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9 Articles in Volume 8, Issue #9
Fibromyalgia: Fibromyalgia Medical Education
IV Ketamine Effect on Post-Concussional Migraine
Management of Chronic Headache
Multidisciplinary Pain Clinics vs Opioid Treatment for Chronic Pain
Neurodevelopmental Basis for Chronic Regional Pain Syndrome
Neuromuscular Training in Pain Management
Opioid-induced Sexual Dysfunction
Sphenomandibularis Muscle and Retro-Orbital Headache
Therapeutic Laser Evolution—Part 2

Neurodevelopmental Basis for Chronic Regional Pain Syndrome

A primer on the first level of evaluation in the practical application of neuropostural evaluations (P.A.N.E. process).

In my previous two articles for this journal, (July/August and September 2008 issues),1,2 I presented my neurobiological theories on the etiology of chronic pain syndromes (CPS) and a means of implementing those theories using gait and orthopedic technology. I call this multilevel method of diagnosis "Practical Application of Neuropostural Evaluations," or the P.A.N.E. process for short. In this article, I'll present the first level of evaluation for diagnosing the chronic pain patient.

Theory and Organization of the P.A.N.E. Process

The P.A.N.E. process is organized around developmental and survival priorities. The first three levels in the process are related to neurological functions. Evolution has created both anatomic and functional hierarchies within the central nervous system.3 The various functions of the brain, in turn, are distributed through these developmental layers in specific ways and best described as stratification of functions. The layers are not independent of each other, but work together like the members of a symphony orchestra to give us the incredibly diverse capabilities of our human brain. This functional hierarchy has to be intact for us to operate at our biological and mental best, and it is the first priority to check in matters of chronic illness. I have also concluded that hierarchical organization is not “hard-wired” into the brain, but results from parallel organization and neuronal and synaptic plasticity, which can become disorganized causing severe loss of functional capacity.4 It is my theory that loss of hierarchical order is associated clinically with autonomic dystrophy and functional collapse of basic biological regulating mechanisms.

Dystrophy has been recognized since the Civil War as a severe pain syndrome and which modern pain theory considers is due to loss of central inhibitory mechanisms within the acute pain circuitry.5 However, pain problems are the tip of the iceberg with respect to dystrophy. It is my experience that there is also loss of normal homeostatic adaptability leading to environmental intolerance, altered control of blood flow distribution causing poor exercise tolerance, reduced wound healing, potential collapse of the neuroendocrine and immune systems, and other forms of biological dysfunction beside the pain issues. I believe it is therefore critical to determine whether or not the central hierarchy is intact before embarking on any surgery or therapeutic endeavor. This is another reason why I have made primitive reflex testing the first level in this algorithm. I want to remind the reader that dystrophy is a disorder with a spectrum. Long before a patient shows the classic symptoms, he can be developing the central neurological changes leading to loss of hierarchical control as a precursor to the overt disease. This is the time to find the problem and deal with it, rather than after you have done a major procedure and unanticipated complications ensue.

This article concerns the first priority in the neurological hierarchy: autonomic homeostasis. It is first because, developmentally, the autonomic nervous system is the oldest part of the nervous system.6 To my knowledge, the P.A.N.E. process is the first clinical algorithm designed to evaluate this most basic level of human biology. In testing the associated involuntary, neurological functions, I have found that about 70% of the patients that I see with CPS have neurological dysfunction at this level.

P.A.N.E. Process Considerations

CRPS is fundamentally a neurological condition regardless of what “hurts.” Neurological diagnosis is critical in resolving the associated health issues. In general, western medical neurological diagnosis is inadequate in diagnosing CPS because it is usually limited to finding neuropathy. Western clinicians are caught up in the traditional symptom-directed, pathoanatomic algorithm. One might ask: Where is the pathologic anatomy in fibromyalgia? The traditional Western Medicine algorithm doesn’t work in solving CPS because:

  1. the CPS patient typically has minimal objective pathology,
  2. we ignore the incredible “compensatory survival dynamics” inherent in brain processing,7
  3. standard diagnostic technology (PET, fMRIs, etc.) can not show the status of brain processing, only that it is overactive.3,8-10

Central neural processing is reflexive in 70% of the brain and is affected by “neuritis” of afferent inputs (afferency). Pain is a reflex11 with afferent, central and efferent components. Obviously, a problem is best solved at its source, (e.g., at the keyboard rather than at the printer) yet neuritis is typically not diagnosed.3,11

Since Hughlings Jackson, MD’s pioneering work, brain processing is accepted as following developmental lines. Evolution has created a hierarchy of developmental stages which have to be intact for optimal processing of reflexive functions to occur.12 Chronic states of elevated neural anxiety due to survival stress come at the expense of over-utilization of key neurotransmitters (serotonin, dopamine, nitric oxide, etc.) This explains where the Serotonin has gone in fibromyalgia.8,13,14 What causes these states of metabolic activity? I am proposing that threatened fundamental biological functions—such as bite, balance, breathing, or blindness—activates survival metabolism in the reflexive parts of the brain.15 When these frequently asymptomatic conditions are misdiagnosed (who in our modern world worries about their “bite”?), the chronic stress can lead to depletion of neurotransmitters and set the stage for altered pain processing and altered homeostasis.

Based on my experience with motor reflex testing, I propose that depletion of neurotransmitters drives the brain’s processing back into the primitive developmental layers normally seen only in infancy. I call this “functional regression” and have found that it is reversible if the cause is treated. The problem remains: how does the clinician evaluate the status of reflexive processing in the brain? How does the clinician locate the cause of brain stress, so that it can be addressed? I believe that the P.A.N.E. process being presented in this series of articles is a step forward in answering these questions.

P.A.N.E. Process Overview and Order of Testing

This overview presents the components of P.A.N.E. process and the order in which they are performed. Due to the wide variety of potential causes of chronic pain, this process provides a troubleshooting guide to converge on the underlying problem(s).

  1. Standard neuropostural inspection (optional)
  2. Gait observation (optional)
  3. “Wall test”— if positive, continue neurological tests; if negative, skip to ortho exam16
  4. “Light/dark test”— if positive, continue to the postural cervical segmental dystrophy (PCSD) tests (described in the following section); if negative, skip to spine tests.17
  5. PCSD tests of the primitive reflexes (the subject of this article)
  6. “Spinal Scratch” tests of the cervical and lumbar dermatomes, rarely thoracic (subject of a forthcoming article)
  7. Dynamic neural tension tests of the median, radial, and ulnar nerves in the arms; abduction-scratch in legs; and provocative withdrawal (“touch and go”) tests for the peroneal and posterior tibial nerves.
  8. Priority postural compensation areas using kinesiological testing of shoulders, allergy, GI, hands, feet. These are areas likely to cause postural compensation.
  9. Tests for kinetic chain (core) stability (regional weakness, lumbar and cervical)
  10. Kinesiological joint-specific exam13
  11. Orthopedic joint exam

Postural Cervical Segmental Dystrophy (PCSD) Tests

I am now going to discuss the most unique and exciting part of the P.A.N.E. process, namely, the postural cervical segmental dystrophy (PCSD) tests (P-tests for short). These PCSD tests help locate the origin of the primitive motor reflex changes that present in chronic pain conditions. These tests are therefore the bridge between the neurophysiological theories about hierarchical control I have been discussing and practical application in the clinic. With current existing technology, we cannot image synapses and pathways, but we can see and feel motor reflexes. It is my contention that motor behavior reflects underlying neurological controls and that you can reach a neurological diagnosis by evaluating tangible motor actions.12

Each stage of the developmental hierarchy is characterized by unique motor reflexes and, as each stage replaces an older one, the older reflexes disappear.12 Re-appearance of older reflexes implies regression of the central hierarchy18 and is bad news. Re-appearance of neonatal (primitive) reflexes means that the regression has gone back to its oldest developmental stage of the brain18 and is very bad news. I associate the re-emergence of primitive reflexes with a state of reflex dystrophy in the nervous system—with or without classic symptoms.

I have taken these concepts one important step further. Through trial and error in performing thousands of motor examinations and confirmatory xylocaine nerve blocks, I have associated specific patterns of primitive reflexes with specific areas of neurological injury. The PCSD tests—discussed in subsequent sections—address the problem of diagnosing specific neurological dysfunctions in the involuntary nervous system. This allows for improved diagnosis and treatment of the dystrophy. The PCSD series of eight tests (also interchangeably referred to as P-tests) are designed for diagnosing these most basic levels of neurological injury. To understand what these tests accomplish, an important concept to review is segmental theory.

Segmental Theory

Embryologically, the earliest precursor to the spine and its related structures organizes around a bar of cartlilage tissue called the notochord.19 The primitive spine then divides into blocks of multi-potential cells called somites. Each somite gives rise to ectoderm, mesoderm, and endoderm. These, in turn, yield the vertebrae, muscle, skin, organ, and nerves associated with each of the 33 spinal segments. The distribution of a nerve to the skin is called a dermatome; to a particular muscle, a myotome; and to bones and connective tissue, a sclerotome. Although precordial nerve tissues start off with a specific somite, they migrate through the developing embryo and become widely dispersed. However, early relationships persist in the function of these structures and are still important in maturity. These relationships are important in making neurological diagnoses in that there are related body areas that do not follow standard neuroanatomical distribution. For example, the C-5 segment may relate to the sinuses and allergy, and C-6 to the stomach.

Unlike bones and muscles, nerves communicate and can distribute information back to the spinal area of origin and even to the opposite extremity. This is particularly true of reflex actions. All reflexes have an afferent and efferent limb, but some are ipsilateral in that the afferent and efferent go up and down the same side. I call these ipsisegmental. Some reflexes cross over the spinal cord to react on the opposite extremity; these are transegmental reflexes. Classic reflex dystrophy is a transegmental reflex. The initiating afferent injury is on the opposite side of the symptoms, which is why we physicians have had so much trouble locating the cause of this disorder: we typically don’t look where there are no symptoms.

The first six PCSD reflex tests—numbers 0 to 5—are ipsisegmental, while those numbered 6 and 7 are transegmental. This becomes important when applying xylocaine sensory blocks and acupressure techniques during diagnosis.

Segmental theory goes further. Keep in mind that the basic cell of the nerve system is the neuron. In neural anatomy, all peripheral nerves are made up of axons which are not independent structures19 but are extensions of neuron bodies that live in the central nervous system like the roots of a tree. Like those tree roots, nerves are very much interactive with their central neurons. Current theories in peripheral nerve surgery are emphasizing these relationships and are including spinal diagnosis with peripheral nerve conditions. One such theory is called the “double-crush syndrome,” where spinal disease initiates the dysfunction and a peripheral nerve entrapment finishes off the nerve. Neither condition by itself would necessarily cause a problem.20

In consideration of recent interest in chronic pain conditions, new research is showing a significant relationship between degenerative disc disease in the spine and autonomic disorders like reflex dystrophy.21-24 The connection is not on the basis of nerve compression and I personally feel that we are back to those primitive segmental relationships since the notochord and the precursor sympathetic ganglia form around each other in early embryological development.20,25-27

Confirming Reflex Processes

The examiner has to be able to reverse a “positive” result to prove that it is truly a reflex process.5 I use xylocaine nerve blocks, acupressure techniques, tongue blades for clenching in cases of TMD and, where appropriate, 4% xylocaine spray for sphenopalatine blocks when testing for allergy.

In order to implement these tests effectively, you will need to know—in addition to the manual skills previously addressed—something of the neuro-anatomy of the body, the derivation and makeup of the reflexes used in this testing, and the environmental conditions that influence primitive reflexes. The goal of the P.A.N.E. process exam is to identify neuropostural injuries, namely, conditions that induce central compensations in the neuroposture at the expense of increased brain stress. Since neuroposture is a reflexive process, postural injuries are mostly abnormal reflexes.

There are many different types of reflexes utilized for many different purposes. Remember that 30% of the human nervous system is involved in conscious, voluntary matters and 70% is busy with involuntary reflexive regulation. A comprehensive dissertation of all of the reflexes of the body is outside the scope of this article. Suffice it to say that reflexes originate from the spinal, supraspinal, and supratentorial regions of the central nervous system. The basic purpose of the P.A.N.E. process examination is to determine the anatomic site of origin of an observed abnormal reflex so that the whole reflex can be corrected at its source.

Defensive Motor Behavior

In addition to developmental motor reflexes, the P.A.N.E. process makes heavy use of defensive reflexes such as flexion/withdrawal, threshold/ provocative reflexes, and inhibition reflexes.12 Flexion/withdrawal reflexes are probably the most universal of all defensive motor reflexes. Even the simplest of animals exhibit withdrawal behavior when subjected to noxious stimulation. The critical issue with these reflexes is understanding how they produce medical problems. This has to do with thresholds of response. Like the alarm on the car, these reflexes are life-preserving and essential, but they have to function within a certain range of appropriate sensitivity. If the alarm keeps going off for no reason, it becomes a nuisance rather than an asset. In my experience, neuritis, inflammation, and mechanical trauma can increase the reactivity of our neurological alarms.

Understanding the basic kinesiology of the flexion response helps to explain the health problems we see when the reflexes are not working at appropriate thresholds. In order to pull your hand back from the hot stove, you first have to tighten your neck so that your shoulder can pull against the neck, so the elbow can pull against the shoulder, and so on down the line. When the alarm is momentary, no harm is done other than you go into reverse for a moment. But when the alarm is sustained, the flexion response becomes chronic and now we have that painful, stiff neck to contend with. You can stretch your neck all day, but the muscles won’t relax until you shut off the alarm.

Another category of defensive reflex motor behavior illustrates the amazing complexity of the brain, even with seemingly simple reflexes. I am referring to inhibition, namely those occasions when the brain says “no, don’t do it!” A simple example of inhibition is the weakness caused by trying to squeeze a hot potato. Other types of inhibition are very useful for diagnostic purposes, such as the weakness caused by trying to exert muscle action that places more pressure on an irritated nerve. These are neural tension tests and they help to locate regions of neuritis in peripheral or spinal nerves. The principle of neural tension is a subject called neurobiomechanics. As we move our spine or extremities, nerves have to glide along their beds like the cuff on a long sleeve shirt. This takes pressure off the nerve and avoids an otherwise momentary loss of blood flow in the nerve. There is considerable clinical data now to show that the earliest stage of nerve entrapment is not pinching or compression, but loss of glide. This leads to intermittent traumatization of the nerve with repetitive motion.28 This has significant clinical import in understanding and treating common nerve conditions like carpal tunnel syndrome.

Another variant of the use of inhibition for diagnostic purposes are various kinesiological muscle tests where the patient is asked to provide isometric effort against the examiner’s resistance in a provocative position that causes the muscle to put pressure on a nerve. Like that proverbial hot potato analogy, the brain will not let the muscle contract and there is apparent weakness in that position but not other positions of the same muscle.28,29

Examples of the tests that I use would be supination resistance test for the radial nerve and the elbow flexion test for the ulnar nerve. For our purposes, the key here is that neural tension tests are negative with normal nerves. These various reflexes demonstrate that the brain is not just a simple computer, but can anticipate and plan protective strategies while maintaining neuroposture.

An additional variant of defensive reflexes occur when we combine maneuvers. An example is provocative withdrawal. I apply momentary deep pressure by touching or scratching over a nerve and then test for a withdrawal response. Normal nerves can tolerate a push without triggering a withdrawal response. These are very helpful tests in locating a specific area of nerve entrapment, whereas neural tension tests tend to apply to the whole length of a given nerve and are not specific to an anatomic spot.

The highest level of defensive reflexes involves phenomena the neurotherapists call cerebral-cerebellar strategy. In the interest of survival, the brain is constantly anticipating what is coming next from the environment. The brain pre-plans movements and reactions in accordance with physical liabilities. It is known that the brain plans around postural weaknesses, predetermining how you will land if you fall. Experience in sports medicine has shown that one tends to keep re-injuring the same side. It is my theory that neuropostural reflex testing may be another important avenue to consider in injury prevention.

Diagnosing Disorders of the Autonomic Nervous System

Let us return to the original subject, which is my methodology of using primitive reflexes to diagnose disorders of the autonomic nervous system. Primitive motor reflexes come in different categories and are widely used in evaluating children with developmental motor problems. Examples are attitudinal reflexes like asymmetric tonic neck reflex, symmetrical tonic neck reflex, and tonic labyrinthine reflex (our old neck-flexion-labyrinthine tests), righting reflexes like optical righting reaction, labyrinthine righting reaction, body-on-head righting reaction, the Landau reaction, neck-on-body righting reaction, and body-on-body righting reaction. I make particular use of primitive balance and protective re-actions like tilting reactions, postural fixation reactions, parachute reaction, and stepping reflexes. The bottom line is that these reflexes are not part of normal adult neuroposture and so their re-appearance in the adult is a sign of loss of hierarchical organization in the brain and dystrophy.

PCSD Test Protocols

From extensive clinical experience, I have derived eight simple reflex tests based on the foregoing—each with an association to certain causative pathologies. My experience over the past 35-plus years indicates that these tests are clinically useful in returning the central hierarchy to normal order when the cause is finally treated. This gives the clinician some control over actually treating chronic pain syndromes rather than just managing them with analgesics and anti-depressants.

I shall present the reflex tests in the order I perform them in the clinic rather than in numerical order. While there is no priority associated with the tests themselves, this order eliminates the need for the patient to shift back and from sitting to standing and vice versa.

It would be useful at this juncture for the reader to review the mechanics of neuropostural motor testing described in my previous article in the September issue of PPM.2 Remember that the PCSDs are neuropostural motor tests and not strength tests. Further, the examiner’s technique is critical in performing these tests.

The following sections will present the eight reflex tests. The primary purpose of each PCSD test is listed below:

PCSD-0. TMJ/TMD, lateral cervical and supraclavicular allodynias.

PCSD-1. Radial supinator tunnel entrapments; radial neuritis.

PCSD-2. Dysfunction associated with with pronators, supinators; gastrointestinal problems.

PCSD-3. Pronator syndromes, Raynaud’s phenomena, and Morton’s neuroma of the foot.

PCSD-4. Pronator syndrome.

PCSD-5. TMJ as well as pronator and supinator syndromes.

PCSD-6. Carpal tunnel syndrome, classic reflex sympathetic dystrophy (RSD).

PCSD-7. Dystrophy.

PCSD-0 Test

This test will reveal the existence of temporal mandibular joint disorders (TMJ/TMD) and lateral cervical and supraclavicular allodynias. Allodynias are areas of sensitized skin. The skin over the side of the neck and collarbone are particularly vulnerable to allodynias because of the density of skin nerves in these areas. This is a rare test. Reversal is with local skin blocks.

Skin scratching, as used in the PCSD tests, deserves a little discussion. Normally, adults like scratching and do not withdraw from it. Infants, on the other the other hand, do not like scratching and will pull away from it—always in the opposite direction of the stimulus. Dystrophy patients withdraw from scratching in the same manner as the infant. I apply the scratch in PCSD tests in the same direction as the push in order to amplify the weakness, if present. To verify results, I apply the scratch on the opposite side of the first maneuver and repeat the test. The second scratch should reverse the effect.

For this test, the patient is seated with arms abducted and straight out from sides, horizontal with the floor. The hands are palms down. The scratch stimulus is applied to the dorsal surface of the forearms while the examiner simultaneously applies downward pressure on the wrists. See Figure 1.

PCSD- 5 Test

This is the best test for TMJ, also pronator syndrome and supinator syndrome. Supinator syndrome occurs where the radial nerve passes under the proximal edge of the supinator muscle called the Arcade of Frohse on the radial neck and becomes the posterior interosseus nerve. In the very common finding of TMJ/TMD, the use of a tongue blade placed in the patient’s mouth can immediately reverse the reflex. This test is performed in the classic parachute posture. To an infant, it means he is falling and activates recovery responses. I have discussed the role that TMD plays in balance disorders, so the effect of the neuroposture is enhanced when TMD is present

For this test, the patient has arms abducted as in the PCSD-0 test, but forward flexed 45 degrees, and slanted downward 30 degrees. Thumbs are rotated towards the floor. The examiner pushes downward on the wrists. See Figure 2.

Figure 1. PCSD-0 test demonstration. Figure 2. PCSD-5 test demonstration. Figure 3. PCSD-7 test demonstration. Figure 4. PCSD-3 test demonstration.

PCSD- 7 Test

This test is equally divided between radial nerves in the forearms and deep branch peroneal nerves on the dorsum of the foot on the same side. You confirm the test by acupressing the same nerve on the opposite side. Both the radial and peroneal nerves of the foot are very touchy and produce dystrophy when irritated. The PCSD-7 reflex is derived from stepping reflexes in infancy. The peroneal nerve runs down the dorsum of the foot with the dorsalis pedis artery. It is vulnerable to shoe pressure where it runs over the prominence of the second cuneiform bone of the midfoot. Be aware that allergy can aggravate a radial nerve because of a combined effect with the sinuses, C-5 segment in the neck, and the radial nerve. This reflex is also a very common finding.

For this test, the patient’s arms are still abducted to 90 degrees but are now parallel with each other pointing straight forward. Scratch is applied to the dorsum of the forearms with downward pressure applied on the backs of the wrists with the palms face down. This is a transegmental reflex so that acupressure applied to the opposite radial nerve from the weak side and the test repeated should reverse the result. See Figure 3.

PCSD- 3 Test

This tests for variants of stepping reflexes and is positive with pronator syndromes, Morton’s neuroma of the foot (pinched interdigital nerve in the webspace between the third and fourth toes), and Raynaud’s phenomena. The latter is a sympathetic vascular disorder where the patient’s fingers turn white and painful in response to cold exposure. I believe Raynaud’s phenomena is associated with pronator syndrome, thoracic outlet syndrome, and disorder of the second thoracic segment.

PCSD-3 testing is performed in the same position as PCSD-7 testing, except the scratch is applied to the outside of the forearms and the maneuver is directed at pushing the hands together instead of downward. See Figure 4.

PCSD- 1 Test

This test is based on the reciprocal movements of the crawling we see in infancy and is the best test for radial supinator tunnel entrapments. First, confirm the “positive” exam result with the resisted supination test and/or radial nerve xylocaine block. Also note that an allergy can amplify a radial nerve finding due to its affect on the C-5 segment. Confirm this using a 4% xylocaine topical spray into the patient’s nostrils in order to obtain a temporary spenopalatine nerve block.

The test is performed with the arms of the patient extended in front of him but lowered at a 30 degree angle and the wrists are dorsiflexed. The examiner applies a light scratch to the dorsum of one hand and the palmar side of the other. Then the examiner tries to bend the wrists downward to determine if there is any weakness from either side. Weakness from the side with the dorsal scratch indicates radial neuritis. See Figure 5.

Figure 5. PCSD-1 test demonstration. Figure 6. PCSD-2 test demonstration. Figure 7. PCSD-4 test demonstration. Figure 8. PCSD-6 test demonstration.

PCSD- 2 Test

This test is positive for problems associated with pronators, supinators, and, surprisingly, gastrointestinal problems such as gastritis. Forearm nerve entrapments weaken the wrist stabilizers. I have no idea why gastrointestinal problems result in a positive PCSD-2 test except they do. I give the patient two or three TUMS® and repeat the test. A positive test can be treated with Prevacid® (lansoprazole) and a medical consult might be indicated.

For this test, the patient holds his arms like the PCSD-7 test, except the wrists are turned outward and the palms are down. The scratch is applied to the outside of the hands followed by the examiner trying to twist the hands radially inward. See Figure 6.

PCSD- 4 Test

This test is useful for determining pronator entrapment. Pronator syndrome is an entrapment of the median nerve in the proximal forearm. The median nerve innervates the hand intrinsics along with the ulnar nerve (the latter is never involved in the PCSDs or dystrophy). There are four structures which can put pressure on the nerve as it courses from the medial arm to the antecubital fossa on the front of the forearm: the ligament of Struthers, the lacertus fibrosis, the ulnar head of the pronator teres muscle, and the fibrous arch of the sublimis muscle.

This test requires a change of position and is based on hand intrinsics. These are subtle tests and have to be performed with finesse. The arms are adducted to the sides, the elbows are flexed to 90 degrees while the wrists are straight, and the fingers are spread wide as possible (abducted). The palms are facing each other. The examiner grasps the hands with his thumbs and index fingers just distal to the metacarpophalangeal (MP) joints of the patient’s hands. Consistent hand placement is a must, and the scratch is applied along the upper side of the index fingers. The examiner then attempts to squeeze the fingers of the patient together (into adduction). A positive test indicates that one hand is much weaker than the other (asymmetry). The weak side is the one that has the pronator entrapment. It is essential to confirm positive findings with provocative/withdrawal tests performed by pressing the pronator. See Figure 7.

PCSD- 6 Test

This test is used for carpal tunnel syndrome, classic reflex sympathetic dystrophy (RSD), occasionally pronator and, rarely, Morton’s neuroma in the foot. Median nerve entrapment at the carpal tunnel affects the fine hand manipulation and grasping. In particular, the median nerve controls the thumb.

Like the PCSD-4 test, this test is very commonly positive because carpal tunnel injuries are so prevalent. One difference between PCSD-4 and this PCSD-6 test is another transegmental reflex as in PCSD-7.

For this test, the scratch is applied along the underside of the little fingers and, as in the PCSD-4 test, the examiner attempts to squeeze the fingers of the patient together (into adduction). With a positive result, the cause is the carpal tunnel on the side opposite the weak hand (transegmental). To confirm a positive test, the examiner will acupress the opposite wrist while pushing on the other since the injured carpal tunnel is in the opposite wrist from the weak hand. It is also essential to confirm positive findings by performing the provocative/withdrawal test by pressing on the wrist with the suspected carpal while pushing in on the opposite one. See Figure 8.


The most unique parts of the P.A.N.E. process are the PCSD tests (also referred to as P-tests). They can be used to test for autonomic dysfunction—also known as autonomic disregulation. They are used to locate the origin of the motor reflex changes that help solve chronic pain syndromes. Please keep in mind that positive PCSD test results always mean dissociation of the central processing hierarchy due to stress-related regression. This means that the individual is in what I call dystrophy—with, or without, classic symptoms. Because dystrophy (chronic regional pain syndrome) is such a medical disaster, addressing the cause of a positive exam is the first priority in treating these patients. It is critical that surgeons not operate on those patients that have positive PCSD test results. If the patient’s biological homeostasis is not intact, it is likely that the operation will not have a successful outcome.

I am presenting these theories of the neurobiological basis for chronic pain syndromes in the hopes of stimulating dialog with my peers. In particular, controlled studies need to be performed to establish the validity of the P.A.N.E. process.

My next article will discuss the radicular syndromes and associated “R-tests” that I have developed to diagnose radicular pain of the neurospinal complex. I will discuss how spinal conditions relate to chronic pain syndromes—even without classic compressive radiculopathy.

Last updated on: December 13, 2011
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