Dr. Fred Clary's Functional Analysis Chiropractic Technique

Atlas vertebra realignment and achievement of arterial pressure goal in hypertensive patients: a pilot study.

Bakris G,
Dickholtz M,
Meyer PM,
Kravitz G,
Avery E,
Miller M,
Brown J,
Woodfield C,
Bell B.

1Department of Preventive Medicine, Rush University Hypertension Center, Chicago, IL, USA.

Anatomical abnormalities of the cervical spine at the level of the Atlas vertebra are associated with relative ischaemia of the brainstem circulation and increased blood pressure (BP). Manual correction of this mal-alignment has been associated with reduced arterial pressure. This pilot study tests the hypothesis that correcting mal-alignment of the Atlas vertebra reduces and maintains a lower BP. Using a double blind, placebo-controlled design at a single center, 50 drug naive (n=26) or washed out (n=24) patients with Stage 1 hypertension were randomized to receive a National Upper Cervical Chiropractic (NUCCA) procedure or a sham procedure. Patients received no antihypertensive meds during the 8-week study duration. The primary end point was changed in systolic and diastolic BP comparing baseline and week 8, with a 90% power to detect an 8/5 mm Hg difference at week 8 over the placebo group. The study cohort had a mean age 52.7+/-9.6 years, consisted of 70% males. At week 8, there were differences in systolic BP (-17+/-9 mm Hg, NUCCA versus -3+/-11 mm Hg, placebo; P<0.0001) and diastolic BP (-10+/-11 mm Hg, NUCCA versus -2+/-7 mm Hg; P=0.002). Lateral displacement of Atlas vertebra (1.0, baseline versus 0.04 degrees week 8, NUCCA versus 0.6, baseline versus 0.5 degrees , placebo; P=0.002). Heart rate was not reduced in the NUCCA group (-0.3 beats per minute, NUCCA, versus 0.5 beats per minute, placebo). No adverse effects were recorded.

We conclude that restoration of Atlas alignment is associated with marked and sustained reductions in BP similar to the use of two-drug combination therapy.

Journal of Human Hypertension advance online publication, 25 January 2007; doi:10.1038/sj.jhh.1002133.

Hyperventilation Syndrome: A Diagnosis Begging for Recognition


GREGORY J. MAGARIAN MD; DEBORAH A. MIDDAUGH MD, and DOUGLAS H. LINZ MD, Portland
Topics in Primary Care Medicine


"Topics in Primary Care Medicine" presents articles on common diagnostic or therapeutic problems encountered in primary care practice. Physicians interested in contributing to the series are encouraged to contact the series' editors. --BERNARD LO, MD, STEPHEN J. McPHEE, MD Series' Editors


Refer to: Magarian G J, Middaugh DA, Linz DH: Hyperventilation syndrome: A diagnosis begging for recognition (Topics in Primary Care Medicine). West J Med 1983 May; 138:733-736. From Ambulatory Care and Medical Services, Veterans Administration Medical Center, and the Division of General Medicine, Department of Medicine, Oregon Health Sciences University, Portland. Supported in part by HEW grant No. 1-028-PE10051-02. Reprint requests to Gregory J. Magarian, MD, Ambulatory Care Service (llC), Veterans Administration Medical Center, Portland, OR 97207.



Beginning with the American Civil War, military physicians seeing soldiers under the stress of combat have described a syndrome characterized by breathlessness, lightheadedness or dizziness, pronounced fatigue and exercise intolerance, numbness and paresthesias and chest pain. Rarely have organic diseases been found to account for the symptoms in such cases, yet despite reassurance, symptoms commonly persist for prolonged periods despite removal from the apparent stress setting. This syndrome has been given many names including irritable heart, soldier's heart, Da Costa's syndrome, effort syndrome, neurocirculatory asthenia and, more recently, hyperventilation syndrome.

Since the original descriptions in soldiers, it is now recognized that hyperventilation occurs in many persons under stresses of daily living. It is manifest not only in those overtly stressed, anxious and depressed but also in those who appear outwardly calm as they "bottle up" their feelings, often because of undeveloped or lack of acceptable emotional outlets. Physicians and lay persons alike readily recognize acute hyperventilatory attacks occurring under acute stress. However, chronic or recurrent hyperventilation problems often are unrecognized probably for a variety of reasons, including the frequent lack of obvious overbreathing, a tendency to focus on one or two complaints that alone are not particularly suggestive of hyperventilation, minimal discussion of the topic in medical school and cursory coverage in medical textbooks.

Physiology of Hyperventilation Although precise delineation of the relationship between physiologic responses and symptoms of hyperventilation is lacking, an understanding of known physiologic mechanisms does provide insight (Table 1). Hypocapnea and respiratory alkalosis develop rapidly upon onset of hyperventilation and can easily be maintained indefinitely, by nearly imperceptible hyperventilation, such as by taking an occasional deep breath while maintaining a normal respiratory rate. Without knowing this, physicians may directly observe the subtle, chronic form of hyperventilation without recognizing it or, upon considering the diagnosis, inappropriately reject it because the anticipated hyperventilatory respiratory pattern is not present.

TABLE 1.--Physiologic Responses Associated With HyperventilationHypocapnic, respiratory alkalosisHyperadrenergic state Increased oxygen binding to hemoglobin (Bohr effect) Hypophosphatemia Initial vasodilatory, later vasoconstrictive cardiovascular responses Reduced cerebral perfusion Possible coronary vasospasm

Stress is often associated with a hyperadrenergic state that is known to provoke hyperventilatory responses in humans. Beta-blocking drugs may reduce not only stress levels but also ventilatory responses to catecholamine stimulation and have recently been shown to improve performance levels in stressful situations.

Respiratory alkalosis increases the avidity of oxygen binding to hemoglobin such that oxygen becomes less readily released to tissues (the Bohr effect). Hypophosphatemia develops rapidly and persists for the duration of respiratory alkalosis, probably related to intracellular shifts of phosphorus. With persistent hyperventitation, hypophosphatemia would impair generation of 2,3-diphosphoglycerate (2,3- DPG), further reducing oxygen availability for tissue utilization.
It is estimated that a 2 percent reduction in cerebral blood flow occurs for every decline of 1 mm of mercury in arterial carbon dioxide tension. This, along with the Bohr effect, leads to reduced cerebral oxygenation. Cerebral hypoxia, however, produces a vasodilatory response that may compensate for the initial reduction in cerebral perfusion.

Cardiovascular responses are variable and seem to be in large part related to the duration of hyperventilation. The initial response is a reduction in systemic vascular resistance and blood pressure with an increase in heart rate and cardiac output. Within four to seven minutes of sustained hyperventilation, however, this response diminishes or disappears.

Finally, several investigators have shown coronary vasoconstriction induced by hyperventilation in some patients with Prinzmetal's angina and others with fixed coronary occlusive disease.
PathogenesisHow does the hyperventilation syndrome develop? Although hyperventilation may have organic or physiologic causes, the syndrome of hyperventilation is usually associated with emotional triggers and thoracic breathing tendency. Indeed, many persons who are anxiety-laden, stressed or depressed have hyperventilatory breathing patterns and complain of their inability to obtain satisfying deep breaths. Anxiety, anger and other emotions produce increases in both rate and depth of respirations probably mediated by a hyperadrenergic state. Once hyperventilation is initiated, persisting stresses of everyday living or the stresses of new bothersome symptoms from hyperventilation create the potential for a self- perpetuating cycle of chronic hyperventilation (Figure 1 ). Persons who hyperventilate more commonly exhibit obsessional behavior, excessive body consciousness, phobias, feelings of inadequacy and maladjustments in many stages of life. Lum believes that an exaggerated tendency to breathe using thoracic musculature is an important factor allowing for the development and, once developed, the persistence of the hyperventilatien syndrome.

Symptoms and Signs of Hyperventilation SyndromeAmong the most difficult and frustrating. patients for physicians are those with multiple complaints involving many organ systems who, despite seeing numerous physicians, fail to obtain a satisfactory explanation or relief from their symptoms. They often have a "positive review of systems." After numerous physicians have been seen and multiple diagnostic tests have been done, which have excluded organic disorders, such patients are often dismissed as having nothing wrong with them or having a severe neurosis, anxiety, depression, hypochondriasis or hysteria, despite the persistence of symptoms that may be disabling in their work and other aspects of everyday living. Unfortunately, this scenario continues to be a common occurrence and is the frequent setting in which the hyperventilation syndrome is recognized, months or years after its onset. Previous studies have shown that 5 percent to 10 percent of patients seeking care from primary care physicians have at least some complaints related to hyperventilation.

TABLE 2.--Signs and Symptoms of Hyperventilation SyndromeGENERAL Weakness, fatigue, sleep disturbances, blurred vision

PSYCHIATRIC Anxiety, depression, phobias, feeling far away, sensations of unreality
NEUROLOGIC Paresthesias in extremities or periorally, lightheadedness, dizziness, disorientation, impaired thinking, seizures, syncope, headaches
CARDIOLOGIC Palpitations, chest pain
RESPIRATORY Dyspnea often without provocation characterized as being unable to take a satisfying deep inspiration, exaggerated thoracic breathing, sighing, yawning
GASTROINTESTINAL Dry mouth, bloating, belching, flatulence
MUSCULAR Cramping, spasm, musculoskeletal chest wall pain (chest wall syndrome)

The hyperventilation syndrome may be associated with a myriad of symptoms (Table 2), affecting both men and women equally. The most frequent complaints for which medical attention is sought are lightheadedness or dizziness, dyspnea and chest pain. Substantial weakness, exercise intolerance, fatigue and peripheral or perioral numbness and tingling, occurring in isolation or in concert with other hyperventilatory symptoms, are almost always present. Many patients have multiple other complaints. When symptoms are taken in isolation, the syndrome is often not considered. However, when taken together, the entire symptom complex often makes the diagnosis rather obvious.

The dizziness of hyperventilation may be described as lightheadedness or an unsteady, giddy feeling, similar to drunkenness or vertigo. In one review of 104 patients who presented to a specialty clinic for the evaluation of dizziness, 23 percent had hyperventilation as the sole or prominent contributing factor. There may also be some degree of disorientation and mental impairment.
Breathlessness is a common complaint and is usually described as the inability to inhale a satisfyingly deep breath. It may be manifested by periodic, predominantly thoracic deep breaths, sighing and yawning. Sighing dyspnea is not a manifestation of cardiac failure. Although the hyperventilation syndrome rarely is associated with an obvious increase in respiratory rate, astute observers usually will note an increase in thoracic respiratory efforts. Paradoxically, whereas many people take deep breaths in an effort to relax, they may be provoking the very state they wish to avoid. The dyspnea of the syndrome may arise from fatigued respiratory muscles, overworked from chronic, excessive respiratory efforts. Since this type of dyspnea rarely occurs in the absence of other related symptoms, it is important that other manifestations of the hyperventilation syndrome be sought in all cases of otherwise unexplained dyspnea.

Gastrointestinal manifestations include dry mouth, bloating, belching and flatulence, related to aerophagia associated with overbreathing. Depression with attendant anorexia and weight loss may mimic systemic disease.

Cardiovascular symptoms of the syndrome are primarily palpitations and chest pain, which may mimic angma. Continuous ambulatory electrocardiographic monitoring of hyperventilators has shown frequent sinus tachycardia and supraventricular arrhythmias, even during sleep. Hyperventilatory symptoms without apparent provocation may occur during these times.
The chest pain of hyperventilation is variably described. It may be sharp and stabbing, thought to be related to pressure on the diaphragm from gastric distention or diaphragmatic hypertonicity related to a generalized hypertonic muscular contractile state. Other types of chest pain have features that may strongly suggest angina including location and radiation patterns. The pain may be described as dull, gnawing, burning or constricting and localized to the precordial or retrosternal area but is often rather diffuse and of greater duration than is typical of angina pectoris. It is not predictably associated with events that usually provoke angina, frequently occurring at rest or after exertion, and is not reliably relieved by nitroglycerin. Occasionally, "pseudoischemic" electrocardiographic patterns may be seen in patients with chest pain from hyperventilation. It currently remains uncertain whether hyperventilation- induced coronary vasospasm and myocardial ischemia contribute to the chest pain associated with the hyperventilation syndrome. Unfortunately, a diagnosis of noncardiac chest pain, while initially gratifying, usually does not result in a significant reduction in outpatient clinic or emergency room visits as symptoms often persist. Therefore, in evaluating chest pain, the historical data base should include questions directed toward the possibility of hyperventilation lest the etiologic basis of the chest pain be dismissed as noncardiac, yet unrecognized as hyperventilatory.

Other symptoms of hyperventilation are usually present but rarely offered voluntarily. Apart from other disorders the patient may have, the physical examination is often normal. Patients often do not appear overtly anxious though they are frequently depressed. Obvious hyperventilation is usually lacking although occasional deep breaths, sighing or yawning and palpable chest wall tenderness may be noted. The diagnosis of chest wall syndrome requires exclusion of the hyperventilation syndrome which may be its basis.
It is critical to recognize that the presence of the syndrome does not exclude the presence of an organic disease. In fact, reaction to the symptoms of an organic disease may be a prime factor provoking hyperventilation.

Management of Hyperventilation SyndromeAs many patients with the syndrome have had symptoms for months or years and have seen other physicians without appreciating the cause of their symptoms, it is important that the patient be confronted with the cause-and-effect relationship between hyperventilation and their symptoms. A hyperventilatory trial is crucial for therapeutic success. This can be accomplished by having the patient breathe deeply at a rate of 30 to 40 times per minute. Most patients with the hyperventilation syndrome will recognize at least some of their symptoms within several minutes and often in seconds. This recognition and subsequent explanation of hyperventilation greatly enhances the potential for improvement. An explanation and reassurance without the patient actually experiencing the cause-and- effect relationship of overbreathing at the time is often without therapeutic benefit.
After provocation of symptoms .during a hyperventilatory trial, breathing into a lunch bag-sized brown paper bag will result in resolution of those symptoms that are directly related to hypocapnea. Dyspnea and chest pain, however, may persist in that they are not caused by hypocapnea, but more likely by the excessive use of thoracic musculature.

Because many patients have experienced substantial adverse effects on their employment and social interactions it is beneficial for a spouse or a friend to be present during a hyperventilation trial. Family and friends may be highly skeptical that something as simple as overbreathing can be having such devastating effects on the patient and indirectly upon them as well. Convincing both the patient and others provides support for the patient as he or she attempts to regain control.

Although some believe bag rebreathing is of little value, we have found it to be useful, allowing patients an escape from symptoms. Initially, we encourage patients to attempt bag rebreathing, relax and get away from the situation that may have triggered the response. As a result, patients appreciate a newfound control. This greatly reduces the anxiety and stress that fuel the hyperventilation cycle.

Long-term control may be achieved by relaxation therapy and retraining patients to become diaphragmatic rather than thoracic breathers. Referral to behavior modification experts may be of value in particularly difficult patients with long-standing symptoms. In anxious and depressed persons with chronic hyperventilation we have rarely seen substantial benefit from the use of anxiolytic or antidepressant medications when the hyperventilatory component was unrecognized or being inadequately addressed. in conjunction with therapeutic measures directed toward the hyperventilatory tendency these drugs may be of additional benefit though we often find them unnecessary.

GENERAL REFERENCES Evans DW, Lure LC: Hyperventilation: An important cause of pseudoangina. Lancet 1977; 1: 155-157
Heistad DD, Wheeler RC, Mark AL, et al: Effects of adrenergic stimulation on ventilation in man. J Clin Invest 1972; 51:1469-1475
Lary D, Goldschlager N: Electrocardiographic changes during hyperventilation resembling myocardial ischemia in patients with normal coronary arteriograms. Am Heart J 1974; 87:383-390
Lurm LC: Hyperventilation: The tip of the iceberg. J Psychosom Res 1975; 19:375-383
Magarian GJ: Hyperventilation. syndromes: Infrequently recognized common expressions of anxiety and stress. Medicine 1982; 61:219-236
Pfeiffer JM: The aetiology of the hyperventilation syndrome. Psychother Psychosom 1978; 30:47-55

As previously stated, in the subluxated patient, the brain is not processing or organizing the flow of sensory impulses in a manner that gives the individual good, precise information about himself or his world. Thus any efferent output will be inefficient and lead to eventual dysfunction and limitation.

The chiropractic subluxation is any afferent-based program that leads to long-term pathology and inefficiency. The interference in the nervous system is on the afferent side NOT the efferent side. It just may not be the area of pain, or motor unit fixation, or wedge on X ray, or the loss of a lateral curve that, if corrected, will give the CNS the best information about its internal and external environment and allow it to produce the most efficient output. It just may be the wedge on X ray or the listing just may change from day to day.

Critical Thinking: Critical thinking is the intellectually disciplined process of actively and skillfully conceptualizing, applying, analyzing, synthesizing, and/or evaluating information gathered from, or generated by, observation, experience, reflection, reasoning, or communication, as a guide to belief and action. In its exemplary form, it is based on universal intellectual values that transcend subject matter divisions: clarity, accuracy, precision, consistency, relevance, sound evidence, good reasons, depth, breadth, and fairness. It entails the examination of those structures or elements of thought implicit in all reasoning: purpose, problem, or question-at-issue; assumptions; concepts; empirical grounding; reasoning leading to conclusions; implications and consequences; objections from alternative viewpoints; and frame of reference.

Neuronal Fatigue

Not only does neurophysiological partitioning siphon off available ATP to other more important circuits within the CNS, dysponetic processing secondary to subluxation can also reduce intracellular energy reserves of neurons, with a consequent decrement in neuronal performance, such as a reduction in action potential amplitude or a reduction in maximum frequency of activation. When a neuron transmits more frequently or more continuously than appropriate to its physical design, and is required to repolarize its membrane and resynthesize transmitter more rapidly than its capacity, fatigue may occur as it does at any cell. The possible sites of this fatigue lie within the mechanisms for polarizing the membrane and for synthesizing transmitter substance.

Continued activation of circuits in the neocortex, limbic system, thalamus, hypothalamus or reticular activating system as a consequence of dysponetic processing (secondary to subluxation) can generate fatigue of neurons in any CNS area. Any circumstances that diminish or impair restorative processes within the organism, such as sleep deficits, debilitating active dis-ease, injury or drugs, facilitate the development of neuronal fatigue.

When energy reserves (ATP) within a neuron are reduced sufficiently, the energy available for repolarizing the membrane after each transmission of an action potential is reduced, with resultant impairment of the repolarization process. Impaired and inefficient neuronal performance results. A lengthened repolarization time reduces the maximum frequency of transmission of action potentials and an incompletely repolarized membrane would reduce the magnitude of the action potential.

Declining ATP resources within a neuron also reduces the energy at hand for synthesizing neurotransmitters and receptor function. The result is a reduction in the excitatory or inhibitory effect of the neuron.

The central theory of biology is evolution through natural selection. Frankly, if we assume a stationary environment, natural selection improves the ability of an average organism to reproduce fertile offspring. Consequently we arrive at the notion of evolution as an energy efficiency optimization process. These plastic changes have to happen at the microscopic cellular level (DNA expression).

Since the CNS controls and regulates all physiological process of the human body, these optimizations must occur at the microscopic cellular level in the nervous system first.

All these changes can be explained by considering the process of energy efficiency of neural communication and neural processing. Energy (available ATP) is finite. It is reasonable to assume that the limiting factor for this energy efficiency optimization process is the use of available ATP. Thus, to optimize neurological programs, the CNS will shunt and mobilize ATP to the areas of greatest physiological need in the CNS. This is neurophysiological partitioning.

Immediate energy-efficient processing of information can explain seemingly independent physiological processes. In the context of energy, neural processing is rather expensive. The adult human brain accounts for 20 percent or more of our total energy use. In young children, whose brains are nearly as large as an adult, the energy use by this organ can account for nearly 50 percent of the ATP use. Recent studies have shown that 85 percent of the energy used by the brain goes toward restoring the ion fluxes across neuronal membranes that are the biophysical basis of computation and communication in the neocortex. Thus information processing, although perhaps five or six orders of magnitude more energy efficient than man-made computation, is a considerable expense for the organism. Our survival and dominance as a species is dependent on the energy efficiency of CNS processing.

This is chiropractic’s greatest challenge and opportunity for increasing human potential. Increasing the efficiency of CNS processing is the chiropractor’s true goal.

Long ago I stopped blaming my computer for all the errors it produced. If the hardware and software were in working order, the machine would simply produce from the input loaded into it. Similarly, the thalamus (as the integrator and filter of all sensory information, except smell) is the primary focus of the functionally based chiropractor. L5 cannot even misalign chronically without cortical firing. Sensory cortical firing originates with thalamic firing into the sensory cortex. Our perceived and unperceived reality begins and stops at the thalamus.

Paradigm: A set of assumptions, concepts, values, and practices that constitutes a way of viewing reality for the community that shares them, especially in an intellectual discipline.

A philosophical and theoretical framework of a scientific school or discipline within which theories, laws, and generalizations and the experiments performed in support of them are formulated; broadly : a philosophical or theoretical framework of any kind.

Since the late 1960s, the word paradigm has referred to a thought pattern in any scientific discipline or other epistemological context.

Philosopher of science Thomas Kuhn gave this word its contemporary meaning when he adopted it to refer to the set of practices that define a scientific discipline during a particular period of time. Kuhn himself came to prefer the terms exemplar and normal science, which have more exact philosophical meanings. However, in his book The Structure of Scientific Revolutions Kuhn defines a scientific paradigm as:

• what is to be observed and scrutinized,
• the kind of questions that are supposed to be asked and probed for answers in relation to this subject,
• how these questions are to be structured,
• how the results of scientific investigations should be interpreted.

Paradigm Shift : When anomalies or inconsistencies arise within a given paradigm and present problems that we are unable to solve within a given paradigm, our view of reality must change, as must the way we perceive, think, and value the world. We must take on new assumptions and expectations that will transform our theories, traditions, rules, and standards of practice. We must create a new paradigm in which we are able to solve the insolvable problems of the old paradigm.

Evidence or Eminence Based Medicine?

“Power to corrupt, and absolute power corrupts absolutely.”

• The Entire Chiropractic Profession has only 70 full time researchers

· The drug company Pfizer has 12,000 full time researchers

• Less than 5% of full time DC Faculty at chiropractic institutions are involved in chiropractic research
• The total budget (for Everything) for all our chiropractic institutions is a mere $224 million
• Of that $224 million of the total budget, our chiropractic institutions spend only $4 million on research programs
• Harvard University receives $739 million a year from the NIH alone just to do research
• In the entire 100+ year history of the chiropractic profession, chiropractic has received less than $10 million from the federal government to do research
• The top 25 medical schools received $6 Billion from just the NIH in 2000 alone

What are the results?

When one begins comparisons with medical / allopathic procedures, the statistics really begin to spin one’s head. Using a baseline figure of one per one million as an estimate of stroke incidence attributed to cervical manipulations (not just chiropractic, but all such procedures), one finds a:

· Two Times greater risk of dying from transfusing one unit of blood

· 100 Times greater risk of dying from general anesthesia

· 160-400 Times greater risk of dying from the use of NSAIDS

· 700 times greater risk of dying from lumbar spinal surgery

· 1000-10,000 times greater risk from traditional gall bladder surgery

· 10,000 times greater risk of serious harm from medical mistakes in hospitals

The 225,000 deaths per year attributed to medical iatrogenesis (allopathy) have propelled it to the third leading cause of death, after heart disease and cancer.

Absolute, testosterone charged, black and white statements by heroic allopathic physicians will have to give way to the gray world of reality and hard numbers brought to us by evidence and real science – rather than Eminence based medicine and allopathic-religious superstitions.

Dysponesis: Chiropractic in a word

by Christopher Kent, D.C., FCCI and Patrick Gentempo, Jr., D.C.

Medical practitioners seem to be obsessed with the diagnosing and naming of specific "conditions," while often overlooking the underlying cause. This has resulted in a myopic assessment of patients which could be partially responsible for medical malpractice being the third leading cause of preventable death in this country [1].

Dysponesis does not mechanistically describe a specific "condition," but rather relates to human homeostasis and dis-ease. It relates to human health as a functional whole, rather than a sum of independent parts. It is philosophically and scientifically appropriate for a chiropractor to diagnose a patient with dysponesis secondary to vertebral subluxation complex. All that is necessary are the tools and the understanding.

Dysponesis is defined by Doreland's Medical Dictionary as follows:

A reversible physiopathologic state consisting of unnoticed, misdirected neurophysiologic reactions to various agents (environmental events, bodily sensations, emotions, and thoughts) and the repercussions of these reactions throughout the organism. These errors in energy expenditure, which are capable of producing functional disorders, consist mainly of covert errors in action-potential output from the motor and premotor areas of the cortex and the consequences of that output.

Physicians Whatmore and Kohli, who first described dysponesis, observed that "Most diseases consist of physiologic reactions that lead to organ dysfunction. These physiologic reactions constitute the response of the organism to some noxious agent, whether microbial, chemical, or mechanical." [2]

D.D. Palmer emphasized the importance of "tone" in the dynamics of health and disease. "Life is an expression of tone. Tone is the normal degree of nerve tension. Tone is expressed in function by normal elasticity, strength, and excitability...the cause of disease is any variation in tone." [2] B.J. Palmer acknowledged the role of muscular function in maintaining life. "Life is motion; motion is life. The absence of motion is death...in human beings, motion is produced by muscles...that which moves muscles is nerve force." [3]

Traditionally, the vertebral subluxation consists of a loss of juxtaposition of a vertebra with the one above, the one below, or both, to an extent less than a luxation. Furthermore, there is occlusion of opening, impingement of nerves, and interference with the transmission of mental impulses. [5] A contemporary definition of the vertebral subluxation complex proposes five components: spinal kinesiopathology, neuropathology, myopathology, biochemical changes, and pathology. [6] It is significant that both definitions incorporate both structural and physiological factors.

The term "dysponesis" is derived from "dys" meaning faulty, and "ponos" meaning effort, work, or energy. It is important to remember that motor dysfunction results from nerve interference. Neurological dysfunction is, by definition, an element of the vertebral subluxation described in chiropractic. According to D.D. Palmer, vertebral subluxations may be caused by trauma, poisons, or autosuggestion. Whatmore and Kohli note that "The agent to which the organism is reacting can be an environmental event, a bodily sensation, an emotion, or a thought." Dysponesis effectively expresses, in contemporary terms, the essential elements of the vertebral subluxation complex.

A clinical challenge to the chiropractor is determining the presence and correction of vertebral subluxations. Many D.C.s feel uncertain about their analytical strategies for determining if a patient is subluxated, and if the subluxation was corrected following an attempt at adjustment. Fortunately, technology exists to objectively assess muscular activity as it relates to subluxation.

A clinical challenge to the chiropractor is determining the presence and correction of vertebral subluxations. Many D.C.s feel uncertain about their analytical strategies for determining if a patient is subluxated, and whether the subluxation was corrected following an attempt at adjustment. Fortunately, technology exists to objectively assess muscular activity as it relates to subluxation.

Dysponesis defined

Dysponesis is a reversible pathophysiologic state. It is composed of neurophysiologic reactions to various agents, and the repercussions of these reactions throughout the organism. The neurophysiologic reactions consist mainly of covert errors in energy expenditure. [2] To the chiropractor, it is essential to develop clinical strategies which are effective in disclosing these covert errors in energy expenditure and correcting them.

Whatmore and Kohli describe the factors which determine the specific effects that dysponesis will have in a given person:

1. The inherited constitutional characteristics of the individual.

2. Acquired characteristics of the individual, resulting from the person's total past experience.

3. Activity going on within the neuronal networks of the nervous system at the time he or she is subjected to dysponetic influences.

4. The duration, magnitude, and distribution of the particular dysponesis present at that time.

These authors developed diagnostic strategies for the assessment of dysponesis using multi-channel surface electrode electromyography. Today, better technology makes assessment of dysponesis practical in the clinical setting. Modern surface EMG equipment is capable of performing static surface EMG measurements, as well as graphing the real time action of muscle groups being assessed.

Surface EMG techniques have the ability to disclose "covert errors in energy expenditure" in asymptomatic patients, permitting the chiropractor to intervene with appropriate adjustments before pain or pathology become evident. Protocols for SEMG in chiropractic practice have been published in peer reviewed scientific journals. [7,8] Furthermore, there are over 300 scientific papers in the indexed scientific literature on surface EMG.

Dysponesis embodies the tenets of traditional chiropractic philosophy and the technology of the 21st century. Acknowledging the devastating effects of the vertebral subluxation upon human health, the chiropractor now has the clinical and intellectual tools to effectively lead humanity into a healthful and fulfilling 21st century.

References

1. Dye M: "Silent danger of medical malpractice: third leading cause of preventable death in U.S." Public Citizen May/June 1994, p. 10.

2. Whatmore GB, Kohli DR: "Dysponesis: a neurophysiologic factor in functional disorders." Behavioral Science 13:102, 1968.

3. Palmer DD: "The Chiropractor's Adjustor." Portland Publishing House. Portland, OR. 1910.

4. Palmer BJ: "The Law of Life." Audio tape of lecture delivered at the Palmer School of Chiropractic. Davenport, IA.

5. Stephenson RW: "Chiropractic Text-Book." The Palmer School of Chiropractic. Davenport, IA. 1927.

6. Flesia J: "Renaissance--A Psychoepistemological Basis for the New Renaissance Intellectual." Renaissance International. Colorado Springs, CO. 1982.

7. Kent C, Gentempo P: "Protocols and normative data for paraspinal EMG scanning in chiropractic practice." Journal of Chiropractic Research and Clinical Investigation. October 1990.

8. Kent C, Gentempo P: "Dynamic paraspinal SEMG: a chiropractic protocol." Chiropractic Research Journal Volume 2, Number 4, 1993.

(CHRISTOPHER KENT, D.C., a 1973 graduate of Palmer College of Chiropractic (PCC), and the ICA's 1991 "Researcher of the Year," was a principal investigator in the PCC research department, assistant professor of diagnosis and X-ray, and president of the faculty senate. A member of the editorial review board for the Chiropractic Research Journal, he has published more than 50 articles in various chiropractic publications, including popular and peer-reviewed journals. He served as an item consultant and reviewer for the National Board of Chiropractic Examiners and as a consultant to the FDA panel on review of neurological devices. Dr. Kent, a Diplomate of the Academy of Chiropractic Radiology, serves as chairman of the ICA College of Chiropractic Imaging. A former associate professor at Palmer College of Chiropractic-West, he has conducted postgraduate programs for PCC, PCC-W, Cleveland, Life-West and Texas Chiropractic Colleges.

PATRICK GENTEMPO, Jr. D.C., a 1983 Life Chiropractic College graduate, is president and co-founder of the seminar group Paradigm Partners, Inc., and chairman of E.M.G. Consultants, Inc. Dr. Gentempo has authored or co-authored more than 30 papers in popular and peer-reviewed journals on a variety of subjects. He is on the post-graduate faculties of leading chiropractic colleges and gives over 40 seminars a year both nationally and internationally. His unique and well-attended presentations combine educational, motivational and inspirational elements, blending the science and philosophy of chiropractic in objective and rational terms.)