Sequential Development of the Neuropathy

Arterial, Venous, and Nervous Systems

Chiropractic theory equates any deviation in mechanical co-ordination of physical movement between spinal segments as evidence of a functional derangement of primary importance in any disease process.

In order to understand the new objectives of a chiropractic analysis, it will be necessary to define the role of physiological indicators in the diagnosis of a localized neuropathy and posit the classification of forms of neuropathy. This will enable us to present the hypotheses of the mechanics of the disease process as it might appear in classic form.

Definitions of the following types are not intended to be so wide as to embrace variations which admittedly occur outside such theoretical classification. They are intended only to aid the reader in understanding the underlying principles.

Through the full spectrum of functional derangement, from simple fatigue at one extreme, to advanced degenerative diseases at the other extreme, there is one common denominator – neural interpretation of stress of cellular activity, either structural or functional, via direct or indirect communication.

The nervous system, acting in its capacity as coordinator of all functional activity, exhibits a high degree of adaptability to a wide range of micro-trauma or physical insult to its integrity. It is of interest here to attempt only a classification of the events which follow the stress-insult of injury which exceeds the normal adaptative capacity of such functional integrity.

Two mechanisms of neural control – vasomotor control of thermal regulation and spatial or positional orientation of spinal movement – are used as indicators of the efficiency of adaptation to stress. Both mechanisms have been part of the chiropractic diagnostic armamentaria since its inception. The state-of-art has steadily progressed, and present evaluation is a continuum of earlier explorations.

The degree to which each of these systems of neural control is capable of producing a uniform and appropriate response to thermal and mechanical stress stimuli is known to be indicative of the progression or regression of any disease process.

Using these mechanisms as isolated examples, a sequence of events can be described which may follow a stress-insult of injury. These events have been evaluated in the past decade from clinical data.

It must be understood that it is only for academic reasons that there is justification to try to divide or isolate nerve circuits according to the functions which they perform. At no time is it permissible to speak of independent nerve circuit action, since the basic function of neural control is total integration of all functional activities.

Classification of the forms of neuropathy of segmental reflex mechanisms can be made according to type and kind of resultant dysfunction of elements controlled by such mechanisms.

Three major divisions of “stress-insult” may be identified;

1. Micro-trauma of cellular tissue (as opposed to nervous tissue). The injury of stress damages tissue beyond its capacity for the immediate recovery of its bio-chemical equilibrium, and this requires time for repair. Neural control “recognizes” such injury by reducing functional demands and initiating responses which set the organism on “guard” against future exposure to new trauma, i.e., local inflammation.

2. Trauma extensive enough to damage nerve endings. Injury to nerve tissue is of far greater significance than injury to any other type of tissue as it has the potential capacity to modify the neural image of appropriate control of functions which are contained within the nerve circuits with which it is connected, for example, the entire neuromere. Whether or not a given injury will produce a neuropathic change in nervous function appears to be dependent on the following:

(a) The order of prime importance of the function under control of the neural network containing the injured elements.

(b) The degree of dependency on summation between inter-segmental links of a given reflex mechanism necessary to produce co-ordinated impulse

characterization.

(c) The number of fibers affected in the injury.

The probability of the neural elements degenerating sufficiently to establish a neuropathic behavior can be estimated by consideration of these three factors.

3. Referred, or second-order trauma.

In so far as every hypothetically discrete neural reflex mechanism is in reality interrelated and interdependent with other reflex mechanisms, traumatic dysfunction in one zone will result in some degree of aberration in associated zones. The degree of aberration will depend on the strength of association and this will be symptomatically interpreted in hyper- or hypo-function, depending on the innate nature of the individual mechanisms to stimulate or inhibit.

Micro-trauma, the first classification, could, under different circumstances, be included within the normal range of adaptation. However, it is listed as the first phase of a neuropathology for the obvious reason that in most instances a stress episode is composed of a series of injurious events occurring almost simultaneously. Placing the organism on “guard” therefore, only acts to set the stage on which the neuropathy can develop; locating the neural components on centre stage, so to speak, in a manner which makes such components extremely vulnerable to injury.

As noted in number two above – local nerve trauma – the primacy of the function under control is an important factor in the consideration of the probability of establishing a neuropathy in a reflex mechanism. In the emergency type reactions to stress, either localized or general, primary functions (such as vasomotor control of blood volume and distribution, tone of digestive tract, secretion of hormones, conversion of stored energy, and the increase of sensory and motor responsiveness) dominate the neurological scene increasing the probability of their being injured by subsequent stress factors.

It is imperative that the reader be able to distinguish the difference between the deviation in function as classified in number one and number three (local or distant) above, and number two. Number one and number three in reality, represent only a restriction or incoordination of neural activity. Number two represents the distinct loss of functional identification and control of peripheral tissues, all of which results from cellular damage of a neural control mechanism.

A distortion of the neural imagery contained within a nerve circuit will be shown to exhibit the capacity to exist as a separate and distinct entity in comparison to its previous integration with associated networks. Peripheral manifestation of its existence is always observed as a complete dissociation between the neural mechanism and the cellular elements normally under its control. We will demonstrate that this becomes the self perpetuating vicious cycle – with or without the local subluxation within the cycle.

Regardless of the manner in which it was set into motion (thermal, mechanical or chemical stress) the segmental neuropathy, once established becomes self-supporting in the sense that the initiating factor need not remain as part of the abnormality for the process to continue to exist and extend itself.

Such a peculiar characteristic behavior defies any explanation based on old concepts; explanations which are still in vogue today to describe this type of neuropathy. The popular concept of nerve “lesion” as used in orthodox medicine, or nerve pressure, once commonly used in chiropractic to explain dysfunction of a motor unit as muscular activity for example, more aptly defines the “side effects” of normal neural components to abnormal stress. They have been forced into extremes of functional adaptation simply by being in contact with the neuropathy. Continuous strain is imposed onto these associated networks until a new conditioned reflex of the total complex is impressed as a new behavior pattern upon the central nervous system.

Deviation from the normal range of neural co-ordination usually results in a diminution of control of respective functions. It is as though the nerve networks become insensitive to fine increments of functional changes under their control. The total process – the neuropathic element, and constellation of associated aberrant neural mechanisms – progresses toward higher degrees of abnormality or regresses to dissolution and return to normal depending on the degree of strain produced on the organism and the inherent ability of its adaptation.

Early in the development of chiropractic it was as difficult to explain clinical successes as it was to explain clinical failures, because the theories were based on orthodox concepts of neurology and pathology.

Orthodoxy denies the existence of a qualitative factor superimposed on the quantitative response of a neuron to a given stimulus. Yet clinical evidence illustrates the role of deranged neural function in the eventual debility of any organ or tissue. In the eighteenth century, researchers recognized that a damaged or injured nerve element was potentially more dangerous, from the standpoint of ultimately producing degeneration and pathologies in the tissues supplied by the nerve, than complete severance or immediate destruction of the nerve. Although a qualitative tone to the impulse would aid in explaining neural interpretation of varying stimuli, qualitative characteristics have not been observed through experimentation. While measurements are not yet fine enough to prove such a conjecture it is the present belief that qualitative characteristics are an inherent property of all neural activity. It is this factor which ultimately brings to reflex neural control an image of the cellular behavior of the tissues in which most nerve fibres terminate at the periphery.

As cellular bio-physical and bio-chemical behavior moves through the entire spectrum of processes concerned with its normal adaptability to stimuli, the tone of neural response (to stimuli for which it is specifically sensitive) is modified. A graded variance of neural tone could be estimated to affect the conduction velocity of the impulse. It is reasonable to suppose that the conduction velocity of impulse transmission would reach its highest value at the center of the spectrum of cellular activity wherein optimum physical and chemical equilibrium exists. Above or below this optimum it is equally reasonable to suggest that the conduction velocity will diminish in decrements to a base value. It is probable that one of the reasons that such changes in conduction velocity nave not been observed, is due to the fact that stress associated in the methods of experimentation have reduced the elements to this base value.

For our purpose it is sufficient to use the antidromic impulse associated in the vasomotor control of dilatation of blood vessels in the skin as a model which quite adequately describes the neural capability of qualitative action. The neural mechanism of motor-receptor units, designed to control function, has, in addition to “memory” of the appropriate response to specific demands, an impressed image of the cellular physio-chemical characteristics peculiar to the specific tissues involved in the given function.

The biological integrity of any tissue is identified through its cellular response to the command of the nerve impulse. It is, in effect, controlled by the specificity of that impulse which is created and generated by neural elements containing the image of that tissue.

Final decision on the validity of this hypothesis must at this time be left to the future. It is more important to satisfy the purpose of establishing this concept – to give meaning to chiropractic principle and a better understanding of its clinical application. Having described the neuropathy of any neural mechanism as the primary locus for deranged function there remains only a need for description of the role of such a neuropathy in pathology.

In 350 B.C. Aristotle considered the warmth of the body to emanate from the heart. Fever then resulted from an abnormal heart action. In 1648 vital spirits were cited as the cause. About 1773 friction of the blood was named. That the central nervous system was an influencing factor was not discovered until 1852 when the vasomotor control mechanism of thermoregulation was described. Fever is accepted today as resulting from the “setting” of the human thermostat in the brain at a higher value, adjusting vasomotor function accordingly. There still remains the question as to why the thermostat behaves in this manner. Reasons are advanced that a fever state is a natural defense mechanism in combating infection. Others wonder at the role of toxins circulating in the blood stream as possibly being the contributing factor deranging the central control of thermoregulation.

From our foregoing definition of the form of neuropathy observed on segmental levels of the spinal cord, one must now recognize clinical evidence of generalized hypertension of the small arteries of the skin, and relative hypo-tension of the superficial capillary bed in fever states as exhibiting the same type of behavior as seen in the segmental derangement. That fever is associated with infectious diseases, toxemias etc., cannot refute the primacy of the neural involvement as being a first order of pathological events. This neural involvement only identifies the bacteria or toxin as a nerve irritant or as an element in the advanced stages of a pathological process which has expanded unobserved through successive stages of debilitating associated neural mechanisms concerned in the process of immunity. The bacterium, virus or toxin “invades” the organism and a “battle” between organism and invader ensues. The presence of an “invader” and the pathological forms which the “battle” may take are valuable only as indicators of the course and development of the final stages of the pathological process, (the debilitation of neural control). If there is an “invader” it is the original segmental neuropathy. If there is a “battle” between organism and invader it is a battle fought deep within the nervous system between the original neuropathy and “healthy” associated neural mechanisms of control. The appearance of the microbe only testifies to the fact that the original neuropathy was successful in debilitating associated healthy mechanisms, thus extending its influence throughout the nervous system to involve the processes of immunity.

Just as fever and the microbe are indicators of the extension of the neuropathy throughout the nervous system, similarly, symptomatology of all other functional derangements or pathologies can now be viewed as indicators of neurological aberration. Classification of symptoms into diseases would serve a more worthwhile purpose if such classification was directed toward the evaluation of the particular course of development which the neuropathy was taking in its extension into associated fields of neural control.