Rheumatism by Dr. Lance Christiansen: Difference between revisions
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The following information concerning the chronic, inflammatory disease of rheumatism was obtained from reading countless texts, journal articles, and on-line sources during a career in medical science and especially during the last eight years during which time I have conducted a clinical, academic and epidemiological study of rheumatic fever. In addition, and perhaps the most important, was the information I learned from patients who had had rheumatic fever. | The following information concerning the chronic, inflammatory disease of rheumatism was obtained from reading countless texts, journal articles, and on-line sources during a career in medical science and especially during the last eight years during which time I have conducted a clinical, academic and epidemiological study of rheumatic fever. In addition, and perhaps the most important, was the information I learned from patients who had had rheumatic fever. | ||
Much of the medical knowledge I accumulated was during my medical education, but much more was developed and accumulated during a thirty-year career as a general practitioner in medicine. I owned my own clinic, I saw 230,000 patient visits, at least 2000 house calls, and treated males and females, of all ages, for all diseases. 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 much of the information in this article. In addition, my clinic was located in an economically depressed area of S.W. Washington State, wherein there was a mini-epidemic of rheumatic fever during 2004-2006 and at least ten people, who were my patients, and who had chronic rheumatism, died of recurrent rheumatic fever. That experience, and the intellectual study that it stimulated, led to a epidemiological study wherein I traveled to twelve countries and visited hospitals and clinics and people on the street. All together, the experiences I have mentioned provided the knowledge to write this article. | Much of the medical knowledge I accumulated was during my medical education, but much more was developed and accumulated during a thirty-year career as a general practitioner in medicine. I owned my own clinic, I saw 230,000 patient visits, accomplished at least 2000 house calls, and treated males and females, of all ages, for all diseases. 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 much of the information in this article. In addition, my clinic was located in an economically depressed area of S.W. Washington State, wherein there was a mini-epidemic of rheumatic fever during 2004-2006 and at least ten people, who were my patients, and who had chronic rheumatism, died of recurrent rheumatic fever. That experience, and the intellectual study that it stimulated, led to a epidemiological study wherein I traveled to twelve countries and visited hospitals and clinics and people on the street. All together, the experiences I have mentioned provided the knowledge to write this article. | ||
Between 2002 and 2005 I conducted a three-year clinical investigation in order 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, but their neuropathic pain was caused by rheumatic autoimmune-mediated, vasculitic neuropathy of the terminal nerves of the sacral plexus in the piriformis canal and the brachial plexus in the axillary canal, respectively. | Between 2002 and 2005 I conducted a three-year clinical investigation in order 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, but their neuropathic pain was caused by rheumatic autoimmune-mediated, vasculitic neuropathy of the terminal nerves of the sacral plexus in the piriformis canal and the brachial plexus in the axillary canal, respectively. | ||
Revision as of 04:38, 29 March 2010
| Rheumatism by Dr. Lance Christiansen | |
| ICD-10 | M79.0 |
|---|---|
| ICD-9 | 729.0 |
| MeSH | D012216 |
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Overview
The following information concerning the chronic, inflammatory disease of rheumatism was obtained from reading countless texts, journal articles, and on-line sources during a career in medical science and especially during the last eight years during which time I have conducted a clinical, academic and epidemiological study of rheumatic fever. In addition, and perhaps the most important, was the information I learned from patients who had had rheumatic fever.
Much of the medical knowledge I accumulated was during my medical education, but much more was developed and accumulated during a thirty-year career as a general practitioner in medicine. I owned my own clinic, I saw 230,000 patient visits, accomplished at least 2000 house calls, and treated males and females, of all ages, for all diseases. 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 much of the information in this article. In addition, my clinic was located in an economically depressed area of S.W. Washington State, wherein there was a mini-epidemic of rheumatic fever during 2004-2006 and at least ten people, who were my patients, and who had chronic rheumatism, died of recurrent rheumatic fever. That experience, and the intellectual study that it stimulated, led to a epidemiological study wherein I traveled to twelve countries and visited hospitals and clinics and people on the street. All together, the experiences I have mentioned provided the knowledge to write this article.
Between 2002 and 2005 I conducted a three-year clinical investigation in order 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, but their neuropathic pain was caused by rheumatic autoimmune-mediated, vasculitic neuropathy of the terminal nerves of the sacral plexus in the piriformis canal and the brachial plexus in the axillary canal, respectively.
During the above investigation I attracted 700 miserable, painful patients. Eventually, I learned that they all had had meaningful, repeated Streptococcus pyogenes infections (tonsillitis, sinusitis, bronchitis, pharyngitis, impetigo, and vaginitis) and many of them had, when they were younger, rheuamatic 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 writings by Sir William Osler, from his text, cited below, however, that there are subacute and less than subacute states of rheumatic fever with more subtle systemic symptoms and signs of rheumatic disease.
I conducted serology tests (ASO adn 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 that were really cases of rheumatic fever, the great majority of the 700 patients, mentioned above, who had chronic neurological and arthritic pain, and other common diseases, were qualified to have had mild and severe septic responses to Streptococcus pyogenes infections. The septic responses were caused by rheumatic, systemic autoimmunity: acute rheumatism. As the elevated rheumatic, autoimmune disease naturally decreased after infections by Streptococcus pyogenes abated, due to the protective aspect of the immune response, patients had chronic rheumatism. I learned that future infections by Streptococcus pyogenes would cause repeated rheumatic stimulation establishing a chronic, autoimmune disease process: rheumatism.
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 animals, it seems that Streptococcus pyogenes causes a universal zooinosis, and therefore a universal, chronic, autoimmune disease among most vertebrates, including humans: rheumatism.
Rheumatism is a specific term for a chronic, systemic, inflammatory, autoimmune-mediated disease process caused by the immune system's response to Streptococcus pyogenes infections, for instance, tonsillitis, pharyngitis, peridontal disease, bronchitis, laryngitis, sinusitis, vaginitis, pyoderma, impetigo, a systemic inflammatory response syndrome, SIRS, with what is termed, popularly, "flu-like symptoms", but which is mild rheumatic fever, high-grade rheumatic fever and scarlet fever. Acute rheumatism was the common term for rheumatic fever, the most elevated level of rheumatic autoimmunity, up through the early decades of the 1900's.
Current medical opinion provides the knowledge that certain virulent infections in a well Streptococcus pyogenically sensitized individual (Acute Rheumatic Fever (Carapetis, JR.,et al., Lancet Jul 9-15; 366(9480): 155-68) can develop high-grade rheumatic fever, which is known to be an an inflammatory, autoimmune disease process. It has not been clinically recognized, however, that all infections by Streptococcus pyogenes cause an inflammatory autoimmune response and it slowly, but surely causes pathological damage to the body's tissues and therefore organs in a somewhat subtle, varying, but progressive fashion and causes, over time, the clinical signs and symptoms of rheumatism. Eventually, in all individuals, the target-organ damage caused by rheumatism is thought to be what is commonly termed the aging process.
High-grade rheumatic fever decreased in incidence starting in the early 1900's, in modern, industrialized societies, secondary to the improvements in living conditions brought on my advances of the industrial revolution. Advances included larger homes that caused decreased crowding, smaller family size, more hygienic living habits, the common use of soap, home bathing facilities, clothes washers, dish washers, the pasturization of milk, and the use of antibiotics for respiratory infections starting in the 1930's. The environmental changes resulted in fewer and fewer Streptococcus pyogenes infections, and more importantly, perhps, infections with less virulence, so by 1970 rheumatic fever was a relatively rare disease in modern, developed countries. Simultaneously, the citizes of modernized countries experienced a life-expectancy increase; in the USA the life expectancy increased from forty-seven in 1900 to about seventy-seven in 2000: an increase of about thirty years, an increase of 64% over a 100 year period. There has to be a logical reason for the increased longivity. The reason, mainly, was less Streptococcus pyogenes infections and lesser levels of rheumatic autoimmunity, including rheumatic fever, a disease that often caused the death of children and younger people, three to fifty years of age, and increased, remarkably, the average longivity of the population. There were other positive factors also, better food supply, vaccines for other diseases, etc.
Rheumatic autoimmunity causes, initially and continually, an inflammatory vascular disease that results in inappropirate intra-arterial thrombosis. The immune system reacts to it with a localized inflammatory response so that 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.
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, physicians did not completely adopt 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.
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. However, since acute rheumatic fever, and moreso, chronic rheumatism are both systemic disease processes with multitudes of target-organ manifestations they simply were not recognized, or ceased to be recognized, by the members of the specialty-oriented medical community. Individuals in the medical specialties concentrated on various target-organ manifestations of rheumatism and developed disease-altering treatments such as CABG, angioplasty/stent procedures, many other surgical procedures such as cholesystectomy and partial colectomies (ulcerative colitis, diverticulitis, colon polyposis), the use of NSAIDS, Streroid anti-inflammatory medications and countless other chemotherapeutic drugs.
During the development of "specialty medicine", rheumatology was "elbowed" into dealing with connective tissue only. The medical 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 elements of its understanding had been provided by investigators in prior eras, by microbiological breakthroughs, and by the initial insights made in autoimmune disease concepts.
Even though high-grade rheumatic fever greatly decreased in incidence, from 1900 until 2000, 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, they still cause pathological, rheumatic, systemic, inflammatory, autoimmune-mediated responses within "all" individuals in human society, but at a lesser level of intensity in modern, developed countries.
The clinical understanding of high-grade rheuamtic fever decreased in modern countries so that, nowadays, the average physician has virtually no, or little, knowledge of acute rheumatic fever at this time, threrefore, the knowledge of the much lower grade, chronic rheumatic autoimmunity and its target-organ manifestations, is virtually null in medical science and along the way, rheumatism as a chronic disease concept was dismissed as a serious medical subject.
Because of the belated full acceptance, by the medical community, of the cause of acute rheumatic fever, just as it was becoming less and less common in the late 1940's and 1950's, the wisdom concerning lesser, chronic levels of rheumatic autoimmunity was never established in modern medicine even though as early as the late 1700's the "clinical cause" 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 rheumatism. 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 or other description of a respiratory disease. Galen knew, that when people developed contagions that caused the development of phlegm, or 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), angina, pericarditis, pleurisy, tendonitis, ligamentitis (for instance plantar fasciitis) are examples of modern names for target-organ manifestations of rheumatism.
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 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 were shouldered out of dealing with infectious diseases, or problems of the body's organs, by the other specialty-segregated physician groups and so they deal with "connective tissue" 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.
As a vestige of past wisdom, many individuals feel that arthritis, neuropathy, and tendonitis has 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 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 (Kasper,D., et al., McGraw-Hill, 2005) the author describes rheumatoid arthritis as a systemic, autoimmune disease (it is in the section of the text about autoimmune diseases), and in prior editions it indicates, that at times exacerbations appear sometime after a feverish affliction. In the edition mentioned above, the 16th Edition, the following is mentioned: "In approximately 10% of individuals the onset is more acute, with a rapid development of poly arthritis, accompanied by constitutional symptoms, including fever, lymphadenopathy, and splenomegally." It describes that rheumatoid arthritis, better termed rheumatoid disease, 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.
The connections, mentioned above, of an acute disease triggering vasculitis, arthritis, neuropathy, myocardial infarction, anemia, pericarditis, and osteoporosis describes many of the same causes of pain that are historically attributed to rheumatism. The acute disease process mentioned, is a mild case of acute rheumatic fever, the systemic, inflammatory, autoimmune disease process that post-dates, from a week to five weeks, the Streptococcus pyogenes infection that triggers the rheumatic, autoimmunological response.
Within the text, Rheumatic Fever and Streptococcus Infection (Massell, B., Harvard Press, 1997) 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, therefore, so it would not be surprising that those low-grade respiratory infections and the somewhat higher grade infections would be missed, forgotten, or just thought to be mild, pesky, previous or concomitant problems.
Individuals who develop high-grade rheumatic fever would seemingly represent a different, and separate, acute disease process, but it also has symptoms and signs of vasculitis, arthritis, pericarditis, subcutaneous nodules, and neuropathy, but it has other more serious manifestations of acute rheumatism, for instance, rheumatic carditis, heart failure, cardiac arrhythmias, lassitude, stupor, coma, chorea, seizures caused by rheumatic encephalitis, kidney failure, etc. Since rheumatic carditis is a life-threatening target oran manifestation, and since it can cause acute rheumatic myocarditis, endocarditis and cardiac arrhythmias, most medical attention to rheumatic fever is provided by cardiologists who specialize in disease altering procedures, but who rarely think about cardiac, rheumatic, autoimmune disease. The rest of the target-organ manifestations of rheumatic fever have been inappropriately disconnected from the acute disease process.
Like most diseases, rheumatic fever (acute rheumatism) exists as a lower-grade, more 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, even though 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 that in high-grade cases has serious, acute, somewhat focused, cardiac, autoimmunological sequela.
Frequently, the target-organ manifestations of rheumatic autoimmunity, rheumatism, clinically appear as seemingly isolated maladies. Examples of some of them are:
The rheumatic diseases including rheumatoid (rheumatic) arthritis, psoriasis and its arthritis, lupus erythematosis, Sjogren's syndrome, scleraderma, ankylosing spondylitis, dermatomyositis, myositis, Wegener's granulomatosis, and others. Osteoarthritis is simply rheumatic arthritis that appears due to an individuals stress on the meniscus, usually the medial meniscus, when they have more subtle signs and symptoms of rheumatoid (rheumatic) arthritis in other joints.
Peripheral Neuropathies: Sciatic back pain (sciatic, posterior femoral cutaneous, pudendal neuropathy), femoral neuroapthy, carpal tunnel syndrome, ulnar neuropathy, peroneal neuropathy, meralgia paresthetica, and tarsal tunnel syndrome. Fibromyalgia is a dispersed neuropathy of the bilateral brachial plexus and the terminal nerves of the sacral plexus. The femoral nerve and the lateral femoral cutaneous nerves can be involved. Various cranial neuropathies such as rheumatic, trigeminal neuropathy, Bell's palsy, hearing deficits, vertigo, 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.
Endocrinopathies: diabetes, Addison's disease, Cushing's syndrome, hypothetically, polycystic ovary disease, testicular failure, hypothyroidism, hypoparathyroidism, and pituitary abnormalities of various types.
Benign Tumors and cancer of various types. Yes, cancer of all tissue types are target-organ manifestation of the systemic autoimmune disease of rheumatism. The rheumatic neuropathies often appear before, or concomitantly, with cancer and they are termed, in that case, paraneoplastic neuropathy. Often the neuropathy is sciatica. Ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, and many rheumatic conditions such as dermatomyositis, lupus erythematosis, are paraneoplastic rheumatic conditions. I estimate that most individuals who develop cancer have rheumatoid (rheumatic arthritis).
Vasculitides: Peripheral artery disease, carotid stenosis, aneurysm development, CVA's, and kidney vascular abnormalities are all caused by rheumatic vascultis, the primary lesion of rheumatism.
Central Neuropathies: autism, ADHD, depression, schizophrenia, manic-depressive illness, disassociative reactions, etc. are manifestations of "rheumatism of the brain".
Gastrointestinal 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 development, 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, 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 (McRae, T., D. Appleton-Century Co., 1935). 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.
Within the first edition of the Encyclopedia Britannica(By a Society of GENTLEMEN of Scotland., In Three Volumes, Edinburgh: Printed for A.Bell and C. Macfarquhar; And fold by Colin Macfarquhar, at his Printing-office, Nicolson-stree, M.DCC.LXXI.), 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 is provided. It mentions fever, chills, rapid heart rate, fatigue, lassitude, gastrointestinal problems, the 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-1600's knew that repeated "...lesser but neglected colds." could cause the systemic disease of rheumatism, but in the modern day, pundits of evidence-based medicine (they gave up on scientific medicine, I surely think) 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 (even if those common tests are often inadequate or inconclusive).
The above pundits should read articles and texts by Gene Stollerman, M.D. and Benedict Massel, M.D., two of the last physicians who treated many, individuals 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. 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. That semantic error, using the term disease, when the cause of the 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 "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 eara, about 1600, and that a modern approach to medical science was not possible without the insights first developed by 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 person 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, for all diseases, who happened to practice in an area where rheumatic fever was active, who could put the advances in immunology together 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 of the painful symptoms of rheumatism is to use analgesics, such as acetaminophen, and non-steroidal anti-inflammatory medications (NSAIDs), 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.
If individuals know they have had rheumatic fever, 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. Certain organizations are working on the development of a vaccine for Streptococcus pyogenes.
"Rheumatism" and weather
There has long been said to be a link between "rheumatic" pain and the weather. There appears to be no firm evidence in favour or against, 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.""
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 weather often is connected with clear, high-pressure weather patterns. 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 from Mexico, usually individuals from the more economically poor class, have been vectors for virulent strains of Streptococcus pyogenes and they have probably been one of the causes of the increased level of rheumatism as indicated by the increased incidence of fibromyalgia, explosive emotional behavior (Tourette's syndrome) in the United States.
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]
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
- e-medicine article on Non-Articular 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