomic, physiologic, and biochemical alterations inherent in subluxation degeneration and parallel changes involved in normalization of structure and function through adjustive procedures.”

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The remainder of the Subluxation page contains the collected articles
written about the subluxation complex, including the:

• anatomical structures involved,

• degenerative changes that occur after a joint remains fixated over time,

• neurologic consequences following that fixation and/or inflammation,

• improvements that occur following chiropractic care,

• and the evolving development of subluxation theories.

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REFERENCES:

1. Models of Vertebral Subluxation: A Review.
   J Vert Sublux Res. 1996 (Aug); 1 (1): 1–7
   

2. Review of the Literature Supporting a Scientific Basis
   for the Chiropractic Subluxation Complex
   J Manipulative Physiol Ther 1985 (Sep); 8 (3) Sep: 163–174
   

3. The Vertebral Subluxation Complex PART 1:
   An Introduction to the Model and Kinesiological Component
   Chiropractic Research Journal 1989; 1 (3): 23–36
   

4. The Vertebral Subluxation Complex PART 2:
   The Neuropathological and Myopathological Components
   Chiropractic Research Journal 1990; 1 (4): 19–38
   

5. The Subluxation Complex.
   In: Gatterman MI,ed.
   Foundations of Chiropractic Subluxation.
   St. Louis, MO: Mosby, 1995
   

6. A Psychoepistemological Basis for the New Renaissance Intellectual.
   Renaissance International, Colorado Springs, CO, 1982
   

7. The Vertebral Subluxation Complex:
   An Integrative Perspective
   ICA International Review of Chiropractic 1992 (Mar): 25–27
   

8. Immobilization Degeneration and the
   Fixation Hypothesis of Chiropractic Subluxation
   Chiro Res J 1988; 1 (1) Spring: 21–46

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Since 3–06–1997

Updated 11-11-2023