Chapter 1:
Basic Principles and Practice of Chiropractic

From R. C. Schafer, DC, PhD, FICC's best-selling book:

“Basic Chiropractic Procedural Manual”

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The Causes of Disease: An Overview 
  Environmental Factors 
  Constitutional Factors
The "Chiropractic" Subluxation 
Primary Neural and Homeostatic Mechanisms 
Fixation-Related Articular Therapy 
  Historical Perspective 
    Medical Pioneers 
    Chiropractic Pioneers
Adjusting Rational
  Segmental Hypomobility 
  Fixation Metamorphosis 
  Joint Play Restrictions 
  Segmental Hypermobility 
  Adjustive Therapy
Major Causes of Joint Fixation Development
  Muscle Fixations 
    Muscle Tonicity vs Phasic Contractions 
    Characteristics of Perivertebral Muscular Fixations 
  Ligament Fixations 
  Articular Fixations 
  Bony Restrictions 
  Maladaptation During the Aging Process 
  Biomechanical Compensation 
  Autonomic Aberrations 
  Potential Contributory Causes of Joint Fixation Development 
Review of Subluxation Effects On, In, or Near the IVF
  Constant Articular Mobility is Normal 
  Clinical Expressions of Fixation 
  IVF Content and Size Alterations 
  Factors Changing IVF Diameter and Their Consequences 
  Vertebral Unit Microtrauma: General Considerations 
  Nerve Root Insults 
  Ganglion Irritation/Pressure 
  Nerve Compression 
  Axoplasmic Transport Alterations 
  Cerebrospinal Fluid Flow Alterations 
  Meningeal Irritation 
  Nerve Root Course Considerations 
  Altered Nerve Root Angle 
  Circulatory Alterations 
  Local Toxicity 
  Distal Neurocirculatory Expressions 
  Mechanoreceptor Responses and Reflexes 
  The Posterior Rami 
  Tissue Defense

Chapter 1: Basic Principles and Practice of Chiropractic

This introductory chapter describes the general causes and effects of the subluxation complex. The role of subluxation as an etiologic or perpetuating factor in disease is determined by the extent of the neuropathologic and/or biomechanical processes involved and how they relate to the creation, maintenance, or progress of such disorders.

The study of pathology shows that disease is not a static state. It is a process, and as such it manifests in certain signs, symptoms, functional alterations, and morphologic changes. These occur as an action of the body to motor responses of a somatic, visceral motor, or vasomotor nature that begin by noxious sensory stimulation. Such initial sensory irritation arises from the environment, are of a varied and complex nature, and their effects depend on an inherent or conditioned resistance of the organism at a given time. It can therefore be said that disease states essentially depend on irritations from the environment overcoming constitutional resistance and response mechanisms and reserves, with the nervous system acting as the mediating factor between. As life is a stimulus-response phenomenon in its normal homeostatic functions, disease can be considered an abnormal response to stimuli that is beyond the capacities of the organism to adapt.


The general etiology of disease has been traditionally considered an irritation brought about by trauma, poison, or autosuggestion. Today, we might say physical injury; chemical, thermal, and/or pathogenic irritation; and psychologic overstress. Current pathology categorizes causes in somewhat different areas such as environmental or constitutional factors.

Environmental Factors

The four major environmental factors are

(1) physical trauma;
(2) various parasitic, bacterial, viral, rickettsial, or fungal infections;
(3) harmful inanimate substances such as foreign bodies or chemical toxins; and
(4) nutritional abnormalities from
    (a) deficiency and/or in excess in various ingested food substances or
    (b) tissue deficiency from impaired absorption, metabolism, or blood supply.

Constitutional Factors

The two major constitutional factors are

(1) the inheritance of genetic abnormalities and
(2) nongenetic factors that may lower a person's resistance to disease by impairing his constitutional health, particularly as a by-product of previous disease states.

Because of the general environmental and constitutional factors involved, the proper treatment of disease would thus be to remove these irritations from an individual's environment and enhance resistance to disease by improving constitutional health.


The processes described above, however, are complicated by one's nervous system that reacts to irritations uniquely, according to conditioned or genetic constitutional factors, that may establish certain neurologic patterns of response. There may then be created a habituation (self-perpetuating) of certain neurologic responses and, therefore, the establishment of physiologic and structural alterations acting as an intrinsic source of neurologic irritability that persist after the initiating stimulation has decreased. This internal source of sensory stimulation may produce motor responses giving rise to clinical symptoms and signs.

The physical changes secondarily created by these reactions or primarily by structural injury, disease, anomaly, etc, may act as a physical source of neuropathologic reflexes and may be called a "chiropractic" subluxation. That is, a structural state characterized by an abnormal physical relationship between adjacent anatomic structures whose contiguous tissues elicit neurologic responses that may clinically be manifested as symptoms, signs, functional changes, and morphologic alterations of a disease state but less than that of complete structural disruption.

It can therefore be readily acknowledged that to discuss the "chiropractic" subluxation in general terms is difficult. Thus, to clarify the issue in a cause and effect manner, the remainder of this chapter will describe primary neural and homeostatic mechanisms, fixation-related articular therapy, the foundation of chiropractic clinical rationaler, the major causes of joint fixation development, and potential contributory causes of joint fixation development. These topics will be followed by a summary review of subluxation-fixation effects on, in, or near the intervertebral foramen (IVF).


Each moment the nervous system receives thousands of signals from a variety of sensory organs, integrates the data, prepares necessary responses, and initiates responses through a multitude of motor and/or autonomic mechanisms. A specialized network of nerve fibers permeates the body to do this in a manner that some fibers receive and respond to stimuli from the external and/or internal environments, some transmit signals to and from integrating and coordinating centers, and some conduct messages from centers peripherally to the complex of muscles, vessels, and glands to produce an action.

This explanation describes normal neural function, but it does not explain what happens if some process or mechanism fails. In more instances than not, that is the concern of the doctor of chiropractic. Healthy homeostatic mechanisms are the ideal for which all DCs strive. This is especially true in family practice where much more than orthopedic and trauma-related disorders are seen. Working as partners in distinctive roles, the nervous system and the endocrine system provide almost all functional control for body processes.

The basic function of the nervous system is to control rapid activities of the body such as muscle contraction, swift visceral events, and the rate of endocrine secretion, states Guyton, the renowned physiologist. The endocrine system, in contrast to the nervous system, principally regulates the slower metabolic functions of the body to prolonged physiologic activities.

The general design of the body is an organic matrix of synchronized master tissues and vegetative systems. The quick-acting master tissues specialize in receiving messages from the external and internal environments and reacting to them (eg, nerve and muscle tissue). Specialized peripheral receptors (eg, the telereceptors and contact receptors) become impressed by stimuli from the external environment, while deep proprioceptors in muscles and joints and the interoceptors and chemoreceptors of the viscera are sensitive to stimuli arising within the internal environment. In this context, the slower-acting vegetative systems (eg, digestive, respiratory, circulatory, excretory systems) provide the basic utilities of life necessary for cellular nutrition, growth, or repair and the removal of waste products.

Vegetative systems are directed and regulated primarily by the sympathetic and parasympathetic divisions of the autonomic nervous system (ANS), whose activities are modified, harmonized, coordinated, and integrated by centers within the central nervous system (CNS) to meet the constantly changing needs of the body relative to its internal and external environment. It is this way that homeostasis is maintained.


One or more vertebral segments may be held in a state of extension, flexion, or lateral flexion when the patient's spine is in a neutral posture. This is the classic picture of a chiropractic "subluxation." For an articulation to remain in an abnormal state of "subluxation," something must hold it there to restrict its mobility or it would spontaneously reduce itself and produce little clinical concern. This "holding" or "mobility hindrance" mechanism is commonly called a "fixation." Thus,

(1) if a subluxation (a malposition less than that produced by a dislocation) exists, a fixation must also exist, and
(2) a fixation can exist even when the articular surfaces are in an ideal relationship during the static resting posture. Thus, a fixation is a dynamic factor; a subluxation, a static factor.


Although an intrinsic articular holding mechanism is commonly called a fixation, this term too can cause confusion if it always implies a state of complete immobility. In this chapter, the editor will use the term fixation in its traditional sense in motion palpation referring to any physical, functional, or psychic mechanism producing a loss of segmental mobility within the normal physiologic range of motion. Thus, ankylosis would be considered a fixation in its purest sense a 100% fixation. Most fixations found clinically, however, will be far less than complete (ie, in the 20%–80% range of normal mobility). Thus, an accurate synonym for the term "fixation" would be "mobility impairment."

A single vertebra cannot become subluxated or fixated; rather, only articulations can subluxate or become fixated. As fixation-subluxations occur between two normally articulating surfaces, we speak of adjusting or mobilizing vertebral motion units (two apposing vertebral segments), not a single vertebra. Thus, articulating surfaces subluxate, bones do not. Lax terminology has led to much confusion in describing a subluxation complex.

A state of subluxation or incomplete luxation in the surgical sense of the word is difficult to achieve in gliding joints, and all spinal zygapophyses are gliding joints. Terminology is one reason chiropractic theory has had such a difficult time being accepted generally by many within the scientific community. It is thus paradoxical that the term subluxation, in the classic chiropractic sense, has forced its presence on all health-care professions and is becoming widely used in circles beyond the chiropractic profession. At the same time, chiropractors now understand that the term is a misnomer when all its pathophysiologic components are considered. For example, a vertebra may be in a hypomobile state of "fixation," unilaterally or bilaterally, while the segment is well within its normal range of motion during the resting position yet be considered an articular aberration causing or contributing to pathologic expressions.

Historical Perspective

The correction of malaligned or immobile articulations is far from a new art within health care. One of the earliest indications of its use is confirmed in the ancient Chinese document Kung Fou, written about 2700 B.C. Manipulation was also practiced in various forms by the ancient Japanese and Indians of Asia, as well as the early Babylonians, Syrians, Hindus, Tibetans, and Polynesians.

Greek papyruses dating back to at least 1500 B.C. explained maneuvering the lower extremities in the treatment of low-back disorders. In later Greece, the celebrated physician Hippocrates (460 to 377 B.C.) wrote at least 70 books on healing, including Manipulation and Importance to Good Health and On Setting Joints by Leverage. The discoveries and refinements of Hippocrates were used and improved by such famous Greek and Roman physicians as Herodicus, Serapion, Galen, and Celsus, and the Swiss-born Paracelsus.

Historians also record that manipulative therapy has been practiced by the natives of Tahiti for centuries. Some North American Indians known to have used manipulative therapy include the Sioux, Winnebago, and Creek tribes. Tribes of Mexico and Central America known to have used the art include the Aztec, Mayan, Toltec, Tarascan, and Zoltec cultures. The mysterious Inca Indians of South America are known to have developed manipulative methods to a respected art.

Manipulative therapy was repressed in Europe by the medical hierarchy during the Dark Ages, but it later resurfaced among "bonesetters" during the Renaissance. Years later in the British Medical Journal of January 5, 1865, the famous surgeon Sir James Paget wrote "Cases That Bonesetters Cure." Nevertheless, even this recognition did little to stimulate objective investigation by the medical aristocracy of the era who was narrowly schooled in the use of drugs, bleeding, and purging. To them, the art of manipulation was unknown and thus shunned –a subject to be feared in silence and condemned in public.

With the birth of osteopathy and chiropractic in the late 19th Century, the correction of malaligned fixated articulations was given a scientific basis and direction that have been continually refined to its present state-of-the-art. Even this approach, however, was strongly opposed by political medicine of North America until the last decade or so. This opposition, however, was not as severe in Europe or among a very small group of American orthopedists early in this century.

Medical Pioneers

While manipulative techniques were publicly criticized by spokesmen for the American Medical Association for most of this century, its use was openly advocated within professional surgical and orthopedic circles during the first half of this century. For example, manipulative techniques were frequently advocated in several major professional references during the 1920–1940 period by Bankart, Marlin, Mennell, and Coulter. Several of these texts and papers referred to the manipulative procedures of Sir Robert Jones, which were widely used in the 1920s. Today, the art of manual (manipulative) medicine is still rarely, if ever, taught in undergraduate medical courses in America, but its application is strongly encouraged in postgraduate programs designed for allopathic-oriented physical therapists.

Without an in-depth knowledge of chiropractic or osteopathic education, several allopaths considered authorities in their field recognized the void being filled by chiropractors and osteopaths in the early part of this century and tried to warn their colleagues of the potential of these maverick professions. Within a 1920 paper published in International Clinics, for example, Magnuson/Coulter wrote:

Unless the medical profession wakes up to the fact that our bodies are built on mechanical principles and that many things that we have groped in the dark about are due to a mechanical fault of one kind or another, we are doing our patients grave injustice, neglecting our duties as physicians.

These and similar warnings generally went unheeded. For example, the treatment of articular sprain is almost identical in general medical practice today as it was 60 or more years ago: immobilization, elevation to reduce swelling, bed rest, and possibly the application of some form of heat during rehabilitation. Many years ago, Jostes tried to warn his colleagues of the fallacy of this limited approach in a 1938 paper published within the Journal of Bone and Joint Surgery. Note how he describes the basic chiropractic rationale in his remarks:

Sprains involving joints vary in severity from marked stretching to actual tearing of capsule and ligaments, with certain degrees of subluxation.... Given a sprain involving a deeper joint, with marked muscle spasm and some degree of deformity, the carrying out of this routine of immediate immobilization and prolonged rest may afford little correction or relief. Rather, more logically, in such cases one would be prone to manipulate gently the involved joint, in order to correct whatever degree of malalignment or subluxation may have occurred incident to the tearing or stretching of the ligaments or capsule. In this manner, the normal relations of the joint are restored, the torn soft tissues are morecorrectly approximated, and the muscle spasm is more effectively and permanently allayed.

Under traditional orthodox care, Jostes further stated that such patients were being condemned by negative radiographs and left to "wander through many hands until they are finally consigned to the diagnostic category of neurotics or malingerers." He affirmed that periodic sessions of steady traction and gentle manipulation maneuvers without anesthesia, but under a state of self-induced relaxation, resulted in the "successful restoration of normal alignment" and "the obliteration of the painful and deforming muscle spasm." Only then, he concluded, are heat and rest effective therapeutic aids.

Forty some years ago (1949), Coulter, a specialist in tropical medicine, wrote in a paper called "Manipulation." In it, he reported:

In recent years much progress has been made in the investigation of the proper use of manipulation. There is now no justification for condemning manipulation because harm has been done by improper manipulation and because fantastic claims are made for it. It is now possible with a correct diagnosis to use manipulation as a useful adjunct in the treatment of certain conditions.

Chiropractic Pioneers

Several clinical studies were conducted in early chiropractic to validate partial or complete segmental fixation. Gillet and Liekens did much in Europe to develop a system of dynamic motion palpation, and many of their findings have recently been confirmed by Wiles, Faye, Grice, and others in North America.

Stress-view roentgenography has also been used extensively to evaluate the existence of segmental fixation in the spine. The first system found in the editor's literature search was developed by Vladef in Detroit in the 1940s and early 1950s and expanded by Rich at Lincoln Chiropractic College in the 1950s through cineroentgenography. In more recent years, studies by Illi, Carrick, Giles, Good, Banks, and Henderson have offered helpful reconfirmations. Likewise, the works of Vernon, Burnarski, Cox, Mannen, and others have shed much light on this subject (see Bibliography).

As the findings of Gillet/Liekens were reported, some basic chiropractic assumptions were confirmed and others were discarded in light of the new knowledge obtained. It was found, for example, that two basic concepts withstood the assault of the knowledge obtained year after year. These ideas involved vertebral position and motion:

  1. Position.   It was determined that a subluxated vertebra was not an incomplete luxation in the strictest sense. The involved segment(s) had not displaced from its physiologic boundary nor had it exceeded its normal limits of motion. Thus, when a "subluxation" is adjusted, it is not replaced, relocated, or reduced in the same context as would be a dislocation. Rather, it is "freed" in some degree to function normally (mobilized).

  2. Motion.   Vertebral movements arc about an axis of motion from one direction to the other. It was found that the basic movements of spinal segments are rotation about the longitudinal axis, lateral flexion (side bending, tipping) toward the right or left, posterior-anterior flexion, anterior-posterior extension, and long-axis lengthening (traction). Factors inhibiting movement within any one or more of these directions were found that set up a state of abnormal biomechanical translation and rotation leading to biomechanical and subsequent physiologic dysfunction.


Most chiropractors link the common forms of isolated joint motion restriction to an intra-articular cause such as a subluxation, a loose body, or an adhesion, or to a periarticular cause such as shortened ligaments, spastic muscles, contractures, or marginal osteophytes. On the other hand, most allopaths with an interest in manipulation still agree with Coulter's 1949 limited comment that "One of the most common indications for manipulation is the restoration of normal mobility where the limitation of motion is due to adhesions. In other words, the object of the manipulation is to break or stretch fibrous tissue binding the structures together and limiting their motion."

Coulter stressed that manipulation of a joint with limited motion does not restore function, but it often makes the restoration possible. He never clarified this obscure statement.

The general chiropractic viewpoint has more closely resembled that of Jones who stated that adhesion formation conveys a less accurate picture of the pathologic process than the phrase adherence of capsular plications. Jones believed that the impression that adhesions form only as the result of injury or infection was erroneous: "The joint itself may be perfectly normal and the source of the adhesions is entirely extra-articular." According to Jones' findings, it was recurrence and persistence of serofibrinous exudation that provides the key to the problems of adhesion formation. He gives the following causes, limited as they may be, which coincide with some findings of such chiropractic authorities as Janse and Gillet for continued or recurrent exudation –whether the fixation is in a spinal or extraspinal joint:

1.   Disuse with continued venous stasis.

2.   Recurrent edema.

3.   Recurrent trauma from daily passive stretching or repeated manipulation.

4.   Constant trauma from immobilization in a position of strain.

5.   Infection near a joint.

6.   Continued irritation of foreign bodies near a joint.

Segmental Hypomobility

Some pioneer chiropractic educators viewed a subluxation solely as a static malalignment and demanded that only this concept be taught. However, contemporary research has shown that a spinal or extraspinal articulation may become hypomobile, totally or partially, in its neutral position, or it may be fixed anywhere within its range of flexion, extension, lateral bending, or rotational motion. Thus, a fixation is not synonymous with subluxation but a state superimposed on or independent of subluxation.

According to the fixation hypothesis, static anatomical relationships may be near normal but dynamic relationships may be far from normal. The subluxation complex, therefore, must be studied in vivo and the reason postmortem studies have failed to validate the chiropractic approach is explained.

In compensation for a local area of fixation, adjacent joints are forced to assume roles of increased mobility (hyperkinesia), leading to clinical instability. Also, when a unilateral articulation is partially restricted, its contralateral partner is forced to assume the role of both through pivotal hypermobility about an abnormal axis. Invariably, this will be at the site of symptoms rather than at the site of the cause for abnormal movement (fixation). Gillet reported that one exception to this is in the suboccipital area, which he felt was often involved in a state of muscular fixation. Janse often described cases of occipitoatlantal articular "jamming."

Fixation Metamorphosis

Giles offers a hypothesis that the main stages of segmental hypomobility evolve as follows:

  1. Decreased mobility or vertebral fixation of a motion unit in its normal physiologic range of movement causes sluggish circulatory flow. The motion unit is normally dynamic, and the following structures may be found in the IVF: the anterior or motor nerve root, posterior or sensory root, part of the posterior nerve root ganglion, recurrent meningeal nerve, spinal ramus artery, intervertebral vein, lymphatic vessels, nervi nervorum, nervi vasorum, vaso vasorum, and vaso nervorum.

  2. Sluggish circulatory flow in the vertebral veins and arteries produces venous stagnation. Venous stagnation from arterial backup in turn produces local toxicity. Toxicity, due to the buildup of metabolic waste products in the area of the IVF, alters the normal pH of the local fluids which in turn causes a breakdown of Kreb's cycle.

  3. A breakdown of Kreb's cycle, due to decreased oxygen and toxicity, produces a partial breakdown of the sodium pump mechanism, resulting in an ionic imbalance. Ionic imbalance, as the sodium pump can no longer maintain normal ionic equilibrium, results in some degree of erratic nerve conduction and edema in the tissues of the immediate area. Erratic nerve conduction may be exhibited in the nerves passing through the involved IVF and immediate area. CSF stagnation possibly occurs in association because of the intimate relationship between spinal fluid and venous blood, contributing to toxicity in the nerve root area.

Joint Play Restrictions

Besides normal active and passive ranges of motion, there is a third type of motion called "joint play." Many articular fixations begin as restrictions in joint play. This small but precise accessory movement within synovial joints can be induced only passively. Although joint play is necessary for normal joint function, it is not influenced by a patient's volition. Thus, joint play can be defined as that degree of end movement allowed passively that cannot be achieved through voluntary effort. In other words, total joint motion is the sum of the voluntary range of movement plus or minus any existing joint play.

Joint play occurs because normal joint surfaces do not appose tightly. As joint surfaces are of varying radii, movement cannot occur about a rigid axis. The capsule must allow some extra play for full motion to occur. Besides translatory and rotational joint play, a degree of distraction must exist. If one of these involuntary movements is impaired for some reason, the articular surfaces become closely packed (compressed) and mobility is restricted. Added to this is the factor that there are small spaces created by articular incongruities necessary for hydrodynamic lubrication. Thus, prolonged compression leads to poor lubrication and possibly ischemia, likely progressing to degenerative joint disease due to abrasion irritation.

While joint play cannot be produced by phasic muscle contraction, voluntary action is greatly influenced by permitted joint play. Loss of joint play results in a painful joint that becomes involuntarily protected by secondary muscle spasm. Thus, motion palpation to detect restricted mobility and joint play is an important part of the biomechanical examination of any painful and restricted axial or appendicular joint. Pain and spasm result when an involved joint is moved (actively or passively) in the direction in which normal joint end-play is restricted. Once normal joint play is restored (eg, during adjustive mobilization), the associated pain and spasm subside.

Joint play should exist in all ranges of motion normal for a particular joint. That is, if a joint functions in flexion, extension, rotation, abduction, and adduction, the integrity of joint play in these directions plus distraction should be evaluated. It is not unusual for joint play to be restricted in some planes but not others.

Segmental Hypermobility

Spinal instability is that state of a vertebral segment in which it cannot maintain its normal relationships with its contiguous structures under normal loading or mobility conditions for the individual. The results are likely chronic irritation of the nerve, root, or cord; severe pain; and progressive degenerative alterations.

Because severe segmental instability requires stabilization, the priority question to be answered in diagnosis is locating and determining the primary problem or maladaptation that is overloading and chronically stretching the involved motion unit. A hypermobile motion unit is obviously not tightened by manipulation. However, it is often self-correcting once its cause is removed.


Segmental hypermobility is allowed by ligament laxity, disc degeneration, and remolding of the posterior articulations. That is, a hypermobile subluxation indicates laxity of the holding elements –a positional relationship of two vertebrae in which their bodies or the apophyseal joint surfaces or both are in a position that they would never occupy during any phase of a normal movement. The immediate cause can be trauma, disease, or iatrogenic from misapplied surgery or manipulation.

Such hypermobility may be primary (ie, localized trauma or pathology limited to one or more motion units) or secondary. The most common secondary cause is that found in compensation above and below an area of spinal hypomobility (fixation). This subluxation complex is a dysfunction discernible through motion palpation. Secondary factors also include changes induced by a primary problem often far removed from the spine such as lower-limb asymmetries, eccentric weight bearing, misuse or overuse of spinal tissues associated with postural-occupational overstress, and system-oriented disorders such as hypoglycemia that may increase the degree of spinal curvatures through chronic fatigue.

Implications in Disc Disease

Several authorities believe that the first sign of disc disease is that of abnormal motion on flexion. Macnab attributes most pains associated with disc lesions to be from repetitive sprain due to chronic hyperextension of the posterior vertebral joints and the resulting arthritis. Farfan believes the more advanced changes found in disc disease (eg, marginal osteophytes, degenerated facets, pseudospondylolisthesis) are also due to mechanical overstress. Macnab and Farfan consider these changes to be the result of segmental hypermobility. Keep in mind that this instability is often the product of adjacent motion-unit hypomobility.

Roentgenographic Findings

Hypermobility is the variant of subluxation most apparent in stress-film roentgenography. The overt structural signs include traction spurs, interruption of Hadley's S curve, excessive centrum shift at extremes of flexion and extension, abnormal opening and closing of disc space during lateral bending, appearance of segmental hyperextension on neutral lateral films, change in articular relations to the joint-body line, reactive spondylosis and arthrosis, etc.

Segmental hypermobility is particularly obvious in spondylolisthesis, laterolisthesis, and retrolisthesis. It is also seen in excessive disc-space gaping in the sagittal or frontal plane. Instability in these cases becomes even more obvious at the extremes of movement, hence the value of carefully conducted stress films if they are not clinically contraindicated.

Chronic subluxations appear to follow a progression. For example, a spondylolisthetic segment may have started with fairly normal mechanics in childhood, then slowly become hypermobile because of accumulated stress, and become symptomatic in middle age.

Adjustive Therapy

Aside from severe trauma (eg, whiplash), segmental hypermobility appears to be the frequent effect of adjacent articular fixation as the result of soft-tissue (muscle and/or ligament) shortening. Buerger has shown that there appears to be a lack of stimulation of joint mechanoreceptors which normally inhibit nociceptive afferents. Lack of articular mobility prevents normal input to the neuronal pool thus blocking pain-conducting afferents from conducting impulses to higher CNS centers.

The importance of freeing articular fixations (eg, by chiropractic adjustments, passive mobilization) is brought out clinically. Mennell states that normal muscle function depends on normal joint function, and vice versa. If joint motion is not free, the involved muscles that move it cannot function. Thus, impaired muscle function leads to impaired joint function, and, conversely, impaired joint function leads to impaired muscle function (ie, disuse atrophy). In this clinical cycle, muscle and joint function cannot be separated from each other functionally. The earlier a fixation is corrected, the less chance there is for chronic degenerative changes to occur and the greatest change in mobility can be noted after adjustment.

Although nociceptive impulses cannot be measured directly in a clinical setting, an accompanying reflex (spontaneous activity of segmental muscles) can be measured by EMG recordings. It has been shown by Thabe that local joint restriction induces abnormal EMG changes and that adjustive therapy normalizes this response concurrently with the correction of joint malfunction.

Adjustive mobilization of spinal fixations has also been demonstrated in EMG studies by Rebechini-Zasadny and associates that showed a positive gain in muscle strength. Vernon's team has shown a significant but short-term increase in serum beta-endorphins (resembling that following acupuncture) immediately after adjustive therapy. Besides the control of pain, endorphins have broad effects in multiple body systems that are currently undergoing extensive study.

In support of the supposition that significant fixation is primarily articular in nature, Thabe reports that specific adjustive techniques can make this correction where local anesthetic injections and general mobilization did not. In addition, Mayer and associates found that oral anti-inflammatories do not improve symptoms associated with segmental cervical hypomobility.

Acute inflammation tends to develop into chronic inflammation that may continue for decades. Thus, it is necessary to treat each acute injury until all tenderness, signs of swelling, immobility, pain, etc, are eliminated. Partial treatment is not adequate.


Gillet classified four general types of fixations:

(1) muscular,
(2) ligamentous,
(3) articular, and
(4) bony.

It is clinically important to attempt to judge the degree of fixation and the nature of the fixative element to determine the minimum amount of force necessary during an adjustive thrust to release the fixation if it is logical to do so. Breaking severe ankylosis, for example, would usually be contraindicated. This judgment is necessary whether the cause is a spasm, shortened ligaments, interarticular adhesions, or another ameliorative factor.

Physiologic stretching, compression, and stimulation of the contents of the IVFs are normal and essential to maintain a healthy state of the structures involved. For this not to occur in the spine, or any extraspinal synovial joint, produces effects similar to those seen following prolonged immobilization of a limb: disuse atrophy, ligament shortening, circulatory stasis, neurotrophic changes, etc.

The atrophy of disuse is one of degeneration: a pathologic state producing minimal nerve excitability. This is undoubtedly why we find an acute subluxation-fixation producing far more clinical expressions than a chronic subluxation-fixation, and its effects tend to reflect signs of hyperactivity (eg, spasm, warmth, hyperesthesia, visceral hyperfunction). On the other hand, a chronic subluxation-fixation tends to express signs of hypoactivity (eg, weakness, coolness, numbness, visceral hypofunction, musculoskeletal degeneration).

These changes can be related to either the effects of neural facilitatory or inhibitory effects within the anterior, lateral, and posterior columns of the spinal cord. For example, facilitation would respectively manifest as motor excitation (eg, hypertonicity, spasm), sympathetic vasomotor excitation (eg, warmth), and sensory excitation (eg, pain, hyperesthesia). In contrast, inhibition would exhibit as motor depression (eg, hypotonicity, weakness), sympathetic vasomotor depression (eg, coolness, trophic changes), and sensory depression (eg, anesthesia).

The Belgium researchers (Gillet et al) gave no more importance to the intervertebral disc (IVD) in the production of spinal fixations than any other ligamentous structure. They believed that the integrity of the IVD is generally more of a passive factor than an active one. Motion palpation studies have not confirmed that true IVD lesions are as common as generally accepted in the medical community and to a large extent within our own profession.

Clinicians should not overlook the basic premise of biologic function; ie, life (health) is a stimulus-response mechanism. Without stimulation, life deteriorates. Thus, the proprioceptive impulses originating from the mechanoreceptors of mobile joint surfaces is an important means of maintaining the integrity of neural conductivity and the responsive function of the receptors within the spinal cord and higher centers of the CNS. When these circuits are dulled from disuse or hampered by some other factor (eg, certain drugs) normal adaptation and homeostasis cannot be expected.

Muscle Fixations

In the context of spinal fixations, the term spasm was used by Gillet to describe the state of a muscle or muscles that fixate vertebrae and hinder their normal movement. Yet, he does this with misgivings because such contractions are somewhat different from the spasms and cramps occurring in other muscles of the body. For example:

  • Spasms and cramps occurring in other parts of the body (eg, calf "Charley horse," intestinal colic, diaphragmatic spasm of "windedness") are acute contractions that may be extremely painful. In contrast, the spasms associated with spinal fixations, usually, are sensitive only to deep pressure and otherwise may go unnoticed by the patient.

  • Except spastic paralysis (eg, poststroke), spasms in other parts of the body usually have a short duration. In contrast, the spasms associated with spinal fixations may endure for months or years without change. In spite of the chronicity, the muscles involved do not necessarily degenerate or become fibrotic as other muscles normally do under such conditions. Why this occurs is unknown. One authority theorizes that it may be a natural physiologic reaction, similar to muscle "splinting," as an aid to maintain biomechanical equilibrium.

The cardinal sign is that these perivertebral "spasms" can be palpated. The more common ones are of the rotatores, multifidi, interspinales, intertransversarii (cervical), obliquus capitis (atlas-axis), levatores costarum, spinalis groups, and different portions of the quadratus lumborum. Although areas of spasm can sometimes be palpated in the large muscles of the back, they are rarely responsible for individual fixations.

Gillet's findings only tended to affirm B. J. Palmer's theory of a single segmental subluxation (the "major" concept) rather than Carver's hypothesis of abnormal curves of the spine (summation of the whole area) being the focus for pathologic expression. Much more research is necessary for uncontested confirmation of either theory. It is likely that either or both concepts may manifest in a given clinical picture.

Muscle Tonicity vs Phasic Contractions

When hypertonicity is sufficient and unilateral, the motion unit involved tends to be pulled into a sustained position of functional action. This appears likely because each vertebral segment is "balanced" at rest in a state of physiologic equilibrium between its extremes of motion.

In healthy skeletal muscles, there is a combination of two major neurologic factors at work:

  • The sustaining or resting tone (tension, firmness) of a muscle (an involuntary mechanism) is controlled by the sympathetic nervous system through low-frequency asynchronous impulses from the spinal cord. Its purpose is to keep the muscular system in a neurochemical and functional state of readiness to act and maintain static postural equilibrium (sustained by the stretch reflex). It is active during both rest and work, and is especially developed in the antigravity muscles.

  • The voluntary and involuntary gross contraction of a muscle, under the control of both the cerebrospinal motor system and cord reflexes, directs all postural, ballistic, and tension movements. It is electrically subdued during rest and while in the relaxed upright position if the body is well balanced over weight-bearing joints. Voluntary muscle contraction is normally superimposed on the involuntary intrinsic tone of the muscles involved in any musculoskeletal action.

The palpable spasm associated with a vertebral fixation, postulated Gillet, could be an involuntary state of abnormal hypertonicity rather than a cord reflex initiating a spasm via a phasic contraction as seen in typical spasms and protective "splinting." His theory could explain why the hypertonic muscles associated with fixations are tender to palpation but not otherwise painful.

Characteristics of Perivertebral Muscular Fixations

The major features of muscle-related articular fixations are:

  • They are usually palpated as taut muscle fibers underneath hyperesthetic skin. If the patient's overlying skin and subcutaneous tissues near the related spinous process are rolled between the thumb and index finger, acute tenderness will be reported by the patient.

  • They exhibit restricted mobility from the start when challenged, and the end-feel exhibits a little "give" with a rubbery end block.

  • They are released by adjustment and almost immediately become nontender and relaxed. The segment to which they are attached becomes mobile with the proper adjustment.

  • They are usually secondary to another area of fixation or the result of a reflex (somatosomatic or viscerosomatic); thus, they will likely recur if the primary fixation or some other focus of irritation is not corrected.

Besides being the most numerous, fixations of muscle origin are the most pathognomonic of overt symptoms –yet they are the most open to change by either direct or indirect methods. They also are the type in which the vertebral "displacement" factor is the most visible because the spasm or hypertonicity involved is usually unilateral. The more acute the condition, the less degeneration will be found in the muscle(s) responsible and the more change can be observed after an adjustment either locally or through the correction of more chronic primary fixations.

If resulting from a somatosomatic reflex, many related fixations disappear spontaneously after the correction of primary ligament and articular fixations. Gillet reported that there seems to be an important specificity between primary chronic fixations and acute muscular (reflex) fixations. This specificity can be surprising in its remote location, sometimes going from L5 to the lower cervicals without an apparent neurologic or biomechanical explanation. Another common example frequently reported is an upper-cervical major fixation producing low-back muscular fixations which, in turn, results in low-back pain and dysfunction.

Ligament Fixations

An early physiologic change seen with chronically fixated vertebral articulations is the shortening of ligaments. This occurs because ligaments tend to adapt to the range of motion used. That is, they shorten to the degree necessary to remove excessive slack. Thus, in complete or multimuscular fixations, associated ligaments and related soft tissues distinctively shorten.

Total functional fixation (pseudoankylosis) is often found at the occipitoatlantal, lower thoracic, and sacroiliac articulations. In many instances, however, mobility is not restricted in all directions. The type of thrust used for correction should be designed to stretch the shortened ligaments by, for example, repeated nontraumatic traction on the insertions of the involved ligaments.

The most pertinent characteristics of ligamentous fixations, which are often major fixations, are that they usually are:

  • Motion palpated as an abrupt hard block within a normal range of motion exhibiting no end play.

  • Either bilateral (with one side tighter than the other) or in the median line and found to improve only slightly immediately after each treatment.

  • The reflection of a degenerating chronic muscular fixation complex or the effect of ligament trauma and are overlaid with atrophied subcutaneous tissues.

In some purely muscular chronic fixations, the spastic or hypertonic muscles involved tend to degenerate and become fibrotic to resemble ligaments. As most deep spinal muscles are underlaid and/or overlaid with ligaments, it is often difficult to determine which structure is responsible for the fixation. Fortunately, the type and direction of a corrective thrust is nearly the same, and even the amount of demonstrable change that can be expected from a fibrosed muscle or a shortened ligament is the same. Thus, from a clinical viewpoint, a fibrotic muscle fixation can be classed as a ligamentous fixation. Gillet believed that this type of fixation is the most common but not the most symptomatic.

Articular Fixations

Complete (total) articular fixations are common in the human spine. Despite cause, they appear to be the result of intra-articular joint "gluing" similar to that seen in adhesive capsulitis and multiple-ligament shortenings. Overt pathology does not appear to be related as the fixation is eventually mobilized by a course of chiropractic adjustments.

In total articular fixations, one lateral pair of articulations (inferior and superior facets) of the bilateral posterior articulations may be the seat of fixation and the other not. The contralateral pair may be initially normal, but as the involved zygapophyses become more immobilized because of the fixation of their contralateral counterparts, they also become functionally incapable of motion. In time, the pathologic effects of disuse can be expected in the initially normal contralateral zygapophyses.

In total fixations in which the fixative element is the product of degeneration of the interarticular and periarticular soft tissues, with the probable development of "adhesions," the major corrective effect of the chiropractic adjustment is produced by the forced opening of the apposed facets.

Unilateral total fixation may exist whenever reflex fixations are found. However, total unilateral fixations in the spine function differently than total unilateral fixations in the sacroiliac joints. In total unilateral fixation of a sacroiliac joint, the contralateral articulation is not restricted in movement and typically adapts by becoming hypermobile and, in time, acutely overstressed in an attempt to serve the role of both joints. This reciprocity of immobility and hypermobility is found in all types of fixations –an important point to remember.

In total fixations between vertebrae, Illi states that the adaptive segmental hyperkinesis takes place in the articulations above and below, or in contralateral articulations. In partial fixations, it takes place on the yet mobile side of segments unilaterally fixated.

Gillet found that few spinal fixations can be explained by shortening of the capsular ligaments, although practically all other spinal ligaments can be involved. When apophyseal capsular shortening occurs, one might think that it would result in an articular-like fixation. However, Gillet did not find this to be true; ie, there is still a certain amount of torsion possible.

In summary, the major characteristics of articular (total) fixations are that they:

(1) are felt during motion palpation as being completely immobile in all directions and are asymptomatic;
(2) are painful when challenged by the palpator; and
(3) progress to true ankylosis. Thus, they are irreversible in the terminal stage.

Bony Restrictions

Bony blocks from outgrowths may be obvious during palpation. If they are near the periphery of a joint, however, they may be recognized only by the sudden arrest of otherwise free motion. An abrupt hard halt in motion usually signifies bone-to-bone contact, signaling that further movement should not be conducted. Such an approximation will be felt before the end of normal motion occurs when hypertrophic bone growth (eg, an osteophyte, a malunited fracture, or myositis ossificans) has developed. If force continued beyond the point of a bony block is painless, neuropathic arthropathy should be considered. In true ankylosis, there is no mobility whatever and adjacent joints are often hypermobile in compensation. Roentgenography is usually necessary for diagnosis.

Authentic ankylosis is one type of total fixation. It is invariably the result of a local bone disease process or severe trauma and rarely correctable by adjustive therapy. On the other hand, Gillet believed that a fibrous type of pseudoankylosis is far more frequent, especially in the midthoracic spine during middle age or in the elderly. This is likely the result of a general degeneration of the perivertebral muscles and ligaments. Although this fibrous condition can be improved, it takes many months of treatment to produce even a meager amount of normal motion.

In differential analysis, muscle spasm is distinguished from bony outgrowth as a cause of limited joint motion by several features. Bony outgrowths allow perfectly free motion up to a certain point, after which motion is arrested suddenly, completely, and without great pain. Muscular spasm, on the contrary, checks motion slightly from the onset. Resistance and pain gradually increase until the examiner's efforts are arrested.

Maladaptation During the Aging Process

Connective tissues tend to lose their youthful degree of flexibility, elasticity, viscoelasticity, and plasticity during the aging process. The rib cage especially tends to become tough and tight, and the spine is forced to use whatever compensatory mechanisms are available.

When the forces of adaptability are meager, we may see the unfortunate picture of a cervical spine that has had to distort itself to a great degree to "catch up" the lost balance that stopped at the lower thoracic spine. There also is the biologic necessity to maintain, if possible, level eyes. This sometimes forces a high degree of lateral flexion at the occipitoatlantal articulations –with all the danger of nerve compression and/or irritation we know is possible in this highly vulnerable area of the spine.

Biomechanical Compensation

The law of reciprocation should be remembered during examination. When an articulation cannot carry out its normal function (motion), at least one other articulation is forced to compensate by excessive motion, which may include eccentric and/or out-of-plane movement. This added role within the counterpart joint or an adjacent articulation in the kinematic chain leads to inflammation once homeostatic reserves are surpassed. Thus, a site of fixation is typically asymptomatic while the compensating hypermobile joint can be highly expressive. In such situations, it would be contraindicated to adjust the already hypermobile joint even if it is the focal site of clinical symptoms and signs.

Because of this compensatory factor, vertebral position derangements are often only of an adaptive type; ie, they exist in compensation to motion overstress applied to another articulation. If the stress applied on the compensatory hypermobile segment is prolonged, the greater the degree of related neuromuscular overstress. We often see this with the neuromuscular complaints of someone who has engaged in an unaccustomed activity such as shoveling, painting the ceiling, weekend gardening, or after exercise by someone in poor physical condition.

Autonomic Aberrations

Although there is a tendency of some within chiropractic to narrow their practices to the treatment of neuromusculoskeletal disorders, Gillet reported and many others strongly believe that a subluxation complex is involved in many organic functional disorders. They propose that many of these disorders are due more to faults in autonomic innervation than to irritation or compression of the cerebrospinal nerves.

Why should a subluxation affect the smaller autonomic nerves without seemingly producing greater harm to the extremely larger motor and sensory nerves? Gillet answers by calling attention to the position of the vertebra in fixation, whose motion may be blocked either within or beyond the normal range of motion. The latter occurring when an articulation is forced into a compensatory movement that it would not normally take. This type of subluxation was frequently described in pioneer chiropractic literature. The topic has been absent in recent years because it has not conformed to the data about normal vertebral motion.

Gillet stated that when such abnormal motion is forced to occur, the facets are displaced, the IVFs are abnormally closed and their contents are impinged. Processes leading to neurologic, circulatory, and osseous degeneration in this area are formed that involve the most vulnerable tissues first. If occurring in the thoracic spine, said Gillet, this could produce visceral symptoms without intercostal neuralgia –a condition that could be called a pathologic subluxation in contrast to the physiologic subluxation in which motion is restricted within the normal range of motion. In the latter, one might expect to find minimal compression or stretching of the involved IVF contents. Unless highly severe, fixations producing sympathetic disorders seem to produce fewer secondary contractions in the long spinal muscles and, therefore according to Gillet, produce far less postural distortion.

Potential Contributory Causes of Joint Fixation Development

In several writings, Janse and Gillet agreed with Jones' earlier findings that disuse of a joint causes slight adhesions which are due to exudation from venous stasis. These adhesions will be greater if there is also immobility of the muscles (eg, bracing, spasm), which increases the exudation from the lack of normal muscle contractions that aid venous and lymphatic circulation. After manipulation, wrote Coulter, the most important after-treatment is moderate active exercise.

Disuse with Continued Venous Stasis

There is no doubt that a common cause of articular fixation and the resulting motion restriction is disuse. Many occupations require certain joints to move only in one or two planes but not in all planes available. For example, a joint that is continually flexed but rarely extended will exhibit normal or abnormal joint play in flexion and frequently restricted joint play in extension. A similar situation occurs in a joint frequently abducted but rarely adducted or frequently rotated toward the left but rarely to the right.

Immobilization of a joint and its surrounding soft tissues produces bone atrophy. Several studies conclude that exercise is the best prevention against osteoporosis. However, as long ago as 1934, Key and associates reported in Archives of Surgery (28:943) that voluntary exercise is the only agent that will lessen or prevent bone atrophy. To prevent joint adhesions, they stated that it is important in postfracture management to immobilize the fracture by complete fixation of adjacent joints so that active exercise of other joints of the extremity can be done painlessly.

Recurrent Edema

Jones reported many years ago that there is no more potent factor in adhesion formation than recurrent edema. He called this the "glue" of which adhesions are made. Such an adhesive-like substance was frequently mentioned in the writings of Janse many years later. Jones directed attention to the edema caused by the removal of a plaster cast from the lower limb, which gradually increases during the day and subsides during the evening. This edema disappears only when the distended tissue spaces are obliterated by the return of muscle tone through active exercise.

Manipulation of any joint with adhesions while the limb is still subject to recurrent edema was strongly advised against by Jones: "Not only does the edema produce fresh adhesions, but since the adhesions themselves are edematous, there is a greater exudation when they are torn than if the circulation is first restored to normal. The swelling must be controlled by external pressure and exercise, and if any adhesions still remain, a manipulation may then be successful."

Recurrent Trauma from Passive Stretching

Jones listed recurrent trauma as another cause for the formation of joint adhesions. He believed that this was usually the result of daily passive stretching or repeated manipulation. The reader might be reminded here of the advice of Firth who strongly advised his students to:
"find the subluxation, fix it, and leave it alone."

Violent stretching of adhesions and taut tissues within and around a joint produces small hemorrhages and an inflammatory reaction with edema and the formation of subsequent adhesions and induration. At times, this overstress may lead to a degree of myositis ossificans. However, this potential should not restrict the judicious use of gentle stretching, massage (manual, mechanical, electromechanical) and active exercise during rehabilitation of joints exhibiting reduced mobility.

Concern must be given to do enough but not too much at any one time. Jones stated over 65 years ago, and many chiropractic clinicians still believe, that it is often better to perform several well-tolerated but incomplete adjustments at intervals of several days, to allow for tissue compensation, than attempt to make a full correction with a singular adjustment. Empiric findings show that the beneficial result of manual articular correction may be neutralized if it is followed by repeated passive and forceful tissue stretching and/or compression.

It was reported by Jones that recovery may be delayed for several months, or even indefinitely if an involved limb is allowed to swell because the vessels remain dilated, the tissue spaces remain patent, and every swelling of the limb encourages further swelling. Thus, a vicious cycle is established. For this reason, an elastic bandage over a cotton bandage should be applied immediately after a plaster cast or firm brace is removed and kept in position for about 6 weeks while the patient walks and exercises. Coulter recommended that the support should be removed once or twice daily for superficial stroking massage and mild active exercise of the part. After the 6-week period, the tendency to edema disappears as does the slight residual stiffness of the joint.

Prolonged Dysfunction from Immobilization

Another cause listed by Jones for the formation of adhesions is the continual trauma of the immobilization of a joint in a position of stress (eg, hyperflexion, hyperextension). When this occurs, an almost intractable stiffness can result. Coulter believed that these strained positions cause traumatic synovitis with recurrent exudation, leading to the formation of adhesions. In this context, Janse wrote extensively on the microtraumatic effects of postural and overtly traumatic overstress placed on the soft tissues (muscles, ligaments, vessels) near the intervertebral foramen and around the apophyseal joints. The typical reactions of synovial joints to overstress are essentially the same whether they are spinal or extraspinal.

Gillet's Postulates Regarding Common Trauma

Ligaments are not normally tender unless they are in a pathologic state. Trauma less than that producing fracture or dislocation produces an inflammatory reaction similar to that caused by a bacterial infection. The reaction to bacterial invasion is designed to contain and wall off the area to prevent further spreading of the infection. After injury, normal localization processes serve to contain the products of the injured tissues but the resolution of inflammation can be especially harmful if joint mobility has not returned to normal. This occurs because normal periarticular soft tissues are flexible, elastic, plastic, and generally richly vascular. Scar tissue, on the other hand, tends to be stiff, unyielding, and poorly vascularized. For this reason, reinjured joints that are not properly attended initially are extremely slow to heal.

More than one tissue is usually affected by a single traumatic incident, and treatment should be specific for each tissue affected. Determining the cause is not an easy task. For example, tender hypertonic perivertebral tissues found in the upper thoracic region of the spine may be from:

(1) overworked tissues (eg, unaccustomed activity of chopping wood or lifting),
(2) unusual sustained postures (eg, prolonged spinal extension as in painting a ceiling),
(3) a viscerosomatic reflex (eg, lung or heart disease),
(4) excessive compensatory segmental hypermobility owing to one or more fixated lower cervical or midthoracic vertebral motion units, or
(5) a combination of two or more of these factors.

Case management can be considered as a progression through two phases. The first goal is to reduce swelling and relieve associated pain and soreness by R-I-C-E (rest, ice, compression, and elevation) and other physiotherapeutic measures when appropriate. The second objective is to promote healing, movement, and strength (eg, by adjustments, massage or vibropercussion, stretching, passive and active exercise, and other standard regimens). It is imperative that any attending neurologic disorder in the spine be relieved because this often disrupts the reflex feedback cycle that prolongs the effect and also eliminates a possible source of a secondary or contributing subluxation complex.


Spinal manipulation has been placed on a scientific plane essentially because of chiropractic. The primary but not sole role of this art and science encircles, but is not restricted to, events occurring at or near the intervertebral foramen (IVF).

Spinal segments are designed to move in their anatomical planes of articulations (unless the motion is blocked). It is at the level of the apophyseal facets that most subluxations occur to influence the IVFs far more than any other articulations of the spinal column; ie, IVD interfaces, costovertebral articulations.

The cross-sectional area of an IVF normally allows sufficient room for its neural contents during the dynamics of daily life. IVF narrowing occurring during spinal extension movements has little if any adverse neural effects in the normal spine. Thus, channel contents are normally free to adjust to movements throughout the normal range of regional motion. Pathologic changes in and near the foramen, however, may reduce its dimensions and lead to compression or tension, but, as Sunderland points out, friction over osteofibrous irregularities or traction on one or more nerve roots fixed in the foramen by an adhesion is more likely.

A normal vertebral motion unit adapts under mild–moderate stress to changes occurring in adjacent IVDs, ligaments, fascia, muscles, tendons, and other associated tissues producing some mild degree of fixation. Nevertheless, adjacent IVFs must alter in size in compensation because of the impaired articular mobility. As a rule, two IVFs become smaller than normal and the other two become larger. Nerve roots and other contents of the affected IVFs suffer compression insult at the smaller foramina and stretching forces at larger foramina. Potential motor-unit events produced by a subluxation complex are shown in Table 1.1.

     Table 1.1. Potential Motor-Unit Events Resulting from Subluxation
Articular and Para-Articular Changes        Meningeal traction
  Bony foraminal encroachment               Minute hemorrhages
  Changes resulting from mechanical         Minute tearing of dural root sleeve
    deformation                               attachments in or near IVF
  Eccentric zygapophyseal cartilage         Paravertebral pain and tenderness
    compression                             Pedicle kinking
  Joint capsule overstress, resulting       Sclerosis
    in capsule thickening, reduced          Transudation
    mobility                                Traumatic edema
  Trauma to periosteal margins pro-
    ducing proliferative changes            Proprioception and Autonomic Changes
  Traumatic edema                           Reflexes to motor components
                                            Abnormal or subnormal somatomotor
Circulatory Changes                           reflexes
  Arteriovenous stagnation                  Abnormal or subnormal visceromotor
  Cerebrospinal fluid flow alterations        reflexes
  Changes resulting from ischemia           Stimuli interpreted as peripheral
  Interference with IVF interstitial          sensory stimulation
    fluids                                  Misinterpreted somatosensory re-
  Interference with nerve root intra-         flexes
    cellular fluid                          Misinterpreted viscerosensory re-
  Sluggish lymphatic flow                     flexes
                                            Visceromotor reflexes
IVD Changes                                 Circulatory dysfunction
  Anular fiber overstress                   Smooth muscle dysfunction
  Eccentric compression                     Secretory dysfunction
  Nuclear displacement                      Trophic dysfunction
  Loss of optimal hydrostatic loading       Musculoskeletal
    ability                                 Visceral
  Protrusion or herniation
                                            Toxic Metabolic Products and Effects of
Paraforaminal Soft-Tissue Changes           Venous Stagnation from Arterial Backup
  Adhesions                                 Acetylcholine inhibition
  Altered nerve root level                  Cellular malnutrition
    Encroachment symptoms                   Creatinine
    Traction symptoms                       Hypoxia
    Pedicle kinking                         Inflammatory residues
  Atrophy                                   Ionic imbalance
  Contractures                              Lactic acid buildup
  Ganglionic compression or irrita-         pH changes
    tion                                    Urea
  Hyper- or hypo-tonicity                   Uric acid

Studies by Drum, Hargrave-Wilson, Kunert, Burke, Gayral/Neuwirth, and others have shown that a subluxation complex, often leading to spondylosis, can produce a variety of apparently unrelated disturbances. Most remote effects can be grouped under the general classifications of root neuropathy, basilar venous congestion, cervical autonomic disturbances, CSF pressure and flow disturbances, axoplasmic flow blocks, irritation of the recurrent meningeal nerve, Barre-Lieou syndrome, and/or the vertebral artery syndrome.

Constant Articular Mobility is Normal

During spinal motion, which occurs even in sleep because of breathing, cineroentgenography and surgical animal studies show that the superior and inferior posterior articular facets constantly glide on one another and establish a mild but normal stream of complex proprioceptive signals to higher CNS centers. In addition, the IVFs are constantly opening and closing –thus mildly squeezing and stretching the contents of the IVFs. This latter phenomenon, the continual dynamic mechanical action of mild traction and compression, is believed to help "milk" cerebrospinal fluid (CSF) around the spinal cord and peripherally along the spinal nerves. When spinal mobility is induced, the alternating compressing and stretching actions initiated occur only for a few seconds at any specific direction because of the different dynamic movements produced and varying postures assumed during normal activity that alter the lines of force. The effect can be likened to mild circumducting massage and should not be confused with prolonged or severe compressing and stretching actions. The point to be made is that the area is constantly dynamic, structurally and functionally.

This CSF-pumping action should not be overlooked in treating chronic neurologic disorders –a point frequently emphasized by Leo Spears, DC, who founded the hospital and sanitarium bearing his name in Denver and received world-wide attention for his treatment of poliomyelitis, cerebral palsy, muscular dystrophy, multiple sclerosis, and other similar disorders. Unfortunately, the import of Spear's findings as well as those of thousands of DCs during the 1920s–1950s in treating such disorders have been neglected in recent years by those professing a more limited "musculoskeletal" philosophy in chiropractic.

Clinical Expressions of Fixation

Gillet's studies continually verified several major characteristics of fixations. One was that the pathogenicity of a fixation varies inversely to the degree of existing fixation. In a unilateral incomplete fixation, for example, signs of irritation are found on the movable (contralateral) side of the vertebra and not on the side of fixation. In partial bilateral fixation in which some movement occurs in the A-P plane, the signs of irritation will be bilateral and often to the same degree on both sides. In total fixation, rarely are there signs of irritation at the level of the involved segments with one notable exception: the occipitoatlantal articulation.

Another finding of Gillet's team was that if an area of the spine in fixation was actively or passively flexed or rotated several times, skin temperature readings increase immediately and then decrease with rest. This supports the hypothesis that the site of fixation, especially if degeneration has occurred, will exhibit signs and symptoms of hypofunction (eg, anesthesia, paresthesia, vasodilation, stasis). It also helps to explain why a complete fixation (eg, an ankylosed articulation) is not painful but important clinically because of the extra motion forced on adjacent mobile articulations in the kinematic chain and by the secondary fixations produced.

If a unilateral fixation allows some contralateral movement, motion occurs around an abnormal axis that, if forced, produces a distinct pivoting-type of aberrant joint separation rather than the normal translatory gliding or sliding of articulating surfaces. Oblique x-ray films of the spine, for example, will reveal reduced facet mobility on the side of fixation and separation of the facets contralaterally which widen further when the patient's spine is forced into various postures.

IVF Content and Size Alterations

It has been explained that each IVF is functionally dynamic: widening and narrowing vertically and horizontally with various types of spinal motion, thus serving as a dynamic channel for nerve and vessel shifting and allowing compression and stretching of the lipoareolar bed. From one-third to one-half of the foraminal opening is occupied by the spinal nerve root and its sheath, with the remaining portion filled primarily by fat, connective tissue, and various vessels. One should keep in mind that the following important structures are found in the IVF and always subject to abnormal tensile and compressive forces:

  • The anterior and posterior nerve roots

  • A portion of the dorsal root ganglion

  • A bilaminar sleeve of dura and arachnoid membrane, extending to the ganglion

  • A short continuation of CSF-containing subarachnoid space, which ends just after the ganglion

  • The recurrent meningeal nerve

  • The spinal ramus (radicular) artery and intervertebral vein

  • Lymphatic vessels

Factors Changing IVF Diameter and Their Consequences

Six abnormal factors commonly modify IVF diameters. They are

(1) the incongruity of facets (subluxation);
(2) changes in the normal static curvatures of the spine;
(3) the presence of induced abnormal curves of the spine;
(4) degenerative thinning, bulging, or extrusion of the related IVD;
(5) swelling and sclerosing of the capsular ligaments and the interbody articulation; and
(6) marginal proliferations of the vertebral bodies and apophyseal articulations.

These factors singularly or in combination can insult the viable contents of the IVF and subject its contents primarily to:

  • Compromise by nerve root pressure, traction, or torque.

  • Intraforaminal and paraforaminal edema.

  • Constriction of the spinal blood and lymph vessels, which can result in stasis.

  • Changes in local tissue chemistry due to metabolic and trophic effects.

  • Induration and sclerosing of the periarticular ligaments with incarcerating insult upon the contained receptors.

  • Forcing foraminal contents into protracted constriction and/or an altered position.

Other factors are undoubtedly involved. Note that nerve tissue normally tolerates slow compression without offering obvious symptoms. Thus, acute phenomena are usually the result of friction, severe or repeated trauma, and/or encroachment from degenerative thickening or exostosis.

Vertebral Unit Microtrauma: General Considerations

The zygapophyseal articular complex of a subluxated-fixated vertebral motor bed is initially subjected to the stress of prolonged "off centering" and is attended by the following aspects of microtrauma through the resulting aberrant motion:

(1) minute hemorrhage, transudation, exudation, and arteriovenous stagnation from the sluggish circulatory flow resulting from the motion unit's decreased mobility and the arterial backup;
(2) para-articular and paraforaminal traumatic edema;
(3) eccentric compression stress upon the IVD and the apophyseal cartilages;
(4) possible separation of minute fasciculi of the retaining fibers of the anulus, joint capsule, dural root sleeve, and nerve root sheath;
(5) stress insult of the proprioceptive bed;
(6) minute crushing of the periosteal margins with resultant proliferative irritation; and
(7) minute tearing of the attachments of the dural root sleeves if they fasten to the lining of the IVF.

Thus the following pathologic changes typically occur:

  • Extravasation and edema, along with the precipitation of fibrinogen into fibrin, result in interfascicular, foraminal, articular, and capsular thickening, "gluing," and adhesions. This restricts facet glide, mobility of the foraminal contents, and the competent movement of the vertebral segment within its articular bed. Whenever extravasation occurs, mineral salts normally precipitate with infiltration. Sclerosing is a common consequence.

  • Binding adhesions may also develop:

    (1) between the dural root sleeves and the nerve roots within the IVF and

    (2) between the spinal nerve root sheath and the inner margins of the IVF. When subjected to microtrauma, connective tissues undergo rapid and extensive degenerative changes featuring loss of functional integrity and their normal physical properties.

There is no doubt that overstress and traumatic edema often produces paraforaminal adhesions. The result is a painful restriction of the normal back-and-forth glide of the nerve root within the IVF. Symptoms simulate low-grade radiculitis; eg, increased pain on movement, straining, andstretching, along with pain on changing positions and when placing the involved area in extension.

Nerve Root Insults

The point cannot be overemphasized that disturbances of nerve function associated with subluxation-complex syndromes can manifest as abnormalities in sensory interpretation, motor activity, and/or autonomic aberrations. These disturbances may result from one of two primary mechanisms:

(1) direct nerve or nerve root disorders or
(2) noxious reflexes.

Sensory Manifestations

When direct involvement occurs on the posterior root of a specific neuromere, it usually manifests as an increase or a decrease in cutaneous awareness over the dermatome; ie, dysesthesia in the area supplied by this segment. Such expression is usually tested with a cotton wisp and sterile pinwheel or dull pin. Foraminal occlusion and other irritating factors reflected as tenderness are frequently witnessed.

Common upper-extremity examples include abnormal sensitivity produced on the posterior and lateral aspects of the thumb and radial side of the hand when involvement occurs between C5–C6. At other times, this root involvement may cause hypertonicity and sensations of deep pain in the muscles supplied; eg, C7 involvement, with deep pain in the triceps and supinators of the forearm. Direct pressure over the nerve root or its distribution will usually be acutely painful.

Cyriax lists the major signs of nerve pressure as:

(1) pain on stretching the nerve,
(2) the provocation of paresthesia (eg, pins and needles) on motion,
(3) swelling and tenderness over the nerve sheath,
(4) postural deformity, and
(5) evidence of secondary parenchymatous changes in the nerve (eg, impaired conduction during electrodiagnosis).

Motor Manifestations

Nerve root insults from a subluxation complex also may be evident as disturbances in motor reflexes and/or muscular strength. Examples of these reflexes include the tendon reflexes such as seen in the reduced biceps reflex when involvement occurs between C5 and C6, the reduced triceps reflex when involvement occurs between C6 and C7, or the reduced patella and Achilles tendon reflexes when involvement occurs between L4 and L5. These reflexes also should be compared bilaterally to judge whether the hyporeflexia is unilateral. Unilateral hyperreflexia is pathognomonic of an upper motor neuron lesion. Muscle strength against resistance should also be tested.

Autonomic Manifestations

Prolonged or severe nerve root irritation also may produce evidence of trophic changes in the tissues supplied. This may feature atrophy, especially if circumference of an involved limb is measured at the greatest girth in the initial stage and this value is compared to measurements taken a few weeks later. For this reason, the circumference of the thigh, leg, forearm, and upper arm should be measured and recorded during any examination for a neuromusculoskeletal disorder.

Because autonomic pathways innervating musculoskeletal tissues are intimately connected with spinal nerves, these systems do not operate in isolation. Structural disorders in the spine frequently cause, contribute to, or mimic such "functional" disorders as Meniere's disease, causalgia, shoulder-arm syndrome, asthma, sphincter spasms, cluster headaches, angina, and a large variety of referred pains and areas of referred tenderness. Disorders affecting these nerves play an important role in many remote reflexes, often mimicking visceral disease.

Ganglion Irritation/Pressure

Because of its juxtaposition to the IVF, potential irritation or compression of a posterior root ganglion should be considered. The ganglion of each spinal nerve commonly lies near or within the upper medial aspect of the IVF, a precarious position.

If the transverse diameter of the IVF becomes modified, the ganglion can be subjected to compression or tensile forces and irritation. This is especially common at the cervical level where it tends to occupy the medial limits of the IVF and is thus likely to become involved in any changes in IVF diameter (viz, unilateral spasm, trauma, spondylosis). An acute whiplash-like mishap to the cervical spine, for example, especially of the hyperextension type, may force the vagus and superior cervical sympathetic ganglion against the transverse processes of the atlas and axis, often provoking bizarre autonomic reactions (ie, a parasympathomimetic syndrome).

Nerve Compression

Many subluxation syndrome effects can be attributed to nerve root compression. Sharpless, Luttges, Sunderland, Pleasure, and several others in recent years have contributed greatly to our understanding of the phenomena involved.

Nerve roots are normally well protected from trauma by the bony border of the IVF and the tough fibrous dura. However, Schaumberg shows that when distorted by degenerative bone and joint disease or space-occupying lesions, these same protective layers may be the cause of damage to the delicate neural elements. Thus, direct nerve pressure may come from the malaligned osseous segment itself or from various soft-tissue lesions causing or affected by structural faults such as contractures, adhesions, inflammatory residues, atrophies, and cysts or tumors of related tissues.

Sharpless reports that the posterior nerve roots are about five times more susceptible to compression block than a peripheral nerve. As little as 10 mm Hg pressure held for only 15–30 minutes reduces the compound action potentials of posterior roots to about half their initial value. This effect is thought to be from mechanical deformation rather than the attending ischemia because the larger fibers are blocked first. Anoxia affects small fibers first.

When exiting IVFs, nerve roots pass near the inner edge of the superior articular process. In subluxation, this process overrides the surface of the inferior process and can produce direct irritation of the root by the inferior process, with or without compression. Direct compression also can result when the root is caught between the inferior process and the body of the superior vertebra or trapped between a hypertrophied inferior process and the superior body. Olsson and coworkers, however, reported that mechanical pressure on a root occurs more often from the formation of edema within the nerve sheaths and epineurium, despite the cause.

Oppenheimer, Hadley, and others found that a large number of patients suffering from pain and discomfort suggestive of rheumatism or arthritis was the result of nerve root compression arising from narrowing of the IVF. They explained the primary causes as discogenic disease, inflammatory swelling, and penetration by an articular process.

Sunderland reported that IVF narrowing results from normal extension or any number of pathologic changes in and about the foramen that reduces its dimensions or leads to nerve compression. Thus, the same effect would exist in a subluxation fixed in extension or be achieved in some other manner causing IVF narrowing.

Subarticular Entrapment.   This type of compression usually occurs from arthritic hypertrophy of an articular facet and is often associated with advanced spondylosis. The resulting bony mass can compress the nerve root lying beneath the medial border of the superior articular facet. The root is caught between the posterior aspect of the vertebral body and the facet. Pang, Chrisman/Gervais, and Davis report that besides somatic sensory and motor manifestations, hearing, visual, and equilibrium disturbances may be associated.

Axial Compression on Discs.   When a person arises to an upright position, axial compression in the spine does not cause a problem with healthy well-hydrated discs. If unloaded disc space narrows considerably because of weakened restraints, the vertebral canal can be narrowed by several mechanisms. Typically, these include posterior subluxation of the superior vertebra, anterior subluxation of the inferior vertebra, a diffuse posterior anular protrusion or rupture, kinking of the ligamentum flavum, thickened capsules from laminae shingling, arthritic hypertrophy of the superior processes, or a combination of these factors.

Pedicular Kinking.   Root kinking is a condition associated with chronic IVD degeneration in which the disc space has thinned and the vertebral bodies approximate each other asymmetrically because of lateral disc collapse or a laterally tilted vertebral body (eg, scoliosis). As the superior vertebral body descends, it may impose its pedicle on the nerve root. Macnab believes that the most common mechanism in the cervical spine is from the nerve root being entrapped in the gutter formed by a wide lateral protrusion of the disc and the superior pedicle.

Spinal Canal Stenosis.   Spinal stenosis can produce a bony root entrapment syndrome as it progresses. Narrowing of the spinal canal will generally occur either laterally or in the midline of the canal. When occurring laterally, root compression result from foraminal impingement, pedicular kinking, or subarticular entrapment. If occurring in the midline, compression of the cord or cauda equina may result.

Diverse Clinical Manifestations.   Spinal nerve pressure or irritation may manifest as near or remote sensory, motor, autonomic, or combined signs and symptoms, and their initial effects are often interacting. In studying the effects of injured and compressed nerves, Granit and associates found that nerve impulses initiated in a motor root are transmitted to the sensory fibers in a cut or compressed region of the nerve and can be picked up in the sensory root of the same segment. In acute disorders, Causey/Palmer found that the failure to conduct an impulse after local pressure is applied to a nerve was caused by local anoxia. Rydevik affirmed that this was true but also learned that biomechanical nerve-root deformation was an additional factor in inducing weakness and altered sensibilities.

Axoplasmic Transport Alterations

Research has established three important facts:

(1) nerve roots are highly susceptible to compression, the slightly peripheral spinal nerves are not;
(2) nerve roots become highly vulnerable to IVF compression when the roots are subjected to traction and the IVF is narrowed; and
(3) spinal nerves, while not highly susceptible to compression, are highly susceptible to axoplasmic transport block.

Much of the protein synthesized within a nerve cell body moves along with other materials, such as neurotransmitters, out from the cell body and along the nerve fiber (anterograde material transport system). Two mechanisms have been isolated and are characterized by their rates despite fiber size. Guth initially recognized this total system for transporting the "trophic" substances normally carried by efferent nerves. It is also recognized that there is a retrograde flow of substances; ie, from terminals toward the nerve cell body.

Ochs, Korr, Fernandez, Rainer, Sjostrand, and several other researchers have found that any type of neuronal constriction, compression, or ischemia will cause a local transport block and an accumulation (damming) of the fluid proximal to the restriction. Weiss had earlier explained this as a form of persistent endoneurial edema found just proximal to a compressed area.

Pressures successful in blocking axoplasmic flow are far below those necessary to block nerve conduction. Thus, it has been hypothesized that some effects previously attributed to root compression may be effects from interference with normal axoplasmic flow.

Cerebrospinal Fluid Flow Alterations

Disorders classified under the category of CSF flow alterations relate to the mechanical effect on the flow of CSF within the CNS and perhaps within the peripheral nerves sheaths (as previously described). Stagnation possibly occurs in association because of the intimate relationship between spinal fluid and venous blood. It can be presumed that this contributes to stasis toxicity in the nerve root area.

Freedman shows how biomechanical aberrations of the spinal column may adversely affect CSF flow and CNS function. It is thought that this factor may be a common physiologic denominator within various (although seemingly different but often equally effective) chiropractic adjustment technics.

CSF Flow.   According to some researchers, minute pressure on meninges can alter the flow of CSF and interfere with the system's ability to remove wastes and provide nutritional substances to the cord and related nerves. This may be either the result of direct mechanical pressure or impairment of motion necessary for proper inflow and outflow of this nutrient fluid.

Steer/Horney investigated whether CSF passes peripherally from the spinal cord to peripheral nerves. To test the possibility, blue powder suspended in CSF was introduced into the lumbar subarachnoid space of pigs and sheep. Nerves and other tissues were examined 4–21 days later. Particles of dye were found widely distributed; eg, far into the brachial and lumbosacral plexuses, thoracic nerves and muscles, skin, and the jugular vein. Yet, this would not prove CSF flows directly into spinal nerves because diffusion could occur via lymphatics and capillaries.

Occipital Subluxation Effects.   Almost any situation causing constriction in the connecting area between the cerebral subarachnoid space and the vertebral canal can limit the escape of CSF into the inferior vertebral canal. This results in a degree of increased intracranial pressure. An occipitoatlantal subluxation, for example, may cause the dura mater of the cisterna cerebellaris to be pressed against the posterior medullary velum and partially occlude the foramina of Luschka and Magendie and interfere with flow from the 4th ventricle. The resulting increase of intraventricular fluid accumulation can produce a variety of symptoms such as deep-seated stubborn "internal pressure" headaches; nausea; a tendency toward projectile vomiting; bizarre and unusual visual disturbances; and protopathic ataxia.

Meningeal Irritation

Spinal dura matter contains an intrinsic nerve supply that is highly significant. Meningeal rami are derive from gray communicating rami and spinal nerves. Each spinal nerve contributes sensory fibers to meningeal rami. Several meningeal rami enter each IVF, and most are located anteriorly to the sensory ganglia within the IVF. Bridge found that these intrinsic nerve fibers reach the anterior surface of the dura by three main courses. Here the nerves divide into ascending and usually longer descending filaments running longitudinally and parallel on the dural surface, with a large number of fibers intercommunicating from adjacent segments. Finer filaments penetrate the dural substance where they subdivide.

Most of these fibers, reports Kimmel, penetrate the dura near the midline, while others enter laterally near the exiting spinal nerve roots. At each segmental level, two or three nerves pierce the spinal dura and contain only small-diameter nerve fibers. In contrast, Edgar/Nundy could find no definitive nerve endings, but the nerves could be traced to the posterior aspect of the spinal dura.

These observations help to clarify the wide distribution of back pain often found following protrusion of a single IVD. Also, biomechanical errors in motion and position readily place compressive or tractional forces on the meningeal coverings of the cord and/or dural root sleeves that may produce mechanical pressure on the neurons and retard CSF flow emanating from the cord itself. These factors may, therefore, elicit abnormal neurologic motor effects or sensory interpretations. Autonomic disturbances also may be associated.

Nerve Root Course Considerations

Nerve root course can be significant when sharp deviations occur. For example, cervical nerve roots are normally located anteriorly and inferiorly to their facets. In the thoracic spine, they lie directly anterior to the facets. In the lumbar spine, the roots course anteriorly and superiorly to the facets, beneath the pedicles. These routes should be visualized during palpation and adjustment procedures.

With regional modifications, a typical IVF is generally elliptical in shape when viewed laterally. The diameter of its vertical axis is about double its A-P dimension. This allows adequate space for changes in vertical dimension (eg, dynamic axial traction or compression and moderate disc flattening) without injury to IVF contents if adequate fat and fluid are present. In contrast, reduction of an already short transverse diameter can produce many noxious effects. For this reason, disc collapse vertically is often asymptomatic, while only slight posterolateral intervertebral disc protrusion into the IVF can produce severe symptoms.

The Cervical Area.   Cervical foramina are designed more in the shape of rounded gutters than orifices, averaging 1 cm in length. There is no true IVF between the atlas and the occiput or between the atlas and axis. The C1 nerve exits over the superior aspect of the posterior arch of the atlas in the vertebral artery sulcus. The C2 nerve exits between the inferior aspect of the posterior arch of the atlas and the superior aspect of pedicle of the axis. It then precariously crosses the lateral atlantoaxial joint, anterior to the ligamentum flava. The C3–C8 nerves exit through short oval trenches, which increase in size as they progress caudally. Cervical nerves uniquely fill the transverse diameter of their IVFs. Thus, any prolonged factor or event reducing this dimension (eg, subluxation, osteophytes, IVD herniation, edema) will undoubtedly compromise the integrity of the IVF contents.

Nerve sheaths in the cervical region are not firmly attached to their respective foramina. Only the C4–C6 cervical nerves commonly have a strong attachment to the vertebral column, and this is at the gutter of the transverse process. Sunderland states that this has relevance to any local lesion that may fix, deform, or otherwise affect the nerve and its roots to the point of interfering with their function. This fact also may be important to traction injuries of nerve roots.

The Thoracic Area.   The pedicle notch of the vertebra above is fairly deep in the thoracic region, while that of the vertebra below is relatively shallow. The result of this design is a pear-shaped canal with sharp bony edges that predispose to fibrotic and osseous changes from chronic irritation. The vertebral body and the disc of the superior vertebra form most of the IVFs anterior boundary in the thoracic region.

The Lumbar Area.   A lumbar IVF is shaped like a kidney bean when viewed laterally. It takes considerable posterolateral disc protrusion to encroach the nerve (but not its sheath) exiting at the same level because the lumbar IVFs are comparatively large. When IVD protrusion does cause trouble, it is usually from pressure from the vertebra above on the laterally placed nerve root. The course of the medial branch of the lumbar dorsal ramus and its accompanying vessels through the osteofibrous tunnel, and the intimate relationship of the neurovascular bundle to the capsule of the apophyseal joint, is a potential site of adhesion and entrapment following pathologic changes involving the joint.

Altered Nerve Root Angle

Disrelationship between position level and course direction of nerve root origin (spinal cord) and nerve root exit (IVF) is always an important consideration. Whenever there is subluxation or the presence of abnormal curves, the relative levels of points of nerve root origin and exit are altered and the root becomes vulnerable to encroachment compression or irritation. This especially results whenever the normal curves of the spine are grossly altered (eg, cervical kyphosis, lumbar lordosis, scoliosis especially at the cervicobrachial area and lumbosacral junction).

When nerve roots are forced to assume an unusual approximation to a wall of their IVF, root angles are altered. After that, only slight added deviation may precipitate a nerve root irritation syndrome. In addition, a spine affected with partial fixation of several segments will suffer marked tension on the dural root sleeves and related spinal nerve radicles, especially the cauda equina, whenever subjected to stressful flexion, extension, or rotation.

When one or more vertebral segments are functionally embarrassed for any reason by abnormal motor action, added articular and proprioceptive responsibilities are imposed on the segments above and below the involved area. Thus, there is an extension of harmful effects that will likely have noticeable complications.

In addition, bipedism requires the neurologic development of an ascending and descending reticular activating mechanism. It may be assumed that spinal and pelvic interosseous incongruity may overstimulate the ascending portion of the reticular activating mechanism. Excessive psychic stress, by way of the descending portion, may also provoke overstimulation of the cellular elements in the anterior and lateral horns and produce abnormal somatic and autonomic reactions.

Circulatory Alterations

Impaired segmental mobility (eg, vertebral fixation) of a vertebral motion unit within its normal physiologic range of movement may cause sluggish lymphatic or vascular circulation that is further influenced by mechanical pressure. This can produce chemical or physical changes within involved tissues such as anoxia, toxicity, swelling, edema, etc, and the consequent disruption of normal function.

Local irritation at the site of segmental malalignment and the decreased ability to exercise within its normal physiologic ranges lead to an edematous inflammatory reaction disturbing the normal exchange of nutrients and waste products between capillary and extracellular fluid. Added to this stasis is the probable factor of lactic acid buildup in the area because of leakage from the surrounding hypertonic muscles.

Local Toxicity

Venous stagnation from arterial backup produces local toxicity at the spinal level. While toxic metabolic end products (eg, urea, uric acid, creatinine, lactic acid) accumulate in the stagnant tissue and congested capillary beds, there is also a corresponding decrease in nutrient and oxygen concentration in these fluids. Thus, the nerves emanating from the involved area will be deficient in necessary nutrients and possibly hypoxic as well.

Accumulation of metabolic debris in the area of the IVF, may also alter the normal pH of local fluids causing a breakdown of Krebs' cycle due to decreased oxygen and toxicity causing a partial breakdown of the sodium pump mechanism. The result is an ionic imbalance. As the sodium pump can no longer maintain a normal ionic balance, the imbalance results in a degree of erratic nerve conduction and edema in the tissues of the immediate area. This erratic nerve conduction may be exhibited in all fibers passing through the involved IVF and immediate area.

When toxicity occurs in either the central or peripheral nervous systems, the formation of acetylcholine at the level of involvement results in further disturbances due to increased nerve conduction impairment. This situation, along with the toxicity effects on the nerve itself, results in abnormal membrane permeability contributing to the complex picture of dysfunction.

Distal Neurocirculatory Expressions

Because of the effects of subluxation-complex microtrauma and the consequent pathologic changes involved, the neurologic insult may result in:

(1) modification of the basic chronaxie;
(2) alteration of normal impulse amplitude, wave length, and force intensity; and/or
(3) lengthening of the refractory period.

Neurologic expressions of a subluxation are not always shown by the response the nervous system makes to irritation discernible in the immediate area. It can be an intrinsic source of irritation. Again allow the author to emphasize that this altered state of nerve-fiber threshold and the impulse proper can readily lead to remote dysfunction of sensory, motor, vasomotor, and spinovisceral responses. Possible distal manifestations of vertebral subluxations are shown in Table 1.2.

     Table 1.2. Possible Distal Manifestations of Vertebral Subluxations
  Acroparesthesia                    	Neuralgia and neurodynia
  Angioneurotic edema                	Pain and tenderness
  Cutaneous discolorations           	Cutaneous and subcutaneous
  Cutaneous flushing or pallor       	Deep muscular
  Decreased electrical resistance    	  Somatic
   of skin                           	  Visceral
  Dermatographia                     	  Periosteal
  Fasciculation                      	Postural fatigue
  Formication                        	Abnormal somatospinal reflexes
  Gastrointestinal sphincter spasm   	Abnormal viscerospinal reflexes
   or inefficiency                   	Diaphragmatic dysfunction
  Hyper- or hypo-esthetic areas      	Gait disturbances
  Hyper- or hypo-hidrotic areas      	Lymphatic traction or compression
  Hyper- or hypo-peristalsis         	Mediastinal displacement
  Hyper- or hypo-reflexia            	Nerve traction or compression
  Hyper- or hypo-thermic areas       	Organic displacement
  Hyper- or hypo-tonicity            	Respiratory inhibition
  Hypertrophy or atrophy             	Sustained postural stress
  Increased flare to scratching      	Vasculature traction or compression
  Increased or decreased gastro-     	Visceral support stretching or
   intestinal secretions             	 shortening
  Increased or decreased glandular   	Visceral traction or compression
   secretions                        	Visceroptosis
  Increased or decreased strength    	Proliferation or degeneration
  Local swelling                     	Sluggish movements
  Malcoordination                    	Tics
  Mucous membrane congestion or      	Tingling
   blanching                         	Tremor
  Myocardial spasm or inefficiency

Somatosensory Responses.   Related somatosensory dysfunctions include varying degrees of discomfort and pain, tension, superficial and deep tenderness, periosteal tenderness, hyperesthesia or hypesthesia, haptic sensations, acroparesthesia, formication, flushing, numbness, coldness, and postural fatigue.

Somatomotor Responses.   Related noxious somatomotor reflexes include painful muscle spasms (especially proximal); abnormal muscle tone (from hypotonicity to spasm), weakness, atrophy, or degeneration in long-standing cases; sluggish and uncoordinated movements; paralyses; trigger points; and fasciculations, tics, and tremors.

Visceromotor Responses.   Related abnormal visceromotor responses may be exhibited in several ways. Typical examples include:

  • Dysfunction in the spinovisceral field frequently give rise to visceral smooth-muscle abnormalities, glandular and mucous membrane secretory malfunctions, and sphincter spasms of the detrusor muscles and myocardium when severe.

  • Dysfunctions in the vasomotor field may include angioneurotic edema, vasospasm, flushing or blanching, mucous membrane congestion, urticaria and dermatographia. Changes in the circulation of the skin can sometimes be crudely measured indirectly by various heat sensitive devices, thermography, or infrared photography. Such changes parallel circulatory changes in the deeper tissues as they too are affected by similar vasomotor responses.

  • Alterations in the ability of skin to secrete oils or perspiration can be crudely monitored by various electrical resistance instruments. These secretory errors also may indicate similar changes in deeper visceral tissues. Either hyperhidrosis or dryness, as well as hyperesthesia or hypesthesia, in a local area near the spine signals altered vasomotor activity in the subsequent spinal segment. Hyperesthesia and hyperhidrosis are usually associated with an increased flare (red response) from scratching and a decrease in electrical skin resistance.

  • Alterations in the quality of tissue may result from trophic disturbances such as atrophies, degenerations, thinning or discoloration of the skin, or other changes reflecting viscerotropic abnormalities.

Mechanoreceptor Responses and Reflexes

When kinetic dysfunction occurs (hypermobility, hypomobility) within any joint (spinal or extraspinal), the early significant effects likely to occur are those of proprioceptive irritation or lack of input to the CNS. In the spine, the musculoskeletal tissues (particularly the ligaments and paravertebral/intervertebral muscles) are richly endowed with proprioceptive receptors. Common consequences include:

  • First, when overly stimulated by stretching, these neurons interpret impulses as somatic sensory stimulation that may be perceived as pain. They also send reflexes to their motor components, producing changes within the paravertebral muscles or elsewhere in the soma supplied by the segment.

  • Second, they may be interpreted as viscerosensory stimuli, whose visceromotor responses alter circulatory changes, smooth muscle activity, glandular secretions, or trophic activity in the musculoskeletal tissues or viscera supplied.

It is this ability of the proprioceptive sensory beds to influence motor changes of a somatomotor or visceromotor nature that is perhaps the most universal effect of vertebral subluxation-fixations.

The Posterior Rami

Although the spinal roots as a whole are the major concern in any form of IVF syndrome, posterior rami branches are often involved in minor–moderate musculoskeletal complaints of the posterior neck and thoracic region of the back. The posterior rami turn sharply backward to supply the spinal muscles and skin of the back.

Tenderness and warmth over the rami of the posterior division have particular significance during spinal palpation. Sensory nerve distribution runs in a zone extending from the posterior scalp to the coccygeal area and then laterally to the greater trochanter. See Table 1.3.

     Table 1.3. Distribution of Spinal Nerve Somatic Rami

C1Adjacent muscles, filaments to capsule of atlanto-occipital joint and connections with the anterior branch of C2.
C2The posterior branch supplies and overlying skin, adjacent muscles, and adjacent facet joints. The anterior branch (greater occipital nerve) passes horizontally across the inferior oblique muscle beneath the semispinalis capitis as it transverses vertically and then proceeds within the fascia of the trapezius to the scalp where it divides into numerous twigs that extend as far anterior as the coronal suture. Filaments supply the occipital and superficial temporal arteries. Impulses initiated at the C2 level of the cord in the greater occipital nerve merge with those of the C2 level spinal nucleus of the trigeminal. Thus, this nerve is often involved in suboccipital pain and occipitofrontal headache.
C3The posterior branch supplies overlying skin and superficial musculature. The anterior branch divides with one branch winding around the facets of C3 and another communicating with the greater occipital nerve.
Posterior cervical plexusThis plexus is formed by the posterior rami of C1–C3 and sensed as a mass of neurovascular tissue lying beneath the semispinalis capitis muscle and as such is quite vulnerable to cervical strains, whiplash-type trauma, and subluxation syndromes.
C4–T1Medial branches essentially supply overlying skin and superficial muscles, and the lateral branches essentially supply the deep muscles of the cervical region. As the nerves cross around the faces of the articular masses between the superior and inferior articular facets, these nerves are quite vulnerable to entrapment. The posterior rami of C8 follows a groove in the superior aspect of the 1st rib and is often involved in a cervical rib or scalenus anticus syndrome.
T2–T6The posterior branches of the upper thoracic nerves are accompanied by the posterior arterial branch of the thoracic aorta as they pass posteriorly via an osseofibrous canal located about 2 cm from the midline. A shorter segment lies transversely between the costotransverse ligaments prior to dividing about 2.5 cm from the midline into terminal branches. The medial branches pass medioinferiorly, send twigs to nerves above and below, and supply adjacent muscles, ligaments, and joint capsules. Cutaneous branches must pierce the trapezius (3–4 cm from the midline) and pass laterally to supply the overlying skin. Thus, numerous areas of possible entrapment occur in the course of these nerves.
T7–T12The posterior divisions of the lower thoracic nerves differ somewhat from those of the upper thoracic nerves. The medial branches are essentially muscular and supply the supraspinous and interspinous ligaments, but they have no cutaneous twigs. The larger lateral branches take an oblique course, emerge from the sacrospinalis, and follow the thoracolumbar fascia.
T7–T12, continuedSmall, short trunk sinuvertebral nerves enter the canals and are distributed to the vertebral arches and posterior facets, veins, sheath surrounding the dura matter, and communicate with the sympathetic chain. Thus, these nerves have two components: one from the spinal nerve and the other from the sympathetic chain. The spinal nerve portion arises just lateral to the posterior root ganglion and is often double. The fine sympathetic twigs arise from the rami communicantes.
L1–L5The relatively small posterior division of lumbar nerves splits from the anterior division at almost a right angle as it projects backward and enters the posterior compartment via an osseofibrous tunnel as it forms partnership with other members of the neurovascular bundle. Some branches quickly course medially (about 5 mm from their origin) and divide into a medial branches and lateral branches:

1.   Medial twigs to supply structures around the apophyseal joints such as the multifidus, interspinales, and erector spinae muscles; articular capsules; and the ligamentum flava, interspinous, and supraspinous ligaments. This supply covers an area that extends about 3 cm from the midline. Collaterals extend to communicate with two or more segments above and below.

During their course, the medial fibers become flattened against the osseofibrous tunnel. This tunnel is about 6 mm long and is located at the inferior border of the transverse process at the root of the articular process. Thus, this is a common site of irritation and entrapment in which pain is referred to the tissues supplied.

2.   Lateral limbs course obliquely inferolaterally over the back of the blunt transverse processes and project to supply the muscles lateral to the apophyseal joints and the intertransverse, iliolumbar, lumbosacral, and posterior sacroiliac ligaments.

The lateral branch of the posterior ramus of L5 nerve descends vertically in a groove on the sacral ala just lateral to the S1 articular process to join the lateral branch of S1. The medial branch of L5 curves medially under the lumbosacral apophysis and sends branches medioinferiorly and posterior into the local multifidus muscles and lumbosacral ligaments.

S1–S4These nerves form a plexiform arrangement on the back of the sacrum. The lateral branch of S1 joins with that of L5. The lateral branch of S2 projects downward over the sacrum just lateral to the 3rd and 4th foramina and joins the lateral divisions of S3 and S4. All these nerves lie between the interosseous and overlying sacroiliac ligaments, which are supplied by the lateral branches of the L5–S3 posterior rami. The fine medial branches of S1–S4 supply the multifidus muscle.

Note: Above data adapted with modifications from Bradley.

A few posterior rami intermix branches, but most remain segmental. The anterior rami course ventrally and laterally, entering plexuses or connecting with sympathetic fibers via the rami communicantes, whereafter their specific identity is lost. In the sacral region, the anterior and posterior rami, respectively, exit the bony canal through the anterior and posterior foramina.

Sunderland emphasizes that the passage of cutaneous branches through the muscles and fascia of the back should not be overlooked as potential sites of entrapment. Such entrapment frequently involves the greater occipital nerve and the cutaneous branches of the posterior rami of the L1–L3 nerves.

Tissue Defense

It requires more than an invasion of a pathogenic organism to cause an infectious disease; ie, inadequate tissue resistance and immunologic reserves are also necessary for invading organisms to survive and multiply.

The idea of "improving natural resistance to disease" was at the foundation of many pioneer chiropractic concepts. While allopathy has traditionally emphasized the virulence of the invader, chiropractic has emphasized the resistance of the host. This hypothesis was based primarily on empiric findings by pioneer chiropractors. They were later substantiated considerably by the studies of Zhigalina, Gondienko, Speransky, and others. Studies of the effects of axoplasmic flow interruption have added even greater validity to the chiropractic approach.


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