| ###Reflex Sympathetic Dystrophy Syndrome - RSDS, Complex Regional Pain Syndrome - CRPS
Many diseases (including RSDS/CRPS) trace their origin to a breakdown in the stress response system of the body. The human stress response system (primarily the sympathetic nervous system which is the more active portion of the autonomic nervous system) is designed to protect the body from real or perceived threats. This is the fight, flight, or fright system. This system is designed to have a physical reaction to a short-term stress. When a threat is perceived, the body reacts with a "mass discharge" of norepinephrine from the adrenal glands. Norepinephrine helps to protect the body by changing the allocation of circulation and by changing carbohydrate metabolism. This is a protective mechanism that is designed to change the body's focus for approximately 20 seconds to survive a threat. Norepinephrine increases the flow of blood to the large muscles at the expense of the digestive system, small muscles, nerves, bone, and skin. Not only is the heart rate increased but also the pulse volume of the heart is increased by as much as 50%. Norepinephrine causes the release of insulin and the breakdown of glycogen, the "storehouse of sugar." The insulin allows the large muscles to utilize the blood sugar more efficiently.
This stress response system was well adapted for human life 50,000 years ago when stresses were of short duration and were handled with a physical response. However, in the modern era, stress is rarely short-term and usually cannot be dealt with a physical response. Those areas of the body, which are denied adequate circulation by the stress response system, have no problem tolerating insufficient circulation of 20 seconds. However, these areas cannot tolerate continued insufficient circulation for extended periods of time. Many different diseases are caused by insufficient circulation to the digestive system, small muscles, nerves, bone, and skin. In essence, this is a stone-age physiology in a space age world.
Under normal circumstances, the circulation to a given part of the body is determined by demand, since supply is adequate. The autonomic nervous system and various neuropeptides control the flow of blood. VIP (vasoactive intestinal polypeptide) increases the blood flow to the intestinal tract. The flow of blood to the skin, nerves, bone, and small muscles is increased by CGRP (calcitonin gene-related peptide). This increased flow is decreased by neurons releasing substance P, which causes the mast cells to release a proteolytic enzyme, which destroys CGRP. In a "normal" human, there is a balance between norepinephrine/substance P, decreasing the blood flow to these various tissues and organs, while CGRP and VIP increase the blood flow.
Norepinephrine is destroyed on a system-wide basis by catecholamine-O-methyl transferase (COMT). The amount of COMT made by an individual's body is determined by their genetic makeup. There are two COMT alleles, valine and methionine. The valine COMT produces a normal amount of COMT. The methionine COMT produces much less COMT. The COMT genes follow Mendelian genetics. Dr. Jan Zubieta performed the pioneer investigation into the action of these genes. He found that persons with a low/low COMT (met/met) or low/high COMT (met/val) genes were less able to tolerate pain than persons with a high/high COMT (val/val) gene. PET scans showed that this occurred because the people with met/met COMT or met/val COMT made less beta-endorphins. In addition, the decreased COMT levels allowed the norepinephrine produced by the sympathetic nervous system to last much longer in their bodies. He found that approximately 25% of the people in the United States have met/met and val/val COMT genes, while 50% of the people have met/val COMT genes. When he studied those patients complaining of severe pain, he found that their genetic makeup was usually met/met COMT or sometimes met/val but only extremely rarely val/val COMT.
When norepinephrine is released from the adrenal glands in patients with val/val COMT, it remains very active for approximately 20 seconds and semi-active for several minutes. However, in patients with met/met or met/val COMT, the norepinephrine remains very active for 2 or 3 minutes and semi-active for at least 6 minutes. In addition, he found that people who had val/val COMT were able to tolerate much more pain than people who had met/met COMT. PET scans confirmed that this was probably due to the normal production of beta-endorphins in response to pain. It has been found that the bulk of patients with diseases such as Fibromyalgia and RSDS and other forms of severe chronic pain usually are patients with less than normal levels of COMT.
The increased duration of the action of norepinephrine causes ischemia in the skin, nerves, bone, small muscles, and in the intestinal tract. This ischemia causes pain, which liberates substance P, the chemical transmitter of pain. Substance P causes the mast cells to produce a proteolytic enzyme that destroys CGRP, which results in increased ischemia and, therefore, increased pain. This becomes a circle of continually worsening ischemia and pain.
In addition, the longer duration of norepinephrine causes a marked increased liberation of insulin. This places an increase stress on the beta cells in the Islets of Langerhans, which produce the insulin. This requires an increased supply of oxygen at the very time that circulation to this area is being decreased. Of the entire body, the three areas, which are the most sensitive to oxygen deprivation, are the central nervous system, the peripheral nervous system, and the Islets of Langerhans. This decreased oxygen causes increased reactive oxygen species, which cause mutations in the mitochondrial chromosomes and interferes in the production of ATP and, therefore, decreases the production of insulin.
There is an increasing body of scientific evidence that ischemia in tissues is the etiology of disease. Ischemia causes a buildup of reactive oxygen species (ROS) and changes the local pH of tissues. Since the circulation is decreased, there is an accumulation of CO2. The CO2 combines with water to become carbonic acid. As the pH decreases, various deleterious changes occur.
The decreased oxygen has been shown to be responsible for an increase in tumor necrosis factor alpha, vascular endothelium growth factor, and various cytokines. These substances are responsible for such varied disease such as Rheumatoid arthritis, endometriosis, and diabetic retinopathy, as well as, worsening RSDS/CRPS. TNF alpha has been shown to increase insulin resistance throughout the body, which makes the symptoms of RSDS much worse. Increased insulin resistance causes increased blood glucose. It has been demonstrated that when the blood glucose is higher than 130 mg%, COMT is deactivated. This allows for increased norepinephrine activity, which exacerbates the signs and symptoms of RSDS.
Many of these diseases affect women more that men. This is probably because men have a better oxygen supply to the periphery of their bodies. In general, men have higher blood pressures, than women. Men have more muscle than women and, therefore, have more myoglobin, which holds oxygen in the muscles. In addition, men have more hemoglobin than women. Women have 12 to 14 mg% hemoglobin in their blood while men have 14 to 17 mg%. Diseases such as RSDS, Fibromyalgia, and Chronic Fatigue Syndrome affect mostly women.
In bone, the decreased oxygen and decreased pH are responsible for a breakdown of the bone matrix. Bone is a matrix of hydroxyapatite and collagen held together with copper in a matrix maintained by a Piezo electric current. The stress side of the bone has a negative charge and the compressive side of the bone has a positive charge. Osteoblasts, which are responsible for the building of bone, go primarily to the negative (stress) side of the bone. Osteoclasts, which are responsible for the remodeling of bone, go primarily to the positive (compressive) side of the bone. This loss of bone shows up first in the areas of increased oxygen use. Therefore, it is seen as subchondral cystic degeneration beneath cartilage or where there is an attachment of muscles, tendons, or ligaments. With time this becomes more generalized and is seen as osteopenia and, eventually, as osteoporosis. If these subchondral cysts are in a line, a pathological fracture may occur.
The cartilage has no intrinsic circulation and derives all of its nutrients and rids itself of its waste products into the underlying bone. However, if the underlying bone no longer exists and is now a subchondral cyst, the cartilage begins to degenerate. This is seen as degenerative joint disease or arthritis. These bone cysts increase in size with low barometric pressure, which is why RSDS patients' pain is many times radically increased with rainy weather.
The skin, being deprived of adequate circulation, begins to break down and is seen as nonhealing ulcerations, nonpruritic lichenification, and occasionally cellulitis.
Cells in the small muscles, being deprived of adequate circulation, begin having small areas of cell death. This is seen clinically as tremors, fasiculations, or in diseases such as RSDS or Fibromyalgia.
The nerves in the central nervous system and peripheral nervous system, being deprived of adequate circulation, begin to degenerate. Myelin is extremely sensitive to oxygen deprivation. As the myelin degenerates the nerves transmit with less than normal stimulation (hyperesthetic). With continued hypoxia, the nerves only transmit with more than normal stimulation (hypoesthetic). Eventually, with continued hypoxia, the nerves will not transmit (anesthetic). Saltatory conduction suffers and nerve conduction velocity is decreased. Since nerve conduction velocity only tests the A-beta fibers and only show decreased nerve conduction, these studies are useless in early RSDS. The hyperesthetic nerves will result in a normal reading. Many times, this causes intense frustration on the part of the RSDS patient since they would be told that the NCV testing did not indicate malfunctioning nerves.
One of the aspects of this situation, which is usually overlooked, is that the nerves are the source of the neuropeptides, which counteract norepinephrine. Nerves throughout the body create CGRP and VIP. However, when the nerves do not receive adequate oxygen to function normally, they do not make adequate amounts of the neuropeptides.
Norepinephrine is destroyed by COMT. However, patients with chronic pain do not have adequate COMT. The only other substance, within the body, which is known to destroy norepinephrine, is melatonin. The problem is that melatonin is produced by the pineal gland in the presence of adequate VIP and cAMP (cyclic adenosine monophosphate), which are produced by nerves. Since these nerves are not receiving adequate oxygen, the VIP and cAMP are not being produced in adequate amounts to create the melatonin to destroy the norepinephrine. In addition, melatonin is produced after 4 P.M. due to the body's circadian rhythm. At approximately 4 P.M., the body's blood cortisol level, blood beta-endorphin level, and blood pressure decrease. At approximately 4 A.M., these levels increase. This helps explain why chronic pain patients have insomnia and increased pain in the evening and are able to sleep better during the daytime.
This inability to produce adequate VIP and cAMP creates diseases as diverse as migraine headaches, Irritable Bowel Syndrome, and asthma. Many RSDS patients suffer from these diseases without realizing that they are all connected.
Migraine headaches occur due to a lack of glycogen. The brain utilizes glycogen for energy. Glycogen requires one half of the oxygen to metabolize as does blood glucose. However, the body requires VIP to create glycogen. Therefore, if there is not adequate VIP the brain is forced to utilize blood glucose, which requires more oxygen to metabolize, at a time of decreased oxygen supply.
Irritable Bowel Syndrome occurs when there is insufficient VIP in the intestinal tract. This causes hypoxia in these tissues.
Medical literature has shown that asthmatic patients have markedly decreased VIP producing nerves, in their lungs.
VIP and beta-endorphins determine the immune system function of the body. These neuropeptides are diminished in RSDS, which causes RSDS patients to be prone to illness such as the flu and slow to recover from these illnesses.
Many RSDS patients are also diagnosed as having Raynaud's Disease or Phenomenon. Raynaud's Disease/Phenomenon is caused by a lack of CGRP producing neurons in the skin. RSDS has the same pathology.
Normally, dynorphins, beta-endorphins, and enkephalins inhibit the release of norepinephrine. However, in patients with insufficient amounts of COMT, the production of these neuropeptides is diminished. As was seen earlier, these are patients who experience significant amounts of pain. If this type of patient is seen by a physician and complains of moderate to severe pain, the physician is liable to write a prescription for a morphine derivative mediation. These medicines may dull the painful sensations, however, they actually make the chronic pain syndrome worse. This is also true of the nonnarcotic drugs, which function in the body as a narcotic, such as Ultram. All of these medicines decrease the production of dynorphins, enkephalins, and beta-endorphins. Studies have shown that narcotics increase the release of norepinephrine 200 to 300%. Even worse reactions have been found if the patient misses a dosage of the narcotic or intentionally tries to diminish the amount of daily intake of the narcotic. It has been found that reduction of the daily intake of narcotics doubles the output of norepinephrine.
Patients in our clinic are never prescribed narcotics, except during the course of reduction of their previously prescribed narcotics. When a patient arrives at our clinic utilizing narcotics or other deleterious medications, they are prescribed a slow reduction to prevent exacerbations of the RSDS, due to the withdrawal of the medications. It is necessary for the patient to be off all narcotics to be able to return to a normal pain-free life.
I am the inventor and patent holder of the methodology of what is in the FDA approved physical therapy system known as the Dynatronic STS. This system involves two simultaneous, separate interferential treatments. STS treatments are designed to normalize the abnormal autonomic nervous system. The current working hypothesis is that the STS treatments are effective due to a combination of the following aspects of the treatments: low frequency electrical current passing through long sections of nerves; electrode pad placement (including acupuncture and reflexology points); production of cyclic adenosine monophosphate; the choice of the peripheral nerves being stimulated so that there is a cross-over effect in the Central Nervous System; leakage of action potentials from the nerves being stimulated into nerves entering the sympathetic ganglia; the quadrilateral location of stimulation; creation of action potentials through sympathetic nerve fibers, in the peripheral nerves being stimulated; creation of action potentials in peripheral nerves being stimulated; activation of the sodium pump, in the nerves being stimulated; production of ACTH; production of dynorphins, enkephalins or beta-endorphins; creation of action potentials in sympathetic fibers within the peripheral nerves being stimulated, which enter the sympathetic ganglia directly; analgesia causing a reduction in the production of substance P; and/or the production of circulation altering neuropeptides such as vasoactive intestinal polypeptide(VIP) and calcitonin gene-related peptide (CGRP).
There are literally thousands of different combinations of beat frequencies and electrode pad placement protocols, which are utilized for our patients. The choice of electrode placement and beat frequency is unique to each patient and changes as often as necessary. Many times, these are changed on a daily basis to respond to the ever-changing RSDS symptoms.
An indication of autonomic nervous system (ANS) dysfunction is an alteration of the heart rate variability (HRV). HRV not only shows the relative control of the heart by the sympathetic and parasympathetic nervous system but also shows the heart rate variability compared to normal for that type of patient (based upon sex, age, marital status, etc.). Multiple HRV testing has shown that even the first STS treatment decreases the dominance of the sympathetic nervous system control of the heart and partially or fully normalizes the variability in the heart rate.
An indication of ANS dysfunction is nonhealing skin ulcerations. It has been found that STS treatments cause nonhealing ulcerations to granulate and heal. This has been documented with dated photographs.
Another indication of ANS dysfunction is the skin temperature and the skin temperature differential between the left and the right side of the body. Decreased skin temperature is an indication of decreased circulation into the skin vascular bed. The skin vascular bed circulation is increased by CGRP. In the absence of increased ambient temperature, if the skin temperature is increased, that is caused by an increased liberation of CGRP. Skin temperatures are taken from the lower and upper body. The palmar surface of the thumb should be approximately 91 degrees Fahrenheit. The plantar aspect of the big toe (hallux) should be approximately 83 degrees Fahrenheit. If there is a greater than a one-degree difference between the right and left sides and/or there is a lower or higher temperature of the fingers or toes, it indicates an ANS dysfunction. In the Peripheral Neuropathy study by Dr. Guido (published in the American Journal of Pain), it was shown that STS treatments normalize the actual skin temperature and also decrease the side-to-side variance of skin temperatures. That study also demonstrated that STS treatments radically increase the time and quality of sleep in chronic pain patients, indicating an increased production of melatonin. Medical literature has been demonstrated in multiple studies that a decreased endoneurial circulation causes decreased nerve conduction velocities (NCV). It has also been demonstrated that increased CGRP results in increased endoneurial circulation and normalization of decreased nerve conduction velocities. In the Guido study, 59% of the patients who had pre study and post study NCV had nerve conduction improvement. This indicated that adequate CGRP was produced by the STS treatments. |
제 목 : RSDS-CRPS 3rd
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