The spinal dysarthric subluxation may be either a cause or an effect, and the immediate causes may be divided into two major categories: the unequal or asymmetrical muscular efforts upon the joint structures and the inequality in the supporting tissues of a particular joint such as the cartilage, intervertebral disc, ligaments, etc. Some form of internal or external stress is necessary to produce a subluxation to a degree sufficient to cause a state of neurodysfunction.

The general cause-and-effect relationships involved in subluxation complexes are shown in Figure 18.11.

Trauma.   Frank trauma may cause inflammation, degeneration, etc, and particularly the muscular splinting reaction that muscles make when their surrounding tissues are injured. This alters the position and motion of the structural tissues that are related. Sustained microtrauma, though of a less acute nature, may cause a slow continual irritation and eventually create degenerative pathologic changes which similarly alter muscular reaction. The obvious trauma of a fall or blow which surprises a joint with the intrinsic muscles unprepared will cause a joint sprain with ligament injury. A sudden slip during a lift is equally damaging to the unprepared or weak joint. Watkins reminds us that the slower trauma of occupational strain is not as easy to visualize. He reminds us of the game of youth in trying to hold an axe at arms length to the side for 1 minute. Within 2 minutes, the shoulder aches but the big "catch" is at the lumbosacral level in following hours and days.

Postural Distortion Phenomena.   Postural compensations for either mechanical activity or structural changes in the skeleton itself are referred to as postural distortion phenomena. These changes, as well as other causes of subluxation, often result in a series or combination of minor mechanical errors which together may be termed scoliosis, kyphosis, lordosis, distortion, or similar terms. Such a distortion phenomenon is dependent upon the ability of the spine to adjust to any interference in the body's vestibular, visual, or proprioceptive adaptation which is incompatible with the normal balance of the musculoskeletal system to gravity. Whether this structural imbalance creates disturbances or appears asymptomatic is dependent upon the neurological irritation developing within the tissues affected. They may not elicit apparent disturbance at a given time; but, rather, at a later date when they overcome the adaptation and resistance of the individual.

Biochemical Reactions.   The acute or chronic hypo- or hyper-tonicity of musculature may be due to various biochemical changes within the above-mentioned tissues. This may be brought about by foreign bodies, by either local or general pathologies which may cause anoxia, ischemia, toxicity, etc, or by systemic fatigue-producing activities, nutritional deficiencies or excesses, caustic chemical exposure, ingestion of harmful chemicals, inhalation of noxious gases, microorganism toxins, abnormal glandular activity, excessive heat or cold, or electric shock affecting the chemical environment of cells histologically.

Psychomotor Responses.   These responses refer to the reaction of musculature to emotional effects on the nervous system as the body depicts its psychologic stresses. They may be environmentally, socially, or intrinsically initiated.

Paralytic Effects.   Primary disease of the neuromuscular system itself (eg, paralytic diseases) affects musculoskeletal tone and strength, thus affecting position and quality of motion.

Somatic and Visceral Responses.   These responses refer to the secondary reactions of the muscular system to somatic or visceral sensory irritation which may develop elsewhere in a given neurological segment. Our embryologic nature is such that the various components of a given vertebral segment and its ramifications or neuromere may be influenced by sensory stimuli that arise from any tissue supplied by these components. The somatic or visceral sensory neurons that enter into a given neurological segment and cause somatic or visceral motor response may cause a similar response throughout the various ramifications of that segment. This, of course, depends upon certain states of sensitivity or facilitation, certain convergencies or divergencies within the nervous system, and particularly upon the intensity and duration of the initiating stimulation. Therefore, could well be a visceral sensory irritation in the intestinal tract or other viscus that is causing motor changes not only in the internal organs, but also in the vascularity and the musculature of the body. These changes may result in motor alterations in the tone of muscles, consequently resulting in a spasm or splinting action. If long standing, degenerative changes, atonicities brought about by atrophy, contractures, or other pathologic changes within the musculature may develop which can influence the mechanics of the vertebral segment(s) involved.

      Abnormal Structural Support

Mechanical errors in position or motion may also be brought about by structural alterations in the supporting tissues of the joint itself. These in turn may be brought about by:

(1)   Genetic and developmental abnormalities causing asymmetry of the vertebrae, cartilage, muscular structure, etc.
(2)   Various acquired disease processes within the joint such as arthritic degeneration, avascular necrosis, or a neuropathic process that causes the cartilage, bone, ligaments, or musculature to be structurally altered.
(3)   The resolution of macro- or micro-traumas, strains, sprains, or of other primary pathology may cause fibrosis, degeneration, or other retrograde changes of a structural nature within the joints themselves.

These same processes not only develop within the vertebral column and its paravertebral tissues but also in the musculoskeletal tissues of the appendicular skeleton. Thus, similar lesions may exist remote from the spine which perpetuate neuropathic responses by their presence. When the cause is within the structures of the vertebral column, the effects are more evident because of the close anatomical proximities and the functional importance of normal motor-unit motion or integrity to the various components of the nervous system.

      Stress Factors Resulting in Subluxation

Depending on the degree of stress produced, any internal or external stress factor involves the nervous system directly or indirectly, resulting in decreased mobility of the vertebra of the involved neuromere. This decreased mobility may be the result of:

(1)   muscle splinting, especially on the side of greatest stimulation according to Fluger's Law or
(2)   from abnormal weight distribution to the superior facets and other structures of the vertebrae involved. , resulting in decreased mobility of the vertebra of the involved neuromere. This decreased mobility may be the result of:

Fluger's Law states that if a stimulus received by a sensory nerve extends to a motor nerve of the opposite side, contraction occurs only from corresponding muscles; and, if contraction is unequal bilaterally, the stronger contraction always takes place on the side which is stimulated. When affecting one or more vertebrae, this state of decreased mobility of the motor unit encourages nerve dysfunction leading to pathologic processes in the areas supplied by the affected nerve root or neuromere depending upon the degree and chronicity of involvement.

      Indicative Criteria

The importance of a subluxation depends on its clinical features and whether the lesion and its neurogenic responses are affecting the health and performance of the individual to a significant degree. Minor mechanical errors in positions and motion occur in all of us as do consequent neurologic irritations from their effects. We are all subject to environmental irritations and respond to them in a manner that creates errors in musculoskeletal symmetry in the body, resulting in errors of position and mechanics of related anatomic structures. These in turn cause or perpetuate neurologic aberrations of motor reflexes. However, these motor responses may be of a temporary nature for the body is capable of correcting minor mechanical faults within its structure. On the otherhand, certain forms of lesions cannot be corrected without proper professional attention. It is not so much the presence of a subluxation that is significant but how it is affecting the total economy of the body and how involved it is in the production of aberrant neurologic responses and the creation of a state of dysfunction. These effects may be determined by a proper diagnosis and spinal analysis.


Classification of Selected Causes of Spinal Pain:

      Vertebral Causes of Spinal Pain

Pain can be perceived in the vicinity of the spinal column by a number of factors such as:

(1)   mechanical irritation of the nerve roots,
(2)   mechanical irritation of any of the involved pain-sensitive soft tissues,
(3)   edema and vascular distension,
(4)   reflex spasm of the paravertebral muscles,
(5)   chemical irritation of any of the involved pain-sensitive tissues by the effect of inflammatory exudates, (6)   by referred pain from viscera or distant structures, and
(7)   psychic mechanisms.

Typical classes include:

• Traumatic:   eg, dislocation, fracture, sprain, strain, subluxation.

• Infection:   eg, brucellosis, Escherichia coli, staphylococcal, tubercular.

• Developmental:   eg, hypermobility, kyphosis, lordosis, scoliosis, spondylolisthesis, various anomalies.

• Degenerative:   eg, apophyseal osteoarthritis, cauda equina disorders, degenerative disc lesions, hyperostosis, joint instability, nerve root compression, spinal cord diseases.

• Tumor:   eg, carcinoma (secondary), myelomatosis.

• Inflammatory Arthropathy:   eg, ankylosing spondylitis, collagen diseases, fibrositis, focal sepsis, gouty rheumatism, muscular rheumatism, osteochondritis, panniculitis, psoriasis, regional ileitis, Reiter's disease, rheumatoid arthritis, ulcerative colitis.

• Metabolic:   eg, osteomalacia, osteoporosis.

• Systemic:   eg, secondary involvement of primary infection and general disease processes such as actinomycosis, alkaptonuria, blood dyscrasias, brucellosis, cancer, gout, influenza, smallpox, typhoid fever.

• Idiopathic:   eg, Paget's disease, rare bone diseases.

• Miscellaneous:   eg, psychogenic conversion syndromes; iatrogenic causes such as unskilled or illadvised manipulation, myelography, surgery with subsequent adhesions, and poorly fitted or prolonged use of supports.

      Disorders Simulating Spinal Pain

• Cervical Pain:   eg, malignant lymphadenopathy, pancoast tumor, subarachnoid hemorrhage, vertebral artery syndrome.

• Thoracic Pain:   eg, aortic aneurysm, bronchial carcinoma, cardiac enlargement, coronary artery disease, gallbladder disease, herpes zoster, hiatus hernia, lung disease.

• Lumbar Pain:   eg, aortic obstruction, colon carcinoma, disseminated sclerosis, endometriosis, hip disease, pelvic carcinoma, obstruction of iliac arteries, pancreatic carcinoma, peptic ulcer, rectal carcinoma, renal disease, short leg, spinal cord tumor.

• Miscellaneous:   eg, visceral diseases causing referred pain to the spine or pressure erosion; central nervous system diseases such as meningitis, poliomyelitis, syringomyelia, tetanus, spinal subarachoid hemorrhage; psycogenic causes; iatrogenic manifestations.

As a primary concept of chiropractic clinical science, spinal dysarthric subluxations may result in the development of disease states locally within the vertebral motor unit itself or throughout the body. These primary and secondary effects of subluxations may be divided into three major categories:

1. The mechanical effect, motion, and balance of the local segment, or the effect upon the skeleton elsewhere, due to compensatory distortions and alterations as the proprioceptive mechanism would correct its mechanics to the presence of structural imbalance.

2. The effect of any localized condition occurring within the articulations due to interarticular stress and trauma (often microtrauma) such as irritation, inflammation, swelling, necrosis, and degenerative changes.

3. The neurologic effects of subluxation effects may be grossly differentiated as nerve pressure, nerve stretch, nerve torsion, circulatory changes, meningeal irritations, cerebrospinal fluid flow alterations, alterations of proprioceptive responses and reflexes, traumatic insult to the rami communicantes or sympathetic ganglia, etc. Neurologic effects are undoubtedly the more important of the three.

Many spinal subluxations have more than one immediate cause and effect. Therefore, a complicated far-reaching series of interacting and interdependent changes occur which may be designated as a subluxation syndrome. As a cause-effect interrelationship, it is hypothesized that, once initiated, this biomechanical impropriety becomes an etiologic "vicious cycle" from cause to effect and from effect back to cause which, if not interrupted by corrective effort, will carry on to an ultimate and perhaps fatal conclusion.

      Structural Alterations

The primary physical and mechanical factors that often negatively influence the body are gravity, pressure, weight load, inertia, compression, elasticity, leverage, movement, stretch, expansion, and contraction. With these forces in mind, a subluxation may be grossly determined by its structural alterations and manifestations. For example:

Postural Analysis.   Postural faults, which may be either the cause or result of vertebral subluxations, are readily visualized in postural analysis. Pressure or stretching stress of viscera leads to disturbed visceral function and abnormal reflexes. Abnormal body mechanics affecting the thoracic and abdominal cavities interfere with normal function by:

(1)   abnormal efferent visceral stimuli reaching organs from the faciliated segment,
(2)   abnormal tensions and stretching of visceral supports, nerves, blood and lymph vessels,
(3)   venous pooling as the result of inactivity, diaphragm dysfunction, organ displacement, and sustained postural stress, or
(4)   abnormal vasomotor impulses to blood vessels. Blocking stress or irritation of blood vessels leads to ischemia or congestion. There are many general effects to the body as a whole besides these local effects because each abnormal stress results in abnormal discharges of afferent impulses to the central nervous system with consequent hormonal reactions systemic in character. Also considered must be the associated emotional stress as the result of the local stress which contributes to the clinical picture.

Physical Examination.   Palpable alterations in the normal anatomic relationships of one joint to another are frequently found. These mechanical changes may occur in the static recumbent, sitting, or standing positions, or in various ranges of motion as the segments and their supporting tissues are put through either active or passive positions of motion. Subluxations are also evident by the presence of certain objective or subjective signs and symptoms when the joint and tissues are put through certain kinetic or orthopedic tests. Stress, strain, and sprain at the area of the zygapophyses and the attending inflammatory reaction may give rise to a radiculitis of moderate disposition.

Mechanical spinal disturbances can adversely affect the body in a number of ways such as:

(1)   load stress on muscles leading to hypertrophy or atrophy and alterations of local muscle strength,
(2)   leverage stress at joints leading to weakness or sprain of ligaments, articular and intra-articular cartilage damage, and synovitis, and
(3)   compression stress or irritation of nerves leading to increase or decrease of conduction with consequent trophic changes.

Roentgenology.   Subluxations visualized on x-ray films exist as disrelationships in the normal structural relationship of one joint to another. This may not be evident in a given view, but in the view best depicting the mechanical fault. Sometimes they may only be evident on views when an area is put through various positions of motion. Compression stress on bone leads to sclerosis or alteration of its normal shape and internal architecture, and pressure stress on connective tissues leads to thickening or thinning. Combinations of factors influence cartilage degeneration such as severe isolated or repeated minor trauma, chronic mechanical stress or tension, local circulatory excesses or deficiencies, idiopathic biochemical factors, developmental anomalies or malformations, nutritional factors, and the inherited cellular quality of the cartilage.

Criteria.   Such structural faults are not, of course, the major criteria upon which a subluxation's presence and importance are based for the body is able to adapt to structural faults and diminish their influences upon it. Consequently, the signs and symptoms of neuropathic processes are more significant than the structural alterations. The major importance is not the positional relationship of osseous segments, but the significance of soft-tissue and functional changes that are causing or are affected by the alteration. The position of the segment is important because it suggests or reflects changes in the neuromusculoskeletal and visceral systems.

      Events at the Interverterbral Foramen

There are 115 diarthroses within the spine and pelvis vulnerable to the "off centering fixation" of subluxation. Each of these articulations is an organ of proprioceptive sensitivity which under articular strain is insulted and provoked to express pain. As mentioned, a working hypothesis regarding spinal dysarthrias is that the vertebral displacement fixation causes adjacent areas of the spine to become hypermobile, resulting in stress of adjacent motor units. Neurologic feedback may causes the elicitation of ACTH and a resulting increase in the production of corticosteroids as an adaptative mechanism, according to the Hans Selye stress syndrome, and this may also be reflected by possible blood sugar changes.

Contents of the Intervertebral Foramen.   Each foramen is dynamic: widening and expanding with spinal motion, serving as a channel for nerve and vascular egress and ingress, and allowing compression and expansion of the lipoareolar bed. The following structures are usually found in the IVF: anterior and motor nerve root, posterior or sensory nerve root, part of the dorsal nerve root ganglion, recurrent meningeal nerve, spinal ramus artery, intervertebral vein, lymphatic vessels, nervi nervorum, nervi vasorum, vaso vasorum, and vaso nervorum.

Factors Which Change the Diameter of the IVF.   In review, the factors modifying the diameters of the IVFs are

(1)   the disrelation of subluxation,
(2)   changes in the normal curves 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 articulations.

Consequences of IVF Diameter Alteration.   These factors mitigate the viable contents of the IVF and subject its contents to physiologic compromise which results in nerve root pressure, traction or torque, constriction of the spinal blood vessels, intraforaminal and paraforaminal edema, induration and sclerosing of the periarticular ligaments with incarcerating insult upon the contained receptors, forcing of the foraminal contents into protracted constriction and altered position, and such other consequences.

Effects of Microtrauma.   Initially, subluxation is attended by the following aspects of microtrauma:

(1)   minute hemorrhage, transudation, and arterial-venous stagnation from the sluggish circulatory flow as the result of the motor unit's decreased mobility and arterial backup,
(2)   para-articular and paraforaminal traumatic edema,
(3)   eccentric compression stress upon the intervertebral disc and the zygapophyseal cartilages,
(4)   possible separation of minute fasciculi of the retaining fibers of the annulus, 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 as they attach to the lining periosteum of the IVF.

In consequence, the following pathological changes occur:

(1)   Extravasation and edema, along with the precipitation of fibrinogen into fibrin, result in interfascicular, forminal, and articular adhesions that restrict fascicular glide, ingress and egress of the foraminal contents, and the competent motoricity of the vertebral segment within its articular bed.
(2)   Whenever there is extravasation, mineral salts are precipitated and infiltration and sclerosing result.
(3)   Binding adhesions may develop between the dural root sleeves and the nerve roots within the inter-radicular foramen and between the spinal nerve root sheath and the inner margins of the IVF.
(4)   When subjected to microtrauma, mesenchymal connective tissue undergoes a relative rapid and extensive degenerative change with loss of functional integrity and substance.

Altered Nerve Root Level.   Induced disrelation between level and direction of nerve root origin (spinal cord) and nerve root exit (IVF) is an important factor. Whenever there is subluxation, change in normal curves, or presence of abnormal curves, the relative levels of points of nerve root origin and exit are altered. Hence, the position, direction, and course of the nerve roots and trunk within the IVF become abnormal. Compression or irritation is thus more likely. In addition, a vertebral column affected with partial fixation of several segments when subjected to flexion, extension, and circumduction efforts will be attended by marked tension upon the dural root sleeves and the related spinal nerve radicles, especially the cauda equina.

Proprioceptive Responses and Reflexes.   Perhaps the most significant effect is that of proprioceptive irritation. The musculoskeletal tissues and particularly the ligaments and paravertebral or intervertebral musculature of the spine are endowed with proprioceptive neurons. First, when overly stimulated by stretching, these neurons interpret the stimuli as somatic sensory stimulation which may be perceived as pain. Second, they may also send reflexes to their motor components and cause muscular changes within the paravertebral muscles or elsewhere in the soma supplied by the segment. Third, they may be interpreted as visceral sensory stimuli, whose visceral motor response alters circulatory changes, smooth muscle activity, glandular secretions, or trophic activity in the musculoskeletal tissues or viscera supplied by a given neurologic segment or within the cord itself. It is this vast ability of the proprioceptive sensory beds to influence motor changes, both of a somatic-motor or visceral-motor nature, that is perhaps the most universal effect of vertebral subluxation.

Intraneural Effects.   It is probable that any interference with or abnormality of:

(1)   the interstitial fluids in which the nerves lie and/or
(2)   the intracellular fluid of the nerve itself in the nerve axoplasm will cause a breakdown of the sodium pump mechanism which will prevent the normal flow of impulses along the nerve fibers concerned. These abnormal impulses refer to an overaction or underaction in the rate of impulse frequency along a nerve. Once a threshold stimulus has been reached, a nerve will fire in accordance with the all-or-none law.

Circulatory Changes.   Decreased mobility (vertebral fixation) of a motor unit within its normal physiologic range of movement causes sluggish circulatory lymphatic or vascular supply may be influenced by mechanical pressure therefore causing chemical or physical changes within tissues such as anoxia, toxicity, swelling, edema, etc, and the consequent derangement of normal function brought about by these metabolic disorders. Local irritation at the site of misalignment and hypomotoricity causes an inflammatory reaction with edema leading to a disturbance in 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 as a result of acid leaking from the surrounding hypertonic musculature.

Local Toxicity Effects.   The venous stagnation from arterial backup produces a local toxicity. 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 emitting from the involved area will be deficient in necessary nutrients and quite possibly hypoxic as well. The buildup of metabolic waste products in the area of the IVF, may also alter the normal pH of local fluids causing a breakdown of Krebb's cycle, due to decreased oxygen and toxicity, which causes a partial breakdown of the sodium pump mechanism, resulting in an ionic imbalance. As the sodium pump can no longer maintain a normal ionic balance, ionic imbalance results in some degree of erratic nerve conduction and edema in the tissues of the immediate area. This erratic nerve conduction may be exhibited in all nerves passing through the involved IVF and immediate area. When toxicity occurs in the central and peripheral nervous systems, the formation of acetylcholine at the level of involvement will be interferred with and result in further disturbances due to increased nerve conduction impairment. This situation along with the toxicity effects upon the nerve may well result in a disorder in membrane permeability leading to dysfunction.

Ganglion Irritation/Compression.   Irritation/compression of the dorsal root ganglion may be a factor. The general sensory dorsal root ganglion of each spinal nerve lies within the upper medial aspect of the IVF. Whenever its position is altered or the diameters of positions of the IVF are modified, the ganglion may be subject to compression and irritation. For example, an acute whiplash-like mishap to the cervical spine, especially of the hyperextension type, may force the vagus and the superior cervical sympathetic ganglion against the transverse processes of the atlas and axis, provoking the bizarre autonomic reactions that not uncommonly attend this condition.

Meningeal Irritations.   Mechanical errors in motion and position may cause tractional effects upon the meningeal coverings of the cord or dural-root sleeves which may produce mechanical pressure upon the neurons emitting from the cord itself. These may, therefore, cause the elicitation of abnormal neurologic motor effects or sensory interpretations.

Cerebrospinal Fluid Flow Alterations.   These refer to the mechanical effect upon the flow of cerebral spinal fluid within the central nervous system and perhaps within the peripheral nerves themselves. Cerebrospinal fluid stagnation possibly occurs in association because of the intimate relationship between spinal fluid and venoid blood, contributing to toxicity in the nerve root area. According to some researchers, minute pressure on meninges alter the mechanics or flow of cerebrospinal fluid and interfere with its ability to remove wastes and provide nutritional substances to the cord and nervous system. This may be either the effect of direct mechanical pressure or impairment of motion necessary for proper inflow and outflow of this nutrient material.

Paraforaminal Adhesions.   Paraforaminal adhesions in consequence to stress and traumatic edema often result in a painful restriction of the normal back-and-forth glide (1/4 to 1/3 inch) of the nerve root within the IVF. Symptoms simulate a low-grade radiculitis: increased pain on movement, straining, and stretching; pain on changing positions and when placing the involved part in extension.

Care must be taken in the differential diagnosis of visceral disease and referred pain from somatic structures on the basis of pain and muscle rigidity alone. Often, the referred symptoms from lesions in widely separated groups of structures can be almost identical. The symptoms of many diseases can be mimicked by spinal lesions, and vice versa. A complete case history and clinical examination is required to rule out these possible conditions or determine their relationship with a subluxation syndrome.

All subluxations do not show all the neurological and structural features that have been discussed, and the profession has found that all the causes and effects of a subluxation syndrome are not of equal significance. Structural alterations and neurologic effects may arise from specific segments and/or musculoskeletal lesions that are, in turn, mechanically altered by errors in position or motion elsewhere in the musculoskeletal system. Major subluxations are often found to be specific positional errors which originate from alterations in the integrity of the structural supporting tissues of the joint itself. As such, they are beyond the capacities of the muscular system to correct by its own functional adaptations.

      Potential and Scope of Reactions

Whenever abnormal function is manifested clinically, it can be assured that some degree of pathology is present. Changes may manifest not only in adjacent parts but also in areas far remote from the site of irritation. If an intrinsically irreversible change occurs at any point as a result of local irritation, the result is a degree of loss of a particular function plus the establishment of new pathological excitations which draw other parts into the pathologic process. In the nervous system, "localization of effect" does not exist. This is not to say that every active means of producing a transformation of the normal nervous state will be reflected in the same manner in the various pathologic progressions because the neurologic element is highly complex in its manifestations.

When the neurologic element is disturbed, symptoms and signs display themselves in those tissues and functions most predisposed and vulnerable. The agents that serve to maintain life stimuli and harmonize the forces between the internal and external environments are the:

(1)   skin,
(2)   musculoskeletal proprioceptor bed, and
(3)   special senses.

Any unfavorable impression upon these three sensor systems provokes somatic and visceral syndromes to some degree, and vice versa. The vital organs are also concerned with harmonizing internal and external environments by the shifting of blood from periphery to center and reverse under varying conditions; ie, visceral disturbances affect somatic structures.

During its function, the nerve impulse creates a multitude of cellular reactions and responses in addition to those of even the most intricate, subtle, and variable sensations and motor activities. Once this is appreciated, we must add the complexities of trophic effects, neuroendocrine interrelations, biochemical affinities, proprioceptive buildup, summation increments, facilitation patterns, the input of the ascending and descending reticular activating mechanisms, genetic neurologic diatheses, synaptic overlaps, demoralization and disintegration of synaptic thresholds, the neurologic spread and buildup, reflex instability, predisposition to sensorial aberrations, undue cerebrovisceral or viscerocerebral inter-reactions, psychosomatic overtones, and those many phenomena that science is only beginning to appreciate or are beyond our present understanding. This underscores the fact that the quality of nerve function relates directly or indirectly to practically every bodily function and contributes significantly to the beginning of physiologic malfunction and the development of pathologic processes.

      The Neurodysthrophic Processes

Disease is a byproduct of the interaction of irritants, forces, and processes both within and without the patient, and all these factors have their influence of the patient's total adaptation. However, these factors are not all equal in their importance in a given patient, and a differential diagnosis is necessary to qualify which are of paramount importance in an individual case.

Predisposition to malfunction and disease is created by definite combinations of internal nervous relations and not merely by an undermining of the general state of health. Present clinical state-of-the-art holds that any nerve point, including the peripheral nerve structures, may become the initiator of neurodystrophic processes and serve as a temporary or permanent originator of such processes. Speransky states that neurodystrophic processes are not confined to a limited sphere, they enter into the composition of all pathologic processes without exception, are not separable from them, and consequently, do not constitute and cannot constitute a separate chapter in pathology. Pathologist Boyd boldly states, "Disease is function gone wrong".

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