Reviews4

Sponsored Links

Chronic Obfuscation – A Review of OSLER’S WEB: Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic
By Hillary Johnson.
Crown. 720 pp. $30.

Circa 1984, around the time when San Francisco immunologist Jay Levy was investigating the cause of the “gay pneumonia,” University of California medical school professor Carol Jessop began seeing women patients who presented a baffling array of signs and symptoms: fever, lymphadenopathy, sore throat, visual and other neurological disturbances, and paralytic muscle weakness. The worsening of these symptoms upon minor physical exertion formed a common denominator in all cases. But when Jessop began subjecting the patients to exhaustive tests to rule out autoimmune and other diseases, male colleagues scoffed, calling the tests “million dollar workups on neurotic women.” That derisive attitude set the tone for both medical and media discussions of an enigmatic illness for years to come. The problem was exacerbated by the 1988 Centers for Disease Control case definition — set in stone in the Annals of Internal Medicine — when the C.D.C.’s Gary Holmes labeled with the word “fatigue” a crippling disease of probable infectious etiology.

“Chronic Fatigue Syndrome” (C.F.S.) is a name that reveals just how tenuous the connection between words and their referents can be. It is difficult to imagine clinical severity after hearing a name that denotes tiredness. In Osler’s Web, Hillary Johnson provides a well-documented account of the politics behind that prejudicial choice of a name. Written in the style of Randy Shilts’s AIDS epic, And the Band Played On (and edited by that volume’s editor, Michael Denneny), Johnson’s book is a thorough medical and political history of this decades-old (and variously named) syndrome during the epidemic years of 1984-1994. Beginning with Jessop’s experience, it reports on vast cluster outbreaks of C.F.S. in the eighties.

But the most provocative portion of Johnson’s discussion concerns the federal research establishment’s attempt to manufacture a mental disorder out of a physical symptomatology. In meticulous detail, Johnson shows how bias in the choice of patients, value-laden selection of C.F.S.-related data and prejudicial allocation of research funds permitted government researchers to conclude that C.F.S. was a psychiatric condition, or rather, something more akin to a behavioral problem. If Johnson is correct, then the government’s conclusion is a classic illustration of the Thomas Szasz thesis: The concept of mental illness is often a political tool with which society dismisses its inconvenient members.

Johnson cites the voluminous evidence independent researchers have gathered in support of the claim that C.F.S. is a disease that attacks both the immune system and the brain — including viral markers that reveal a patient’s inability to maintain latency of ubiquitous viruses (i.e., some viruses infect 95 percent of the population, but lie dormant prior to conditions of immune suppression) and brain abnormalities as evidenced on M.R.I. (shows structural defects) and SPECT (reveals functional defects). The brain abnormalities resemble those observed in AIDS. The disease’s clinical severity also emerges from the stories Johnson relates of formerly active men, women and children who, after contracting the malady, became homebound, suffered dementia or seizures, or faced confinement in nursing homes.

Osler’s Web juxtaposes evidence for the disease’s gravity, prevalence and contagion with an account of ongoing government efforts to control the nature and availability of information about C.F.S. Representative of official bias was the C.D.C.’s tepid response to a 1985 cluster outbreak in Incline Village, Nevada. Where clinician and C.F.S. researcher Paul Cheney had already identified over 150 cases, Holmes and Jon Kaplan of the C.D.C., working within the same patient population, claimed to have confirmed only fifteen cases. The discrepancy resulted from Holmes and Kaplan having selected out all patients displaying concomitant pathology, as though it were coincidental rather than a natural outcome of the disease process itself. For instance, patients with bacterial infections were excluded, even though infections might be expected under conditions of immune suppression. Selection bias characterized government research, surveillance and grant allocation from that point on. Cheney’s partner, for instance, had observed an increase in lymphomas in his epidemic population. When he complained that Holmes was ignoring this evidence, Holmes wrote, “The identification of…lymphomas that occurred in your patients (and) MRI abnormalities…moves such patients out of the CFS category.”

But the central villain of Osler’s Web is Stephen Straus, head of the medical virology section of the National Institute of Allergy and Infectious Diseases (NIAID). Johnson discovered that Straus, who was considered by his superiors to be an expert on the disease, omitted from consideration not only patients with post-C.F.S. lymphomas but those with such classic C.F.S. complications as seizures and, indeed, with any objective signs of disease. He then circularly concluded that C.F.S. is a subjective condition.

Straus became the establishment’s C.F.S. oracle. According to Johnson, he voted in favor of the C.D.C.’s obfuscatory name, “Chronic Fatigue Syndrome,” peer reviewed prospective journal articles, supervised the dissemination of dubiously informational C.F.S. pamphlets to physicians and negatively influenced the allocation of federal research money. He thereby set the parameters for professional and lay discourse, insuring that it would be conducted only in terms of psychopathology. Moreover, Straus staunchly maintained this stance in spite of opposition to his conclusions from within the psychiatric community itself. In the end, the psychopathological paradigm of C.F.S. became an article of faith among those in mainstream and academic medicine — physicians who disagreed were threatened with professional ostracism — rather than an issue to be assessed in light of all available evidence.

Evidence that C.F.S. was an illness didn’t come from federal research money, since N.I.H. grants were dispersed according to the principle that C.F.S. was not a bona fide disease. Promising grant proposals of dissenters from this clinical orthodoxy were passed over, and one casualty was that the cancer link with C.F.S. was never explored. Indeed, Johnson forcefully accuses both the N.I.H. and the C.D.C. of gross misuse of Congressionally appointed funds earmarked for C.F.S. Misappropriation of funds at the C.D.C. and biased selectivity in grants at the N.I.H. went hand in hand — no amount of money devoted to C.F.S. research seemed to prove helpful in understanding the disease, since the infrastructure was predisposed to dismiss it. Institutionalized intransigence became increasingly obvious as patients — medical professionals among them — sent written complaints to Anthony Fauci, head of NIAID and Straus’s boss. According to Johnson, Fauci defended his subordinate’s cavalier response to C.F.S. by citing studies by Connecticut psychiatrist Peter Manu, who, having failed to select his patients according to any known diagnostic criteria for C.F.S., concluded that C.F.S. was a somatization disorder — a physical manifestation of a mental problem. And, in a move that strikingly illustrates Szasz’s thesis, NIAID deputy director Jim Hill even suggested that those who criticized Straus were more likely to have a psychiatric component to their disease than those who agreed with him.

One of Osler’s Web’s genuine strong points is its illustration of a propaganda system at work. Studies citing negative findings in C.F.S. were readily published, while studies reporting positive physiological findings were turned down (e.g., by Lancet and The New England Journal of Medicine) or were published after being held to higher standards of verification than were papers on other diseases. Johnson illustrates how, in turn, this professional skepticism influenced the mainstream media and hence public perception. Time, The New York Times, The Washington Post and television networks seized upon the negative reports and on the pronouncements of government-paid scientists as those of unimpeachable authority. Insidiously, the patient organizations themselves were co-opted. According to Johnson, the largest of these organizations, the formerly ACT UPish C.F.I.D.S. Association, even came to permit government censorship of its journal in the name of “peer review.”

Sponsored Links

Johnson has worked from written documents, taped interviews and published journal articles, and she offers an impressive accumulation of well-substantiated facts. But her analyses are inadequate. She criticizes the new, 1994 case definition for its treatment of the disease as a subset of fatigue; criticizes the C.D.C. surveillance method of looking for the prevalence of fatigue in American society; criticizes Straus’s intent to “define the disease… out of existence by embracing all who claimed fatigue under its umbrella”; but fails to state precisely what is wrong with these approaches. For the error here is fundamentally one of logic.

Put most starkly, some members of the federal system take an accident, fatigue, as the disease’s essence — and from this a variety of unrelated diseases, linked by a shared symptom, are identified as one. Such was the error of Peter Manu, whom federal scientists frequently cite as an authority on the disease. From my own reading of Manu, it is apparent that he selected into his practice people with fatigue associated with depression. Since the usual prescription for fatigue is more exercise, many of Manu’s patients, predictably, responded to a regimen of graded workouts. Manu went on to use this experience as the basis for patronizingly reassuring publications about C.F.S. — a disease that, in fact, worsens with exercise. Manu’s error was to identify two different diseases by a shared property, diseases so distinct that neuroendocrine studies have shown marked physiological contrasts between them. In other words, he committed the Fallacy of the Undistributed Middle. Such reasoning is only one of the damaging consequences of the name “Chronic Fatigue Syndrome.” The conflation of C.F.S. and chronic fatigue permeates medical journals and federal discussions of the disease and permits patients who fail to respond to standard fatigue therapies to be dismissed as malingerers and somatizers.

Fatigue is not a disease. It is a symptom of many diseases. Since there is no single underlying condition behind fatigue, by equating C.F.S. with unexplained fatigue, federal officials can say that there is no single underlying condition behind C.F.S. While there is nothing unreasonable about the claim that C.F.S. has multiple causes (exposure to toxins can trigger reactivation and hence chronicity of latent viruses, and it is probable that a number of viruses could cause the chronic postviral syndromes that are now classified as C.F.S.), what is unreasonable is the notion that C.F.S. is many unrelated diseases grouped by their shared symptom, fatigue. After excluding patients with the disease by excluding the whole complex of classic symptoms and complications that accompany C.F.S., federal officials went on to include those who don’t have the disease via the symptom of fatigue. With the latter they “recognize” the disease without recognizing it: A truly effective system of repression is one that propagates the impression of its openness and fairness.

Osler’s Web harbors its own internal contradictions. Most striking, in light of Johnson’s criticism of the “insidiously benign name,” is the book’s frequent use of the term “fatigue” to describe the disease’s main component (relapsing of flu and neurological symptoms upon exertion, which leaves patients bedridden for days, weeks or years). Johnson fails to note that there is no necessary connection between a need for rest and tiredness: Rest might equally well serve to curb the exacerbation of pain and, speaking in more conceptually rigorous terms about C.F.S., of exertion-induced complications. While Osler’s Web thoroughly debunks the myth that any of these complications — paralytic muscle weakness, blurred vision, dementia — typify the habitual, volitional idleness that the term “chronic fatigue” suggests, by adopting “fatigue,” if only as a synthesizing placeholder, Johnson vitiates her own case against the name. Patients who criticize the name must take responsibility to eliminate the term, and doing so would be in keeping with the spirit of the namesake of Johnson’s book: It was the Canadian clinician Sir William Osler (1849-1919) who championed research into disease phenomena, as opposed to the deductive approach of following out the logic of unthinkingly adopted concepts, which is among the tactics that have hindered meaningful research on C.F.S., so called.

That federal officials ignored disease phenomena and rarely examined patients is Johnson’s explanation of why they are resisting acknowledging the disease. Yet her explanation is inadequate, since the question of their motivation remains. The book presents strands of a cultural analysis (e.g., Straus’s ill-concealed sexism) and hints of economic analyses (she names physicians who are more concerned with the potential insolvency of insurance companies than with patient well-being). And much of the story unwittingly illustrates Thomas Kuhn’s characterization of normal science as inherently resistant to novelty. The thin line between normal science and propaganda is also evident from Johnson’s account. But Osler’s Web never quite achieves the synthetic grasp of concepts necessary to address properly the pervasive policy abuse it so convincingly exposes.

Osler’s Web also suffers stylistically from an accumulation of detail that, at times, serves no very evident purpose. Roughly one fourth of the book is devoted to the search for a retroviral cause of C.F.S. Since no such virus has yet been found, the book strikes an inconclusive note, rather like a postmodern novel. If Johnson is hinting that more money for viral studies should be allocated to independent researchers, she should have argued her case directly.

Sponsored Links

In the end, Osler’s Web is a kaleidoscope of tantalizing analytical fragments incompletely integrated. Yet too much theory might have overwhelmed a general reader, and this issue needs disclosure, not in some cloistered academic setting but in a public forum. Something appeared in the eighties that was more efficient at triggering the syndrome than any viral or toxic agent had been in the past, and C.F.S. is now a widespread, if still hidden, disease. At a time when the do-gooders at the C.F.I.D.S. Association are taking seriously books on spontaneous New Age recoveries in patients abducted by space aliens, Johnson has given us a fast-paced, highly readable political expose, with a wealth of raw material for further constructive and penetrating critiques.

________________________________________

Maryann Spurgin formerly taught philosophy.

________________________________________

CFS case criteria

The CFS case definition currently in use has been defined by the CDC Fukuda et al., 1994.  This definition was presented as a means intended for research. A first set of criteria, [Holmes et al., Ann Intern Med 1988; 108:387-9]  was hereby revised and replaced.

A study comparing the two CFS-definitions found the 1988-definition more likely to include cases arisen as infectious diseases,  Arpino et al., 1999.,  and to be more disabled and longtime sufferers,  De Becker et al., 2001, and  Jason et al., 2001.

Diagnostic criteria set by Trans-NIH working group for research on CFS, diagnostic.criteria.NIH06.txtDr. Reeves (the CDC) answers questions relating to the current CFS definition, reeves.etal06.txt.

A pediatric case definition for ME and CFS, jason.etal06.txt.

The amount of scientific literature on CFS/ME has not grown at a pace comparable to that on FM. The apparent stagnation over the past decade suggests that if this domain of research is to survive, aggressive efforts may be required to promote a more inclusive case definition, friedberg.etal07.txt,friedberg.etal.07.txtfriedberg.etal07.pdf.

Recently an epidemiological definition was proposed, osoba.etal07.txt.

 

Oxford Criteria

In 1991 psychiatrists (of British origin mainly) lauched their own CFS-criteria, the Oxford criteria [Sharpe et al., J R Soc Med, 1991 Feb; 84(2):118-21], oxford.criteria91.txt.  By this criteria CFS is defined less strict omitting the 8 minor criteria required by the CDC-definition, including patients with fatigue as their only symptom (e.g. psychiatric patients). The absurd situation imposed by this psychiatric CFS case definition is brilliantly enlightened,  Jason et al., 1997.

The problems inherent in present case definition(s),  Jason et al., 1999, and  Jason et al., 2000.

A discussion on the importance of the CDC-defined diagnosis compared to the absence of symptoms other than fatigue, letter.stouten04.txtletter.stouten04.pdf  reply,  letter.bleijenberg.etal04.txtletter.bleijenberg.etal04.pdf.

 

2003 – Canadian Case Criteria for CFS

A Canadian clinical working case definition for CFS was published in 2003,  ME/CFS, Canadian clinical definition, 2003,  Carruthers et al., 2003 Carruthers et al., 2003 (pdf).   The editorial in connection with the new guidelines,  editorial, JCFS, 2003.  A short summary of the Canadian guidelines, carruthers.etal.short03.txt  and  canadian.guidelines.summary04.txt.  The Canadian guidelines request laborious testing, a problem in clinical practice according to Dr. Shepherd, comment.canadian.guidelines04.txt.

 

The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)nightingale.definition06.txt, Definitions and aetiology of Myalgic Encephalomyelitis (ME): how the Canadian Consensus Clinical Definition of ME Works, carruthers06.txt.
Comparing the Fukuda et al. criteria and the Canadian Case Definition for CFS, jason.etal04.txt,  jason.etal04.pdf,   d Both definitions select individuals who are significantly different from psychiatric controls with chronic fatigue, and the Canadian criteria select cases with less psychiatric co-morbidity, more physical functional impairment, and more fatigue/weakness, neuropsychiatric, and neurological symptoms.

 

The NICE trial in the UK does not stick to strict CFS diagnostic criteria, cfs-definition07.txt.

Sponsored Links

 

Future CFS Definition(s)

Identification of ambiguities in the 1994 CFS research case definition and recommendations for resolution, reeves.etal03.txt,  reeves.etal03.pdf. The Swedish CFS research team’s results raise fundamental questions about the 1994 Centers for Disease Control criteria as (1) there was no empirical support for the requirement of four of eight cardinal CFS symptoms; (2) these eight symptoms were not equivalent in their capacity to predict fatigue; and (3) no combination of symptoms was markedly more heritable, sullivan.etal05.txtsullivan.etal05.pdf.

 

Three methods for improving the 1994 CDC-diagnostic criteria:  identification of new diagnostic symptoms, the use of severity ratings for symptomatology, and the identification of standardized measures that differentiate cases of CFS from other conditions, king.jason04.txtking.jason04.pdf.

Based on a great number of earlier results Jason et al. defined 4 subgroups within an empirical CFS definition, jason.etal07.txtjason.etal07.pdf.

 

Is there a test for CFS ?

An unverified spectroscopic diagnosis of CFS in serum samples has been suggested, sakudo.etal06.txtsakudo.etal.06.txtsakudo.etal06.pdf. With FM unverified findings of urine markersribel-madsen.etal07.txt.

A new era with the introduction of a test for identification of CFS by means of gene expression, kerr.etal.06.txtkerr.etal06.txtkerr.etal06.pdf, and xie.etal06.txt.

Who gets the syndrome ? No one can yet answer that question, hempel.etal07.txthempel.etal.07.txthempel.etal07.pdf.

Failure to recover from acute infection with Mononucleosis was not related to body weight, schur.etal07.txtschur.etal07.pdf.

 

CFS in International Classification of Diseases (ICD)

CFS is classified (coded) in WHO’s (1992) ICD-10 (International Classification of Diseases) as G93.3, a subcategory under diseases of the brain,  (i.e. a neurological disease). On the classification issue following a WHO note 23 Jan 2004, who.classification.us04.txt. The WHO website on this issue, who.guide.online.link04.txt.

In the US a modification of the previous WHO coding ICD-9, a so called ICD9-CM is still in use (CM  “Clinical Modifications”).  This results in difficulties in relation to CFS, as this disease is not covered by the ICD-9.  However, the US has adopted the ICD-10 (including clinical modifications) supposedly to be in use by 2004.  A short note on the classification of CFS and ME by the WHO, codes.who.explanation04.txt.

An alternative to WHO, e-medicine classification, e-medicine.cfs07.txt.

 

CFS/ ME in UK Classification

In 2004 the British WHO-associated office finally accepted the correct CFS/ ME code as G93.3, who.coding.cfs.me04.txt.  Dr. Charles Shepherd wrote to the UK National Health Service to make this institution change its information on the coding question, classification.cfs.complaint04.txt. The correct WHO classification of CFS is now a fact even in the UK as shown by their statement 24, Jan 2004, who.classification.me.cfs04.txt.  Some interesting considerations over the ME-term endings “itis” and “pathy”, who.classification.consideration04.txt.

A short summary of the ICD-10 coding of CFS, as opposed to the coding of Neurastenia written by a CFS/ME-activist,  ICD-10, clarification, and   ICD-10, Neurastenia.

Problems may arise in the future if WHO supports a “wider” fatigue definition as opposed to a “narrow” fatigue definition. This relates to the future ICD-11 coding of CFS Skapinakis et al., 2003,   Skapinakis et al., 2003 (pdf).

Framework

FOUNDING PRINCIPLES AND M.E. SOCIETY DEFINITIONAL FRAMEWORK — DISCUSSION

M.E. Is Not Fatigue

  1. Use of the word “fatigue” either to name this illness or to describe this illness is erroneous. Patients and patient groups who want to “change the name” must first take responsibility accurately to describe the symptomatology. This is a disease wherein extending beyond a certain threshold of activity leads to severely disabling symptoms and physical dysfunctionality, possibly resulting from low cardiac output (see ourCardiac Insufficiency Hypothesispage), symptoms which can be described in specific, accurate terminology without reference to broad or demeaning terminology such as “fatigue” or “poor stamina.” M.E. is a disease, and patients are sick, with often excruciating symptoms that can be clearly articulated. The defining characteristic of M.E. is that patients relapse with physical exertion and develop disease progression  and severe physical dysfunctionality with continued physical exertion. Hence, the defining characteristic is exercise intolerance, post-exertional muscle weakness, generalized weakness, faintness, and pain; and post-exertional relapsing of symptoms. In some cases symptoms remit with rest, and in other cases they do not. Recent research has shown that viruses, an upregulated RNase L pathway, and mitochondrial dysfunction lead to low cellular energy in the heart, which results in diastolic dysfunction with reduced stroke volume and low cardiac output, and that postural stress and exercise exacerbates cardiac insufficiency in this disease. So if a patient improves with exercise, that patient does not have M.E. and may have some illness other than M.E. (for example, arthritis, depression, osteoporosis, and a number of other medical conditions do improve with exercise).

In addition to the above central characteristic, Ramsay described three main components of M.E.: (1) Muscle weakness and a delayed or impaired recovery of muscle function after exercise. This has been explained by lactic acid build up as well as cardiomyopathy and microcirculatory impairment under our research-updated interpretive hypothesis. (2) Circulatory impairment. This could include both macrocirculatory problems such as low cardiac output and microcirculatory problems such as coagulopathy, abnormal erythrocyte morphology, and other factors affecting the circulatory system such as dysautonomia and low plasma and/or erythrocyte volume, resulting in exercise and orthostatic intolerance. (3) Cerebral involvement: encephalopathy, encephalitis (see our reference to Dr. Bruce Duffy’s QEEG work below), neurological, and neuropsychiatric impairment. While all three must be present for a diagnosis of M.E., some patients’ symptoms may be brain predominant, others muscle predominant, etc. The 2003 Canadian Consensus Panel Case Definition for ME/CFS requires more narrow selection criteria than the 1994 CDC “CFS” case definition to make the diagnosis, including post-exertional malaise and fatigue, sleep disturbance, and pain; neurological, neurocognitive, dysautonomic, neuroendocrine, cardiac, and immune manifestations. It might be useful for researchers to stop using the CDC’s 1994 selection criteria for doing studies and to use the newer, 2003 ME/CFS selection criteria, as well as to subset M.E./CFS according to presentation of illness, degree of illness, and research findings to achieve more consistency in the research data.

While the word “fatigue” was occasionally used both by Ramsay and in the Canadian definition,  “fatigue” is too broad and inaccurate a term. There are more specific ways of describing the symptoms, such as dramatic loss of muscle power after exercise, delayed recovery of muscle function, orthostatic faintness, cardiac output problems, and other more specific terminology than “fatigue.” In 1921, Muscio suggested that “fatigue” should be banned from strict scientific discussion. The defining characteristics of M.E./CFS can be easily outlined without reference to “fatigue.”  What all patients must have, at least according to both of these definitional frameworks, is an abnormal muscle metabolism — a delayed or impaired recovery of muscle function after exercise, which patients experience as paralytic muscle weakness and pain, not “fatigue.” Tissue hypoxia-ischemia with its resulting elevated lactic acid can lead to muscle weakness and pain, and tissue hypoxia-ischemia destroys the respiratory chain and affects the mitochondria, which cannot function without adequate oxygen. According to recent research, mitochondrial dysfunction leads to diastolic dysfunction and low cardiac output – a heart that cannot meet the demands of physical exertion.  Dr. Paul Cheney has shown that mitochondrial dysfunction results in poor filling properties in the heart (because it takes more energy for the heart to relax and fill with blood than it does for it to squeeze and pump blood), resulting in reduced cardiac output and hence severe functional impairment in ME/CFS. Cardiac muscle pathologic changes have been documented in the research by Dr. A. Martin Lerner, and recent research by Dr. Cheney has also documented cardiac muscle pathologies.  A disease this severe should be given a more serious name than “fatigue.”

Symptoms

The symptoms of the disease are exacerbated by physical exertion, mental exertion, mental stress, or orthostatic stress. In severe cases, even slight orthostatic stress triggers relapses. Symptoms may range from mild, to severe, to life-threatening (such as tachyarrythmias or siezures). The level of activity that precipitates these symptoms may vary greatly in afflicted individuals, and the symptoms that relapse may vary. They may include: sore throat, flu, fever, chills, body aches, sweats, low body temperature, lymphadenopathy, muscle weakness, muscle pain, hypoglycemia, weight change, nausea, vomiting, vertigo, chest aches, chest pain, cardiac arrhythmia, resting tachycardia (this has been explained as compensating for low stroke volume to help increase cardiac output), orthostatic tachycardia, orthostatic fainting or faintness, opthalmoplegia, eye pain, stroke-like episodes, difficulty swallowing, paresthesias, peripheral neuropathic pain, polyneuropathy, extreme pallor, sleep disorder, myoclonus, hyperreflexia, temporal lobe and other types of seizures, cognitive, memory and concentration impairment, attention deficit, anxiety, confusion, disorientation, light/sound sensitivity, blurred vision, wavy visual field, and other visual and neurological disturbances. Allergic hypersensitivity is also common in the disease. The above information is taken from four sources: (1) Ramsay’s observations, (2) the Canadian Clinical Case Definition, (3) patient reports, and (4) reports from other publications.

Turning to those publications:

Case Definitions

  1. Most of the current research articles, especially in America, on findings that fit our above-described M.E. framework were published on under the name “chronic fatigue syndrome” (“CFS”). Unfortunately, because of the broadness of the CDC’s 1994 case definition for  “CFS,” known as the “Fukuda criteria,” “CFS” became something of an umbrella term for a number of diverse diseases. Selection bias became a problem, and everything from depression to viral cardiomyopathy was published on under the name “CFS.” Using the ME/CFS case definitions instead of the U.S. government case definition and conducting research on precise subsets could help remedy this problem. (See our Research-Based Subsets page.)

Currently, two incompatible categories of “CFS” exist: (1) The CFS of the 1994 U.S. government case definition, the Fukuda criteria, which fails to select patients using any past or current research. It does not select for muscle weakness, cardiocirculatory, orthostatic, or neuroendocrine immune disease; it does not describe any published lab work; and it focuses on “fatigued persons,” making post-exertional sickness or malaise optional. These criteria were a government invention and are too broad to define any disease. Dorland’s Medical Dictionary states that to “diagnose” is to engage in “the art of distinguishing one disease from another.” The too-broad Fukuda criteria lump heterogeneous conditions and hence fail in defining a disease. It is widely recognized that the CDC case definition selects a heterogeneous patient population, as does the concept of “fatigue,” which was forced on patients and researchers by Holmes et al. (1988 US government case definition) who were new to the field. (2) The other version of “CFS” is the “CFS” of volumes of articles on cardiac disease, circulatory disease, dysautonomia and endocrine disorders, abnormal muscle metabolism, mitochondrial disease, immune disease, viral and bacterial disease, orthostatic problems, cardiac output problems, etc. Yet none of these telling research findings are listed or required for diagnosis in the CDC’s case definition. We will leave it to the reader to judge whether this is government bureaucratic incompetence or a deliberate attempt to cover up important research. But the newer research-updated Canadian Clinical Case Definition more accurately describes the disease, and should be used for diagnosis and modified and adopted by the government for research.

M.E. and CFS are not two different diseases (even if they are two different case definitions). Disease entities are facts and phenomena, while names and case definitions are mere human constructs. Some constructs are more accurate than others. Some select a different population than others. The name “CFS” and the 1994 CDC Fukuda case definition were constructs that were simply inaccurate — they were too broad, selected a heterogeneous population, and failed to be based on important research findings. The solution to these confusions is to stop using the CDC’s case definition. Recent research findings on cardiac output problems in ME/CFS make the U.S. government’s case definition even more obsolete. Canada, New Zealand, and Australia have begun to use the ME/CFS definition, and in the U.S. a pediatric case definition is in the works for ME/CFS.

As regards naming, there is little research on “myelitis” (although we do not discourage such research). There has been some research on “encephalitis” because systemic herpes infections also infect the brain (in addition to infecting the heart, as Lerner has described). QEEG tests done by Harvard neurologist Frank Duffy, M.D., showed a very high amplitude alpha rhythm and epilepsy-like discharges in the temporal lobes of patients with the disease.  The temporal lobes have a predilection for infection by herpesviruses in herpes encephalopathy and encephalitis. <color=”#31659c”>(For newer research on brain and neurological impairment in ME/CFS, see our Research-Based Subsets page.)

Scientific progress cannot be made when researchers focus on a poorly defined symptom like “fatigue.” The term “chronic fatigue syndrome” focuses on a poorly defined symptom that does not accurately characterize the symptomatology experienced by patients, promotes misunderstanding, and contributes to the disparaging manner in which patients are treated by physicians. The name has negatively impacted the quality of medical care patients are able to obtain. Many researchers, patient groups, and authors of government documents in the UK, Australia, New Zealand, Canada, and the U.S. have chosen to use the name ME/CFS as an interim compromise and to link this encephalopathy/cardiomyopathy disease worldwide until a more suitable name that eliminates the terms “chronic” and “fatigue” can be found.

M.E. Is Not “Medically Unexplained”

3. Unlike somatization disorder, M.E./CFS is not “medically unexplained.” M.E./CFS is a disease which, like lupus, has no single marker. While M.E./CFS is a multi-system disease with many organ and bodily systems affected, producing a myriad of symptoms, and while no single etiology has been found for M.E./CFS, many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research articles. Circulatory impairment, which the CDC case definition fails to mention, has been explained in terms of coagulopathy (Berg) and/or abnormal erythrocyte morphology (Simpson), low plasma and/or erythrocyte volume (Streeten), and low cardiac output (Cheney). Brain/neurological impairment has been documented by numerous researchers.  There are well-documented, scientifically sound explanations for why patients are often bedridden and unable to maintain an upright posture.  We ask the reader to visit our Cardiac Insufficiency Hypothesis page, our home page, our References page, and our Research-Based Subsets page to study these scientifically sound medical explanations.

The most compelling research to date that explains the severe physical dysfunctionality in ME/CFS is the research on low cardiac output available on our cardiac page. Writer Laura Hillenbrand, in her 2003 article in the New Yorker,  stated: “I was sure that being moved would kill me.” In 2005 and 2006, research finally showed that in ME/CFS, cardiac output is sometimes too low to meet the demands of movement, and any attempt to exert oneself beyond one’s own capacity for cardiac output – that is when demand exceeds cardiac capacity – would indeed result in death. Studies on dogs have shown that when the demands of the body exceed cardiac output by even 1%, the organism dies. ME/CFS patients reduce demand and reduce their exertion level to stay within the bounds of their low cardiac output to stay alive.

Etiology

  1. M.E./CFS appears to be a “different insult/same result” disease, and no single viral, bacterial, or environmental etiology is likely to be found, although we are open to any discovery to the contrary. However, as Ramsay states, “the particular invading microbial agent is probably not the most important factor . . . the key to the problem is likely to be found in the abnormal . . . response of the patient to the organism.” Identifying and treating infections early in the disease is important to halt any aberrant immune responses. While the insults may be different, there may be a common pathophysiology.

Inappropriate Treatments

  1. Cognitive Behavioral Therapy (CBT), Graded Exercise Therapy (GET), and antidepressants are not effective treatments for M.E. In fact, these therapies generally make M.E. worse. For an excellent criticism of the CBT/GET studies from the Canadian Clinical Case Definition, see cfids-cab.org/ccpc-1.html.For Dr. Cheney’s theory on why SSRI antidepressants make ME/CFS patients worse in some cases, order his 2006 lecture, “The Heart of the Matter.”. (See cardiac page.)

Progressive Cases

  1. M.E. can be progressive (going from bad to worse, increasing in scope or severity), degenerative (change of tissue to a lower or less functioning form, as in heart failure), chronic, relapsing and remitting, acute (having a short or a severe course), or lead to terminal complications ending in death.  Many cases of M.E. are progressive and degenerative (around 30% of cases), and some have led to complications that were terminal (seehttp://www.ncf-net.org/memorial.htmat the National CFIDS Foundation Web site). Drs. Arnold Peckerman and A. Martin Lerner argue that the disease is progressive. Leonard Jason, Ph.D., recently published a morbidity and mortality study showing premature deaths from heart failure and cancer. Deaths in England due to heart failure and some due to severe dehydration have been documented. In M.E., as in lupus, patients do not die specifically of the disease, but of complications, often prematurely in their 30’s and 40’s. Some groups, researchers, and films claim that most deaths are from suicide. The IN MEMORIUM list we refer to does not confirm that piece of propaganda.

In her recent paper (Jan 01), “THE LATE EFFECTS OF ME,” the well-known English ME specialist Dr. Betty Dowsett wrote: “…..FINAL STAGE (1,2) After a variable interval, a multi-system syndrome may develop, involving permanent damage to skeletal or cardiac muscle and to other “end organs” such as the liver, pancreas, endocrine glands and lymphoid tissues, signifying the further development of a lengthy chronic, mainly neurological condition with evidence of metabolic dysfunction in the brain stem. Yet, stabilization, albeit at a low level, can still be achieved by appropriate management and support. The death rate of 10% occurs almost entirely from end-organ damage within this group (mainly from cardiac or pancreatic failure). It has to be said that suicide in younger patients and in earlier stages of the disability is related to the current climate of disbelief, rejection of welfare support and loss of educational and employment prospects.”
[Back to Top]

References  (For additional references, see our Research-Based Subsets page and our Cardiac Insuffiency Hypothesis page.)

Cardiac-1

Abnormal impedance cardiography predicts symptom severity in chronic fatigue syndrome

Journal: Am J Med Sci. 2003 Aug;326(2):55-60.

Authors: Peckerman A, LaManca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH.

Affiliation: Department of Neurosciences, CFS Cooperative Research Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA. Contact e-mail: apeckerm@njneuromed.org

NLM Citation: PMID: 12920435

BACKGROUND: Findings indicative of a problem with circulation have been reported in patients with chronic fatigue syndrome (CFS). We examined this possibility by measuring the patient’s cardiac output and assessing its relation to presenting symptoms.

METHODS: Impedance cardiography and symptom data were collected from 38 patients with CFS grouped into cases with severe (n = 18) and less severe (n = 20) illness and compared with those from 27 matched, sedentary control subjects.

RESULTS: The patients with severe CFS had significantly lower stroke volume and cardiac output than the controls and less ill patients. Postexertional fatigue and flu-like symptoms of infection differentiated the patients with severe CFS from those with less severe CFS (88.5% concordance) and were predictive (R2 = 0.46, P < 0.0002) of lower cardiac output. In contrast, neuropsychiatric symptoms showed no specific association with cardiac output.

CONCLUSIONS: These results provide a preliminary indication of reduced circulation in patients with severe CFS. Further research is needed to confirm this finding and to define its clinical implications and pathogenetic mechanisms.

Complete text in PDF Format ]

Index

“This illness is to fatigue what a nuclear bomb is to a match. It’s an absurd mischaracterization.” – Laura Hillenbrand, Bestselling author of Seabiscuit

“The term[s] ‘fatigue’ and ‘chronic fatigue’ never existed in this entity until it was put into [the name] in 1988…The whole concept of fatigue has warped our understanding of this illness.” – Byron Hyde, M.D., The Nightingale Research Foundation, Ottawa, Canada

The M.E. Society of America is an organization that seeks to promote understanding of the disease known as myalgic encephalomyelitis (ME/CFS), a multi-system disease adversely affecting the cellular mitochondria and the heart, brain, neuroendocrine, immune, and circulatory systems. M.E. was first described in the 1950’s following the recognition of many cases around the world, including a number of cases at the Royal Free Hospital in England. Many different viruses, bacteria, or toxins in combination with genetic factors may be involved in the etiology of the disease, which usually begins in childhood or early adulthood with an acute infection. Studying research-based subsets is the key to scientific progress in this area of investigation.  In a number of publications, Dr. A. Melvin Ramsay outlined a definitional framework for M.E. that described abnormal muscle metabolism, circulatory impairment, and cerebral involvement. 

Unfortunately, in 1988, what was historically known both as myalgic encephalomyelitis and as the well-documented epidemic neuromyasthenia was renamed “Chronic Fatigue Syndrome” by employees at the Centers for Disease Control (CDC), who imposed the misleading “fatigue” term onto patients and researchers.  In 1994, more damage was done when the CDC broadened the definition for CFS to include many diverse, unrelated diseases, for which “CFS” became an umbrella term.  Broadening the case definition led to conflicting research data. But there is a more current, research-based case definition available on this Web site compiled by the Canadian Consensus Panel for ME/CFS, which includes neuroendocrine, immune, and cardiocirculatory symptoms as well as abnormal muscle metabolism, circulatory impairment, and cerebral/neurological involvement, and also lists neurally mediated hypotension, postural orthostatic tachycardia syndrome, and cardiac arrhythmia. In one study, this Canadian Clinical Case Definition selected patients who had more physical functional impairment, neurological, and cardiocirculatory symptoms and had variables that significantly differentiated them from a psychiatric comparison group. The ICD-10 code for ME/CFS is G93.3.

Mounting research indicates that orthostatic intolerance, in some cases involving a virally induced dysfunction of the autonomic nervous system, low plasma and/or erythrocyte volume, left-ventricular failure upon postural stress, and diastolic cardiomyopathy is a prominent feature of ME/CFS. For something so severe, the term “fatigue” is vague and inadequate. A more accurate use of language would be to use  “muscle weakness and pain” or “delayed muscle recovery after exercise,” orthostatic faintness, and cardiac output problems to characterize the symptomatology. To access new research on these topics and to view a streaming video of a lecture on CFS and diastolic cardiomyopathy, see our Cardiac Insufficiency Hypothesis page.

There is strong evidence that mitochondrial dysfunction plays a role in the pathophysiology of ME/CFS and of other neurological diseases. Research has shown respiratory chain deficits and damage to the mitochondrial DNA, and, when the degree of illness is severe, acquired myopathic changes in some subsets.

Some have argued that muscle and neuroendocrine dysfunction may follow from inadequate oxygen delivery to tissues, either from coagulopathy, blood viscosity, and deposits of fibrin; or blood with high values of red cells with altered margins – or both. Poor organ perfusion due to low cardiac output has also been described. When the capacity of cells to take up and release oxygen is impaired, the body shifts to anaerobic metabolism, wherein incomplete metabolism of glycogen leads to the formation of lactic acid, which further impairs oxygen delivery.  Brain, nerves, heart, skeletal muscles, and endocrine glands have higher requirements for oxygen and nutrient substrates, require more energy, and react to deficiencies with more serious consequences.

The mitochondria and respiratory chain are adversely affected by tissue hypoxia-ischemia; they are also adversely affected by elevated nitric oxide, another common finding in the disease. Some infectious agents also adversely affect the mitochondria.  Mitochondrial metabolism is the principle source of energy intermediates as well as of free radicals. Acquired mitochondrial defects could be responsible for the neuronal degeneration. Mitochondrial respiratory chain dysfunction has been reported in association with primary mitochondrial DNA abnormalities. But defects in oxidative phosphorylation and increased free radical production have also been observed in diseases that are not due to inherited mitochondrial abnormalities. In these cases, the mitochondrial failure is likely to be an epiphenomenon. As in other conditions in which the respiratory chain is compromised, ME/CFS is a multi-system disease affecting many organ systems of the body. Accumulated damage to the mitochondrial DNA over many years could lead to similar problems as in inherited mitochondrial diseases.

New research is emerging that viruses, an upregulated R-Nase-L pathway, and mitochondrial dysfunction lead to low energy in the heart. Since it takes more ATP energy for the heart to relax and fill than it does for the heart to pump, low energy leads to diastolic dysfunction and hence reduced cardiac output, leading to circulatory impairment, and poor organ perfusion to maintain life-preserving blood pressure. (Again, see our Cardiac Insufficiency Hypothesis page.) Both macrocirculatory and microcirculatory factors have been shown to impair organ perfusion in ME/CFS. The end result of the above-described cascade may be a crisis in the cells of the skeletal muscles, heart, brain, kidney, endocrine, and other systems.

In her recent paper (Jan 01), “The Late Effects of  ME,” the well-known English M.E. specialist Dr. Betty Dowsett wrote: “…..FINAL STAGE (1,2) After a variable interval, a multi-system syndrome may develop, involving permanent damage to skeletal or cardiac muscle and to other “end organs” such as the liver, pancreas, endocrine glands and lymphoid tissues, signifying the further development of a lengthy chronic, mainly neurological condition with evidence of metabolic dysfunction in the brain stem. Yet, stabilization, albeit at a low level, can still be achieved by appropriate management and support. The death rate of 10% occurs almost entirely from end-organ damage within this group (mainly from cardiac or pancreatic failure).”

The M.E. Society of America disseminates cutting-edge research on the disease regardless of the name under which it was published.  We do not play the role of a support group. We are a research-information and advocacy group only.  (Information on obtaining updates from the M.E. Society is available here.)

Lerner

Cardiac Insufficiency Hypothesis

There is new research from a New Jersey team, authored by Doctors Arnold Peckerman, Benjamin Natelson et al., which found left-ventricular dysfunction following exertion and orthostatic stress in patients with myalgic encephalomyelitis/chronic fatigue syndrome. The WedMD article and the press release are available at the link below. In an NIH-funded study on impedance cardiography also linked below, Peckerman and Natelson found that low cardiac output correlated with symptom severity in ME/CFS.

Dr. A. Martin Lerner holds U.S. patents for the diagnosis of  ME/CFS in the chronic mononucleosis subset of this disease using 24-hour Holter monitoring.  He argues that a prominent subset of the disease is a prolonged, chronic mononucleosis following infection with Epstein Barr virus (EBV), Human  Cytomegalovirus (HCMV), or both, and/or possibly Human Herpes Virus 6 (HHV-6).   Viral infection persists in the heart, causing left-ventricular dysfunction, producing exercise intolerance.  Exercise, in turn, worsens the cardiac dysfunction.  He has also postulated that the disease is an early dilated cardiomyopathy that in later stages might result in progressive, end-stage dilated cardiomyopathy, a type of heart failure.  Dilated cardiomyopathy is sometimes viewed as “idiopathic,” or “Idiopathic Dilated Cardiomyopathy” (IDC).  In an editorial response titled “Microbial Persistence and Idiopathic Dilated Cardiomyopathy,” Dr. Lerner has postulated that these viruses may be the etiological link. 

More recently, physicist, physician, long-time ME/CFS researcher and clinician, and heart-transplant recipient Paul Cheney, M.D., Ph.D., has offered an alternative theory that a subset of ME/CFS patients suffer from a diastolic cardiomyopathy, a problem with ventricular filling resulting from mitochondrial dysfunction and low ATP energy in the heart.

To view a streaming video of a three-hour talk by Dr. Cheney on diastolic cardiomyopathy and ME/CFS, click here. This video can be accessed with a broadband connection only. The video cannot be properly viewed using a dial-up modem. Because there may be many people trying to access the video at once, our server may become temporarily overloaded. Please try back again if you encounter this problem or if the video does not play for the full three hours. Note that some of the most informative parts of this three-hour talk occur in the second half when Dr. Cheney discusses and shows charts on cardiac output in litres per minute, comparing ME/CFS patients with controls. To purchase a videocassette of this seminar by Dr. Cheney from the Dallas-Fort Worth CFS group, click here. A detailed discussion of Dr. Cheney’s views is available below in an interview by Carol Sieverling, and is recommended reading along with the Peckerman/Natelson article on impedance cardiography for those who want to study the insightful issues addressed in the video. To purchase a DVD set of another talk by Dr. Cheney illustrating more recent echocardiographic and other objective data on ME/CFS and heart failure, click here.

Some of Dr. Lerner’s significant articles, as well as his patent issued in 2002, are linked below in Portable Document File (PDF) format. These files require an Adobe Acrobat Reader. Most computers come with this program preloaded.  If not, a free Acrobat Reader can be downloaded here.

 

ccpc

The Canadian Expert Consensus Panel has published a medical milestone, the first clinical case definition for the disease known as myalgic encephalomyelitis/chronic fatigue syndrome. This definition is clearly a vast improvement over the CDC’s 1994 case definition for CFS, which led to misunderstanding in both research and treatment modalities by making “fatigue” a compulsory symptom but by downplaying or making optional the disease’s hallmark of post-exertional sickness and other cardinal ME/CFS symptoms. In sharp contrast to the CDC’s 1994 definition, this new clinical case definition makes it compulsory that in order to be diagnosed with ME/CFS, a patient must become symptomatically ill after exercise and must also have neurological, neurocognitive, neuroendocrine, dysautonomic, circulatory, and immune manifestations. In short, symptoms other than fatigue must be present for a patient to meet the criteria. The complete 109-page article “Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols,” was published in the Journal of Chronic Fatigue Syndrome, Vol. 11 (1) 2003, pp. 7-116.
The Canadian Clinical Case Definition is summarized as follows:

1. POST-EXERTIONAL MALAISE AND FATIGUE: There is a loss of physical and mental stamina, rapid muscular and cognitive fatigability, post-exertional fatigue, malaise and/or pain, and a tendency for other symptoms to worsen. A pathologically slow recovery period (it takes more than 24 hours to recover). Symptoms exacerbated by stress of any kind. Patient must have a marked degree of new onset, unexplained, persistent, or recurrent physical and mental fatigue that substantially reduces activity level. [Editor’s note: The M.E. Society prefers to use delayed recovery of muscle function, weakness, and faintness rather than fatigue. Further, we disagree that the muscle dysfunction and post-exertional sickness is unexplained. See our Cardiac Insufficiency Hypothesis page and our Research-Based Subsets page for researchers medical explanations on this website.]

2. SLEEP DISORDER: Unrefreshing sleep or poor sleep quality; rhythm disturbance.

3. PAIN: Arthralgia and/or myalgia without clinical evidence of inflammatory responses of joint swelling or redness. Pain can be experienced in the muscles, joints, or neck and is sometimes migratory in nature. Often, there are significant headaches of new type, pattern, or severity. [Editor’s note: neuropathic pain is a common symptom and should be added here as well.]

4. NEUROLOGICAL/COGNITIVE MANIFESTATIONS: Two or more of the following difficulties should be present: confusion, impairment of concentration and short-term memory consolidation, difficulty with information processing, categorizing, and word retrieval, intermittent dyslexia, perceptual/sensory disturbances, disorientation, and ataxia. There may be overload phenomena: informational, cognitive, and sensory overload — e.g., photophobia and hypersensitivity to noise — and/or emotional overload which may lead to relapses and/or anxiety.

5. AT LEAST ONE SYMPTOM OUT OF TWO OF THE FOLLOWING CATEGORIES:

AUTONOMIC MANIFESTATIONS: Orthostatic Intolerance: e.g., neurally mediated hypotension (NMH), postural orthostatic tachycardia syndrome (POTS), delayed postural hypotension, vertigo, light-headedness, extreme pallor, intestinal or bladder disturbances with or without irritable bowel syndrome (IBS) or bladder dysfunction, palpitations with or without cardiac arrhythmia, vasomotor instability, and respiratory irregularities. [Editor’s note: low plasma and/or erythrocyte volume should be added as another explanation for orthostatic intolerance in this disease. More cardiac symptoms should be listed such as left-side chest aches and resting tachycardias, which, in addition to low blood volume, have also been documented in the research. The full text of the case definition does suggest 24-hour Holter monitoring, and when tachycardias with T-wave inversions or flattenings are present that they not be labeled as nonspecific since they aid in the diagnosis of ME/CFS. The frequent tachycardias seen in ME/CFS have been shown by Dr. Paul Cheney to be a compensatory mechanism that serves to increase cardiac output in the presence of low stroke volume due to diastolic dysfunction in the heart. Orthostatic problems may also be related to diastolic dysfunction as recently shown by Dr. Paul Cheney. See our Cardiac Insufficiency Hypothesis page.]

NEUROENDOCRINE MANIFESTATIONS: loss of thermostatic stability, heat/cold intolerance, anorexia or abnormal appetite, marked weight change, hypoglycemia, loss of adaptability and tolerance for stress, worsening of symptoms with stress and slow recovery, and emotional lability.

IMMUNE MANIFESTATIONS: tender lymph nodes, sore throat, flu-like symptoms, general malaise, development of new allergies or changes in status of old ones, and hypersensitivity to medications and/or chemicals.
6. The illness persists for at least 6 months. It usually has an acute onset, but onset also may be gradual. Preliminary diagnosis may be possible earlier. The disturbances generally form symptom clusters that are often unique to a particular patient. The manifestations may fluctuate and change over time. Symptoms exacerbate with exertion or stress.

This summary is paraphrased from Dr. Kenny van DeMeirleir’s book Chronic Fatigue Syndrome: A Biological Approach, February 2002, CRC Press, pg. 275. A few edits and suggestions were added by the M.E. Society of America. As we have noted, the M.E. Society of America holds that this is the best case definition so far, although it is not perfect. Listing more cardiac and neurological symptoms (e.g., chest pain, left-side chest aches, tachycardia, and neuropathy pain), and emphasizing muscle weakness and faintness instead of fatigue, would have more accurately represented the symptomatology and vastly improved the criteria. Nevertheless, the Canadian Consensus Panel clinical case definition more accurately represents the experience and manifestations of the disease than other current case definitions. Again, for the 30-page diagnostic ME/CFS case definition click here.

Myalgic Encephalomyelitis / Chronic Fatigue Syndrome Panel

1. Dr. Bruce M. Carruthers, lead author of the consensus document; co-author of the draft of the original version of the ME/CFS clinical definition, diagnostic and treatment protocols document; internal medicine.

2. Dr. Anil Kumar Jain co-author of the draft the original version of the ME/CFS consensus document, affiliate of Ottawa Hospital, Ontario.

3. Dr. Kenny L. De Meirleir, Professor Physiology and Medicine, Vrije Universiteit Brussel, Brussels, Belgium; ME/CFS researcher and clinician; organizer of the World Congress on Chronic Fatigue Syndrome and Related Disorders; a board member of the American Association for Chronic Fatigue Syndrome; and co-editor of Chronic Fatigue Syndrome: Critical Reviews and Clinical Advances (Haworth)

4. Dr. Daniel L. Peterson, affiliate of the Sierra Internal Medicine Associates in Incline Village, Nevada; ME/CFS researcher and clinician; a board member of the American Association for Chronic Fatigue Syndrome; and member of the International Chronic Fatigue Syndrome Study Group

5. Dr. Nancy G. Klimas, Clinical Professor of Medicine in Microbiology/Immunology/Allergy and Psychology, University of Miami School of Medicine; ME/CFS researcher and clinician; a board member of the American Association for Chronic Fatigue Syndrome; and member of the federal CFS Coordinating Committee

6. Dr. A. Martin Lerner, staff physician at William Beaumont Hospital in Royal Oak, Michigan; Clinical professor and former chief of the Division of Infectious Diseases at Wayne State University’s School of Medicine; and ME/CFS researcher and clinician

7. Dr. Alison C. Bested, haematological pathologist; former head of the Division of Haematology and Immunology at the Toronto East General and Orthopaedic Hospital; affiliate of the Environmental Health Clinic and Sunnybrrok & Women’s College Health Sciences Centre, Toronto, Ontario; ME/CFS researcher and clinician

8. Dr. Pierre Flor-Henry, Clinical Professor of Psychiatry, University of Alberta; Clinical Director of General Psychiatry and Director of the Clinical Diagnostic and Research Centre, both based at Alberta Hospital in Edmonton, Alberta, Canada; ME/CFS brain researcher

9. Dr. Pradip Joshi, internal medicine, Clinical Associate Professor of Medicine at Memorial University of Newfoundland in St. John’s, Canada

10. Dr. A. C. Peter Powles, Professor Emeritus, Faculty of Health Science, McMasters University, Hamilton; Professor, Faculty of Medicine, University of Toronto; Chief of Medicine and Sleep Disorders Consultant, St. Joseph’s Health Centre, Toronto; Sleep Disorder Consultant at the Sleep Disorder Clinic at St. Joseph’s Healthcare, Hamilton, and Central West Sleep Affiliation, Paris, Ontario

11. Dr. Jeffrey A. Sherkey, family medicine, affiliate of the University Health Network, Toronto, Ontario; and diagnosed with chronic fatigue syndrome nearly 10 years ago

12. Marjorie I. van de Sande, Consensus Coordinator; and Director of Education for the National ME/FM Action Network, Canada

This definition was hosted and coordinated by the National ME/FM Action Network of Canada, led by Lydia Nielson. The M.E. Society would like to thank the Canadian group for the many years of work that went into this important project.

Hillenbrand

We were in Linc’s car, an aging yellow Mercedes sedan, big and steady, with slippery blond seats and a deep, strumming idle. Lincoln called it Dr. Diesel. It was a Sunday night, March 22, 1987, nine-thirty. Rural Ohio was a smooth continuity of silence and darkness, except for a faintly golden seam where land met sky ahead, promising light and people and sound just beyond the tree line.

We were on our way back to Kenyon College after spring break. Linc, my best friend, was driving, his arm easy over the wheel. My boyfriend, Borden, sat behind him. I rode shotgun, a rose from Borden on my lap. Slung over my arm was a 1940s taffeta ball gown I had bought for $20 at a thrift shop. I was 19.

The conversation had dropped off. I was making plans for the dress and for my coming junior year abroad at the University of Edinburgh. My eyes strayed along the right shoulder of the road: a white mailbox, the timid glint of an abandoned pick-up’s tail-light. The pavement racing under the car was gunmetal gray. We were doing 50 mph or so. A balled-up bag from a drive-through burger joint bumped against my ankle.

A deer.

At first, he was only a suggestion of an animal, emerging from the darkness by degrees: a muzzle, a sharp left eye. Then the headlights grasped him.

He was massive — a web of antlers over his head, a heavy barrel, round haunches lifting him from the downward slope of the highway apron. Briefly, his forehooves rested on the line between the shoulder and the highway. I saw his knee bending, the hoof lifting: he was stepping into the car’s path.

In the instant that I spent waiting for the deer to roll up over the car’s hood and crash through the windshield I was aware of my body warm in the seat, Linc’s face lit by the dash, Borden breathing in the back, the cool sulfur glow of the car’s interior, the salty smell of the burger bag. I watched the deer’s knee and waited for it to straighten. I drew a sharp breath.

The bumper missed the deer’s chest by an inch, maybe two. The animal’s muzzle passed so close that I could see the swirl of hair around his nostrils. Then he was gone behind us.

I blinked at the road. My eyes caught something else. A brilliant light appeared through the top of the windshield and arced straight ahead of the car at terrific speed. It was a meteor. It burned through the rising light of the horizon and vanished in the black place above the road and below the sky.

My breath escaped in a rush. I turned toward Linc to share my amazement. He was as loose as he had been, his eyes slowly panning the road, his long body unfolding over the seat. I looked back at Borden and could just make out his face. They had seen nothing.

I was about to speak when an intense wave of nausea surged through me. The smell from the bag on the floor was suddenly sickening. I wrapped my arms over my stomach and slid down in my seat. By the time we reached campus, half an hour later, I was doubled over, burning hot, and racked with chills. Borden called the campus paramedics. They hovered in the doorway, pronounced it food poisoning, and left.

I fell asleep sitting up on my bed, leaning against Borden’s shoulder. In the morning, my stomach seethed. I walked to the dining hall and sat with Linc, unable to eat. In my history seminar, I drank from a water bottle and tried to concentrate. After class, I walked to my apartment and heated some oatmeal. I swallowed a spoonful; nausea rose in my throat and I pushed the bowl away.

In the next few days, everything I ate made my abdomen balloon. I radiated heat, and my joints and muscles felt bruised. Every day on the way to classes, I struggled a little harder to make it up the hill behind my apartment. Eventually, I began stopping halfway to rest against the trunk of a tree.

One morning, I woke to find my limbs leaden. I tried to sit up but couldn’t. I lay in bed, listening to my apartment-mates move through their morning routines. It was two hours before I could stand. On the walk to the bathroom, I had to drag my shoulder along the wall to stay upright. Linc drove me to the campus physician, who ran test after test but couldn’t find the cause of my illness. After three weeks of being stranded in my room, I had no choice but to drop out of college. I called my sister and asked if she could drive me home to Maryland.

I sat in the doorway of the apartment while Borden and Linc packed my sister’s car. As they pushed the last of my belongings into the back seat, a downpour broke over them. We pulled out, and Kenyon was lost in a falling grayness. I turned to wave to Borden and Linc, but I couldn’t see them anymore.

My mother’s house was a dignified Colonial that sat back from the road, behind a pine tree that had been mostly denuded by Hurricane Agnes and an anemic cherry tree that would soon collapse onto the den. In the back yard stood a hemlock that had been missing its upper third since my brother and I accidentally set it on fire. Inside, the house was a warren of small rooms that had suited our two-parent, four-kid, two-Collie family when my parents bought it, in 1971. My father had walked out in 1977, the elder collie had died three days later, and the house had gradually emptied until my departure for Kenyon, which had left only my mother and my cat, Fangfoss.

The sun was setting as we pulled up to the back door. I walked upstairs and lay down in my childhood bedroom, which overlooked the back yard and the charred tree. The next morning, I stepped on a scale. I had lost 20 pounds. The lymph nodes on my neck and under my arms and collarbones were painfully swollen. During the day, I rattled with chills, but at night I soaked my clothes in sweat. I felt unsteady, as if the ground were swaying. My throat was inflamed and raw. A walk to the mailbox on the corner left me so tired that I had to lie down.

Sometimes I’d look at words or pictures but see only meaningless shapes. I’d stare at clocks and not understand what the positions of the hands meant. Words from different parts of a page appeared to be grouped together in bizarre sentences: ‘Endangered Condors Charged in Shotgun Killing.’ In conversation, I’d think of one word but say something completely unrelated: ‘hotel’ became ‘plankton’; ‘cup’ came out ‘elastic.’ I couldn’t hang on to a thought long enough to carry it through a sentence. When I tried to cross the street, the motion of the cars became so disorienting that I couldn’t move. I was at a sensory distance from the world, as if I were wrapped in clear plastic.

I had never been in poor health and didn’t have an internist, so I went to my old pediatrician. I sat in a child’s chair in a waiting room wallpapered with jungle scenes, watching a boy dismember an action figure. When my doctor drew the thermometer from my mouth, he asked me if I knew that my temperature was 101. He swabbed my throat, left for a few minutes, and returned with the news that I had strep throat. Puzzled by the other symptoms, he prescribed antibiotics and suggested that I see an internist.

The doctor I found waved me into a chair and began asking questions and making notes, pausing to rake his fingers through a hedge of dark hair that drifted onto his brow. He ran some tests and found nothing amiss. He told me to take antacids. A few weeks later, when I returned and told him that I was getting worse, he sat me down. My problem, he said gravely, was not in my body but in my mind; the test results proved it. He told me to see a psychiatrist.

I went to Dr. Charles Troshinsky, a respected psychiatrist whom I had seen when I was fifteen, after my high school boyfriend had died suddenly. He was shocked at how thin I was. I was just under five feet five, but my weight had dropped to a hundred pounds. Dr. Troshinsky said that he had seen several people with the same constellation of symptoms, all referred by physicians who dismissed them as mentally ill. He wrote my internist a letter stating that he would stake his reputation on his conclusion that I was mentally healthy but suffering from a serious physical illness.

‘Find another psychiatrist,’ my internist said over the phone, a smile in his voice. How did he explain the fevers, chills, exhaustion, swollen lymph nodes, dizziness? What I was going through, he suggested, was puberty. I had just turned 20. ‘Laura, everyone goes through this,’ he said with the drizzly slowness one uses with a toddler. ‘It’s a normal adjustment to adulthood. You’ll grow out of it in a few years.’ He told me to come back in six months.

‘But I’m not happy with my treatment,’ I said.

He laughed. ‘Well, I am.’

I called his secretary and asked for my medical records. I sat on my bedroom floor and flipped through the doctor’s notes. Couldn’t handle school, he had written. Dropped out.

My next doctor was a plump, pink man with the indiscriminate gaiety of a golden retriever. He was halfway through a hair transplant, and clumps of hair were lined up in neat rows on his scalp, like spring seedlings.

I again tested positive for strep, and he renewed the antibiotics. He ran a blood test for a virus called Epstein-Barr and found a soaring titer, a measurement of the antibody in my system. I had, he said with pep-rally enthusiasm, something called Epstein-Barr virus syndrome. He had it, too, he said, but he had discovered nutritional-supplement pills that cured it. ‘Whenever I feel it coming on,’ he said, ‘I just take these.’ He talked about how much skiing he could do.

I took the supplements. They had no effect. Nor did the antibiotics; the strep raged on. The doctor changed my prescription repeatedly, to no avail.

At the end of one of my appointments, the doctor followed me into the waiting room and asked my mother to make an appointment so that he could test her for strep. She said she felt fine, but he insisted that she might be infected but asymptomatic.

Our appointments fell on the same day. I went in first and sat while a nurse swabbed my throat. A few minutes later, the doctor bounded in, waving the positive-test swab, and bent over to look at my throat. I’d had strep for nearly three months. I dropped my face into my hands. He straightened abruptly and backed out of the room, repeating that the pills would cure the Epstein-Barr. ‘I go skiing a lot!’ he hollered from down the hall.

I was still crying as I paid the bill. The receptionist gave me a sympathetic smile. She understood how I felt, she said, because she had Epstein-Barr, too. ‘It’s amazing,’ she said. ‘The doctor has found that everyone working here has it.’

I sat down. Several other patients were sitting near me, and I asked if the doctor had given any of them a diagnosis of Epstein-Barr. Each one said yes. While we were talking, my mother emerged from the doctor’s office. He had told her that she, too, had Epstein-Barr.

That year, millions of cicadas boiled up from the ground, teemed over tree limbs, and carpeted lawns and roads. The TV news showed people eating them on skewers. Cicadas burrowed into the house, scaled the curtains, swung from our clothes. I sat in bed, watching them bounce off the windowpane and nosedive into the grass, where they flapped and floundered as if they were drowning. Newton, the Dalmatian puppy my mother had adopted, zigzagged around the yard and snapped them out of the air. We called them flying dog snacks.

My world narrowed down to my bed and my window. I could no longer walk the length of my street. My hair was starting to fall out. I hadn’t had a period in four months. My mouth and throat were pocked with dozens of bleeding sores and my temperature was spiking to a hundred and one every 12 hours, attended by a ferocious sweat; in addition to the strep, I now had trench mouth, a rare infection of the gums. Sleeping on my side was uncomfortable because I had little body fat left and my bones pressed into the skin on my hips, knees, and shoulders.

In sleep, I dreamed of vigorous motion. I had swum competitively for 10 years, from age 7 to 17. I had been riding horses since childhood. Smitten with thoroughbred racing, I had spent my mid-teens learning to ride short-stirrup at a gallop, and praying that I wouldn’t grow too tall to become a jockey. At Kenyon, I had been a tennis junkie. Now, as I lost the capacity to move, sports took over my dream world. I won at swimming in the Olympics, out-pedalled the peloton in the Tour de France, skimmed over a racetrack on a Kentucky Derby winner. When I woke, I felt the weight of illness on me before I opened my eyes.

Most of the people around me stepped backward. Linc said my friends asked him how I was, but after one or two get-well cards I stopped hearing from them. Now and then, I called people I had known in high school. The conversations were awkward and halting, and I felt foolish. No one knew what to say. Everyone had heard rumors that I was sick Someone had heard I had AIDS. Another heard I was pregnant.

I missed Borden. At Kenyon, I had often studied in a deli run by a groovy guy named Craig, who cruised around the place in fluorescent-yellow sunglasses. It was there, in September of 1986, that Borden had first smiled at me. He was a senior, with a gentle, handsome face and wavy black hair. He had torn up his knee running track, and to avoid walking he used a battered bike to get around campus. The bike had no chain, so he could really ride it only downhill wiggling it to keep it going when the ground levels out. On the uphills, he stabbed at the ground with his good leg, Fred Flintstone style. Eventually, some frat brothers kidnapped the bike and hung it from a tree over the Scrotum Pole, a stone marker that had earned its nickname during a legendary fraternity vaulting incident.

From the day we met in the deli, Borden and I had been inseparable. Since I left Kenyon, he had sent me off-color postcards and silly drawings, mailed between papers and finals and graduation. I wrote dirty limericks and mailed them back to him.

That summer, he showed up at my door. He got a job as an assistant editor at a foreign-policy quarterly, moved in with my mother and me and took care of me, making plans for the things we’d do when I got better.

Of my friends, only Linc visited. Home for the summer in Chicago, he drove Dr. Diesel fifteen hours to my house, where he would sit in a dilapidated denim armchair at the foot of my bed. The seat on the chair had collapsed, but he sat there anyway, his long thighs pointing up at the ceiling. Each time he saw me after a long absence, a wide startled look would pass over his face. He once said that he could sense the disease on me. I knew what he meant. I was disappearing inside it.

I saw my next physician only once. My jeans slid down my hips as I walked into the exam room, and he watched me tug them up. He asked how often I weighed myself. Often, I replied.

You shouldn’t weigh yourself, he said, and you have to eat. I’m not dieting, I replied. Girls shouldn’t be so thin, he said. I know, I don’t want to be this thin. Yes, yes, but girls shouldn’t be so thin.

After the appointment, I went to the bathroom, and as I opened the door to leave the doctor nearly fell into me. I was halfway home when I realized that he had been trying to hear if I was vomiting.

The next doctor was a pretty, compact woman with a squirrelly brightness. She found that I still had strep and changed the antibiotics. She ran the same tests that everyone else had run, and, again, the results were normal. I fought off the strep, but the other symptoms remained. I kept returning to see this doctor, hoping she could find some way to make me feel better. She couldn’t, and I could see that it was wearing on her.

In September, I was so weak that on a ride over to her office I had to drop my head to my knees to avoid passing out. When the nurse entered, I was lying down, holding my head, the room swimming around me. She took my blood pressure: 70/50. The doctor came in. She wouldn’t look at me.

‘I don’t know why you keep coming here,’ she said, her lips tight.

I told her that I felt faint and asked about my blood pressure. She said that it was normal and left, saying nothing else. She then went to see my mother, who was in the waiting room. ‘When is she going to realize that her problems are all in her head?’ the doctor said.

I returned home, lay down, and tried to figure out what to do. My psychiatrist had found me to be mentally healthy, but my physicians had concluded that if my symptoms and the results of a few conventional tests didn’t fit a disease they knew of, my problem had to be psychological. Rather than admit that they didn’t know what I had, they made a diagnosis they weren’t qualified to make.

Without my physicians’ support, it was almost impossible to find support from others. People told me I was lazy and selfish. Someone lamented how unfortunate Borden was to have a girlfriend who demanded coddling. Some of Borden’s friends suggested that he was foolish and weak to stand by me. ‘The best thing my parents ever did for my deadbeat brother,’ a former professor of his told him, ‘was to throw him out.’ I was ashamed and angry and indescribably lonely.

For seven months I had remained hopeful that I would find a way out of my illness, but the relentless decline of my body, my isolation, and the dismissal and derision I was experiencing took their toll. In the fall of 1987, I sank into a profound depression. I stopped seeing my physician and didn’t try to find a new one. One afternoon, I dug through my mother’s drawer and found a bottle of Valium that had been prescribed for back spasms. I poured the pills onto the bed and fingered them for an hour, pushing them into lines along the patterns on the quilt. I thought about Borden and couldn’t put the pills in my mouth.

I went back to Dr. Troshinsky. He told me to make an appointment with Dr. John G. Bardett, the chief of the Division of Infectious Diseases at Johns Hopkins University School of Medicine. Bardett was the foremost authority in his field, Dr. Troshinsky said. If there were an answer, he would have it.

At Johns Hopkins, after a lengthy exam and review of my records, Dr. Bartlett sat down with Borden and me. My internists, he said, were wrong. My disease was real.

‘You have Chronic Fatigue Syndrome,’ he said. He explained that it was one of the most frustrating illnesses he had encountered in his practice; presented with severely incapacitated patients, he could do very little to help them. He suspected that it was viral in origin, although he believed that the Epstein-Barr virus was not involved; early lab tests had liked the virus to Chronic Fatigue Syndrome, but subsequent research had demonstrated that some patients had had no exposure to the virus. He could offer no treatment. Eventually, he said, some patients recovered on their own.

‘Some don’t?’

‘Some don’t.’

That night, for the first time since March, I didn’t dream of being an athlete. I dreamed of being ill. In my dreams, I was never healthy again.

In the ensuing months, I began to improve. I hitched Newton to a leash and she tugged me through the neighborhood, first one block, then two, then three. My feet, soft from months in bed, blistered. The fever remained, but I was less prone to chills.

In the fall of 1988, Borden began graduate studies in political philosophy at the University of Chicago, and I felt well enough to move there with him. From the airport, we took a cab to Hyde Park, where Borden had rented a one-room apartment. The front door appeared to have been crowbarred for criminal purposes at least once. Inside, there was a mattress splayed across plastic milk crates and a three-legged dresser propped up on a brick. Roaches skittered over the walls and across the floor. The bathtub was heaped with used kitty litter. A weeks-old hamburger sat on the stove, shrunken into a shape that resembled the head of a mummy. The roaches were in various attitudes of repose around it.

We gave the mummy head a proper burial, roachproofed our toothbrushes by storing them in the refrigerator, and tried to make ends meet on Borden’s $9,000-a-year stipend and our savings. The apartment was four flights up, with no elevator, so most days I spent my time inside, reading about the French Revolution and listening to our neighbor throw things at her husband.

I wanted to be useful but I wasn’t strong enough for a conventional job. The one thing I could still do, however, was write. Shortly after arriving in Chicago, while watching a video of the 1988 Kentucky Derby, I had an idea for an article on the impact of overcrowded fields on the race. I researched and wrote the piece, then mailed it to an obscure racing magazine. I got a job offer. Fifty dollars per story, no benefits. I took only assignments that I could do from home and wrote them in bed. The magazine never paid me, but my bylines drew assignments at better publications, ultimately earning me regular work covering equine medicine and horse-industry issues at Equus.

I was growing much stronger, but whenever I overextended myself my health disintegrated. One mistake could land me in bed for weeks, so the potential cost of even the most trivial activities, from showering to walking to the mailbox, had to be painstakingly considered. Sometimes I relapsed for no reason at all. Living in perpetual fear of collapse was stressful, but on my good days I was functioning much better. By 1990, I could walk all over Hyde Park, navigate the stairs of the apartment with ease, and, for half an hour on one blissful afternoon, ride a horse. Three years after becoming ill, I wrote to Linc about the curious sensation of growing younger.

In the summer of 1991, while visiting my mother during Borden’s summer break, he and I decided to drive to New York to see the racetrack at Saratoga. A 10-hour road trip was risky, but I had grown tired of living so confined a life.

As we set out, the skies darkened. By the time we reached the interstate, a ferocious thunderstorm was crashing around us. Rain and hail hammered the roof of the car and gusts of wind buffeted us across the lane. We were caught in speeding traffic, but because the sheets of rain sweeping down the windshield limited visibility to a blurry tinge of lights ahead and behind, we couldn’t slow down or pull over. It was more than an hour before we were able to escape into a rest stop. I sat on the floor of the bathroom, looking out a high window and watching the trees sway. The rain tapered off. My hands were shaking.

We had planned to stop at the New Jersey farmhouse where our friends Bill and Sarah were staying, but we were very late. Borden called them on a pay phone while I waited in the car, watching him through the beads of rain on the windshield. He climbed back in, and we sat with the engine idling. I was frightened by the draining sensation in my body.

Should we turn around? I asked. Borden’s brow furrowed. Sometimes you’ve gotten a second wind, he said gently, as if asking a question. I wanted to believe him, so I agreed. He put the car in gear and we drove in silence. I felt worse and worse. I think we should turn around, I said, struggling to push the words out. We’re closer to Bill’s than we are to home, he said. If we keep going, you can rest sooner. He was scared now, leaning forward, driving fast. We entered New Jersey. We have to turn around, I said. Please. My head was pressed against the window, and I was crying. We’re almost there, he said. We turned into the farmhouse driveway. There were rows of melons in the field.

Bill took us to a guest room. Borden turned on the TV and left me to rest. By the time he returned to check on me, I was sweating profusely and chills were running over me in waves. He took my hand and was horrified: it was gray and cold, and the veins had vanished.

He spread blankets over me and tried to help me drink a glass of milk. I couldn’t sit up, so he cupped my head in his hand and tipped the milk into my mouth sideways. It ran down my check and pooled on the pillow. My teeth chattered so much that I couldn’t speak. Borden called an emergency room. The nurse thought that I was in shock and urged him to rush me in. But we were far from the hospital, and doctors had never been able to help. I was sure that being moved would kill me.

Borden lay down and held me. Wide awake, I slid into delirium. I was in a vast desert, looking down at a dead Indian. His body was desiccated and hardened, his skin shiny and black and taut over his sinews, his arms bent upward, hands grasping, clawlike. His shriveled tongue was thrust into an empty eye socket. I lay there and trembled, whispering I love you, I love you, I love you to Borden through clenched teeth. I’m sorry, he said.

Hours passed. The sun rose over the melon field.

Borden drove me back to my mother’s house. I lay exhausted for three days. When I opened my eyes on the morning of the fourth day, I had a black feeling. I couldn’t get up.

For as long as two months at a time, I couldn’t get down the stairs. Bathing became nearly impossible. Once a week or so, I sat on the edge of the tub and rubbed a washcloth over myself. The smallest exertion plunged me into a ‘crash.’ First, my legs would weaken and I’d lose the strength to stand. Then I wouldn’t be able to sit up. My arms would go next, and I’d he unable to lift them. I couldn’t roll over. Soon, I would lose the strength to speak. Only my eyes were capable of movement. At the bottom of each breath, I would wonder if I’d be able to draw the next one.

The corpse of the Indian hung in my mind. Borden and I never spoke of it, or of the events of that night, and we never spoke of the future. To corral my thoughts, he made lists with me: candy bars from A to Z, Kentucky Derby winners, Vice-Presidents in backward order, N.F.L. quarterbacks, Union Army commanders. Over and over, I asked him if I was going to survive. He always answered yes.

Late one night, as I walked down the hall, I heard a soft, low sound and looked down the stairway. I saw Borden, pacing the foyer and sobbing. I started to call to him, then stopped myself realizing that he wished to be alone. The next morning, he was as cheerful and steady as ever. But sometimes when I looked out the window I’d see him walking around the yard in endless revolutions, head down, hands on his temples.

One afternoon in September, he came in, sat on my bed, and told me that classes were starting and he had to return to Chicago. Before he left, he gave me a silver ring engraved with the words ‘Vous et nul autre (You and no other).’ I slid it on my finger and pressed my face to his chest.

With Borden in Chicago and my mother at work, I needed assistance to get through the day. I went through several helpers hired from nanny services. The first one clattered in with stacks of crimson-beaded Moroccan shoes and harem pants. She dumped them on my bed. ‘Twenty for the shoes, thirty for the pants,’ she said. She prowled through the house, appraising the furniture. ‘How much do you want for your refrigerator?’ she asked.

When I asked the woman who followed to take Newton into the backyard, she opened the front door and shooed the dog onto the street. Lying in bed upstairs, I heard the dog barking gleefully as she galloped westward. I called to the woman but got no response. I sat up and looked out the window. The woman was standing high in our apple tree, mouth open, gaping at the vacant sky. The dog returned; the woman did not.

The third helper sympathized and commiserated, then bustled around downstairs while I lay upstairs in bed. It wasn’t until she abruptly vanished that I discovered she had been packing armloads of my belongings into her car each evening. I went to the closet and found only a hanger where my taffeta ball gown had been.

On a rainy afternoon in January of 1993, I was sitting on the bed reading a magazine when the room began whirling violently. I dropped the magazine and grabbed on to the dresser. I felt as though I were rolling and lurching, a ship on the high seas. I clung to the dresser and waited for the feeling to pass, but it didn’t. At five the next morning, I woke with a screeching, metal-on-metal sound in my ears. My eyes were jerking to the left, and I couldn’t stop them. My eyes, upper lip, and cheeks were markedly swollen.

I went to a neurologist for tests. A technician asked me to lie down on a table. He produced something that looked like a blowtorch and pushed it into my ear. A jet of hot air roared out, spinning the vestibular fluid in my inner ear. It triggered such a forceful sensation of spinning that I gripped the table with all my strength, certain that I was about to fly off and slam into the wall. The tests determined that my vertigo was neurological in origin and virtually untreatable. The doctor prescribed diuretics and an extremely low-sodium diet to control the facial edema, which seemed to be linked to the vertigo. He could do little else.

The vertigo wouldn’t stop. I didn’t lie on my bed so much as ride it as it swung and spun. There was a constant shrieking sound in my ears. The furniture flexed and skidded around the room, and the walls folded and unfolded. Every few days there was a sudden plunging sensation, and I would throw my arms out to catch myself. The leftward eye-rolling came and went. Sleep brought no respite; every dream took place on the deck of a tossing ship, a runaway rollercoaster, a plane caught in violent turbulence, a falling elevator. Looking at anything close-up left me reeling. I couldn’t read or write. I rented audiobooks, but I couldn’t follow the narratives.

Borden called several times a day. He told me about Xenophon and Thucydides, the wind off Lake Michigan, the athletic feats of the roaches. When I asked him about himself, he changed the subject.

On Valentine’s Day, a package from Borden arrived in the mail. Inside was a gold pocket watch. I hung it from my window frame and stared at it as the room bent and arced around it. Weeks passed, and then months. The watch dial meted out each day, the light sliding across it: reddish in the morning, hard and colorless at midday, red again at dusk. In the dark, I could hear it ticking.

Outside, the world went on. Linc got married, my siblings had children, my friends got graduate degrees and jobs and mortgages. None of it had any relation to me. The realm of possibility began and ended in that room, on that bed. I no longer imagined anything else. If I was asked what month it was, I had to think a while before I could answer.

While I was lying there, I began to believe that we had struck the deer back in 1987, that he had come through the windshield and killed me, and that this was Hell.

Two years passed. In late 1994, Borden took his qualifying exams, and left Chicago. When I first saw him, lugging his green backpack, he was so thin that I gasped.

In 1995, by tiny increments, the vertigo began to abate. Eventually, I could read the back of a cornflakes box. My strength began to return. Instead of sitting on the edge of the tub with a washcloth, I could sit on the shower floor while the water ran over me. The first time I showered, dead skin peeled off in sheets. A hair stylist came and cut off eight inches of my hair, which had been growing like kudzu for several years and was now nearing my waist. In time, I could walk down the stairs almost every day. I sat on the patio looking at the trees.

Since my visit to Johns Hopkins, I had searched for an internist I could trust. In 1988, C.F.S. had been officially recognized and described by the Centers for Disease Control and Prevention. Subsequent research suggested endocrinologic, immunologic, and neurologic abnormalities in many C.F.S. patients, though the cause remained elusive. Physicians were becoming aware of the disease, but many of them knew less about it than I did. Others hawked dubious treatments. For a while, I tried almost anything. A few treatments caused disastrous side effects. The rest did nothing.

Then a friend referred me to Dr. Fred Gill, a renowned infectious-disease specialist. He was an angular, elegant man with a neat, Amish-style beard rimming a sharp jawline. As Borden and I told him my story, I found my stomach tightening in anticipation of a dismissive verdict. But Dr. Gill listened for the better part of an hour. When he had finished, he nodded. He couldn’t cure me, he said, but he would do everything he could to help me cope with the illness. In the following years, Dr. Gill managed my symptoms and coordinated my care with other specialists.

Eager to be productive, I called my Equus editor, Laurie Pfinz, and asked if I could write something. She assigned a story on equine surgery and told me not to worry about a deadline. I did the interviews on the phone from bed. Because looking at the page made the room shimmy crazily around me, I could write only a paragraph or two a day. When I could no longer stand the spinning, I’d take a pillow into the yard and lie in the grass with Newton, fixing my eyes on the treetops while she dissected a bone. It took me six weeks to write 1,500 words, but, four years after the abortive trip to Saratoga, I was coming back.

In 1996, with Borden and Fangfoss the cat, I moved into a small apartment in northwest Washington, D.C. One block away stood a fire station, and if Washington has an arson district we were in the heart of it. At the Taiwanese consulate, which was next door, a group of protesters soon set up camp, hauled in a loudspeaker and blasted a Chinese rallying song, sung by shrieky children. They apparently had a loop tape, so the song never ended. It was like listening to a bone saw. After a few weeks, I started dreaming to it.

I turned up my radio and wrote as much as I could, mostly equine veterinary medical articles for Equus. On breaks, I took brief walks. I bought new shoes — I’d been lying around in socks for years – and discovered that my feet had shrunk two sizes. I had lived for so long in silence and isolation that the world was a sensory explosion. At the grocery store, I dragged my hands along the shelves, touching boxes and bags, smelling oranges and pears and apples. At the hardware store, I’d plunge my arm into the seed bins to feel the pleasing weight of the grain against my skin. I was a toddler again.

After years of seeing people almost exclusively on television, I found their three-dimensionality startling: the light playing off their faces, the complexity of their hands, the strange electric feel of their nearness. One afternoon, I spent 15 minutes watching a shirtless man clip a hedge, enthralled by the glide of the muscles under his skin.

On a cool fall day in 1996, I was sifting through some documents on the great racehorse Seabiscuit when I discovered Red Pollard, the horse’s jockey. I saw him first in a photograph, curled over Seabiscuit’s neck. Looking out at me from the summer of 1938, he had wistful eyes and a face as rough as walnut bark.

I began looking into his life and found a story to go with the face. Born in 1909, Red was an exceptionally intelligent, bookish child with a shock of orange hair. At 15, he was abandoned by his guardian at a makeshift racetrack cut through a Montana hayfield. He wanted to be a jockey, but he was too tall and too powerfully built. That didn’t stop him, though. He began race riding in the bush leagues and fared so badly that he took to part-time prizefighting in order to survive. He lived in horse stalls for 12 years, studying Emerson and the ‘Rubaiyat,’ piloting neurotic horses at ‘leaky roof’ tracks, getting punched bloody in cow-town clubs, keeping painfully thin with near-starvation diets, and probably pills containing the eggs of tapeworms.

He was appallingly accident-prone. Racehorses blinded his right eye, somersaulted onto his chest at forty miles per hour, trampled him, and rammed him into the corner of a barn, virtually severing his lower leg. He shattered his teeth and fractured his back, hip, legs, collarbone, shoulder, ribs. He was once so badly mauled that the newspapers announced his death. But he came back every time, struggling through pain and fear and the limitations of his body to do the only thing he had ever wanted to do. And in the one lucky moment of his unlucky life he found Seabiscuit, a horse as damaged and persistent as he was. I hung Red’s picture above my desk and began to write.

What began as an article for American Heritage became an obsession, and in the next two years the obsession became a book. Borden and I moved to a cheap rental house farther downtown, and I arranged my life around the project. At the local library, I pored over documents and microfilm I requisitioned from the Library of Congress. If I looked down at my work, the room spun, so I perched my laptop on a stack of books in my office, and Borden jerry-rigged a device that held documents vertically. When I was too tired to sit at my desk, I set the laptop up on my bed. When I was too dizzy to read, I lay down and wrote with my eyes closed. Living in my subjects’ bodies, I forgot about my own.

I mailed the manuscript off to Random House in September 2000, then fell into bed. I was lying there the following day when the room began to gyrate. Reviewing the galleys brought me close to vomiting several times a day. Most of the gains I had made since 1995 were lost. I spent each afternoon sitting with Fangfoss on my back steps, watching the world undulate and sliding into despair.

In March 2001, Random House released ‘Seabiscuit. An American Legend.’ Five days later, I was lying down, when the phone rang. ‘You are a best-selling writer,’ my editor said. I screamed. Two weeks later, I picked up the phone to hear him and my agent shout in tandem, ‘You’re No. 1!’ Borden threw a window open and yelled it to the neighborhood.

That spring, as I tried to cope with the dreamy unreality of success and the continuing failure of my health, something began to change in Borden. At meals, he sat in silence, his gaze disconnected, his jaw muscles working. His sentences trailed off in the middle. He couldn’t sleep or eat. He was falling away from me, and I didn’t know why.

He came into my office one night in June, sat down, and slid his chair up to me, touching his knees to mine. I looked at his face. He was still young and handsome, his hair black, his skin seamless. But the color was gone from his lips, the quickness from his eyes. He tried to smile, but the corners of his mouth wavered. He dropped his chin to his chest. He began to speak, and fourteen years of unvoiced emotions spilled out: the moment of watching the woman he loved suffer, his feelings of responsibility and helplessness and anger; his longing for children we probably couldn’t have; the endless strain of living in obedience to an extraordinarily volatile disease.

We talked for much of the night. I found myself revealing all the grief that I had hidden from him. When I asked him why he hadn’t said anything before, he said he thought I would shatter. I recognized that I had feared the same of him. In protecting each other from the awful repercussions of our misfortune, we had become strangers.

When we were too tired to talk anymore, I went into the bedroom and sat down alone. I slid his ring from my finger and dropped it into a drawer.

We spent a long, painful summer talking, and for both of us there were surprises. I didn’t shatter, and neither did he. I prepared myself for him to leave, but he didn’t. We became, for the first time since our days at Kenyon, alive with each other.

One night that fall, I walked to the back of the yard. As Fangfoss hunted imaginary mice in the grass, I looked out at the hill behind the house. Beyond it, downtown Washington hummed like an idling engine, the city lights radiating over the ridge. I looked west, where a line of row-house chimneys filed down the hill until they became indistinguishable from the trunks of the walnut trees at the road’s end. Borden came out and joined me briefly, draping his arms over my shoulders, then he went inside. I watched the screen door slap behind him.

As I turned back, I saw a slit of light arc over the houses and vanish behind the trees. It was the first meteor I had seen since that night in Linc’s car. I thought, for the first time in a long time, of the deer.

In the depths of illness, I believed that the deer had crashed through the windshield and ushered me into an existence in which the only possibility was suffering. I was haunted by his form in front of the car, his bent knee, the seeming inevitability of catastrophe, and the ruin my life became.

I had forgotten the critical moment. The deer’s knee didn’t straighten. He didn’t step into our path, we didn’t strike him, and I didn’t die. As sure as I was that he had taken everything from me, I was wrong.

The car passed him and moved on.

What is costochondritis

Frequently Asked Questions

 

What is costochondritis?
cost= rib, chond = cartilage, itis = inflammation
Costochondritis is an inflammation of the cartilage that attaches the ribs to the breastbone

costochondritis

How do you get costochnodritis?
Costochondritis may  be caused by trauma, such as bumping the rib cage; as a result of a viral infection; or as part of an inflammatory disease process. Usually the cause is unknown

Does it go away?
For most people, it goes away in six months to a year;  however, for some people it remains a chronic condition.  Note the costochondritis is most painful in the early stages;  the pain does lessen after awhile!

What does costochondritis feel like?
Costo is an inflammation of the rib cartilage, and is sometimes diagnosed by pushing on the sternum,  (area at the top where your ribs join) or by pushing on any sore spot on your ribs.  Either should cause intense pain.  *However*, not everyone with CC will respond like that.

In the beginning, costo is usually worse,it  feels like there is an elephant sitting on your chest,  it hurts to breathe, ribs hurt all over with intermittent sharp, stabbing pains, and usually a few  “sore spots”  on your ribs, that you would faint if someone poked you there.  You might also feel like you are having a heart attack.   Eventually,  it might go down to a dull, but constant ache, or simply the feeling of sore ribs.  It hurts to wear a bra, and different motions, like picking a child up from the floor, can cause a flare up,  with intense pain.  When it is a chronic condition, it tends to wax and wane, come and go.  It might be better for a while, then you will reach for something in the wrong position and bam!, it is right back again.

My doctor say the pain of costochondritis is benign.  What does this mean?
Benign means nonmalignant.  But, “benign” is often wrongly translated as “harmless and easy to live with”.  Costochondritis is neither!

It feels like I am having a heart attack, what causes this?
When there is that much inflammation and swelling in one area there is no  room for more swelling- the nerves are over reactive and the muscles turn into tight knots – this causes the feeling of  having a heart attack.  You have all of the muscles and nerves running between the ribs themselves, then you also have your chest muscles that are tightening and swollen.  With one on top of your heart and the others on the bottom, there is going to be a heart attack feeling  ( You only have so much room).   However,  cardiac symptoms cannot be ignored, and must be ruled out first!

I am having trouble breathing- does this affect my lungs?
 Costochondritis is simply the swelling of the joints and  has absolutely nothing to do with your lungs and will not hurt them.  When the body is hurt, it automatically keeps everything away from the injured area so that it can heal.  Which is the case with costochondritis – there is the swelling – the body is in fact telling the lung not to expand completely, allowing you that deep breath, due to the fact that when the lungs  expand they press up against the joints where the ribs meet the breastbone.  So our body is trying to heal itself but in doing so it doesn’t allow us to breath properly.   

I feel pain radiating in my shoulders, arms,  or back- what causes this?
Nerves radiate throughout our rib cage and around to the back along our spine,  so the pain/inflammation from the joints can and will radiate from the breastbone all the way to our spines in back.  If there is anything irritating the nerves, then  you might  feel it all the way around.  Down the arms and into the shoulders may be caused from muscle pain which can radiate all over without any rhyme or reason.

Does stress make it worse?
Yes, stress can make it worse, like most health conditions.   Stress causes the nerves to be more on edge and tightens the muscles, both of which trigger our CC pain.  I have found that the pain increases quite a bit in stressful situation versus non stress times.  With stress our bodies go into their fight or flight reaction, which is why some doctors put us on relaxing types of medication so that our bodies won’t go into that reaction, raising the pain level.

How do I treat costochondritis?
Rest, heat or ice on affected areas,  and anti-inflammatories like aspirin, acetaminophen  (Tylenol), Ibuprofen (Advil), or naproxen (Aleve),  or prescription anti-inflammatories.  Most people have not found much to help the pain.   Medications and supplements will be discussed more in  what helps?

What about cortisone shots?
Cortisone shots have been helpful to some people- however, they are a temporary measure to kill the pain and reduce inflammation, and not a cure.  Most have not noticed enough help from them to be considered worth it.  There has been some discussion about cortisone weakening the cartilage.

Go to top of page


What hurts?

            • Sitting at a computer- try putting a binder under your feet (heels down, toes up) to shift your body weight
            • Long drives in a vehicle- try to not “hunch” over the steering wheel
            • Weather-  rainy/humid weather makes a lot of people worse
            • Sneezing/coughing
            • Lifting heavy objects from the floor, or above your head
            • Repetitive motions such a vacuuming, mopping
            • Stress
            • Caffeine

Go to top of page


What helps?

Supplements
 
Some people have had luck with the following supplements

            • Glucosamine/Chondroitin Sulfate (heals cartilage)
            • Ginger Root (inflammation)
            • Evening Primrose Oil (inflammation)
            • Bromelain (inflammation)
            • Vitamin C (boosts immune system)
            • Vitamin E (anti-oxidant, inflammation)
            • Eating fatty fish, such as salmon or sardines for their Omega-3 oils (inflammation)
            • White Willow Bark (inflammation)
            • Goldenseal (inflammation, cleansing, good for viral)
            • Echinacea-(boosts immune system, take for two weeks, two weeks off, etc., will not work as well if taken continuously)
            • Kava Kava (calming)
            • Valerian Root (calming, helps sleep)
            • Grape Seed Extract (antioxidant)

 

Here is one regimen taken with  good results

          •         Glucosamine/Chondroitin Complex (500 mg) 3 x a day
          •          Bromelain (Pineapple enzyme 500 mg) 3 x a day on empty stomach
          •          Vitamin C with Bioflavanoids (1000 mg) 4 x a day
          •          St. John’s Wort (300 mg) 3 x a day (good for nerve pain and depression)
          •          A good multivitamin 1 x a day
          •          B Complex 1 x a day
          •          Traumed brand cream applied to area as needed.
          •          Plain coated aspirin (325 mg) four a day
          •          Hot mineral baths (Batherapy Brand) once or twice a day

My regimen

            •  (started 7-6-98)

 

              • Glucosamine/Chondritin Complex  1500mg/1200mg per day
              • Ginger – two tablets, (550 mg each) morning and evening
              • Evening Primrose Oil (1300 mg) morning and evening
              • Vitamin C -1000mg  three times per day
              • Bromelain- 500mg three times per day,  on an empty stomach

I take a warm shower twice a day, and do light stretches on my back/neck area after each shower; this keeps me flexible.  I also get a swedish massage every two weeks, concentrating on my neck and shoulder area, and work out the neck/shoulder/back area with light weights on a weight machine, to strengthen.

8-28-98
After three days on the above regimen (except for the Bromelain), the dull ache I had constantly in my ribs went away.  It was no miracle cure, I still had a *lot* of pain, but   I would estimate that about 20% of my pain was gone.   A few days later, I woke up with no chest pain at all,  although it came back shortly after I started moving around.  I then added Bromelain, but noticed no difference;  in fact there has not been much of a change since the first week.

9-20-98
I started taking warm baths with Batherapy bath salts once or twice a day,  and using myoflex creme on my ribs, both seemed to help. I had gotten to the point where 40% of my rib pain was gone, but then I stopped the glucasomine/chondroitin and a lot of the pain came back.
I also had to quit working out with the light weights, I was pulling too many muscles, seems like I need to get my neck/shoulders/upper back stretched out-more flexible before I continue with weights.  The massages are helping a lot in this area.  The supplements that seemed to help me the most were the glucasomine/chondroitin, ginger, EPO oil and Vitamin C.

Rx meds

The following is a list of prescription medications that have been prescribed for costochondritis

 

              • Indocin- useful for reducing pain and inflammation, but side effects include liver and kidney damage, and drowsiness
              • NASAIDS-(non-steriod, anti-inflammatory agent) such as Relafen (Nabumetone); side effects include gastrointestinal disorders

 


 
What else helps?

 

              • Acupuncture has helped some people
              • Physical Therapy-  has helped, and has hurt some people.  Check this out carefully!
              • Chiropractors-  once again, some people have been helped, some hurt-  look for a chiropractor who uses an activator, or an adjuster.
              • Massages help the sore muscles around the neck and shoulders a lot of us tend to get from “hunching over”, because it hurts to breathe.
              • There is a book called “Pain Free” by Pete Egoscue, which uses simple but time consuming exercises to get our body back in alignment.  I recommend this book highly for people suffering from muscle pain in their neck, shoulders, arms or upper back, or are having a lot of trouble with their breathing .

 


Email list

There is an email list for people who suffer from costochondritis.  To subscribe, send a  *blank* email to costo-subscribe@egroups.com   To view the archives of this email list, go to   http://www.egroups.com/list/costo/   (you can also subscribe from this website)


 

Links
 


Chat Rooms  (the chat has been discontinued due to lack of participation- perhaps enough interested people can start it again?)

Yes, there is a chat about costochondritis!
Chat

Delphi-Costo Forum-Wednesdays @ 7:00 p.m. , central time


For Women Only

Frequently Asked Questions

I have pain in my breasts, can this be from costochondritis?
Yes, pain in the breasts, can be from nerve pain radiating from the ribs.  However, any pain of this type should be checked out by your doctor.
My costochondritis gets worse just before or during my periods, why would this be?
Prostaglandins are chemicals released at the site of an injury.  The are believed to be
the substances responsible for producing pain and inflammation following tissue damage and in immune reactions.  All the NSAIDs block the production of prostaglandins.

The levels of prostaglandins in the body increase as menstruation approaches, with the highest levels at the onset of the menstrual period. Higher protaglandin levels increase uterine contractions causing cramps and pain. In essence, the uterus squeezes so hard that it compresses the uterine blood vessels and cuts off the blood supply. This situation is similar to when the blood supply is cut off from the heart causing pain (angina). In both instances the result is the same–pain because the muscle does not have sufficient oxygen.

In addition, some of the excess prostaglandins escape from the uterus into the bloodstream where they may affect other smooth muscles. Thus, prostaglandins are responsible for the headaches, dizziness, hot and cold flashes, diarrhea and nausea that can accompany painful periods, and can also increase the pain of costochondritis.

Some women have found relief by taking NASAIDs several days before your period is expected to start,  building up the anti-prostaglandins into your system BEFORE the pain-producing prostaglandins are secreted!   Keep taking until the end of the second day of your period or whenever the pain usually eases up.

 Bras 

            • There is a company that  makes  comfortable cotten bras to size with no hardware, and will do free adjustments for the first two months.  Ask for a soft, wide lycra band at the bottom instead of elastic for free.   Prices start at $26. Go to http://decentexposures.com/

  

            • Bali makes a stretchy, comfortable bra called  “Barely There” that also has no hardware, and a wide band at the bottom.  These can be found in most department stores, or go to  http://www.onehanesplace.com/

Success Stories

Nan
I am a 64 year old woman and have always been physically active and have a pretty stressful job.  On May 22 , 1998, I had severe chest pains at work and was taken to the ER for possible heart attack.  An angiogram showed no blockage or heart problems and I was put on indocin for 10 days after being diagnosed with costochondritis.  My symptoms were chest pain (no redness or swelling), pain in elbows and wrists and labored breathing.

I learned more about costo from the internet and about glucosamine & condroitin as a possible treatment.  I already knew from reading Dr. Andrew Weil’s books that Omega-3 and diet of fatty acids nourish soft tissue and cartilage and that ginger is good as an anti-inflammatory supplement, as well as Vitamin E.  I began all this and cut way down on eating beef and began eating more salmon and sardines. I also used ice packs. I began a steady recovery and went back to work after complete rest for two weeks after being discharged from hospital.  By the end of 5 or 6 weeks I had no symptoms.   Remembering back to February and March that I had constructed a new patio laying 128 twelve inch square cement slabs after removing river stones by shoveling them out , led me to believe this to be the cause of the costo. Why it took so long to reach the pain stage is still a puzzle, but I don’t know what else could have caused this condition.

Costo generally strikes people from 20 to 40 years of age. I think one reason for the complete recovery could have something to do with my age and the fact that I just over did it physically.  I also feel that younger people who contract costo have a weakness in that area already probably caused from poor diet growing up.    Hope this will help others who have suffered much more than I have.


Articles of interest  (various articles collected from a search on the internet)

 Article # 1
 

          •  Ask The Experts (Medicine Net)

Questions & Answers
Question from Chris of Wyoming, USA–November, 1996.
What is costochondritis? What are the health effects, concerns for the long term?
How does someone learn to live with it, or cure it? Is this a genetic disorder?

Dear Chris:

Costochondritis is inflammation of the cartilage at the junction between the ribs
and the breast bone (sternum). Symptoms of costochondritis are pain and
tenderness in the front of the chest wall near the sternum.

Costochondritis is usually treated with ice and/or heat applications, local
injections of anesthetic and/or cortisone, and pain relievers. It can recur.

There is no evidence that costochondritis itself is genetic. Costochondritis can be
associated with other conditions, such as psoriasis, psoriatic arthritis, ankylosing
spondylitis, and Reiter’s syndrome.

MedicineNet is committed to bringing you medical information to help you, your
family, and friends become better informed patients. Please remember,
information is never a substitute for an open doctor-patient relationship.

Thank you for your question.


 Article #2

 

            • COSTOCHONDRITIS

 (Tietze’s Syndrome)

 What is It?

 * Painful inflammation (swelling) of the cartilage of the ribs (attaching ribs to sternum).

 * Commonly affects the 3rd or 4th ribs.

 * Age of onset before 40.

 * Both sexes are affected equally.

 * May mimic cardiac pain.

 Causes

 Cause of the inflammation is often unknown.

 Signs and Symptoms

 1. Pain in the chest wall, usually sharp in nature, especially on pressure.

 2. Pain may occur in more than one location and may radiate into the arm.

 3. Pain worsens with movement.

 4. Tightness in chest.

 5. Affected area is sensitive to the touch.

 Risk Factors

 * Trauma, such as a blow to the chest.

 * Unusual physical activity.

 * Upper respiratory infection.

 Prevention

 Avoidance of activities that may strain or cause trauma to the rib cage.

 Diagnosis and Treatment

 General Measures

 * Rest.

 * Ice packs applied to the affected area.

 * Avoidance of sudden movements that will intensify the pain.

 Medication

 * Mild pain medications, such as aspirin, acetaminophen or ibuprofen may help relieve discomfort.

 * Stronger pain medicines and non-steroidal anti-inflammatories may be prescribed..

 * Steroid injections may be prescribed for some patients.

 Activity

 As tolerated.

 Diet

 No special diet.

 Possible Complications

 None likely.

 Prognosis

 Complete healing. The disorder is benign and the course is usually of a short duration.


Article #3

Costochondritis is anterior chest wall pain associated with tenderness of the
costochondral and costosternal regions. It produces diffuse tenderness without
 swelling in more than one joint in the rib cage. It usually follows unusual excessive
 physical activity or trauma, and is more prevalent in females ages 20-40.


 Article #4

 

            • Costochondritis and PBC….(PBC stands for Primary Biliary Cirrhosis (PBC) , a rare chronic liver disease)

Costochondritis is one of many disorders associated with Auto Immune

Diseases. Normally this disorder will go away on its own.  When

associated with an auto immune diseases such as PBC, it may linger for

years or a lifetime.

Costochondritis is an inflammation of the cartilage that attaches the ribs to the breastbone (costo = rib, chond =cartilage, itis = inflammation).

Costochondritis causes mild to severe pain in the lower rib area or upper breastbone. Some patients fear they are having a heart attack. The most severe pain is usually in the lower rib area between the breast and upper abdomen. The pain may be more noticeable in sitting or reclining positions, and stress is known to aggravate this condition.

Costochondritis may also be caused by trauma, such as bumping the rib cage; as a result of a viral infection; or as part of an inflammatory disease process. Usually the cause is unknown.

Once the diagnosis of costochondritis is made, it usually responds well to a course of a pain-killing, anti-inflammatory medications such as aspirin,  ibuprofen, or any of a number of prescription medications. If this condition doesn’t respond to simple treatment measures, the patient should undergo more tests.  When costochondritis is associated with liver disease, it is more
difficult to treat.

For more info on PBC, go to   http://members.aol.com/pbcers/pbcers.htm


Article #5

Costochondritis
Authored by Lynn K. Flowers, M.D., LCDR MC USNR, Assistant Professor, Eastern Virginia Medical School

   INTRODUCTION

Background:
Costochondritis is a benign cause of chest pain, in contrast to myocardial ischemia or infarction, which is an important consideration in the differential diagnosis of chest pain. Although the term costochondritis is often used interchangeably with fibrositis and Tietze’s Syndrome, these are distinct diagnoses.

Pathophysiology:
Costochondritis is an inflammatory process of the costochondral or costosternal joints that causes localized pain and tenderness. Any of the seven costochondral junctions may be affected and more than one site is affected in 90% of cases. The second to fifth costochondral junctions are most commonly involved.

Frequency:
     In the U.S.: The exact prevalence of a musculoskeletal etiology for chest pain is not known. However, in one clinic  study the overall prevalence of a musculoskeletal etiology for chest pain was found to be about 10%. In a 1994   Emergency Department (ED) study 30% of chest pain patients were judged to have costochondritis.

Mortality/Morbidity: The course is generally self limited, but often with recurrent or persistent symptoms.

   CLINICAL
History: The onset is often insidious. Chest wall pain with a history of repeated minor trauma or unaccustomed activity (i.e. painting, moving furniture, etc.) is common.

Pain description:
          Worse with trunk movement, deep inspiration, and/or exertion
          Better with decreased movement, breathing quietly, or changing position
          Sharp, nagging, aching, or pressure-like
          Usually well-localized, but may extend or radiate extensively
          Can be severe
          May wax and wane

Physical: Pain with palpation of affected costochondral joints is a constant finding in costochondritis. The second through the fifth costochondral junctions are the sites typically involved. More than one junction is involved in >90% of cases.  Surprisingly, patients may not be aware of the chest wall tenderness until examination. The diagnosis should be reconsidered in the absence of local tenderness to palpation. Tietze’s Syndrome is characterized by nonsuppurative swelling, whereas costochondritis has no palpable swelling.

Causes:
The etiology is not well defined. Repetitive minor trauma has been proposed as the most likely cause. Bacterial or fungal infections of these joints occur uncommonly. These patients are more likely to be intravenous drug abusers or postoperative thoracic surgery patients.
  DIFFERENTIALS

  • Abdominal Trauma, Blunt
  • Acromioclavicular injury
  • Anxiety
  • Gout and Pseudogout
  • Herpes Zoster
  • Myocardial Infarction
  • Neoplasms, Lung
  • Sternoclavicular Joint Injury

  WORKUP
Lab Studies:
     There are no specific studies for costochondritis. Labs orders should be guided by the clinical scenario and the most  likely differential diagnoses.

Imaging Studies:
     Chest x-ray should be obtained in the work up of the differential diagnoses.
     Bone (gallium) scans have been used in the U.S., though not an ED study.
   TREATMENT
Emergency Department Care: Reassurance of the benign nature of the condition and adequate pain control are the
important objectives. Narcotic analgesics are not generally required.
Drug Category: Nonsteroidal Anti-inflammatory Drugs –

Provides pain management and anti-inflammatory effects

              Drug Name                                 ibuprofen (Motrin)
               Adult Dose                                 400-800 mg       POq4h-q6h  maximum daily dose 3200mg
               Pediatric                                    10 mg/kg per dose qid
               Contraindications                       hypersensivity to NSAIDS or aspirin
               Interactions                                anticoagulants,aspirin,methotrexate,furosemide, ,                                                                   lithium
                Pregnancy  Precautions            Not recommended during pregnancy
Further Outpatient Care:
     Nonsteroidal anti-inflammatory drugs
     Local heat
     Local infiltration of local anesthetic, steroid, or both, or intercostal nerve block. (Reserved for refractory cases.)
     Biofeedback

Complications:
     Misdiagnosing myocardial ischemia or infarction
     Extensive and expensive negative work-ups

Prognosis:   Excellent
     After one year about one-half may continue with some discomfort, but only one-third report tenderness with palpation.
Patient Education:
     Patients should be given reassurance of the benign nature of the problem and they should be instructed regarding the  avoidance of provoking activities. Patients should have a good understanding of the proper use and potential adverse  effects of NSAIDs.


Article #6

COSTOCHONDRITIS
Costochondritis is an inflammation of the ribs, usually where they attach to the breastbone or sternum.

A person with costochondritis may have pain in the front of the rib cage. Sometimes there is redness and swelling of the tissues around the sternum. The chest pain is described as dull and aching. The pain gets worse if pressure is put on the sore ribs.

It is very important to have all pain in and around the chest evaluated by your healthcare provider. Costochondritis is not life threatening but a heart attack is.

Sometimes a blow to the chest wall will cause costochondritis. Many times it is not known why inflammation sets in.

Treatment for the problem is simple. It includes:

        • anti-inflammatory medication like aspirin or ibuprofen,
        • ice packs over the sore areas,
        • avoidance of movements and activities that increase the pain,
        • rest until movement becomes comfortable, and
        • a gradual return to exercise, using slow stretching to avoid reinjury.Your healthcare provider may suggest cortisone injections if the problem is stubborn.

Tag : what is costochondritis , what causes costochondritis , what is costochondral calcification , what is costochondral chest , costochondritis symptoms