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What is the Vertebral Subluxation Complex?

What is the Vertebral Subluxation Complex?

The Chiro.Org Blog

SOURCE:   ICA International Review of Chiropractic 1992 (Oct): 19-23

Joseph M. Flesia, D.C.

Submitted for your approval is an article written by Joseph M. Flesia, D.C. that is archived on our Chiropractic Subluxation Page. I hope you will find it of interest!

The Vertebral Subluxation Complex Part II:
An Outline

Many correlative and singular studies have been made in the areas of the five components of the Vertebral Subluxation Complex. Some researchers have used the exact titles of the individual components as mentioned in this review. Others report synonymous scientific nomenclature. Ongoing scientific research will and has added more components and subcomponents to the vertebral subluxation complex than presented in this brief outline. However, the following outline will provide the reader an excellent foundation relative to the component basis of the vertebral subluxation complex. This will allow new information to fit into this previously established, scientifically ordered model.

Component #1: Spinal Kinesiopathology (Spinal Pathomechanics, Abnormal Spinal Biomechanics, etc.)

1.   Hypomobility, segmental blockade, fixation: Abnormal restriction of joint motion.

2.   Hypermobility: Abnormal increase in joint motion.

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

4.   Loss of joint play: The loss of normal vertical “joint slack/play” so that the joint becomes hypomobile on the vertical plane.

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

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

Component #2: Neuropathophysiology, Neuropathology

1.   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.

2.   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.

3.   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.

It should be noted that recent studies have shown that discal tissue is supplied by the mechanoreceptor apparatus. A major concern in abnormal mechanoreceptor activity is that it causes abnormal gait, posture and joint kinesthesis resulting in aberrant efferent control to the spine, further debilitating spinal function and health.

Component #3: Myopathology

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)

Component #4 : Histopathology

Basically, histopathology is to be considered as the entire range of the inflammato.ryprocess. 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.

Component #5: Pathophysiology, Pathology

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.

Subluxation Degeneration

Subluxation degeneration is an orthopedic concept introduced in chiropractic in 1977 by Renaissance International. It is a concept meant to convey the orthopedic observation of constant degeneration and regeneration of bone tissue through life. It is a result of uncorrected trauma and the shifting alignment of the body to gravitational stress. All weight bearing joints succumb to this process. It is gravitationally inevitable. The subluxation degeneration concept is expressed through the use of Phase I, 2, 3 & 4 terminology.


1.   The term “Spinal Degeneration” is a medical diagnosis usually relating to some form of osteoarthritis of the spine.

2.   The Renaissance term “Subluxation Degeneration” includes this usual spinal degeneration and the spinal regeneration as a result of architectural changes due to re-adaptation when the spine is out of alignment with gravity.

3.   The four phases of “Subluxation Degeneration” become a radiographic criteria for the doctor and patient to use in order to visualize the long term damage of the vertebral subluxation complex on the spinal structure as a whole.

Phase 1.   Is characterized by mobility aberration, the bony architecture is intact as seen on x-ray and there are the expected initial soft tissue changes in the form of fibrosis.

Phase 2.   Is characterized by all the changes as in Phase 1 plus increased fibrosis, the beginnings of osseous changes as visualized on x-ray (both degenerative and regenerative), disc, joint and bony architecture changes.

Phase 3.   As a result of uncorrected chronic vertebral subluxation complex, (very rarely seen in the office) is characterized by the beginning of fusion, major degenerative and regenerative changes throughout the anterior and/or posterior motion unit.

Phase 4.   Is usually seen in the elderly (severe trauma, disease and surgery will produce exceptions in younger people). Few doctors will ever see a phase 4 in clinical practice. This phase is characterized by all the previous phases plus total fusion of the anterior and/or posterior motion unit and massive bony regenerative changes. See Managing Low Back Pain by W. H. Kirkaldy-Willis, MD, for a complete medical profile of the three medically diagnostic phases of spinal degeneration and their progressive nature as well as the physician’s responsibility to the diagnosis, prognosis and patient recommendations for care.

4.   The first three phases of “Subluxation Degeneration” have been found to alter with “appropriate” chiropractic care.

A.   Appropriate chiropractic care results in most Phase 3′s slowing down. To determine if a Phase 3 does slow down, long term care is required and yearly x-rays are necessary. Six to eight years of elapsed time and yearly x-rays for comparative purposes are necessary in order to observe if there is any slowing of the” subluxation degeneration” process – or not.

B.   Appropriate chiropractic care results in most Phase 2′s stopping. To determine if a Phase 2 does stop, long term care is required and yearly x-rays are necessary. Three to five years of elapsed time and yearly xrays for comparative purposes are necessary.

C.   Appropriate chiropractic care results in most Phase 1′s returning to near normal. To determine if a Phase 1 does return to near normal, long term care is required and yearly xrays are necessary. Twelve-IS months of elapsed time and yearly x-rays for comparative purposes are necessary in order to observe if there is any returning to normal of the “subluxation degeneration” process -or not. Certainly biomechanical changes can be seen long before the clinician is sure of Phase 1 returning to near normal.

It is important to note that not all chiropractic care is designed to alter the spinal biomechanical profile over the long term. If a particular chiropractic “technique” does not alter the spinal bimechanics significantly, other “techniques” that do should be considered by the clinician.

Peripheral to the Spine

Over the years a significant weight of clinical evidence has been accumulated indicating that chiropractic care of the vertebral subluxation complex has a beneficial effect on many and varied conditions distal to the local spinal changes caused by the vertebral subluxation complex. That this” evidence” is considered anecdotal is of little consequence to many health care consumers. Chiropractors are urged to a cautionary approach when naming conditions that can be helped with chiropractic care. The pitfalls here are very painful and obvious.

The major problem in the “Chiropractic Vertebral Subluxation Complex Care of Specific Conditions” is that if that specific condition which may have many and varied causes does not respond to chiropractic, the patient makes the erroneous observation that chiropractic does not work…period.

The greater “clinical observation” is that chiropractic care on a long term basis does help improve the general health index whether or not a specific condition “responds.” Appropriate patient education on a clinical basis is of paramount importance as chiropractors address the health care consumer on the local level.

Certainly, the anecdotal evidence must be considered as a directional vehicle to research efforts rather than of no consequence. It must be kept in mind that no healing art is totally scientificallyproven. The scientific model is an ongoing effort to facilitate the way for the health care practitioner to address the challenges of every day practice that is a dynamic process of “mind set” (philosophy or the lack of it), science and clinical art. Respect for the mass of anecdotal evidence as well as its severe limitations is what is needed in the chiropractic profession to gain its sorely needed increased scientific respectability.

I recommend we stand tall in the face of the challenge of the need for increasing scientific proof and get it. Let the U.S. guide the direction of the research and let the results of the research help guide us in the clinical application of our emerging health care discipline…Chiropractic.

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