Rheumatism by Dr. Lance Christiansen: Difference between revisions
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During the winter of 2002, two more patients, in their forties, failed to experience a decrease in their adverse, neurological symptoms and signs after undergoing lumbar spinal surgery; they were, really, much more symptomatic after spinal surgery than before. That adverse experience, which saddened the patients and made me very disappointed, in addition to the adverse experiences of many other patients who underwent spinal surgery, mentioned above, stimulated me to initiate a clinical investigation to see if I could determine if an ''alternative cause'' could be discovered to account for my patients' lumbosacral/buttock and shoulder/cervical neurological pain beside the venerable, but desultory herniated spinal-disc concept. I thought there was something "rotten (deceitful, mercenary and unscrupulous) going on" within the various professional aspects of "spinal care", in general, and spinal surgery, in particular. | During the winter of 2002, two more patients, in their forties, failed to experience a decrease in their adverse, neurological symptoms and signs after undergoing lumbar spinal surgery; they were, really, much more symptomatic after spinal surgery than before. That adverse experience, which saddened the patients and made me very disappointed, in addition to the adverse experiences of many other patients who underwent spinal surgery, mentioned above, stimulated me to initiate a clinical investigation to see if I could determine if an ''alternative cause'' could be discovered to account for my patients' lumbosacral/buttock and shoulder/cervical neurological pain beside the venerable, but desultory herniated spinal-disc concept. I thought there was something "rotten (deceitful, mercenary and unscrupulous) going on" within the various professional aspects of "spinal care", in general, and spinal surgery, in particular. | ||
I thought about the severe pain that my patients were experiencing and I recalled a ''basic concept in medicine'': Pain (dolor), calor (warmth), redness (rubor), swelling (tumor) and loss of function (functio laesa) are the five signs and symptoms, or factors, of inflammation. Inflammation, itself, is the process by which individuals heal themselves. Pain is the ''only symptom'' of inflammation; the other factors are the ''signs'' of inflammation. During the inflammatory response, pain, at times, is the only noticeable feature of the healing, inflammatory response especially if the injured tissue is deep in the body so it cannot be easily observed. | I thought about the severe pain that my patients were experiencing and I recalled a ''basic concept in medicine'': Pain (dolor), calor (warmth), redness (rubor), swelling (tumor) and loss of function (functio laesa) are the five signs and symptoms, or factors, of inflammation. Inflammation, itself, is the process by which individuals heal themselves. Pain is the ''only symptom'' of inflammation; the other four factors are the ''signs'' of inflammation. During the inflammatory response, pain, at times, is the only noticeable feature of the healing, inflammatory response especially if the injured tissue is deep in the body so it cannot be easily observed. | ||
Acute pain is the most common adverse sensation a person senses when they experience an acute injury such as a laceration, a sprain or a fracture. Over time, acute pain associated with a trauma merges into the pain created by the self-healing, inflammatory phenomenon and pain, therefore, becomes somewhat chronic, but it usually decreases and disappears as the patient heals him/herself. Since the member-patients of my chronic neurological pain investigative group had chronic pain, and it was usually triggered by a traumatic accident, but one connected with relatively mild trauma. I realized that the patients' severe, chronic pain was a symptom of an exacerbation of an existing malady and their pain was a symptom of the inflammatory, self-healing phenomenon. Since the patients' neurological pain was chronic, however, and not decreasing, It seemed that the normal physiological inflammatory healing process was, for some reason, not being successful. | Acute pain is the most common adverse sensation a person senses when they experience an acute injury such as a laceration, a sprain or a fracture. Over time, acute pain associated with a trauma merges into the pain created by the self-healing, inflammatory phenomenon and pain, therefore, becomes somewhat chronic, but it usually decreases and disappears as the patient heals him/herself. Since the member-patients of my chronic neurological pain investigative group had chronic pain, and it was usually triggered by a traumatic accident, but one connected with relatively mild trauma. I realized that the patients' severe, chronic pain was a symptom of an exacerbation of an existing malady and their pain was a symptom of the inflammatory, self-healing phenomenon. Since the patients' neurological pain was chronic, however, and not decreasing, It seemed that the normal physiological inflammatory healing process was, for some reason, not being successful. | ||
Revision as of 20:44, 27 January 2012
| Rheumatism by Dr. Lance Christiansen | |
| ICD-10 | M79.0 |
|---|---|
| ICD-9 | 729.0 |
| MeSH | D012216 |
Editor-in-Chief: Lance Christiansen, D.O.
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==Overview== ( This article undergoing a major edit-January, 2012)
An understanding of the chronic, systemic, inflammatory disease of rheumatism was enabled by my general education in biology at Whitman College, after which, for five years, I was a Naval Aviator in the US Marine Corps and flew many aircraft including the RF-4B Phantom II photoreconnaissance aircraft in a combat environment and older transport with radial, reciprocating engines: a C-119G Flying Boxcar, an aircraft of the "old school", which had to be, completely, "flown" without fancy electronic aids. Surprisingly, perhaps, I surely think that my experience flying complex aircraft enabled me to have certain skills in systems analysis, and an independence of mind, that I subconsciously used during my work in medicine.
After five years active duty in the Marines I remained in the active reserve force as a "weekend warrior" for four years. During that time I resumed my medical education, which consisted of two years of premedical studies at the University of Washington, four years of medical school at the Chicago College of Osteopathic Medicine, three of which I attended on a US Navy scholarship. Thereafter, I completed a one year medical internship at the Oakland Naval Regional Medical Center. I finished my medical education at the age of 38.
After spending five years in the Navy as a general medical officer and flight surgeon, I left active duty, but remained in the Navy Reserves for 7 years. When I left active duty I returned to my home state, Washington, and developed and operated my own clinics for twenty-three years. During that period I developed clinics in three small towns in S.W. Washington that were geographically close together. Eventually, my small town clinic system had 7000 patients enrolled. Naturally, I could not take care of all 7000 patients so I employed physician assistants and for a number of years I employed another physician. The independent clinic situation I developed provided an environment, which enabled me to work and think somewhat independently compared to other medical settings. I, personally, examined and treated patients during, approximately, 220,000 office visits and after-hours urgent care visits and I accomplished at least 2000 house calls. Regularly, I treated males and females, of all ages, for all diseases, the latter, of course, up to my ability. At times, I treated family members for up to four generations. The continuity of medical care that I provided, in a semi-rural setting, enabled me to learn a great amount of medical information not recorded in typical medical texts. In addition, my clinics were located in an economically depressed area of S.W. Washington State and, over time, I learned that poorer people are often sicker people so the clinical elements of their disease processes appeared especially distinct.
From 2002 until 2005, the last three years that I operated my clinics, I conducted a clinical investigation in an attempt to determine the cause of chronic neurological pain, since, over many years, most patients who underwent spinal surgery failed to experience an improvement in their neurological symptoms and signs within a reasonable period, for example, two weeks, after their spinal surgical experience. In addition, surgery for ulnar neuropathy and carpal tunnel syndrome was also, usually, unsuccessful. If a patient underwent a neurological surgical procedure and experienced an improvement in their clinical condition months or years after their surgery that phenomenon did not prove that the surgical procedure aided the patient since many patients experienced an improvement in their symptoms and signs, over time, without any specific treatment.
During my clinical investigation I attracted 700 patients who experienced severe, chronic, neurological pain; many of them, perhaps forty percent, had experienced a failure of neurological surgery to improve their symptoms and signs. Usually their pain, and other symptoms and signs, were localized to the distribution of certain large nerves or plexi, such as a combination of sciatic, posterior femoral cutaneous, and pudendal neuropathy, popularly termed, sciatica. In addition, other patients exhibited femoral neuropathy, median neuropathy, ulnar neuropathy, peroneal neuropathy and brachial plexopathy, but some patients had what appeared to be diffuse pain in many areas of the body and they frequently had been diagnosed, by other physicians, to have fibromyalgia. Most patients exhibited dermatological abnormalities, which reminded me of certain characteristic dermatological features of lupus erythematosis or dermatomyositis. Often patients had had been diagnosed to have rosacea.
During my investigation, I provided my patients, nearly monthly, with repetitious, physical examinations, including repetitious, analytical, neurological examinations and I determined that the patients who had been diagnosed to have fibromyalgia had a diffuse neuropathy-plexopathy wherein the terminal nerves of the sacral plexus, the femoral nerve, and the brachial plexus were anatomical structures that exhibited neurological abnormalities. Eventually, in reference to patients who had been diagnosed with fibromyalgia, II found information within medical texts that indicated that other physicians thought that muscular and/or fibrous tissue pain really originated from nerves, or was referred to nerves, within muscular and fibrous tissues.
For instance, "MUSCLE PAIN, ACHING, AND TENDERNESS Painful Muscles do not always imply muscle disease...disease of major peripheral nerves or of their small intramuscular branches may produce both muscle pain and weakness." ( 1 ) In addition, the following quote gave my findings support: "MYALGIA (Fibrocitis, Myositis) Definition--A painful affection of the voluntary muscles and of the fasciae and periosteum to which they are attached. It is probable that in many cases the fibrous tissue is especially affected--a fibrositis. It is by no means certain that the muscular tissues are the seat of the disease. Many writers claim that in some cases it is a neuralgia of the sensory nerves of the muscles." ( 2 ) Finally, certain authors have indicated that paresthesias are experienced by patients who have been diagnosed to have fibromyalgia: "Fibromyalgia is a commonly encountered disorder characterized by chronic widespread musculoskeletal pain, stiffness, paresthesias, disturbed sleep and easy fatigability along with multiple painful tender points, which are widely and symmetrically distributed...Patients may complain of low back pain which may radiate into the buttocks and legs...patients may complain of numbness of their hands and feet." ( 3 ) The pattern of neurological symptoms and signs, just mentioned: "low back pain which may radiate into the buttocks and legs..." reminds me of the presentation of sciatica syndrome
Fibromyalgia is a painful, somatic syndrome, which has had, historically, many other synonymous names. For instance, "Fibrositis, fibromyalgia, and fibromyositis are synonyms for a disorder associated with pain and tenderness of muscle and adjacent connective tissue." ( 1 ) In addition, Fibrositis is explained within Sir William Osler's text of 1935 in a reasonably thorough fashion:"FIBROSITIS Definition.--An inflammation of fibrous tissue which may occur in many parts of the body , involving ligaments, tendons, muscle sheaths, fasciae, aponeuroses, periosteum, nerve sheaths, or any part where fibrous tissue is found. It is associated with arthritis in many cases and to designate the involvement of special parts certain terms are employed, as synovitis, tenosynovitis, bursitis and perineuritis. Fibrositis is very common and causes many painful conditions often termed myalgia, muscular rheumatism, neuritis, etc." ( 4 ) Paying attention to the above quoted information makes it apparent that muscular rheumatism, fibrositis, fibromyositis myalgia, myositis, neuritis, and fibromyalgia have been used as synonymous names for the same variable condition, which have come into common use in various locations at various times. In this article the term muscular rheumatism/fibromyalgia (a combination of probably the most old and most new synonymous terms) will be used to stand for all the synonymous, syndromic names, above.
Since the signs and symptoms of muscular rheumatism/fibromyalgia are usually anatomically wide-spread the painful somatic condition can be considered, generally, to be systemic in nature. Additional information such as: "It is associated with arthritis in many cases...". And in addition, "Myalgias are also frequent in other rheumatological disorders including rheumatoid arthritis, systemic lupus erythematosis, polyarteritis nodosa, scleroderma, and mixed connective tissue syndrome...", and finally, "Patients with polymyositis and dermatomyositis may have myalgias..." ( 5 ) The above information, taken together, causes, after inductive thought, the the development of the concept: that muscular rheumatism/fibromyalgia's painful clinical presentation is simply a mild presentation of generalized rheumatic disease. Rheumatic diseases are considered to be autoimmune in nature, so therefore, muscular rheumatism/fibromyalgia seems, also, to be a presentation of an underlying autoimmune disease process.
Muscular rheumatism/"...Fibromyalgia is a commonly encountered disorder characterized by chronic widespread musculoskeletal pain, stiffness, paresthesia, disturbed sleep, and easy fatigability...Patients complain of feeling fatigued and exhausted and wake up tired." (3 ) Concerning chronic fatigue syndrome, CFS: "Typically, CFS arises suddenly in a previously active individual. An otherwise unremarkable flu-like illness...leaves unbearable exhaustion in its wake. Other symptoms such as headache, sore throat, tender lymph nodes, muscle and joint aches, and frequent feverishness, lead to the belief that an infection persists, and medical attention is sought." Eventually, "...other features of the syndrome become evident--disturbed sleep, difficulty in concentration, and depression. In addition, patients exhibit, " muscle aches ( 80% ), joint aches (75%), feverishness ( 75%), psychiatric problems (65%, allergies (55%), abdominal cramps (40%), weight loss (20%, rash10%, rapid pulse (10%, weight gain (5%, chest pain 5%, and night sweats (5%)..." Often the patient presents with features that also meet criteria for other subjective disorders such as fibromyalgia and irritable bowel syndrome." ( 3 ) Muscular rheumatism/fibromyalgia and chronic fatigue syndrome appear together so frequently, about 80% of the time, it is probably reasonable to consider them as manifestations of one underlying, autoimmune disease, which is triggered by an infectious disease process of unknown etiology.
Within the section of a reliable text dealing with rheumatoid arthritis (RA) the author indicates that: "In approximately two-thirds of patients, it begins insidiously with fatigue, anorexia, generalized weakness, and vague musculoskeletal symptoms until the appearance of synovitis becomes apparent. This prodrome may exist for weeks or months and defy diagnosis...In approximately 10% of individuals the onset is more acute, with a rapid development of polyarthritis, often accompanied by constitutional symptoms, including fever, lymphadenopathy, and splenomegaly."
Further, concerning extraarticular manifestations, the author writes: "RA is a systemic disease...Rheumatoid nodules develop in 20 to 30% of persons with RA. They are usually found on periarticular structures, extensor surfaces, or other areas subjected to mechanical pressure, but they can develop elsewhere, including the pleura and meninges. Common locations include the olecranon bursa, the proximal ulna, and Achilles tendon, and the occiput." In addition, "Examination of early nodules has suggested that the initial event may be a focal vasculitis...Rheumatoid vasculitis, which can affect nearly any organ system, is seen in patients with severe RA...In its most aggressive form, rheumatoid vasculitis can cause polyneuropathy and mononeuritis multiplex...and visceral infarction." Finally, "Neurovascular disease presenting either as a mild distal sensory neuropathy or as mononeuritis multiplex may be the only sign of vasculitis...Myocardial infarction secondary to rheumatoid vasculitis has been reported, as has vasculitic involvement of the lungs, bowl, liver, spleen, pancreas, lymph nodes and testes." In addition, the author states: "Felty's syndrome consists of chronic RA, splenomegaly, neutropenia, and, on occasion, anemia and thrombocytopenia." Finally, he indicates, "The median life-expectancy of persons with RA is shortened by 3 to 7 years. Of the 2.5-fold increase in mortality rate, RA itself is a contributing feature in 15 to 30%. The increased mortality rate seems to be...attributed largely to infection and gastrointestinal bleeding. Recent evidence has also shown an important role of cardiovascular disease in the increased mortality of RA patients, and this appears to diminish with effective anti-inflammatory therapy. ( 3 )
Patients with systemic lupus erythematosis also experience a wide range of extra-somatic abnormalities such as the development of arteriosclerosis, including coronary artery disease, mental abnormalities, vasculitis, neuropathic abnormalities, and vasculitis. Also, "Systemic symptoms, particularly fatigue and myalgias/arthralgias, are present most of the time...most patients have myalgias without frank myositis." Severe systemic illness...can occur with fever, prostration, weight loss, and anemia in addition to any other organ-targeted manifestations. ( 3 )
Since patients with Muscular rheumatism/fibromyalgia syndrome, chronic fatigue syndrome, rheumatoid arthritis syndrome and systemic lupus erythematosis syndrome have certain key symptoms and signs in common, and since they are all autoimmune disorders, it is probable that they are highly variable clinical manifestations of the same underlying, variable, autoimmune, pathological process. A similar assessment can be made if all of the various rheumatic syndromes such as dermatomyositis, systemic sclerosis, polyarteritis nodosa, palondromic rheumatism, juvenile rheumatoid arthritis, and Sjogren's syndrome are considered since they all have similar systemic findings.
As mentioned above, during the period I practiced medicine, I treated many patients who experienced lumbosacral/buttock (sciatic) and shoulder/cervical pain, with neuropathic signs and symptoms into the appropriate limb, which was often severe and chronic. The adverse condition affected younger persons, from their twenties through their fifties, most frequently, but even teenagers and older people, over sixty years of age, were also frequent victims. Usually, such painful maladies were thought to be caused by the compression of spinal nerves by herniated spinal-discs in the lumbar or cervical region. Some patients had been diagnosed with lumbar or cervical spinal stenosis. In the case of the upper extremity, some patients were diagnosed, in other clinics, with thoracic outlet syndrome. Other painful neurological problems, which I treated somewhat frequently were median neuropathy and ulnar neuropathy. Less frequent neurological maladies were femoral neuropathy, peroneal neuropathy, and meralgia paresthetica, with the latter being neuropathy of the lateral femoral cutaneous nerve. It was not uncommon for patients to give complaints of painful symptoms and signs that, at the time, I considered to be those of fibromyositis or fibrositis even though the term fibromyalgia was growing in popularity. ( 1 ) The reader needs to understand, however, that the above medical conditions are syndromes, not well defined diseases, because their causes are not, absolutely, known.
Many patients, through the years, had failed to experience an improvement in the above-described, painful, somewhat localized, neurologic maladies even if they underwent surgical correction. Individuals who were provided spinal surgery often, eventually, underwent many spinal surgical procedures. One male patient had experienced eight lumbar spinal surgical procedures and one female patient had underwent four cervical and three lumbar spinal surgical procedures; neither patient, unfortunately, experienced an improvement in their neurological symptoms and signs. Usually, I was treating about twenty-five patients who were experiencing chronic, neurological pain and who had experienced the failure of surgical attempts, most commonly lumbar and/or cervical spinal surgery, to decrease their painful symptoms and their abnormal signs.
In addition, through the years,the majority of patients who experienced surgical procedures for carpal tunnel syndrome and ulnar neuropathy did not experience an improvement in their painful condition within a reasonable period after their surgical experience, and they, thereafter, experienced a chronic, neurological pain syndrome.
During the winter of 2002, two more patients, in their forties, failed to experience a decrease in their adverse, neurological symptoms and signs after undergoing lumbar spinal surgery; they were, really, much more symptomatic after spinal surgery than before. That adverse experience, which saddened the patients and made me very disappointed, in addition to the adverse experiences of many other patients who underwent spinal surgery, mentioned above, stimulated me to initiate a clinical investigation to see if I could determine if an alternative cause could be discovered to account for my patients' lumbosacral/buttock and shoulder/cervical neurological pain beside the venerable, but desultory herniated spinal-disc concept. I thought there was something "rotten (deceitful, mercenary and unscrupulous) going on" within the various professional aspects of "spinal care", in general, and spinal surgery, in particular.
I thought about the severe pain that my patients were experiencing and I recalled a basic concept in medicine: Pain (dolor), calor (warmth), redness (rubor), swelling (tumor) and loss of function (functio laesa) are the five signs and symptoms, or factors, of inflammation. Inflammation, itself, is the process by which individuals heal themselves. Pain is the only symptom of inflammation; the other four factors are the signs of inflammation. During the inflammatory response, pain, at times, is the only noticeable feature of the healing, inflammatory response especially if the injured tissue is deep in the body so it cannot be easily observed.
Acute pain is the most common adverse sensation a person senses when they experience an acute injury such as a laceration, a sprain or a fracture. Over time, acute pain associated with a trauma merges into the pain created by the self-healing, inflammatory phenomenon and pain, therefore, becomes somewhat chronic, but it usually decreases and disappears as the patient heals him/herself. Since the member-patients of my chronic neurological pain investigative group had chronic pain, and it was usually triggered by a traumatic accident, but one connected with relatively mild trauma. I realized that the patients' severe, chronic pain was a symptom of an exacerbation of an existing malady and their pain was a symptom of the inflammatory, self-healing phenomenon. Since the patients' neurological pain was chronic, however, and not decreasing, It seemed that the normal physiological inflammatory healing process was, for some reason, not being successful.
The investigation I conducted was, mainly, for the first two and one-half years, clinical and academic in nature. The patients' medical histories and their family medical histories had indicated that most of them, surprisingly, had experienced many of the same, or similar, additional, serious diseases even if their average age was 42. Of the 700 patients who experienced severe, chronic, neurological pain, 70 had had cancer or developed cancer while I was seeing them; 68 patients had experienced, or were experiencing, a cardiac malady and of those, 7 were experiencing cardiac syncope. A meaningful percentage of patients had experienced, or were experiencing, an endocrine problem such as Hashimoto's thyroiditis, hypothyroidism, Addison's disease, Cushing's syndrome, hypoparathyroidism, pituitary abnormalities, or polycystic ovary disease, for instance, all of which are usually thought to be autoimmune in nature. ( 3, 5 ) About ten patients were experiencing a gastrointestinal problems such as ulcerative colitis, Crohn's disease, celiac disease, cholecystitis, or primary sclerosing cholangitis, most of which are also autoimmune in nature. All of the 700 patients were experiencing a rheumatic disease such as rheumatoid arthritis, Sjogren's syndrome, systemic lupus erythematosis, discoid lupus erythematosis, progressive systemic sclerosis, mixed connective tissue syndrome, Wegener's granulomatosis, or osteoarthritis. I had in the past I had treated two patients with dermatomyositis and, in retrospect, they had similar symptoms and signs as many of my investigative patients. The most common rheumatic problem was mild rheumatoid arthritis. The rheumatic diseases, in general, are also considered to be autoimmune in nature. and they frequently feature neuropathic symptoms and signs. ( 3, 5 )
Since many patients in my investigative group exhibited neuropathic abnormalities in more than one limb, I thought that phenomenon indicated that their "underlying" malady was systemic in nature. Since autoimmune disease is caused by autoantibodies, which travel, mainly, throughout the body via the vascular system, I thought autoimmunity was the pathological mechanism by which my patients' painful neurological problems developed, but it also, probably, caused their other, somewhat uniform, disease presentations, which I thought were, really, "target-organ-manifestations" of their systemic autoimmune disease. Eventually, I located articles by respected investigators who indicated that painful neuropathy syndromes could be autoimmune in nature. ( 6, 7 )
Since the patients in my investigative group had chronic neurological pain, and since it had affected their economic lives, their private lives and, often, their family relationships, many were clinically depressed. Those who had been diagnosed with fibromyalgia, really, I felt, had chronic rheumatism/fibromyalgia/chronic fatigue syndrome/depression in a concomitant fashion. I thought that their depression could have an organic cause, but it also, concomitantly, had a situational stress-realted cause. Since investigators, as mentioned above, thought that muscular rheumatism/fibromyalgia had abnormalities of the sensory nerves within muscles, that provided a neurological continuity of concept during my investigation.
Even though I thought that the patients in my chronic neurological pain investigative group were experiencing a chronic autoimmune disease I did not know, however, what caused their autoimmune disease to develop. Since neurological back pain and sciatica syndrome is so common in society, and since rheumatic syndromes, such as rheumatoid arthritis and lupus erythematosis, are very common in society, I decided the cause would probably be an ubiquitous agent, but one which was not known to, frequently, at least, be highly pathological. The patients' concomitant, rheumatic, autoimmune syndromes' signs and symptoms, which were similar, in may ways, to the signs and symptoms of patients with muscular rheumatism/fibromyalgia/chronic fatigue syndrome, which seemed to be autoimmune in nature, caused me to consider that the underlying, pathological mechanism of my patients' chronic, neurological pain was autoimmune in nature.
After examining patients for a long period I noted that they had similar dermatological features. Rosacea, the remains of scarring acne, facial, dermatological abnormalities similar to lupus erythematosis, a great number of nevi on sun exposed surfaces, petechiae, telangectasias, spider nevi, and erythma of the malar region, chin, nose and "v" of the neck, areas where the sun's rays typically strike. Some had lesions with the pattern of the shawl sign of dermatomyositis. All patients had plantar erythema, palmar erythema, and erythematous skin folds of the palms, which reminded me of Pastia's sign of scarlet fever.
After two and one-half years of ten to fourteen hour days I had a breakthrough in my investigation. A thirty-four year old woman had moved to Onalaska, Washington from Plano, Texas. She had a chronic pain syndrome diagnosed as fibromyalgia in Texas a number of years previously and she had been provided Oxycontin for chronic pain and Roxicet for break-through pain. I had about twenty individuals who had been given the same diagnosis prior to their association with my clinic and after thorough examinations I had determined that they had a wide-spread painful neuropathy and that their pain was not caused by abnormal fibrous or muscle tissue primarily. My findings were reinforced by the learned opinions of other investigators as I have indicated above. I examined the above patient and she had the same wide-spread neurological findings: bilateral sacral plexitis, brachial plexitis, and femoral neuropathy. She also had dermatological signs that were similar to systemic lupus erythematosis on her face; she had erythematous, vascular lesions of the upper back and the "v" of the neck that appeared to be similar to the "shawl sign" of dermatomyositis.
After a few visits I asked her when, exactly, her chronic pain started. She indicated it started shortly after she took a job as a motel cleaner. I asked her what her job was before she took the cleaning job. She said she had been off work for a few months since she had been treated for rheumatic fever in the Plano, Texas hospital. I told her that she was probably provided with an improper diagnosis since rheumatic fever hadn't been common in the USA since the 1960's. She indicated she had been hospitalized for seven days, was provided intravenous antibiotics, and that the treating physician told her that her disease could hurt her heart and that she had taken penicillin shots, monthly, for five years after her hospitalization. That statement "got my attention, so I retreated to my study and reviewed rheumatic fever in two texts. ( 3, 9 ) I returned to the examination room and asked her to tell me every detail about her disease. She proceeded to relate a very severe case of acute rheumatic fever. I thought, could all 700 patients in my chronic neurological investigative group have had rheumatic fever? It didn't seem likely, naturally. I tested her serum for ASO and Anti-DNAse B titer and they were positive. She related that she had had a severe flu-like disease with body aches, tiredness, etc. a month, or so before. I placed her on prophylactic oral penicillin therapy.
For the next few months, as I treated the patients in my chronic neurological pain investigative group, I asked each patient if they, or any family members, had a history of experiencing rheumatic fever. Many of the patients, especially if they were born before 1970, or so, knew that they had had rheumatic or scarlet fever and many others knew that a family member had experienced one of the diseases. I learned, over time, that if rheumatic fever is known to be "in a family", probably, many members experienced it even if it wasn't professionally identified. Patients born after 1970 rarely experienced receiving the diagnosis of rheumatic fever, but they had been diagnosed with mononucleosis, viral meningitis, whooping cough, chicken pox, measles, or an allergy to an antibiotic due to the development of a rash
The last three years I operated my clinics I initiated a clinical investigation iAfter I closed my clinics I concentrated, for three years, on academic and epidemiological research. Originally, the clinical investigation that I conducted was focused on attempting to determine if an alternative cause existed for chronic, neuropathic pain, in addition to the generally accepted concept of the herniated spinal-disc. Eventually I learned, as Niels Bohr had learned concerning the unknown issues intrinsically associated with the discovery of atomic fission: "Every great and deep difficulty bears in itself its own solution." ( 1 )
James W. Goding, the author of a chapter in the text, "The Autoimmune Diseases" wrote concerning future approaches to research in autoimmunity: "The "military concept" of a frontal attack seems eerily reminiscent of the ubiquitous "mission statement" that is currently so fashionable in the business world. It usually fails because essential but apparently unrelated information is missing, or simply because the necessary technology is not yet available. The time has to be ripe. Technological progress may make a question suddenly tractable, as witnessed by the occasional simultaneous appearance of a batch of papers on the same hitherto intractable subject. Sometimes major advances are unexpected, unplanned, and even initially unbelievable, coming as the result of asking a totally different question." ( 2 )
I think that the technique of approaching a problem by a "frontal attack", as mentioned above, can be very effective as it proved in the development of the atomic bomb. ( 1 ) The "mission statement", I surely think, was originally used as a preamble for a military organizational plan and it was transferred into the business world by former military men, perhaps, primarily, after the Vietnam War. During my clinical investigation I, more or less, conducted a frontal attack in an attempt to answer the question: is there an alternative cause for patients' chronic neurological pain, except for the herniated spinal-disc concept?
During my investigation I read many types of reasonably current medical texts, but I read older medical texts to which most modern physicians and medical investigators simply do not pay attention. I found that a great amount of clinical, medical information had accumulated, during the last 2500 years, since before the time of Hippocrates. Over the last 350 years, since 1600, a great many breakthroughs have been made in science and medical science in particular. One of the greatest insights have been connected with the microbiological revolution, which Antony von Leeuwenhoek began, in the late 1600's, as he perfected the microscope and became the first microbiologist. After a "pause" of one hundred and fifty years, in the middle of the 1800's, investigators, influenced by the conception advanced by Jakob Henle, finally proved that contagions (infectious diseases) could be caused by bacteria and viruses. William Jenner, Robert Koch, Louis Pasteur, Carlos Finlay, Walter Reed, and many others, led the advancement. Later, after the cause of many infectious diseases became recognized rational efforts towards the development of antibiotics was successfully undertaken by Ehrlich, Domagk, Fleming and others.
During the period I had an active medical practice I had wondering thoughts about many phenomenon. I learned that most diseases are connected, in various ways, to each other. For instance, individuals who experience diabetes are at a high risk to develop coronary artery disease and peripheral neuropathy. In addition, individuals who have ulcerative colitis are more at risk to develop other inflammatory maladies of the gastrointestinal tract and they are, also, at a high risk to develop cancer, they frequently experience neuropathic maladies, and they often co-experience other autoimmune diseases. Similarly, individuals who experience neuropathy are at a higher risk to develop cancer (paraneoplastic neuropathy). In addition, individuals who develop ulcerative colitis are at high risk for developing other autoimmune diseases of gastrointestinal tract, including celiac disease and Crohn's disease and patients with all three diseases feature a higher risk for cancer development and they often experience neuropathic maladies. ( 3, 4 ) In addition, individuals with rheumatic diseases such as rheumatoid arthritis, systemic lupus erythematosis, progressive systemic sclerosis, and dermatomyositis all experience a decreased life expectancy, they all feature accelerated arteriosclerosis, and they all feature neuropathic pain. ( 3, 4 ) Historically, coronary artery disease has appeared in patients who have exhibited "type A" personalities, who have hypertension, elevated cholesterol, and who also have somewhat horizontal earlobe creases. No one knows, however, the nature of the underlying disturbance, which causes the connection and the "type A" personality is hard to define.
Also, I came to realize that since 99% of diseases listed in medical texts have no known cause (they are termed idiopathic diseases), it is more accurate to understand them as syndromes. Syndromes are, simply, adverse medical conditions with somewhat uniform symptom and sign patterns. The word disease is best defined as an adverse medical condition which has consistent symptom and sign patterns, but, in addition, its cause is known. Since the great majority of medical problems have no known cause they are syndromes, therefore, physicians, primarily, do not cure diseases, they alter syndromes, usually for the better. In general, a knowledge of the cause for a disease is a requirement if a cure is to be developed, otherwise medical treatments are, for the most part, syndrome altering in nature.
Prior medical educational and experiential knowledge was important during my investigation, but most of the salient information I learned, which permitted me to develop an understanding of the cause of chronic neuropathic pain, and other associated medical conditions, was gained by repetitiously interviewing patients concerning their, and their family members', medical histories and by repetitiously conducting analytic, neurological, physical examinations. In addition to reading medical information in modern texts, I read parts of many older medical texts, dated from the Hippocratic period, through the Roman period, the Renaissance, and thereafter through the period during which many, great, scientific breakthroughs were accomplished, the 1600's through the early 1900's.
Physicians during earlier eras understood, partially, from a clinical aspect, the disease of rheumatism. For instance Galen, the Greek physician from Pergamum in Asia Minor, now located in Turkey, first coined the word, rheumatismos around two hundred A.D. ( 4, 5 ) The Greek word, rheum, the word-root of rheumatism, is defined in a reliable, medical dictionary to mean: "rheum, rheuma...[Gr. rheuma flux] any watery or catarrhal discharge. ( 6 ) It also seems to refer "a great fluxion which races to various parts of the body, and goes from one to another" ( 7 ) In addition, within the previously cited medical dictionary, the word rheumatism is defined, extensively, and many systemic, pathological manifestations of rheumatism are listed, for instance: apoplectic rheumatism, rheumatism associated with brain hemorrhage; cerebral rheumatism, acute rheumatic fever marked by chorea, delirium, convulsions and coma; rheumatism of the heart, involvement of the heart by the rheumatic fever process; lumbar rheumatism, lumbago; rheumatism confined to the joints is classified as arthritis; muscular rheumatism, fibrositis; and articular rheumatism, rheumatic fever. There are many more, approximately sixteen, anatomically defined symptomatic maladies of a rheumatic nature defined in the above cited medical dictionary. In addition, over time, there have been many synonyms for rheumatic fever, for instance, acute articular rheumatism, acute rheumatism, inflammatory rheumatism, and rheumatic fever; the word, rheumatism, itself, was often used in older, and even in more recently published scientific texts, to mean both acute and chronic rheumatism. ( 8, 9 )
Rheumatism has, for thousands of years, been generally thought to be a widespread, painful condition with, often, a migrating nature. ( 10 ) Again, the terms fibrositis and muscular rheumatism are shown to be synonyms. and results in the understanding that fibrositis, fibromyalgia and muscular rheumatism, describe the same condition. was defined to be a synonym for fibrositis, Fibromyalgia and muscular rheumatism, therefore, are clinical terms describing the same condition.
The following salient information is provided from the chapter on "Medicine", within the article, "of the Rheumatism", within the first edition of the Encyclopedia Britannica published in 1771. The author provides a clinical description of severe, acute rheumatism (rheumatic fever) similar to that provided by Thomas Sydenham during the 1600's. It includes, fever, lassitude, constipation, chest pain, anxiety, fast pulse, absent appetite, etc. Thereafter, the author mentions a ..."racking pain, sometimes in one joint, sometimes in another, but more frequently in the wrists, shoulders, and knees; frequently shifting from place to place, and leaving redness and swelling in the part visited last. The pain is exasperated with the least motion; it sometimes attacks the loins and coxendix. When it seizes the loins, it is called the lumbago; and there is a most violent pain in the small of the back, which sometimes extends to the os sacrum, and it is like a fit of the gravel (kidney stone), only the patient does not vomit. If this disease is unskilfully treated, it may continue several months or years, but not with the same violence, but by fits. If it continues and increases it may cause a stiff join, which will scarce yield to any remedy. Its proximate cause seems to be the inflammation of the lymphatic arteries, of the membranes near the ligaments of the joints, but not so violent as to bring on a suppuration. The blood is like that of persons afflicted with the pleurisy...And Huxham says, that the obstinate rheumatic pains, which remained after the epidemical fever of 1757..." and further, "...Pringle observes, that rheumatisms are generally mild, though they sometimes appeared with all the violence taken notice of by Sydenham...The chronic rheumatism is either the remains of a rheumatic fever, or a continuations of pains that proceeded at first from lesser but neglected colds. The blood in this case is fizzy (anemia). It is an obstinate disease...." ( 8 ) Within a more recent text, published in 1935, Sir William Osler writes concerning the pain that exists during severe cases of rheumatic fever: " Perhaps no disease is more painful; the inability to change the posture without agonizing pain, the drenching sweats, the prostration and helplessness, combine to make it a most distressing affection. ( 11 )
The information in the above paragraph indicates that acute rheumatism (rheumatic fever), in its variable presentations, causes the painful sequela of chronic rheumatism. One of the localized sources of pain, in rheumatism, is lumbago, an older term for low-back pain and sciatica. In older texts, sciatica is termed, "sciatic rheumatism" or "hip gout". ( 8 ) The prior two terms for sciatic neuropathy were used because it was known that all three medical problems, lumbosacral/buttock pain (lumbago), sciatic pain into the leg, and gouty arthritis often appeared in rheumatic patients. It relates that chronic rheumatism can be caused by an acute rheumatic fever episode, but it can also be caused "...from lesser but neglected colds" ( 8 ) Also, it indicates that rheumatic fever can be a highly acute disease, but even acute rheumatic fever "...may continue several months or years , but not always with the same violence, but by fits." ( 8 )
Rheumatism, a commonly used term in medicine before 1920, was often associated with specific, painful, muscular syndromes, for instance: "MYALGIA (Fibrocitis, Myositis) Definition.--A painful affection of the voluntary muscles and of the fasciae and periosteum to which they are attached. It is probable that in many cases the fibrous tissue is especially affected--a fibrositis. It is by no means certain that the muscular tissue is the seat of the disease. Many writers claim that in some cases it is a neuralgia of the sensory nerves of the muscles. The affection has received various names according to its seat, as torticollis, lumbago, pleurodynia...In the acute forms the affection is entirely local. The constitutional disturbance is slight and, even in severe cases, there may be no fever. Pain is a prominent feature and may be constant or occur only when the muscles are drawn into certain positions. It may be a dull ache, like...a bruise, or sharp, severe, and cramp-like. It is often sufficiently intense to cause the patient to cry out...The following are the principal varieties of myalgia: Lumbago...affects the muscles of the loins...stiff neck or torticollis affects the muscles of the antero-lateral or back region of the neck...pleurodynia involves the intercostal muscles on one side...it is more common on the left than the right side...among other forms...are cephalodynia (head ache),...scapulodynia (pain in the scapular region), omodynia (shoulder pain), and dorsodynia affecting the muscles about the shoulder and the upper part of the back." ( 10 )
Since the above concept of rheumatic pain decreased in popularity, over time, by the 1970's, physicians held little respect for the words rheumatism, myositis, myalgia, myofibrositis, fibrositis, or fibromyalgia. Patients, however, during the 1970's, started complaining in greater and greater numbers about diffuse body pains and so, eventually, after the resurgence of such complaints, the diagnostic word (and the development of a rigid, administrative, diagnostic, computer code) fibromyalgia became an accepted syndrome. ( 11 )
After I had hypothesized that the disease was wide-spread, that is, worldly in nature, I conducted an epidemiological investigation. During the epidemiological investigation, I traveled to eighteen countries and spoke with physicians in many locals, but more importantly, with people "on the street". I determined that the great majority the patients who experienced chronic neurological pain were experiencing it as a "target-organ manifestation of rheumatism", which is a chronic, systemic, inflammatory, autoimmune disease caused from infections by "Streptococcus pyogenes".
Rheumatism is usually considered an archaic term in medicine for it is not listed as a subject in most, modern, medical texts. For instance it is not listed as a subject in the text, Harrison's Principles of Internal Medicine, 16th Edition (Kasper,D., McGraw-Hill, 2005).
Within the 12th editon of the same text, published in 1991, the only listing for rheumatism is psychogenic rheumatism and part of the short paragraph explaining it is as follows, "PSYCHOGENIC RHEUMATISM Patients may experience severe joint pain involving a few to several joints without physical findings of arthritis. These patients are often convinced that they have rheumatoid arthritis, systemic lupus erythematosis, or another rheumatic connective tissue disease. This disorder is recognized by the inconsistencies, exaggerations, and emotional lability of the patient during the history and physical examination..." I think that the above synopsis makes obvious the author's lack of observation skills, the author's lack of patient concern, and it is an arch-type example of how some physicians find fault with patients when the physician does not know "what is going on". In addition, physicians who have the above nature seem not to be able to say to a patient, "I don't know".
From, at least, the late 1500's until the early 1900's the terms rheumatism, acute rheumatism, acute articular rheumatism and rheumatic fever were used, at times, in an interchangeable fashion as noted within the chapter "Medicine" and the paragraph, "of the Rheumatism" within the first edition of the "Encyclopedia Britannica" (By a Society of Gentlemen in Scotland, In Three Volumes, Printed for A. Bell and C Macfarquhar, and fold by Colin Macfarquhar, at his Printing-office, Nicolson-street, Edinburgh, M.DCC.LXXI.) As time passed the terms, "acute rheumatism" and "inflammatory rheumatism" were terms frequently used to describe episodes of acute rheumatic fever. One might think that the term rheumatic fever described a disease, at times with a high fever, which was rheumatic in character since other symptoms and signs of the disease were known to be part of the rheumatism concept (arthritis, back pain or lumbago, neuropathies, gastrointestinal abnormalities, cardiac arrhythmias, cardiac enlargement, cardiac valve abnormalities, pulmonary edema, rash, renal and hepatic abnormalities, delirium, stupor, coma, seizures, etc.). It was known in the late 1700's, as quoted in the first edition of the Encyclopedia Britannica, mentioned above, that: "The chronic rheumatism is either the remains of a rheumatic fever, or a continuations of pains that proceeded at first from lesser but neglected colds." The information within that quote indicates that physician-authors of the day, in the late 1700's, knew that acute rheumatism (rheumatic fever) could cause chronic rheumatism, but also they knew that less severe episodes of respiratory disease, "...lesser but neglected colds.", could also cause chronic rheumatism.
Chorea is defined as, "the ceaseless occurrence of a wide variety of rapid, highly complex, jerky movements that appear to be well coordinated and are performed involuntarily...Sydenhams c., an acute, usually self-limited disorder of early life, usually between the ages of five and fifteen, or during pregnancy, and closely linked with rheumatic fever." (Dorland's Illustrated Medical Dictionary, 27th Edition, W.B. Saunders Co., 1985). In older texts such as "Osler's Principles and Practice of Medicine, Eighth Edition" (McCrea, T., Appletonm-Century Co., 1912) the following is written about rheumatism in the section on acute chorea: "Rheumatism.--A causual relationship between rheumatism and chorea has been claimed by many since the time of Bright. The English and French writers maintain the closeness of this connection; on the other hand, German authors as a rule, regard the connection as by no means very close. Of the 554 cases, in 15.5 per cent., there was a history of rheumatism in the family. In 88 cases, 15.8 per cent., there was a history of articular swelling, acute or subacute. In 33 cases there were pains, sometimes described as rheumatic, in various parts, but not associated with joint trouble, the percentage is raised to 21. It is rather remarkable that in our Baltimore series the percentage with a history of rheumatim was the same, 21.6...with the exception of rheumatic fever, there is no intimate relationship between chorea and the acute diseases of childhood...With no disease, not excepting rheumatism, is it so constantly associated. I collected from the literature the records of 73 autopsies; there were 62 with endocarditis. The endocarditis is usually of the simple variety, but the ulcerative form has occassionally been described...pericarditis is an occasional complication of chorea, usually in cases with well-marked rheumatism."
By 1935, when the 12th Edition of Osler's text was published the use, and meanings, of the terms rheumatism and rheumatic fever experienced a segregation and "rheumatism" is not listed in its index. Rheumatic fever, however, is described quite thoroughly (compared to modern texts) since a great amount of clinical knowledge about rheumatic fever, as an acute, a subacute, and less than subacute disease process had been developed. The knowledge that rheumatic fever was caused by Streptococcus pyogenes, a fact discovered by both Alvin Coburn in the USA and Wilfred Collis in England in 1931, was not, however, mentioned in the text, which is an indication of the time it takes for physicians, even highly experienced physicians, to accept new ideas even if they are well proven. The concept of chronic rheumatism still existed, but it was diminishing in the minds of physicians and medical authors, because, in my opinion, the specialty divisions of medicine, which had been experiencing accelerated development for a few decades, decreased the conceptual understanding of systemic disease processes.
Medicine as an art and science, which had its roots in antiquity, was being coerced into following the specialty paradigm wherein disease concepts had to be "fit into" the various specialty divisions that were being developed. Thus, a systemic disease concept, such as rheumatism, slowly disappeared from the minds of physicians and, therefore, medical texts, even though many diseases were, and are, known to be systemic in nature. For instance, within "Webster's Encyclopedic Unabridged Dictionary of the English Language" (Random House, 1989) the following definition for rheumatoid arthritis is provided: "rheumatoid arthritis,...a chronic disease marked by signs and symptoms of inflammation of the joints, frequently accompanied by marked deformities, and ordinarily associated with manifestations of a general, or systemic, affliction."
The following was written, within the prologue, by the editor of the section on "Medicine", in the first edition of the Encyclopedia Britannica, cited above, as he was discussing the various attempts to classify diseases into rational groups: "Of late several attempts have been made to reduce medicine into the form of a regular science, by distributing diseases into classes, orders, genera, and species. Sauvage was the first...Others, as Linaeus, Vogel, Dr. Cullen, Etc., have since endeavored to improve Sauvage's method of classing; but they have contented themselves with an enumeration of the characters and arrangement fo the different genera, without entering into their history or cure. Sauvage enumerates 315 genera, Linnaeus 325, Vopgel 560, and Dr. Cullen has reduced them to 132. The bare inspection of these numbers shews, that physicians are far from being agreed with regard to what constitutes the generic or specific character of a disease. Indeed, we may venture to affirm, that they never will agree upon this point: The diagnostic symptoms of diseases are not so easily discovered as the stamina or petals in a flower, or the number of teeth or toes in a quadraped."
I suggest that the current division of medicine into its current specialty groups is not necessarily rational, but political, at least in many respects, because, for instance, there are various highly variable factors involved in the many specialty definitions. Some are determined, generally, by the age of the patient (pediatrics, geriatrics, internal medicine); some are determined by the organ system attended to (cardiology, psychiatry, nephrology, opthalmology, dermatology, general surgery, orthopedic surgery); some are determined by what high-tech instruments are primarily used (radiology, anesthesiology, pathology); some are determined by the pathological cause of disease (infectious disease specialty); and some are determined by the type of treatment provided (nuclear medicine, oncology). Many of the specialties are further defined by the type of high-tech apparatus that they use: for instance gastroenterologists use colonoscopy and endoscopic techniques most commonly and the various surgical specialties, which are within the organ system specialty groups, use, most commonly, the operating room as do the anesthesiologists.
The family practice specialty is really not a specialty. It is a politically developed specialty that provided general practitioners with the "specialty status" of other physicians. Managed care insurance plans furthered the development of the family practice specialty by mandating that physicians who treated patients "with their insurance plans" had to be specialists. To qualify for various managed care plans, in the early 1990's I had to travel to Atlanta, Georgia and pass a test to be "grandfathered" into the family practice specialty. I functionally, however, remained a general practitioner, that is, a physician and surgeon in medicine.
Specialty physicians limit their practices and therefore their medical thought processes by becoming specialists, as indicated in Dorland's Illustrated Medical Dictionary 27th Edition, cited above: "Specialist... a physician whose practice is limited to a particular branch of medicine or surgery, especially one who, by virtue of advanced training, is certified by a specialty board as being qualified to so limit his practice ." The semi-strict specialty divisions in medicine cause a division of knowledge so that an integration of medical knowledge, over time, has not been managed in medical science since, about, 1920.
Rheumatology has been relegated to deal with abnormalities of connective tissue. One might think that rheumatology was relegated to connective tissue since the various organ systems had been claimed by previously developed specialty groups. It is obvious, however, to any reader of medical texts and medical journal articles, that most rheumatic diseases, such as rheumatoid arthritis, lupus erythematosis, systemic sclerosis, dermatomyositis, Reiter's syndrome, Behcet's sydrome, Sjogren's syndrome, polyarteritis nodosa, Wegener's granulomatosis, mixed connective tissue disease, ankylosing spondylitis, psoriasis, osteoarthritis, and neurogenic arthropathy, all of which have systemic, visceral manifestations, that such clinical syndromes are not necessarily defined to have, only, abnormalities in connective tissue.
The above partial description of the medical specialty groups provides an organizational reason why medical knowledge, historically, during the last ninety years, has been formally segregated so that there is little functional integration of medical knowledge. The lack of integration has resulted in a inhibition in the advancement of knowledge development concerning the causes of, and accurate pathophysiology of, diseases. Without knowing the cause of a disease, cures for them surely cannot be determined. Since fractures, lacerations, burns, sprains, and some infectious diseases have known causes cures for them have been rationally developed. Most other diseases (idiopathic diseases), which are more accurately described as syndromes, since their causes are not known, are provided, by physicians, disease-altering surgery and chemotherapy to alter them, usually for the better. For instance, the use of a diuretic for congestive heart failure and hypertension, the performance of coronary by-pass graft surgery, the performance of a cholecystectomy, and the use of tranquilizers for various adverse mental states, are all disease altering treatments.
Dictionaries, in general, and "Dorland's illistrated Medical Dictionary, 27th Edition", cited above, in particular, tend to preserve the historical meaning, and often the philological evolution, of words, so the word rheumatism is profusely defined. I will select certain aspects of the definition from the above text: "Any variety of disorders marked by inflammation, degeneration, or metabolic derangement of the connective tissue structures of the body, especially the joints and related structures, including muscles, bursae, tendons and fibrous tissue...Rheumatism confined to the joints is classified as arthritis. apoplectic r.,' rheumatism associated with brain hemorrhage. Articular r., acute, rheumatic fever. articular r., acute r, rheumatic fever..."cerebral r"., acute rheumatic fever marked by chorea, delirium, convulsions, and coma..."r. of the heart", involvement of the heart by the rheumatic fever process. "Inflammatory r"., rheumatic fever..."lumbar r"., lumbago..."muscular r"., fibrositis..."subacute r"., a mild but protracted form of rheumatism." Since connective tissue, fibrous tissue, are parts of all organs, the skin, bones, tendons, ligaments, muscles, the heart, kidneys, gastrointestinal organs, the brain, etc., a disease that affects such tissue adversely will be, naturally, systemic in nature.
Hippocrates, or physicians of the Hippocratic persuasion, recorded within the book, The Sacred Disease, published within the text, "Hippocratic Writings", cited above, many case histories, which, in sum, indicate that the patients discussed, who became sick in an epidemic, experienced rheumatic fever. During the second century AD Claudius Galenus, commonly termed, simply, Galen was the first individual known to have coined the word rheumatism (rheumatismos). In the text, "Rheumatic Fever and Streptococcal Infection" (Massell, M., Harvard Press, 1997) the author provides a historical study of rheumatic fever. Guillaume Baillou (1538-1616) in France, during the Renaissance, wrote clearly about rheumatic fever. Later, Thomas Sydenham, during the mid 1600's, differentiated scarlet fever from measles and described rheumatic fever. Even though a great amount of clinical knowledge was gained about rheumatic fever its cause puzzled physicians, and other investigators, for hundreds of years for it wasn't understood that its cause was Streptococcus pyogenes until 1931. "In 1885,...Dr. Alfred Mantle presented a paper on infectious sore throat before the Section on Public Medicine at the annual meeting of the British Medical Association...He concluded that rheumatism was a common complication of infectious sore throat..." Further, "Because of its joint manifestations, rheumatic fever is included by the American Rheumatism Association as one of more than eighty different rheumatic conditions that it classifies." In addition, "Guillaume Baillou (1538-1616,...a Parisian physician apparently was the first to use the term "rheumatism" (rheumatismos) for polyarthritis..." "On the other hand the method by which this affection attacks which is falsely called catarrh; (for the name catarrh signifies distillation from the head) it seems better to speak of the others as rheumatism..." Dr. Baillou goes on to provide a very good description of acute high-grade rheumatic fever similar to that of Sydenham's of the late 1600's. Further, "Many of the tendons of the superficial muscles of this patient were studded with numerous small hard tumors, an appearance I have observed only in one other person...who also labored under rheumatism." Baillou recognized certain systemic features of rheumatic fever: "The whole body becomes painful, the face in some becomes red, the pain rages especially about the joints, so that indeed neither the foot nor the hand, nor the finger can be moved in the least without pain & outcry..." Later, in 1715, Raymond de Vieussens described a patient with acute rheumatic fever, since he was determined during autopsy to have a severely dilated left ventricle, the walls of the aorta were..."thick, very hard, like cartilage; the semilunar valves are markedly stretched & cut off at their tips: all these cuts which bore some resemblance to the teeth of a saw, were in fact osseous." (rheumatic valve syndrome) Later, David Pitcairn, in England, lectured, in 1788, concerning rheumatism and its affect on the heart: "...that persons subject to rheumatism were attacked more frequently than others with symptoms of an organic disease of the heart. Subsequent experience having confirmed the truth of this observation, he concluded, that these two diseases often depend upon a common cause, and in such instances, therefore, called the latter disease rheumatism of the heart." It was not until 1931 that Alvin Coburn in the USA and Wilfred Collis in England determined that Streptococcus pyogenes caused rheumatic fever, and relying on David Pitcairn's judgement, heart disease.
The above information provides the knowledge that physicians in earlier periods, back to the 1500's, used the word rheumatism, rheumatic fever, acte rheumatism and chronic rheumatism somewhat interchangeably for they knew that acute rheumatism would lead to chronic rheumatism and they also knew that a contagion, often connected with tonsillitis, or other respiratory disease presentation, could cause it. Since high-grade, acute rheumatic fever has become so rare in modern counties most currently practicing physicians have lost the clinical knowledge about it. They, therefore, have never gained the knowledge that there are lesser levels of rheumatic fever, as defined in "Osler's Principles and Practice of Medicine", published in 1935, cited above, and therefore they have even less knowledge about subacute and less than subacute rheumatic fever, which is are, semi-chronic clinical subtypes, of rheumatic fever a systemic, autoimmune-mediated, inflammatory disease.
Between 2002 and 2005 I conducted a three-year, clinical investigation in an effort to determine the true cause of most peripheral neuropathies since so many of my patients, through the years, failed to improve after they experienced spinal surgery. I eventually determined that the venerated, herniated spinal-disc concept was flawed, and most of the surgery accomplished for them was, I learned, usually mis-applied. Most patients had suspicious arthritis of the lumbar and cervical spine that featured osteophyte development and bulging of intervertebral spinal-discs, but I learned that typical MRI films did not have the resolution to "see" spinal nerve roots in an analytical fashion. Since the bulging intervertebral spinal-discs are attention-getting on MRI images, and because they do, occasionally, cause symptomatic, spinal nerve root compression, generalizing that almost all bulging intervertebral spinal-discs cause nerve root compression was a classic "red herring". After I managed to determine the cause of the painful neuropathies, I learned that the same disease that causes the neuropathies also causes arthritis of the spine; an anatomical feature of spinal arthritis, herniated spinal-discs, did not necessarily cause the painful neuropathies. There are occassional herniated spinal-discs that cause painful spinal, nerve-root compression, but surgery for them is very common.
Eventually, after a long, investigative period, I learned the most patients' neuroloical pain was caused by rheumatic, autoimmune-mediated, vasculitic neuropathy of the terminal nerves of the sacral plexus located within the piriformis canal, which is located deep in the buttock. Patients who experienced neurological shoulder/cervical pain and who experienced dysesthesias to the appropriate upper extremity, were experiencing rheumatic brachial plexitis. The brachial plexus is located within the axillary canal located deep within the shoulder. I learned that motion of the arm at the shoulder, and of the thigh at the hip, or an accident wherein either of the structures were stressed, would often cause, or exacerbate, patients' neurological symptoms and signs. Patients sensed pain in the lumbosacral region, because of centripetal referred pain from the distal sacral plexus located deep in the buttock. Similarly, they sensed pain in the cervical/shoulder region, because of centripetal referred pain from the brachial plexus located deep within the shoulder.
During the above investigation I attracted 700 miserable, painful patients who had chronic neurological pain. Eventually, I learned that they all had had meaningful, repeated Streptococcus pyogenes infections (tonsillitis, sinusitis, bronchitis, pharyngitis, otitis media, impetigo, and vaginitis) during their lifetimes and often they had experienced chronic tonsillitis. In addition, many of them, who had been born before 1970, had had, when they were younger, rheumatic fever or scarlet fever. Younger patients, born after 1970 had "flu-like" diseases with more mild symptoms and signs than accepted "Jones Criteria" standards for diagnosing rheumatic fever. I learned from information in Sir William Osler's text, Osler's Principles and Practice of Medicine, Twelfth Edition, cited above, that there are subacute and less than subacute states of rheumatic fever with more subtle systemic symptoms and signs than "classic" high-grade rheumatic fever. Such a disease has the same symptoms and signs that are thought to be those of influenza, or "the flu": a respiratory disease, often at least, lethargy, tiredness, at times stupor, body pain, back pain, photophobia, at times, headache, at times, gastrointestinal symptoms and signs, at times, and often a fairly rapid recovery. Often patients who had rheumatic fever had been diagnosed by a physician or by parents to have chicken pox, measles, the flu, mononucleosis and viral meningitis. Often the patients had been very ill, but recovered with care at home.
I conducted serology tests (ASO and Anti-DNase B titers) on over 100 patients and 70 were positive with elevated Streptococcus antibodies on one or more tests. Between the positive medical histories, the elevated serology tests, and those who had medical histories of "flu-like" diseases, chicken pox, measles, mononucleosis, and viral meningitis wherein the symptoms and signs were those of rheumatic fever, the great majority of the 700 patients, mentioned above, who had chronic neurological and arthritic pain, and other similar diseases, were qualified to have had rheumatic fever.
The great minority of cases of rheumatic fever are high-grade and qualify by the Jones Criteria to be that disease. Most cases are much more low-grade and semi-chronic in nature and such individuals develop increased, rheumatic, autoimmunological sensitivity and memory so that they are candidates, in the future, to be at risk for developing acute rheumatic fever. Current medical knowledge (Carapetis, JR.,et al., Lancet Jul 9-15; 366(9480): 155-68) indicates that an infection by a virulent strain of Streptococcus pyogenes, in a well rheumatically sensitized individual, can cause the development of acute rheumatic fever, which is known to be an inflammatory, autoimmune disease process.
The septic responses patients experienced, which frequently took place one to four weeks after an episode of respiratory disease (bronchitis, sinusitis, pharyngitis or tonsillitis) were caused by the rheumatic, systemic, autoimmune response to the autoantigens displayed by Streptococcus pyogenes. As the elevated levels of autoantibodies, and other toxic products, decreases after the peak of rheumatic fever, I hypothesize that patients maintain a low-level of rheumatic autoantibodies within themselves and it causes, over time, the signs and symptoms of chronic rheumatism. Since immunological and autoimmunological proteins circulate through the body via the elements of the circulatory system, rheumatism causes a usually subtle vasculitis, that is, arteritis, phlebitis, and lynphangitis. The much more common low-grade infections by Streptococcus pyogenes, and even the carrier state, cause an exacerbation in rheumatic stimulation, which establishes a chronic, waxing and waning autoimmune disease process within hosts, thus the chronic, autoimmune disease of rheumatism develops and is maintained.
Since Streptococcus pyogenes is endemic in human society, and a Russian Encyclopedia article (V. Nasonova & E. Talahaev) indicates that Streptococcus pyogenes is endemic in domestic vertebratres, and I hypothesize it also exists in wild vertebrates, it seems that Streptococcus pyogenes causes a universal, autoimmunological zooinosis among vertebrates including humans.
As a reminder, the terms acute rheumatism, acute articular rheumatism, inflammatory rheumatism, and rheumatic fever, all describe the same acute, high-grade autoimmunological disease caused, usually in a delayed fashion, from infections by Streptococcus pyogenes. The terms rheumatism and chronic rheumatism refers to tissue damage that usually appears minor for which signs and symptoms are often subtle, are slow evolving, and usually cause little or no dysfunction. Over time, however, they can become highly meaningful and conditions such as hip and knee arthritis, coronary artery disease, peripheral vascular disease, rheumatoid (rheumatic) arthritis, lupus erythematosis, for instance, are an indication of its severity.
The pathological anatomy of chronic rheumatism is often relatively easy to observe since, certain superficial signs of disease, for instance the articular signs of rheumatoid arthritis, dermatological features of lupus erythematosis, dermatological features of progressive systemic sclerosis, rosacea, varicosities of veins, seborrheic keratosis, various types of nevi, Raynaud's phenomenon, palmar and plantar erythema, and livedo reticularis are all manifestations of the systemic disease of rheumatism. Rheumatoid arthritis, historically, was thought to be caused by rheumatic fever. At times it has been termed, arthritis deformans. There have been other more antiquated terms for high-grade rheumatic fever and I hypothesize that two of them are sweating sickness and miliary fever.
It has not been clinically recognized, however, that all infections by Streptococcus pyogenes cause an inflammatory autoimmune response. I hypotheize that Streptococcus pyogenes infections with a high virulence is most meaningful and more frequently cause exacerbations in the rheumatic autoimmune response. In addition, the patients level of rheumatic immunological sensitivity, caused by prior infections, also contributes to the development of an energetic autoimmune response.
After various acute disease episodes, throughout life, and after numerous episode of subacute or less than subacute rheumatic fever ensues during a person's lifetime, rheumatic tissue damage slowly occurs and it eventually rheumatism manifests itself with obvious signs and symptoms of pathological damage to the body's tissues, and therefore organs, in a somewhat subtle, varying, but progressive fashion. Its manifestations are often noted as changes to the skin, tendons, ligaments, nerves and joints so clinical syndromes such as sciatica, brachial plexitis, femoral neuropathy, meralgia paresthetica, carpal tunnel syndrome, ulnar neuropathy, cardiac arrhythmias, headaches, De Quervain's tendonitis, Achilles tendonitis, olecrannon bursitis, rotator cuff abrasions and tears, and Dupuytren's contracture appear. One must remember, however, that rheumatism is a systemic disease process so that all tissues, and therefore organs, are pathologically affected. Therefore, arteriosclerosis, endocrinopathies, renal failure, asthma, allergies, inflammatory bowel syndome, primary sclerosing cholangitis, pancreatitis, osteoporosis, spastic bladder, schizophrenia, obsessive-compulsive behavior, depression, and many, many other pathological conditions are caused by rheumatism. "One must think: each tissue, and therefore each organ, will clinically express the adverse effects of the systemic disease of rheumatism in its own way, thus, many apparent separate diseases develop, over time, in a somewhat random, but often connected, fashion."
High-grade rheumatic fever decreased in incidence starting in the early 1900's within modern, industrialized societies, secondary to the improvements in living conditions which were brought on by advances of basic science that begot the industrial revolution. Advances included larger homes and smaller family size, both of which caused decreased crowding within dwellings, which decreased the spread of Streptococcus pyogenes within families. In addition, more hygienic living habits, the common use of soap, improvements in home bathing facilities, the use of clothes washers, dish washers, and the pasturization of milk all contributed to a decreased spread of Streptococcus pyogenes within society. Later, in the 1930's, the use of broad spectrum antibiotics for respiratory infections was initiated. The environmental changes, and the common use of antibiotics, resulted in fewer and fewer Streptococcus pyogenes infections, but more importantly, perhaps, infections with less virulence, so by 1970 high-grade rheumatic fever was a relatively rare disease in modern, developed countries. Chronic rheumatism also decreased in severity in especially in younger populations, but it still appeared, as a pathological entity, in older people as they lived through the years.
Unfortunately, in 1987 rheumatic fever experienced a resurgence with the first reports appearing in The New England Journal of Medicine with the author, L. George Veasy, MD wrote about a mini-epidemic from the area around Salt Lake City, Utah. Thereafter, numerous mini-epidemics have been reported from many areas in the USA. A mini-epidemic of acute rheumatic fever took place in Lewis and Cowlitz Counties of Washington State during the winter and spring of 2004 and 2005. A few people patients died before that period from rheumatic fever, but I didn't recognize it, but about ten people died out of my patient population of about 7000 during the aforementioned period. A number of patients have died thereafter who lived in the same geographic area. The individuals who died were fairly young, in their thirties to their sixties, they all experienced chronic neurological pain and arthritic symptoms, three of them had had a history of previous rheumatic fever or scarlet fever (Scarlet fever is the same disease as rheumatic fever, except it is caused by a separate sub-species of Streptococcus pyogenes, which develops a somewhat specific rash.) , a number of them had experienced spinal surgery with no improvement in symptoms or signs, and they were taking opiates for their severe, chronic, neurological pain when they died. Unfortunately, the local coroners, neither of whom had much medical knowledge or wisdom, made a determination that some of the patients died from the affects of opiates that they were taking for their chronic rheumatic pain. Some of the patients, on whom I had accurate information, had classic signs and symptoms of acute rheumatic fever so they qualified, by the Jones Criteria, to have had severe, acute, rheumatic fever. They had enlarged hearts and pulmonary edema on autopsy as an indication that they had had acute rheumatic carditis (myocarditis and endocarditis).
One of the painful, clinical, rheumatic conditions, which many children commonly experienced in somewhat earlier times, such as before the 1970's, was growing pains. Growing pains manifest themselves as a painful sensation in the legs, commonly the thighs and knees, and it develops, often, shortly after going to sleep, or lying down, and wakes the young patient who often complains, and even cries, due to the severity of pain. Other clinical manifestations of rheumatism, which children experience, are torticollis (wry neck) and dorsodynia, which is an older term for upper back pain that is usually felt in the scapular region, which, I determined, is frequently a referred pain pattern caused by rheumatic brachial plexitis. Another syndrome children experience, occasionally, is Kawasaki disease. I surely think that Kawasaki disease is a syndrome that is a presentation of rheumatic fever in a child who is "well conditioned" to have a severe rheumatic vasculitic response by having experienced a number of Streptococcus pyogenes infections earlier in life. They could have experienced a chronic infection, which caused an elevated sensitivity to the autoantigens of a virulent subtype of Streptococcus pyogenes. Another syndrome that adults contract is Guillain-Barre' Syndrome. It is a presentation of rheumatic fever wherein the individual experiences an acute, systemic neuropathy and paralysis at some level. Usually they experience a respiratory infection somewhat before their attack and such a pattern of delayed autoimmune disease is classic for Streptococcus pyogenes infections and their delayed rheumatic response.
Simultaneously with the above changes in the frequency of high-grade rheumatic fever, the citizens of modernized countries experienced a steadily advancing life-expectancy; in the USA life expectancy increased from forty-seven in 1900 to about seventy-seven in 2000: an increase of about thirty years, which equates to an increase of 64% over a 100 year period. There has to be a logical reason for the increased longivity. The reason, mainly, I hypothesize, has been a decrease incidence, and severity, in general, of Streptococcus pyogenes infections; a generally decreased level of virulence of Streptococcus pyogenes itself, which resulted in a great decrease in the incidence of acutge rheumatic fever and, therefore, chronic rheumatism decreased in severity in the populations of economically advanced countries. The decrease in the incidence of acute rheumatic fever, a disease that often caused the death of children and younger people, greatly contributed to the increase in human life-expectancy. There were other positive factors also, for instance, a better food supply, vaccines for other diseases, and improved medical care, especially supportive care and disease altering surgical procedures.
Rheumatic autoimmunity causes, initially and continually, an inflammatory vascular condition, which is its main pathological mechanism, that results in inappropirate intra-arterial thrombosis especially at arterial bifurcations. The immune system reacts to localized intra-arterial thrombosis with an enhanced, localized inflammatory response so that inflammatory, intra-arterial, arteriosclerosis lesions develop. As Streptococcus pyogenes infections decreased, as mentioned above, fewer myocardial infarctions developed early in life and coronary artery disease became, to a great degree, a disease of older people, in modernized portions of the world, since it is caused by more subtle, chronic rheumatic autoimmune condition: chronic rheumatism.
In 1931 Coburn in the USA and Collis in England determined, somewhat simultaneously, that Streptococcus pyogenes caused rheumatic fever, but professional inertia being what it is, many physicians did not completely accept their theory until the late 1940's and the early 1950's when rheumatic fever, as a high-grade disease, was becoming less and less common, primarily, because of the above-mentioned improved living conditions and use of antibiotics mentioned above.
Starting in the 1920's, slowly, but then accelerating, especially in the 1950's, medical practice and education became conceptually segregated by means of specialty-organized, procedure-dominated concepts and by the 1960's most physicians were specialists and specialty practice settings and knowledge-states were not conducive to an understanding of systemic diseases. Since acute rheumatic fever, and moreso, chronic rheumatism are basically the same disease, with the former being an acute exacerbation of the latter, the latter, chronic rheumatism, which has a multitude of target-organ manifestations, simply was not recognized, or ceased to be recognized, by the members of the specialty-oriented medical community.
Individuals in the various surgical specialties concentrated on various target-organ manifestations of rheumatism and developed disease-altering cardiac, surgical procedures such as CABG surgery, angioplasty/stent procedures, cardiac valve modification and replacement procedures, and cardiac arrhythmia altering surgery, etc. Surgical procedures to alter, usually for the better, rheumatic pathology to gastrointestinal organs consist of, in part, surgical procedures such as cholecystectomy for cholecystitis, various surgical procedures for ulcerative colitis, redundant colon, Crohn's disease, esophageal strictures, primary sclerosing cholangitis, and gastric and peptic ulcers. The latter two, gastric and peptic ulcers are primarily caused by rheumatic vasculitis, but that condition is exacerbated locally by Helicobacter pylori infection. In general, infections cause a localized exacerbation of rheumatic vasculitis. In addition, organs that function peristaltically, as do most of the gastrointestinal organs, feature compression and abrasion of tissues, which also causes an exacerbation of rheumatic vasculitis, in a semi-localized fashion, within them. Pyrosis, or heart burn, is another clinical entity caused by rheumatic vasculitis. The peristaltic compression causes enhanced rheumatic vasculitis, which is further exacerbated, usually in the distal esophagus, by the effect of hydrochloric acid and digestive enzymes from the stomach on the esophageal endothelium.
In addition, many chemotherapeutic medications were developed so the use of NSAIDS, steroid anti-inflammatory medications, artery dilators, cancer chemotherapy drugs and countless other chemotherapeutic drugs became commonly used to alter the affects of chronic rheumatism on various organs. Both NSAIDS and steroid anti-inflammatory medications are used for acute, rheumatic fever, in addition.
During the development of "specialty medicine", it seems that rheumatology, one of the last specialty groups organized, was "elbowed" into dealing with only connective tissue, perhaps since other groups of physicians had claimed authority of the other organ systems, although most rheumatic syndromes such as rheumatoid arthritis, lupus erythematosis and psoriasis, for instance, are known to be systemic disease processes. The specialty-medicine paradigm that developed, since the 1920's, simply never provided a systemic disease concrept-base so chronic rheumatism has never been understood in a modern, etiological fashion even though all the clinical elements of its understanding had been provided by investigators in prior eras, by the microbiological breakthroughs of the late 1800's through the early 1900's, and by the insights made concerning autoimmune disease concepts. A valuable text that provides a current understanding about the current state of knowledge about autoimmunity is, "The Autoimmune Diseases" Fourth Edition (Rose, N., Mackay, I., Academic Press, 2006).
Even though high-grade rheumatic fever greatly decreased in incidence after1900 lesser levels of rheumatic autoimmunity have still been propagated throughout human society, including modern developed countries, since Streptococcus pyogenes infections still exist endemically, but usually with less virulence, within the populations of all countries. Therefore, since Streptococcus pyogenes infections are endemic at any one time, at some level, in all communities in the world, at some level. For instance, the non-symptomatic carrier state of Streptococcus pyogenes is between 5%-15% of grade school children as per information in the text, "Rheumatic Fever and Streptococcal Infection", cited above. Hypothetically, low grade infections will cause low-grade autoimmunological stimulation within those very mildly sick individuals and they can pass infections on to those around them.
The clinical understanding of high-grade rheuamtic fever (acute rheumatism) decreased in modern countries so that, nowadays, in the USA, the average physician has virtually no, or little, knowledge of acute rheumatic fever at this time. Knowledge, therefore, of the much lower-grade, chronic, rheumatic autoimmunity and its more subtle, slowly-developing, target-organ manifestations has never been developed in modern medical science and along the way, rheumatism as a chronic disease concept, was dismissed as a serious medical subject, even though, as early 200 AD, certain knowledge concerning rheumatism was known, and in the late 1700's the "clinical features" of acute and chronic rheumatism was reasonably well known.
For instance, Galen, the famous Greek physician in the Roman period, who published over 66,000 pages of medical, philosophical, and scientific information, half of which has managed to survive since 200 AD, coined the word rheumatismos. Rheum, in Greek, means to flow, or phlegm. The phrase "a defluxion of rheum" could be used. It was later connected with catarrh, influenza, or the grippe, terms that describe a respiratory disease. Galen knew, I hypothesize, that when people developed contagions that caused the development of phlegm, and, perhaps, chronic phlegm development, they would also, eventually, develop chronic, painful problems that were part of the chronic disease of rheumatism. Arthritis, neuropathy (such as sciatica, carpal tunnel syndrome, ulnar neuropathy, brachial plexitis, for instance), angina, pericarditis, pleurisy, tendonitis, ligamentitis (for instance plantar fasciitis) are examples of modern names for target-organ manifestations of rheumatism.
As mentioned above, within the first edition of the Encyclopedia Britannica, cited above, on page 124, under the chapter on "Medicine", under the paragraph, "Of the Rheumatism", a description of acute rheumatic fever similar to that written by Thomas Syndenham, during the 1600's, is provided. It mentions fever, chills, rapid heart rate, fatigue, lassitude, gastrointestinal problems, sciatic pain (lumbago), and migratory arthritis. It saliently mentions, "The proximate cause is the inflammation of the lymphatic arteries." Further, it mentions, "The chronic rheumatism is either the remains of a rheumatic fever, or a continuation of pains that proceeded at first from lesser but neglected colds."
It appears, clearly, that physicians in the mid-1700's knew that the "Proximate cause (or pathological finding) was inflammation of the lymphatic arteries (arteries) a condition now known as vasculitis, phlebitis, and lymphangiitis. Of course the rheumatic vasculitis that exists in those with chronic rheumatism is somewhat low-grade. They also knew that repeated "...lesser but neglected colds." could cause the systemic disease of rheumatism, but in the modern day, pundits of evidence-based medicine (whose evidence, how was it gathered, who interpreted it?) pontificate to student-physicians that, all "colds" are caused by viruses so upper respiratory diseases, even sore throats and tonsilitis, are not to be treated with antibiotics unless a positive quick strep test or culture is positive. Unfortunately, such tests are often inadequate or inconclusive and since Streptococcus pyogenes can exist intracellularly within the epithelial cells of the pharynx, and even "within" the tonsils, in which case quick Strep tests and cultures will usually, or often, be negative. (Rheumatic Fever and Streptococcal Infection, cited above) One must remember that when a physician is dealing with Streptococcus pyogenes infections one is dealing with a very important aspect of a patient's health.
The term "rheumatism" is still used in colloquial speech and in historical contexts, but it is no longer frequently used in medical or technical literature; it would be fair to say that there is no longer any recognized disorder simply called "rheumatism". The traditional term covers such a range of different problems that to ascribe symptoms and signs to rheumatism, would violate, more than trivially, the artificially developed specialty structure that has developed in modern, western medicine since the 1920's.
One of the first organizations that dealt with rheumatism, in the modern day, was the European League Against Rheumatism. Unfortunately, rheumatologists, to maintain their specialty-mandated specialty status as experts at connective tissue diseases, do not generally deal with infectious diseases or problems of the body's organs even though they also, historically, have dealt with rheumatic fever, which is a high-grade, inflammatory, autoimmune-mediated, systemic disease process stimulated by Streptococcus pyogenes infections and that most "rheumatic diseases" such as rheumatoid arthritis and lupus erythematosis are systemic diseases, per se.
As a vestige of past wisdom, many individuals knew that arthritis, neuropathy, tendonitis, dermatological problems, and many other adverse health conditions had something to do with rheumatism. For instance, during the early 1900's, in America, sciatica was termed sciatic rheumatism or hip gout, eczema of the hands was termed, salt rheum, and gout was termed, gouty rheumatism. Those who understood the collective wisdom of the time knew that the maladies described were part of the rheumatism complex. Old farmers, walking bent over with a cane often have said, "Oh, my rheumatism". Non-articular rheumatism, also known as soft tissue rheumatism, and which is now known as "fibromyalgia", was in prior eras known as "muscular rheumatism". Somewhat surprisingly, that variously described condition is a dispersed rheumatic, sensory neuropathy: bilateral brachial plexitis, sacral plexitis and at times femoral neuropathy that is made more symptomatic by use of the arms and legs. To understand the above pathophysiology an examiner must do an analytic, neurological examination of the brachial plexus, the terminal nerves of the sacral plexus, and the femoral nerve; they must "know" the location of the dermatomes of the body: in SPADES.
Within the chapter on rheumatoid arthritis in Harrison's Principles of Internal Medicine, 16th Edition, cited above, the "NUT" of rheumatism is presented. The author's provides an interesting description: "Rheumatoid arthritis is a chronic multisystem disease of unknown cause." Further, the following is mentioned: "In approximately 10% of individuals the onset is more acute, with a rapid development of polyarthritis, accompanied by constitutional symptoms, including fever, lymphadenopathy, and splenomegally." It describes that rheumatoid arthritis features arthritic aspects, rheumatoid nodules, vasculitis, neuropathy and organ infarction, even myocardial infarction. At times, the text indicates, "Neurovascular disease presenting either as a mild distal sensory neuropathy or as mononeuritis multiplex may be the only sign of vasculitis." Anemia, subcutaneous nodules, and osteoporosis are concomitant features of rheumatoid arthritis. It mentions that pericarditis is found in 50% of individuals with rheumatoid arthritis at autopsy.
Referring to the above description of the "...chronic multisystemic disease..." of rheumatoid arthritis, many signs and symptoms are identical to those found in rheumatic fever: subcutaneous nodules, a feverish disease that exists somewhat before arthritis develops, lymphanenopthy, polyarthritis, splenomegally, vasculitis, neuropathy and organ infarction are all found in acute rheumatic fever patients and some sequelae are found in those with chronic rheumatism.
The connections, mentioned above, of a mild, acute disease triggering vasculitis, arthritis, neuropathy, myocardial infarction, anemia, pericarditis, and osteoporosis describes many of the same pathological features that are historically attributed to rheumatism. The acute disease process mentioned, is, I surely think, a subacute case of rheumatic fever (the type Sir William Osler described in his famous text of 1935), the pathological, systemic, inflammatory, autoimmune disease that post-dates, from a week to five weeks, the Streptococcus pyogenes infection that cased it.
Within the text, Rheumatic Fever and Streptococcus Infection, cited above, the author indicates that fifty percent of Streptococcus pyogenes infections that trigger rheumatic fever have such mild symptoms and signs that patients do not remember them when queried, therefore, it would not be surprising that low-grade respiratory infections and even the somewhat higher grade infections would be missed, forgotten, or just thought to be important.
Individuals who develop high-grade rheumatic fever are often thought to have developed a different, and separate, idiopathic (meaning the cause is not known), acute disease process, but it also has symptoms and signs of vasculitis, arthritis, pericarditis, subcutaneous nodules (which develop due to chronic rheumatism), fever, splenomegally, lynphadenopathy, at times enlargement of the cervical lymph nodes, renal abnormalities, hepatitis, delirium, neuropathy, epistaxis, urticaria (hives) or other rash, and other systemic symptoms and signs, which vary significantly, depending on the severity of the individual disease episode.
Individuals who experience severe cases experience severe pain. Sir William Osler has written the following concerning the pain experienced by patients who have high-grade rheumatic fever: "Perhaps no disease is more painful; the inability to change posture without agonizing pain, the drenching sweats, the prostration and helplessness, combine to make it a most distressing affection ("Osler's Principles and Practice of Medicine, Twelfth Edition, cited above). I learned from experience that when individuals experience severe rheumatic fever, with its severe pain, they will take any thing in an effort to decrease it: opiates, aspirin, ibuprofen, alcohol, cold remedies, etc. Since they become delirious they may behave unwisely and/or behave nastily to those around them. Many patients who die from rheumatic fever, in the past, have been experiencing chronic rheumatism with one of its symptoms being chronic neuropathic pain. Not unusually, they have been prescribed chronic opiates so when they become sick with recurrent rheumatic fever and die, usually at home, their deaths are "blamed" on the opiates they took. A tell-tale sign on examination is, often, however, pulmonary edema and an enlarged heart about 20% above normal. In addition, they often will have a history of a respiratory disease, or a "flu-like" disease, concomitantly or a few weeks before. Possibly, celebrities such as Brittany Murphy (who had the autoimmune target-organ disease of diabetes, her husband (rheumatic fever tends to be a family disease, because Streptococcus pyogenes is very contagious among close-living individuals), Cory Haim, Heath Ledger, Michael Jackson (who had the autoimmune syndrome of vitilago and, perhaps, his quick, stuttering dance steps were, in part enabled by
"Rheumatic fever has various serious manifestations, for instance, carditis, endocarditis (heart valve malfunction), pericarditis, clinical heart failure heart failure, pulmonary edema, rheumatic pneumonitis and cardiac arrhythmias. In addition, it features lassitude, stupor, coma, chorea, and, at times, seizures caused by rheumatic encephalitis. Further, patients experience abnormal kidney function leading to kidney failure, at times; chronic rheumatism is a cause for chronic renal failure. Since rheumatic carditis is a life-threatening target-organ manifestation, and since acute rheumatic myocarditis, endocarditis, pericarditis, and cardiac arrhythmias are aspects of its spectrum, most medical attention in acute rheumatic fever cases is, logically, given to the heart, but in truth, it is a systemic disease process.
For a long period, most medical attention connected with acute rheumatic fever is focused on chronic cardiac valve disease. It is known that individual patients who have had rheumatic fever in the past may have chronically developed cardiac valve abnormalities, with the mitral valve the most commonly abnormal. Most cardiologists, in the modern day, specialize in disease altering procedures to alter the disease of the heart; and they rarely think about, or clinically deal with, acute, systemic, rheumatic fever. The rest of the target-organ manifestations of rheumatic fever have been, more or less, inappropriately disconnected from the acute, disease process and the disease diagnosis that is provided depends on what type specialist attends the patient. If they have meaningful hepatic problems, they may be deemed to have a type of hepatitis. If they have renal failure as a major problem, they may be diagnosed to have acute renal failure. If they have pulmonary failure they may be diagnosed to have interstitial pulmonary disease or, simply, pulmonary failure. Even if they have highly meaningful cardiac problems cardiologists often make the diagnosis of acute heart failure and pulmonary edema, but do not deal with the condition with an etiological approach. The physician, in the modern day, it seems, has the job of providing a "diagnostic code" approved by insurance companies; that is all that is really needed....to get paid.
Like most diseases, rheumatic fever (acute rheumatism) exists as a lower-grade, subtle disease phenomenon most of the time, and relatively rarely, except in certain, favorable epidemiological situations, does rheumatic fever exists in the high-grade state that has the symptoms and signs popularized by the Jones Criteria. Surprisingly, T.Ducket Jones, MD, who invented the Jones Criteria, did not think that Streptococcus pyogenes was the cause of rheumatic fever even in the early 1950's, although, as mentioned above, Alvin Coburn published a monologue that provided proof that it did, in 1931. To keep using the Jones Criteria, nowadays, is improper, I surely think. To think that rheumatic fever is mainly a cardiac disease is also a gross error: it is a systemic, autoimmune disease process, which in high-grade cases has serious, acute, somewhat focused, cardiac, autoimmunological target-organ manifestations.
The rheumatic diseases, which are caused by the autoimmunological response to infections by Streptococcus pyogenes (and perhaps other Streptococcus species) include rheumatoid (rheumatic) arthritis, psoriasis and its arthritis, lupus erythematosis, Sjogren's syndrome, scleraderma, ankylosing spondylitis, dermatomyositis, myositis, Wegener's granulomatosis, and osteoarthritis. They are caused by the autoimmune response to Streptococcus pyogenese infections during the patients' lifetimes. Osteoarthritis is simply rheumatic arthritis that appears in certain joints such as the spine, knees, hips, and hands due to a localized, exacerbation of rheumatic vasculitis that is caused by the mechanical factors of compression and abrasion. For instance, the first three locations feature exacerbated arthritis somewhat commonly due to the compression and abrasion experienced by the joint structures during weight bearing and active use. Individuals' hands, especially womens' hands, often feature arthritis, commonly termed osteoarthritis and rheumatoid arthritis, which are really the same disease state, due to the individual's frequent use, which involves compression and abrasion of the joints, tendons, ligaments and soft tissues of the hands. Also, heat and cold, in general, also cause an exacerbation of rheumatic inflammation in a local fashion. Women are thought to have rheumatoid (rheumatic) arthritis more often then men. Perhaps women use their hands in a more intense and common fashion than most men in the modern day as they do housework and yard work.
Peripheral neuropathies such as lumbosacral/buttock pain with sciatic pain referred down the leg; it is caused by rheumatic inflammation to the terminal nerves of the sacral plexus the sciatic, posterior femoral cutaneous, pudendal nerves. Femoral neuroapthy, carpal tunnel syndrome (median neuropathy), cubital tunnel syndrome (ulnar neuropathy), peroneal neuropathy (lateral lower leg and foot), meralgia paresthetica (neuropathy of the lateral femoral cutaneous nerve), and tarsal tunnel syndrome are all aspects of rheumatism. Fibromyalgia is a dispersed neuropathy of the bilateral brachial plexus, the terminal nerves of the sacral plexus and femoral nerve, and other nerves). Femoral neuropathy can present in a clinically isolated fashion. Various cranial neuropathies such as trigeminal neuropathy can appear as facial pain or the many branches to the meninges can be primarily affected, which, hypothetically, can cause migraine headaches and other clinical types of headaches. Bell's palsy (rheumatism of the facial nerve), hearing deficits, vertigo, Menier's disease, and abnormalities of the motor nerves of the eye are all caused by rheumatic autoimmunity. When neuropathies present more severely they are more systemic in nature so they manifest as the syndromes of multiple sclerosis, Guillain-Barre' syndrome, and, hypothetically, amyotrophic lateral sclerosis.
Rheumatic endocrine abnormalities are common, for instance, diabetes, Addison's disease, Cushing's syndrome, hypothetically, polycystic ovary disease, testicular failure, hypothyroidism, Hashimoto's thyroiditis, hypoparathyroidism, and pituitary abnormalities of various types are usually, more likely, caused by rheumatic autoimmune attack. Hypothetically, children with diabetes probably experienced acute rheumatic fever and the, more or less, acute development of diabetes is one of its sequelae. The others, mentioned above, are due, usually, to chronic rheumatic attack that is caused by rheumatic fever as well as by, or inaddition to, lower grade Streptococcus pyogenes infections during their lifetimes.
Benign Tumors and cancer of various types are rheumatic in nature. Nevi (moles) of various types, freckles, seborrheic keratosis, and many more lesions, usually thought to be benign, are secondary to pathological rheumatic stimulation. Cancer of all tissue types are target-organ manifestations of the systemic autoimmune disease of rheumatism. The rheumatic neuropathies (written about two paragraphs, above) often appear before, or concomitantly, with cancer and they are termed, in that case, paraneoplastic neuropathy. Often the neuropathy is sciatica or the individual has a history of sciatica. Ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, gastritis and esophagitis are also autoimmunological manifestations of rheumatism and like many "systemic rheumatic conditions" such as dermatomyositis and lupus erythematosis, they are also paraneoplastic conditions. I estimate that most individuals who develop cancer have, at least, rheumatoid (rheumatic) arthritis at some level of severity so it, hypothetically, can be thought to be a paraneoplastic, rheumatic disease presentation, also.
Since rheumatism is, first of all, a vascular disease peripheral artery disease of the extremities, carotid stenosis, aneurysm development, CVA's, and kidney vascular abnormalities are all, usually, caused by rheumatic vascultis, the primary lesion of rheumatism. Phlebitis, usually in the lower extremities, is also a manifestation of rheumatic autoimmunity. Lymphedema is probably a condition caused by rheumatic autoimmunity.
Rheumatic central neuropathic conditions are highly variable due to the complexity of the spinal cord and the brain. In recent years there have been breakthroughs that show the "tip of the iceberg, so to speak, in that PANDAS (Pediatric Autoimmune Neurological Deficits caused by Streptococcal infection) is a concept that has wide appreciation. The clinical syndromes, autism, ADHD, Tourette's syndrome (tics, stuttering, stammering, antisocial behavior, explosive personality, coprolallia, echolallia, dysinhibition, etc.), depression, schizophrenia, manic-depressive illness, and disassociative reactions are some manifestations of "rheumatism of the brain", as it were termed in an earlier era.
Gastrointestinal system: target-organ maladies: ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, pancreatitis, peptic ulcers, gastric ulcers (Helicobacter pylori is just an exacerbating problem with rheumatic vasculitis), esophagitis, peridontal disease.
Bursitis: olecrannon bursitis, pre-patellar bursitis, tibial tuberosity bursitis (house maids knee), and subacromial bursitis are examples.
Tendinitis: tendonitis of the long head of the biceps, DeQuervains tendonitis, Achilles tendonitis, and rotator cuff abrasions, tears, etc. Ligamentitis such as plantar fasciitis, deltoid ligamentitis of the medial foot, etc.
Cardiological rheumatic problems: rheumatic cardiac valve syndrome, coronary artery disease, acute and chronic myocarditis (LVH, global cardiac enlargement, and decompensated enlarged heart), pericarditis, and cardiac arrhythmias are all caused by rheumatism. Coronary artery disease and another cardiac problems were termed, "rheumatism of the heart" a concept that was developed by David Pitcairn in 1788 (Rheumatic Fever and Streptococcus infection, cited above).
Kidney: rheumatic vasculitis leading to chronic rhenal failure, gout, and kidney stones.
Special Senses: cataracts, retinitis, iritis, keratokornus, uveitis, subconjuctival hemorrhage, decreased hearing, tinnitis, Menier's syndrome, phorias, tropias, and hyposmia are examples.
Skin: seborrheic keratosis, dermatitis, nevi, angiomas, purpura, urticaria, telangectasias, rosacea, erythroderma, poliosis, vitilago, spider nevi, petechiae, actinic keratosis, Stevens-Johnson syndrome, hypothetically, pityriasis rosea, palmar erythema, plantar erythema, dermographism and others.
Although the above disorders usually are not thought to have much in common etiologically, they are all target-organ manifestations of one variable, inflammatory, autoimmunological disease process: rheumatism. One cannot expect the eye to respond to a systemic disease as the plantar facia responds. One cannot expect the medial meniscus to respond to a systemic, inflammatory disease as the hip joint responds. One should not expect the brain to respond to a chronic, inflammatory, autoimmunological condition as the heart responds. All rheumatic conditions are inflammatory in nature and share two characteristics: they cause chronic (though often intermittent) pain, and they are difficult to treat. They are also, collectively, very common. Aspirin, other NSAIDS, and streroid antiinflammatory medications are used, however, to treat many of them and they "work" reasonably well if taken in adequate doses for protracted periods. Even coronary artery disease, and recently cancer, at times, are prophylactically treated with aspirin.
Since acute rheumatic fever causes a dampening of the protective immune response, hypothetically the innate immune response, "other" infections often develop with acute rheumatic fever (as enumerated by Sir William Osler in his text, Osler's Principles and Practice of Medicine, Twelfth Edition, cited above. Tuberculosis, diptheria, cholera, whooping cough and other diseases are mentioned. Chronic rheumatism also causes a decreased immune response and I surely hypothetically think that tuberculosis, MRSA, Streptococcal necrotizing fasciitis, erysipelas, Lyme disease, herpex zoster, mononucleosis, AIDS, possibly Chigas disease and malaria, are all infectious disease process that take place more commonly in individuals who have high-grade rheumatic autoimmunity: rheumatism.
One can consider that rheumatic fever itself is also an acute aspect of rheumatism and its former name, acute rheumatism, more or less, defines that concept.
interested physicians should read articles and texts by Gene Stollerman, M.D. and Benedict Massel, M.D., two of the last physicians who treated many, patients who had rheumatic fever. Dr. Stollerman has written that physicians should treat patients with pharyngeal infections, after clinical inspection provides a reasonable adjudication that Streptococcus pyogenes could be the causual micorbiological agent, with penicillin. No wonder the American population is becoming populated with millions of cases of fibromyalgia (muscular rheumatism), diabetes, sciatica, autism, MS, cancer, cardiac disease, psychological diseases, and other conditions. One aspect of rheumatic encephalitis is Tourette's syndrome and one of its aspects is antisocial behavior. Our prisons are "filled" with hundreds of thousands of inmates, usually the poorer class of person, who is more likely to have experienced rheumatic fever, and many of them have organic mental problems caused by rheumatic encephalitis.
Since modern, specialty medicine "missed out" on recognizing rheumatism as an abiding, systemic, inflammatory disease that all humans develop, it evolved the concept that the target-organ manifestations of chronic rheumatism were independent idiopathic diseases. The semantic error of using the term disease, when the cause of a malady is not known, led, I surely think, to the general self-deception that physicians knew more about diseases than was true: they were dealing with syndromes, symptom and sign patterns, and not well defined diseases wherein their causes are known. Coronary artery disease is really coronary artery syndrome, for instance. Crohn's disease is really Crohn's syndrome and the list can go on and on since the great majority of the descriptions of "diseases" that fill medical texts such as Harrison's Principles of Internal Medicine, 16th Edition, cited above, are really syndromes: symptom and sign patterns that commonly appear together. Medical science, has, therefore, for the last sixty years developed a multitude of disease altering treatments for various diseases and not curative treatments since the cause of a disease must be known before definative cures can be developed. Modern clinical trials are organized efforts to find a chemical that will alter, significantly, a syndrome for the better; not to cure a disease.
To better understand "where medical science is" at this time, an individual must understand the the scientific revolution of thought started in the modern era, about 1600, and that a modern approach to medical science was not possible without the insights first developed by Antony van Leewenhoek concerning microbiology. Progress was slow, thereafter, so that in 1850, just two long life-times ago, physicians did not know the cause of one disease so all treatments were disease altering. If a patient did not have a laceration, a fracture or a sprain, conditions wherein the cause was known, no curative treatments could be managed. Then the microbiological revolution started in Germany and France with the work of Pasteur, Henle, Koch, Ehrlich, and others. Their breakthroughs stimulated American medical science to become more academic. By the late 1930's sulfonamide and penicillin had been developed and their use was a great boon to physicians and patients alike. It seemed that there was not much further worry about infectious diseases and physicians and medical researches dropped their guard, understandibly.
Autoimmune concepts had been developed early in the 1900's, but the excitement over microbiology and antibiotics and the development of specialty, procedural medicine caused interest in immunology to wane. Interest in immunology re-developed in the 1970's and great progress has been made, but there have been few physicians on the street seeing patients of both sexes, of all ages, and for all diseases, who happened to practice in an area where rheumatic fever was active, and who could put the advances in immunology together, at least in a superficial fashion, with clinical medicine. I hope I have succeeded.
Treatment
Since the etiolgy of rheumatism has not been known, individuals throughout history have used a great number of traditional and more modern treatments for the many symptoms of rheumatism. Modern medical treatment often consists of non-steroidal anti-inflammatory treatments and steroid anti-inflammatory treatments. Both are used for acute, rheumatic fever also. Treatment for the target-organ manifestations of rheumatism are as varied as cryotherapy for dermatological lesions, both cancerous and benign, surgical treatment for rheumatic arthritis as of the knees and fingers, tendonitis of the rotator cuff, and spinal surgery for heriated spinal-discs, which is usually inappropriate. Aaron Filler, M.D. (backpain-guide.com) accomplishes piriformis canal enlargement procedures to decrease the pressure on the terminal nerves of the sacral plexus and often has good results from his procedures when individuals experience recalcitrant sciatica.
Somewhat commonly, initial therapy for mildly painful symptoms of rheumatism is to use non-opiate analgesics such as acetaminophen. Since rheumatism is an inflammatory disease process, of an autoimmunological nature, non-steroidal anti-inflammatory/analgesic medications (NSAIDs) are used, some members of which are aspirin, ibuprofen, naproxen sodium, indomethocin, and diclofenac. Many others exist. Often, more efficacious analgesics are required and if individuals have meaningful pain, opiate analgesics have been safely used for hundreds of years.
Most patients will experience a relief of thier severe neurological pain if they are provided a Steroid injection such as triamcinolone 80 mg. intramuscularly via the upper outer quadrant of the buttock. They should experience reasonable relief in three to four days. They should take aspirin, 325 mg, coated, three times a day and indomethacin 25 mg. three times a day, together, also, and also take ranitadine, 150 mg a day to decrease stomach acid production.
The current practice of providing steroid injections into the spinal space is not needed, because even when it is injected in that area (by an expensive procedure), it will be absorbed by the arterial and venous circulation and spread around the body: it does not matter where it is given and so an intramuscular injection is adequate as long as the dose is high enough. I surely think, for a short period, like three months, a triamcinolone injection can be given every three weeks, or so.
At times a family member, or the patient, can be a Streptococcus pyogenes carrier so I used to see all immediated family members living in the same house and treat them all for a short time with an adequate dose of penicillin.
If individuals know they have had rheumatic fever, or if they have positive or high normal serology tests for Streptococcus pyogenes, ASO, Anti-DNase B, Anti-hyaluronidase, Anti-Streptokinase, for instance, prophylactic use of penicillin VK, G, or amoxicillin can be used to decrease the frequency of high-grade rheumatic fever, by decreasing meaningful Streptococcus pyogenes infections. Keflex or Erythromycin can be used if a person is allergic to penicillin. Certain organizations are working on the development of a vaccine for Streptococcus pyogenes.
"Rheumatism" and weather
For a long period, it has been suspected that there is a link between "rheumatic" pain and the weather. There appears to be no firm evidence in favour or against that idea, but a 1995 questionnaire given to 557 people by R. Jamison, and others, at the Brigham and Women's Hospital's Pain Management Center concludes that "changes in barometric pressure are the main link between weather and pain. Low pressure is generally associated with cold, wet weather and an increase in pain. Clear, dry conditions signal high pressure and a decrease in pain"[2].
Within the first edition of the Encyclopedica Britannica, the following quote is provided: "The rheumatism chiefly attacks persons in the flower of their age, after violent exercise, or a great heat of the body from any other cause an, and then being too sudenly cooled."
Within the text, Rheumatic Fever and Streptococcal Infection, cited above, the following is written: "Haygarth in 1805 was one of the earliest physicians to relate rheumatic fever to the throat when he noted that "persons who have been previously affected with the acute or chronical Rheumatism, the Gout, or sore throat, especially the first, are most liable to suffer attacks of this disease; and ought therefore to be particularly careful to avoid exposure to cold and moisture." In a study of 175 patients with acute rheumatism he observed that sixty-five of them ascribe their disease to "having caught a cold" and he expressed the opinion that the exciting cause was "exposure to cold and moisture.""
Within Sir William Osler's text, published in 1912, cited above, within the section of chorea the following is mentioned, "The cases are most numerous when the mean relative humidity is excessive and the barometric pressure is low (Lewis). Concerning rheumatic fever in the same text, "It prevails in temperate and humid climates...The disease prevails in the more northern latitudes...The general impression is that the disease prevails more in the British Isles than anywhere else...In Norway, where cases of rheumatic fever are notified, there were, for the four years 1888-'92, 13,654 cases, with 250 deaths.,,CHILL--Exposure to cold, a wetting, or a sudden change in temperature are among the factors in determining the onset of an attack, but they were present in only 12 per cent. of our cases.
It is well known by mothers and physicians that respiratory diseases, colds, are more common in the autumn, winter and spring and those are the seasons when rheumatic fever is most common. In the above mentioned text, Rheumatic Fever and Streptococcal Infection, cited above, Bernard Schlesinger indicated, " It is no exaggeration to say that acute nasopharyngeal infection is the most serious menace to the rheumatic child with heart disease."
I do not think barometric pressure affects rheumatism's develoment, especially since it varies continually day in and day out and hour by hour, but cooler and damper weather affects the frequency of Streptococcus pyogenes infections. Damp weather is usually connected with lower barometric pressure and cooler dry weather often is connected with clear, high-pressure weather patterns, in the winter. The fall through the late spring is generally cooler in the northern hemisphere.
It is a sure fact that high altitude areas such as the Rocky Mountain area in the USA has an elevated frequency for the development of rheumatic fever cases for it was proved during the WW II period. Rheumatic fever, acute rheumatism, and therefore the development of chronic rheumatism is not limited, however, to any particular altitude or climate.
The high-altitude area of Mexico features endemic rheumatic fever and I surely think that the great number of immigrants to the USA from Mexico, usually individuals from the more economically poor class, have been vectors for virulent strains of Streptococcus pyogenes and that great immigration phenomenon has probably been one of the causes of the increased level of rheumatism as indicated by the increased incidence of acute rheumatic fever in the USA since 1987, and therefore, the cause of the increase in the incidence of autism, diabetes, and other autoimmunological diseases in the USA during the last thirty years.
Miscellany
A Trod in the West of England is a straight line or Fairy Path in the grass of a field with a different shade of green to the rest. People with rheumatism sought relief by walking along these tracks, though animals are thought to avoid them.[1]
"For the period of 1939-1943, statistics published by the Metropolitan Life Insurance Company indicated that rheumatic fever was the leading cause of death among policy holders for persons from five to nineteen years of age and the second leading fatal disease among twenty to twenty-four year olds." Rheumatic Fever and Streptococcal Infection, cited above.
References
- ↑ Pennick, Nigel (1996). Celtic Sacred Landscapes. Thames & Hudson. ISBN 0-500-01666-6. P. 132.
External links
- BBC "Your Health" website on Arthritis and Rheumatism
- List of plant species that have been recommended as treatments for rheumatism, from Dr Duke's Phytochemical and Ethnobotanical Databases
- Account of Rheumatism from the website of Retirement Matters Ltd of the UK