The following is a nationally published article I wrote in 1987 when PFS was just emerging as a clinical entity. I have updated this article with the latest information and treatment protocols.
By Winston Greene, D.C.
Fibromyalgia syndromes are common noninflammatory, nonarticular musculoskeletal disorders that vary in extent and intensity of involvement. Fibromyalgia (pain that originates from soft tissue) is characterized by chronic aches, pains, and stiffness that can affect articular and periarticular areas, muscles, ligaments, tendons, subcutaneous tissues, and boney prominences. The course and prognosis of Fibromyalgia Syndrome are difficult to ascertain. Current diagnostic and therapeutic strategies are grossly lacking in the medical and chiropractic professions. The purpose of this paper is to present information on 1) recognizing these syndromes, especially in differentially diagnosing these syndromes with respect to intervertebral disc diseases, articular disturbances (arthritides, facet syndrome, etc), and systemic diseases such as lupus, vasculitis, etc., and 2) management of these disorders. This paper will concentrate on those fibromyalgia syndromes where no inflammation is present.
When no cause or contributory disorder is found, Yunus, et. al., prefer the term Primary Fibromyalgia Syndrome (PFS), because inflammation is not present and laboratory investigations and radiographic tests show no pathology. I suggest that PFS can be further classified as Generalized PFS”, which can involve many diffuse areas of the body and other constitutional manifestations such as irritable bowel syndrome (IBS), psycho-neurophysiologic mechanisms, sleep disturbance syndromes, etc. and “Specific PFS” which is a newly proposed term. Specific PFS will involve only one or two main areas of the body, for example, hip and leg muscles with or without other clinical manifestations.
Myofascitis, fibrositis, etc., on the other hand, generally involves muscle spasms (trigger points), acute inflammation of muscles, fascia., nerves or associated connective tissues, positive radiographic findings, and occasionally positive lab results and is usually localized or distributed in a predictable manner.
Reports from various rheumatologists suggest that PFS is a common condition, but is not generally recognized among medical professionals. From a review of the literature it is apparent that fibromyalgia has been recognized probably for over 100 years. However, the syndrome of primary fibromyalgia was first mentioned in the literature in 1981.
Generalized PFS most often affects women in their 20’s to 40’s and is not uncommon in children. Only about 15-20% of cases occurs in men.
Patients complain of chronic diffuse aches, pains, and stiffness in or around nearly any joint and subjective feeling of swelling in articular or periarticular areas. The duration of symptoms may vary from a few months to many years. With generalized PFS usually four or more sites are involved, while with specific PFS only a few sites are involved, usually three or less. With generalized PFS the sites are usually non-related, e.g. low back, shoulders, chest, knees, earaches, dizziness, etc., as compared to specific PFS where the involved sites are related, e.g. low back, hip, thigh, or leg.
Myofascitis and fibrositis, like PFS, present with similar muscle aches, pains, and possibly cramping, usually at only one or two sites. Unlike PFS, however, myofascitis is an “inflammatory process” involving the muscle and its fascia as seen by muscle and fascial biopsies with infiltration of white blood cells. Also, myofascitis tends to be acute, resulting from recent trauma or pathology of spinal joints or IVD (Intervertebral Discs).
It is interesting to note that persistent myofascitis or fibrositis can become chronic. In this chronic state, however, the inflammatory process has resolved and the correct medical terminology is no longer myofascitis or fibrositis. PFS, as noted, is not the correct terminology either. PFS is an idiopathic syndrome with generalized and diffuse muscular aches and pains that does not present a particular pattern of involvement.
In PFS the orthopedic and neurological exams are usually normal, as are muscle strength tests. Laboratory findings including rheumatoid factor and antinuclear antibody tests and radiographic findings are normal.
Patients diagnosed with PFS have symptoms similar to irritable bowel syndrome (IBS) and some researchers state that the two syndromes are almost the same. Some preliminary data suggests that premenstrual syndrome, primary dysmenorrhea, and hypothyroidism are also associated with PFS. Additionally, PFS patients exhibit other symptoms that differentiate it from myofascitis, fibrositis, or specific PFS, such as fatigue, anxiety, depression, poor sleep, and bowel irregularity.
Tignrtis, myofascitis, and bursitis can be distinguished from PFS by the more limited number of symptoms and tender points. Also, lab tests can rule out other similar systemic conditions such as rheumatoid arthritis, vasculitis, and lupus. Osteoarthritis of the spinal or extremity joints may contribute to the symptom picture. Also facet syndromes or IVD syndromes may be factors in producing pain to the back and extremity muscles.
PFS shows: 1) presence of generalized aches and pains or stiffness involving three or more anatomic sites for at least three months; 2) absence of secondary causes, as mentioned before; 3) usually worse in the morning than evening; 4) affected by changes in the weather or physical activities; and 5) usually affects females aged 20-40 years who complain of poor sleep, fatigue, and anxiety. Physical examination is characterized by presence of multiple tender points at various anatomical sites and absence of swelling.
Many patients present with mixed fibromyalgia symptoms. These patients can be diagnosed with PFS but upon further investigation show pathology of the spine and lVD from previous traumas. These pathologies complicate the symptom picture and can determine whether or not a patient is treated successfully.
Some of the features of fibromyalgia were first described in the German literature of the mid-nineteenth century, with emphasis on painful muscle nodules. Many clinicians from that time to the present have postulated the causes of fibromyalgia. However, the cause of the muscle pain and fatigue in patients with generalized PFS remains unknown.
Those patients with fibrositis and specific PFS can be more definitively analyzed. Researchers during this century have described nodules or hardening in the muscles, some the size of plums. Cyriax describes adhesions that follow the entire length of muscle fibers in the hamstring muscles, and many that also perpendicularly or transversely affect the muscles. He states that strain in a muscle causes a few fibers to part causing damage to the fibers. The resultant scar tissue or adhesions mat the fibers together longitudinally and transversely. These microscopic adhesions are only the first part of the fibromyalgia process. Observations of the hamstring muscles in lay people and professional athletes have been made and showed massive transverse lumps or adhesions, sometimes referring pain up into the hip or down as far as the sole of the foot. It has been postulated that the leg muscles of professional athletes endure many traumas and thus, the fibrotic adhesions. But what of the secretary and housewife or the executive – what is the process here? It is not necessary, however, to know what caused this condition, per se, to treat these people. But a casual mechanism should be found to prevent future problems. SEE ADDENDUMS # 1 & 2 BELOW.
Muscle biopsies of PFS patients have revealed no abnormalities of the tissues. Histochemical analysis demonstrated type 11 fiber atrophy and the “moth-eaten” appearance of Type I fibers in some patients. Electron microscopic findings were most impressive and included myofibrillarlysis with deposition of glycogen and the presence of abnormal mitochondria. The cause of these changes is uncertain but may include subclinical of muscle spasm and the resultant ischemic condition that may follow. Kaylan-Rayman and others found swollen capillary epithelial cells in some muscles and hypothesized that hypoxia caused degenerative changes and was a predominant factor in the development of symptoms in PFS). Bengtsson measured oxygenation of muscles of PFS patients with a multipoint oxygen electrode placed on the muscle surface and found ore evidence for the existence of abnormal oxygenation. Abnormal muscle oxygen tension, which indicates an uneven capillary perfusion, was found in all PFS patients. In another study, a decreaRecon levels of ATP and ADP and an increase in levels of AMP and creatin, were found in the painful muscles of all PFS patients. It can be concluded that pronounced changes of high-energy phosphate levels are found only in the muscles with pain, fibrositis and trigger points. These reduced high-energy phosphate levels are probably due to hypoxia, or possibly, to a metabolic change which leads either to a defective synthesis of ATP or to an increased degradation of these substances. These results do not allow a definite conclusion; however, these results do confirm that there are real metabolic changes in painful muscles of fibromyalgia patients.
These mechanisms can apply equally to patients with fibrositis or specific PFS. To differentiate the cause of specific PFS in a few related muscles, stress to these muscles must be considered. Muscle overload from poor posture, IVD and facet syndromes, traumatic accidents, or athletic activity tend to affect only a few muscles at a time with similar resultant metabolic changes in the muscles. However, with the specific form of PFS, if the stress or spasm of the muscle is not relieved it can become fibrotic and the muscle filled with many adhesions. This is not found in the generalized form of PFS. It would appear, therefore, that generalized PFS might be caused by some underlying metabolic disturbances as evidenced by the symptom picture described earlier and by disturbances in hormonal changes or problems of digestion and elimination. Specific PFS and fibrositis are due, primarily, to direct stress in a muscle from whatever cause.
ADDENDUM # 1: Since I first wrote this paper in 1987 more information on the nature and management of PFS has surfaced. Specifically, 1) the metabolic nature of PFS (almost every patient I have examined with PFS symptoms has low body temperatures) and 2) almost every patient has Chronic Fatigue Syndrome (CFS) symptoms as well.
The first priority is to establish a strong working diagnosis. It is important to know, for example, that a patient, who suffered an auto accident, may have underlying PFS (mixed fibromyalgia) which must be recognized after the patient has recovered from the accident. Thus a careful history is paramount.
In PFS, following a firm diagnosis, it should be established that the condition is benign and noncrippling. Observations show that most of these patients respond to reassurance and an explanation of their condition. Exacerbations and remissions may occur. It should be emphasized that the symptoms are not imagined. Rest, relaxation, and the avoidance of anxiety and stress should be emphasized. Patients should remain active and continue working. However, a change from a stressful job may be advisable. Keeping physically and mentally busy is most beneficial to avoid gelling of the soft tissues and to decrease fixation upon the symptoms.
Various stretching exercises are advised to keep muscles supple. Non-straining exercises such as walking and swimming are also most beneficial. Avoidance of chill and the use of heat in the form of a hot shower relieve symptoms in many patients.
Various forms of physical therapy such as massage, ultrasound, and hot packs have all proven to be useful. Good posture at work, play, and during sleep should be emphasized. Corrections of spinal and extremity joint dysfunction help to relieve stress to the soft tissues.
In clinical practice, initial steps are taken to normalize digestion with the use of HCL acid and pancreatic enzymes. Also adequate hydration of the soft tissues via distilled or spring water (2 to 3 ounces every 30 minutes) must be employed. These are probably the single most important factors in managing these patients.
It is likely that most health care professionals have a problem managing this condition because physicians seldom understand that most Americans have digestive problems and are usually in a state of dehydration. If these patients’ digestive processes are improved and proper hydration measures are employed, corrective techniques are more effective.
For pain, aspirin, acetaminophen, or ibuprofen, may be used initially, and does help some patients.
In specific PFS, fibrositis and myofascitis, all of the above therapeutic measures should be employed. Additionally, the use of manual traction techniques via the Leander Distraction Table in the cervical or lumbar spine should be employed. Many times an active IVD lesion or an old IVD lesion that has healed improperly needs to be corrected. These lesions (acute or chronic) can cause reflex muscle spasms, myofascitis, etc. to an extremity. When there is pain in an extremity the soft tissue structures must be examined as an additional source of pathology. The hip muscles, the hamstrings, the adductors, the peroneii muscles, and the calf muscles are often a source of pain in themselves. The same applies to the musculature of the upper extremities.
The treatment of choice for myofascitis, fibrositis, and adhesions in the muscles is specific massage techniques. There are various methods of soft tissue manipulation and all are effective if the adhesions are removed. When the pain from trigger points in the muscles is acute and debilitating, injection with procaine and vitamin B12 can be helpful when done by experienced physicians. This is followed with periodic manipulation of the soft tissue and correction of the spinal lesions.
It has been observed that specific massage, although initially painful, may eventually eliminate the adhesions and hypersensitive findings, as well as the patient’s symptoms. Stockman presented a most detailed account of the use of massage and stated that permanent relief absolutely required that soft tis>Cas0D
ma(60 lation be continued until the adhesions were completely resolved.
Additionally, stretching techniques with the use of a vapocoolant may be advantageous especially when patients are taught to employ stretching exercises at home to maintain muscle flexibility.
ADDENDUM # 2: Particular attention was first directed at normalizing the patient’s low body temperature with Armour’s Desiccated Thyroid (by prescription from a licensed M. D.). We obtained good success with the above treatment protocol when it was coupled with the staggered dosage of the desiccated Thyroid. However, there was something still lacking. Attention should also be directed at the nutritional status of the patient.
In October of 1997 I was introduced to a substance called MSM. MSM is a source of water soluble Sulfur. Sulfur is the 4th most abundant mineral in our bodies and, yet, we obtain very little from our food. Please see SULFUR in the mineral section.
Sulfur (along with Vitamin C) is needed to make good quality collagen. Collagen makes up our soft tissue structures and if there is sulfur lacking in our diets it is only a matter of time before the quality of our collagen is diminished. Specifically, sulfur is needed as a source of SH- or sulfhydryl groups to keep the collagen fibers from sticking or gluing together. When this occurs oxygen and other nutrients cannot enter nor can waste materials be eliminated from the tissues. Therefore, pain and fatigue is the result.
Clinically differentiating PFS with the localized lesions of myofascitis and fibrositis is of paramount importance. On the one hand, patients present with what appears to be a metabolic problem (PFS) and on the other, one of sustained stress to muscles. Many times these symptoms are lumped into one classification and treated with mixed results.
The pathogenesis of PFS is currently unknown but probably related to metabolic disturbances and nutritional deficiencies. The pathogenesis of specific soft tissue lesions is not specifically known, but is probably due to local trauma and/or to spinal disturbances (IVD lesions, etc.) causing sympathetic reflex phenomena to the soft tissues.
A proposed sequential series of PFS causation might be: 1. self-sustaining spasms or nutritional deficiencies — 2. hypoxia (low oxygen) — 3. diminished mitochondria — 4. diminished ATP (energy) production — 5. infiltration of glycogen and collagen deposition — 6. increased fibroblasts and finally — 7. gelling & clumping of the muscle fibers.
The soft tissues now become a foci of pain and pathology. The clinician must develop good palpation skills to effectively evaluate the patient’s condition.
Management of Primary Fibromyalgia Syndrome patients is a challenge and should be conceived as a comprehensive regimen. The same can be said of Specific Fibromyalgic conditions. The results can be most successful and gratifying.
Ahles, T.A., M.B. Yunus, et al, Psychological Factors Associated with Primary Fibromyalgia Syndrome, Arthritis and Rheumatism 27:10, pp. 1101 -1106, 1984.
Bengtsson, A., A.T. Masi, Primary Fibromyalgia, American Family Physician, pp. 115-121, 1982.
Bennett, R.B., Current Issues Concerning Management of Fibrositis/ Fibromyalgia Syndrome, Am. J. Med. 81:15-18,1986.
Blair, L., J. Treadwell, Fibromyalgia or the Fibrositis Syndrome: A New Look, New Zealand Medical Journal, pp. 457-459,1981,
Calabro, J.J., Fibromyalgia (Fibrositis) In Children, Amer. J. Med. 81:57-59, 1986.
Cyriax, i., Illustrated Manual oftsers pedic Medicine, O.M. Publicalions, pp. 17-18,1985.
Kalyan-Rayman, U.P. et al, Muscle Pathology in Primary Fibromyalgia Syndrome: A Light Microscopic, Histochemical, and Ultrastructural Study, J. Rheum, 11:6, 808-813, 1984.
Korr, I.M., The Facilitated Segment: A Factor In Injury to the Body Framework, The Collected Papers of Irwin M. Korr, Amer. Acad. Osteopath. p. 188, 1979,
Korr, I.M., Sustained Sympathetonia As a Factor in Disease, The Neurobiologic Mechanisms in Manipulative Therapy, Plenum Press. New York, pp. 229-256, 1978.
Russell, I.J. et. al. Is There a Metabolic Basis For the Fibrositis Syndrome? Amer. J. Med. 81:50-53,1986.
Simons, D.G., Muscle Pain Syndromes – Part 1, Amer. J. Physical Med. 54:6,289-308,1975.
Simons, D.G., Muscle Pain Syndromes – Part 11, Amer. J. Physical Med. 55:1, 15-39, 1976.
Simons, D.G., Fibrositis/ Fibromyalgia: A Form of Myofascial Trigger Points? Amer. J. Med. 81:93-98,1986.
Tran. T.V, Personal Communications – use of procaine and vitamin 6 12 injections in trigger points.
Wallace, D.J., Fibromyalgia: Unusual Historical Aspects and New Pathogenic Insights, Mt. Sinai J. Med. 51:2, 124-131, 1984.
Yunus, M.B., et al, Primary Fibromyalgia (Fibrositis): Clinical Study of 50 Patients with Matched Normal Controls, Seminars in Arthritis and Rheumatism 11:1, 151-170,1981.
Yunus, M.B. and A.T. Masi, Primary Fibromyalgia, Amer. Family Physician, pp. 115-121, 1982.
Yunus, M.B. et al, Pathologic Changes I in Muscle In Primary Fibromyalgia Syndrome, Amer. J. Med. 81:38-41, 1986.
Winston W. Greene, B.S., B.A., D.C. has lectured on subjects ranging from nutrition and low back pain to sports nutrition and the professional athlete. Dr. Greene received his B.S. degree in Pharmacc7f9d B.A. degree in Zoology from the University of Texas at Austin and his D.C. degree from Texas Chiropractic College in 1983.
PRIMARY FIBROMYALGIA SYNDROME (PFS)
Fibromyalgia and chronic fatigue syndrome share many features.
Although fibromyalgia is a disorder that has many facets, the central cause of the pain of fibromyalgia is a low level of serotonin.
The primary treatment goals in fibromyalgia are to raise serotonin levels, improve sleep quality, and assure adequate magnesium levels.
Individuals with fibromyalgia have altered sleep patterns: reduced REM sleep and increased non-REM sleep.
The severity of the pain of fibromyalgia correlates with the rating of poor sleep quality.
5-HTP has shown considerable benefit in treating fibromyalgia in doubleblind studies.
Although 5-HTP can be effective on its own, we recommend the combination of 5-HTP (100 mg), St. John’s wort extract (300 mg, 0.3-percent hypericin content), and magnesium (150 to 250 mg) three times per day.
Magnesium supplementation has produced very good results in treating fibromyalgia.
a. Sip 2 to 3 oz of distilled or filtered water every 30 minutes, while awake, daily (no well water or water containing fluoride or chlorine); more if you are sweating.
b. Eliminate all refined carbohydrates, alcohol, processed foods, fermented foods, dairy products, and gluten containing grains and caffeine containing foods such as coffee, (except tea), cola and chocolate as much as possible. If you are overweight, insure total daily carbohydrate intake is limited to 60 grams.
c. Eliminate all hydrogenated fats and oils as much as possible. The only oils you should use are extra virgin olive oil, fish oils and coconut oil.
d. Exercise moderately to oxygenate the tissues.
The primary treatment goals in fibromyalgia are to a) raise serotonin levels, b) improve sleep quality, c) assure adequate magnesium levels and d) repair the “leaky gut” that has been implicated as a major cause of PFS.
In addition, there may be recommendations given in the CHRONIC FATIGUE SYNDROME section that are appropriate in any given case. Please follow the relevant recommendations given there if needed.
1. BIO-MULTI PLUS-IRON FREE – 1 tablet, 3 times daily after meals.
2. BIO-C PLUS 1000 – 1 tablet, 3 times daily after meals.
3. M S M POWDER – 1/2 teaspoonful 2 to 4 times daily depending on the severity of symptoms. NOTE: Try to take MSM with your Vitamin C.
4. RIBOSE POWDER – 2 teaspoonsful twice daily preferrably between meals.
5. BIOMEGA-3 – 4 – 5 capsules, twice daily after meals for 1 month, then 4 – 5 capsules once daily thereafter M – F of the week.
FOR THE 1ST MONTH – DETOX PROGRAM
a) M C S – 2 capsules after breakfast and 1 capsule after lunch for 1 month.
b) BETA TCP – 2 tablets, 3 times daily after meals.
c) A D H S – 2 tablets after breakfast and 1 tablet after lunch. Do not take after 1PM.
d) 21ST CENTURY HOMEOPATHICS REMEDY # 1 – Detoxification – 1 capful daily until all the bottle is taken.
AFTER DETOXIFICATION, BEGIN WITH SPECIFIC NUTRIENTS.
Specific Nutrients: When symptoms or condition begins to subside, gradually, as needed, wean yourself from the Specific Nutrients & stay on the Primary Nutrients. If any symptoms re-occur resume Specific Nutrients.
6.. BUTYRIC-CAL-MAG – 2 capsules, 3 times daily with meals for 3 months then discontinue.
7. I P S – 2 capsules, 3 times daily with meals for 3 months then discontinue.
8. MG-ZYME 100mg -1 tablet, 3 times daily with meals.
9. Co Q-ZYME 30 -2 tablets, once daily with a meal.
10. LI-ZYME FORTE – 3 tablets at bedtime for 1 bottle (contains the essential mineral Lithium which is often low in PFS patients. Lithium reduces receptor-cell sensitivity to cortisol thus reducing insomnia).
11. Armour’s desiccated thyroid — dosage as directed (and if axillary temperatures are low).
12. IODORAL – 2 tablets morning & 1 to 2 tablets in the evening.
13. ST. JOHN’S PLUS
Causes of Primary Fibromyalgia:
The cause or causes of primary fibromyalgia are not known; this condition is also sometimes referred to as idiopathic fibromyalgia. Many experts believe that fibromyalgia is not a disease but rather a dysfunctional disorder caused by a constellation of biologic responses to stress in individuals who are more susceptible to such stress because of negative personal histories or genetic factors.
Family Factors. One recent study reported that 28% of the children of mothers with fibromyalgia also develop the disorder. There were no differences in psychological disorders among those offspring with fibromyalgia and those who did not develop it. Another study noted that 66% of parents of children with fibromyalgia reported some sort of chronic pain — with about 10% reporting fibromyalgia. Close-knit families, oddly enough, were more likely to be associated with severe cases of childhood fibromyalgia.
One noted that the severity of the disorder increased in children whose parents were less able to cope with their children’s pain. It is not clear if genetic or psychological factors or both are involved.
Chronic Sleep Disturbance. Some experts believe that disturbed sleeping patterns may be the original precipitating factor for many cases of fibromyalgia pain. In one study, volunteers who did not have fibromyalgia reported fibromyalgia-like pain after they had been subjected to disrupted deep sleep. Disturbed sleep appears to trigger factors in the immune system that cause inflammation and pain.
Abnormalities in the Brain. Studies of hormonal, metabolic and brain chemical activity in fibromyalgia patients have shown a number of abnormalities. Brain scans of fibromyalgia patients have revealed reduced blood flow to certain regions of the brain related to pain sensation. Of particular interest to researchers are possible abnormalities in the brain system known as the hypothalamus-pituitary-adrenal gland axis, which controls important functions, including growth, sleep, response to stress, and depression. One research target is the hormone somatomedin C (also called insulin-like growth factor) which is produced by the pituitary gland in the brain during deep sleep and is responsible for communicating information about pain-producing stimuli to the brain. Very high levels of somatomedin C have been detected in the spinal fluid of fibromyalgia patients. Such increased levels may cause a heightened sensitivity for pain in such patients, who can experience pain even after mild muscular activity. This causes patients to reduce their physical activity, which, in turn, results in muscle weakness, leading to a perpetual loop of muscle atrophy, and increasing pain with less and less physical exertion. The pain also causes on-going sleep disturbance. Excess somatomedin C may be due to a genetic defect or may be derived from early unhealthy sleep habits that, over time, cause hormonal and brain chemical imbalances.
NOTE: It is now known that diets high in carbohydrates increase the release of somatomedin C. Therefore, it is imperative that the patient decrease their intake of carbohydrate foods that have a high glycemic index.
People with fibromyalgia also tend to have low levels of the neurotransmitter serotonin and its precursor; an amino acid called tryptophan. (A neurotransmitter is a chemical in the brain that serves as a messenger between neurons.) Low levels of both these chemicals are associated with depression and other symptoms of fibromyalgia, including gastrointestinal distress, mig??e headaches, and anxiety. Some experts believe that migraine headaches and fibromyalgia are related because of possible defects in the systems that regulate serotonin and another neurotransmitter, epinephrine (commonly called adrenaline). Low levels of magnesium have also been noted in both fibromyalgia and migraine sufferers.
Autoimmunity. Fibromyalgia resembles a number of rheumatic disorders that are known as autoimmune disorders, including rheumatoid arthritis and systemic lupus erythematosus. These diseases occur when a defective immune system produces factors known as autoantibodies, which attack proteins in the body’s own tissue, mistaking them as antigens (foreign proteins). Recently, researchers have identified certain autoantibodies in many fibromyalgia patients that affect neurologic and hormonal systems. There is no strong evidence, however, that a faulty immune system is a primary cause of fibromyalgia. HENCE, the importance of including MSM in your diet.
Post-Traumatic Stress Disorder. One study has indicated that the incidence of sexual and physical abuse is higher in female patients with fibromyalgia than in the general population. This could indicate that post-traumatic stress syndrome may play a role in the development of this disorder in some patients. Post-traumatic stress disorder (PTSD) is an anxiety disorder that is a reaction to a specific traumatic event. Symptoms of this condition, which can occur for years after the traumatic event include emotional withdrawal, hopelessness, irritability, mood swings, sleep problems, inability to concentrate, and an excessive startle response to noise. There is some evidence that PTSD actually results in changes in the brain, possibly from long-term overexposure to stress hormones.
Hypervigilance. It has been suggested that some factor or a combination of factors, such as a genetic susceptibility, bioxperc abnormalities, chronic sleep deprivation, or trauma, causes generalized hypervigilance, an amplification of sensation. People with this condition are oversensitive to external stimulation and are preoccupied with the sensation of pain. One study compared three groups of individuals: those with fibromyalgia; patients with rheumatoid arthritis; and people without these disorders. They were given a questionnaire to assess their response to pain and noise. Of the three groups, the fibromyalgia patients were least tolerant and most attentive to such stimuli.
Muscle Cell Abnormalities. Early research suggested that fibromyalgia is basically a muscular disorder. One relatively recent study reported that fibromyalgia patients had lower levels of the muscle-cell enzyme phosphocreatine and adenosine triphosphate
SEE: HYPOTHYROIDISM in this site.
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THE METABOLIC TREATMENT OF FIBROMYALGIA (1260 p5.68)
Altern Med Rev 1998 Oct;3(5):367-75
Fibromyalgia and the serotonin pathway.
Fibromyalgia syndrome is a musculoskeletal pain and fatigue disorder manifested by diffuse myalgia, localized areas of tenderness, fatigue, lowered pain thresholds, and nonrestorative sleep. Evidence from multiple sources support the concept of decreased flux through the serotonin pathway in fibromyalgia patients. Serotonin substrate supplementation, via L-tryptophan or 5-hydroxytryptophan (5-HTP), has been shown to improve symptoms of depression, anxiety, insomnia and somatic pains in a variety of patient cohorts. Identification of low serum tryptophan and serotonin levels may be a simple way to identify persons who will respond we proo this approach.