SYMPTOMS IN SEARCH OF A DISEASE: NEURASTHENIA, CHRONIC
FATIGUE SYNDROME, AND THE MEANING OF ILLNESS FROM
MODERNITY TO POSTMODERNITY
LISA HELD
A THESIS SUBMITTED TO THE FACULTY OF GRADUATE STUDIES
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS
FOR THE DEGREE OF
MASTER OF ARTS
GRADUATE PROGRAM IN PSYCHOLOGY
YORK UNIVERSITY,
TORONTO, ONTARIO
JANUARY 2008 Library and Bibliotheque et 1*1 Archives Canada Archives Canada Published Heritage Direction du Branch Patrimoine de I'edition
395 Wellington Street 395, rue Wellington Ottawa ON K1A0N4 Ottawa ON K1A0N4 Canada Canada
Your file Votre reference ISBN: 978-0-494-38781-8 Our file Notre reference ISBN: 978-0-494-38781-8
NOTICE: AVIS: The author has granted a non L'auteur a accorde une licence non exclusive exclusive license allowing Library permettant a la Bibliotheque et Archives and Archives Canada to reproduce, Canada de reproduire, publier, archiver, publish, archive, preserve, conserve, sauvegarder, conserver, transmettre au public communicate to the public by par telecommunication ou par Plntemet, prefer, telecommunication or on the Internet, distribuer et vendre des theses partout dans loan, distribute and sell theses le monde, a des fins commerciales ou autres, worldwide, for commercial or non sur support microforme, papier, electronique commercial purposes, in microform, et/ou autres formats. paper, electronic and/or any other formats.
The author retains copyright L'auteur conserve la propriete du droit d'auteur ownership and moral rights in et des droits moraux qui protege cette these. this thesis. Neither the thesis Ni la these ni des extraits substantiels de nor substantial extracts from it celle-ci ne doivent etre imprimes ou autrement may be printed or otherwise reproduits sans son autorisation. reproduced without the author's permission.
In compliance with the Canadian Conformement a la loi canadienne Privacy Act some supporting sur la protection de la vie privee, forms may have been removed quelques formulaires secondaires from this thesis. ont ete enleves de cette these.
While these forms may be included Bien que ces formulaires in the document page count, aient inclus dans la pagination, their removal does not represent il n'y aura aucun contenu manquant. any loss of content from the thesis. Canada Abstract
Disease is an objectively verifiable disorder of bodily functions or systems, while illness is a subjective experience of symptoms. This distinction, rooted in Cartesian dualism, categorizes symptoms as either psychogenic or biogenic. Neurasthenia of the late 19th- and early 20th-centuries, and chronic fatigue syndrome (CFS) 100 years later, have been compared by historians due to their remarkably similar symptom presentation and common etiological controversies. Both have, at times in their histories, been interpreted as psychogenic illnesses and biogenic diseases, making them representative case studies of how the meaning of symptoms influences both the construction of disease and the illness experience. In this thesis I reconstruct the contemporaneous discourses regarding symptomatology, etiology, and treatment for neurasthenia and CFS. Despite remarkably similar symptoms, the meanings ascribed to these symptoms, and thus the illness experience itself, is contingent on sociohistorically-situated factors, rendering the claim that CFS is neurasthenia revisited problematic.
iv TABLE OF CONTENTS
Abstract iv
1. Introduction 1
Neurasthenia and Chronic Fatigue Syndrome: The Case
for Comparison 4
Neurasthenia and CFS: An Overview of Symptoms 7
The Theoretical Underpinnings of Health and Illness
Perceptions 11
Overview of the Current Project 19
2. Neurasthenia and CFS: An Historical Timeline 20
Neurasthenia - What it Was and What it Wasn't 20
The Varieties of Neurasthenia 25
Who Became Neurasthenic 28
The Beginning of the End 31
Somatization in a Post-Neurasthenia World 38
The Bridge Between Neurasthenia and CFS 42
A Mysterious Illness Emerges 46
What's in a Name? 50
Who are CFS Sufferers? 53
Conclusion 56 3. Neurasthenia and CFS: Etiology and Treatment 58 Etiology: The Biological, Psychological, and Social 58
v Biological Theories 59
Psychological Theories 66
Social Theories 71
Treatment Strategies: Biological, Psychological, and Social 76
Biological Treatments 77
Psychological Treatments 81
Social or Lifestyle Treatments 86
Conclusion 91
4. The Socio-cultural Shaping of Illness Representations 93
Negotiating Diagnosis 93
The Importance of Diagnosis: Legitimacy or Stigmatization 102
The CFS Counter-narrative 107
Conclusion 114
5. Conclusion 117
The Meaning of Symptoms 117
Postmodern Medicine: Hope for the Future? 120
References 125
vi Introduction
Were it possible for us to take a glance at the constitution of a man, as man was originally made, we should in all probability find that, in relation to mere anatomical details, there was no essential difference between him and the man existing in the nineteenth century. We might even go farther than this, and, by the most able chemical investigation, analyse tissue after tissue without finding the slightest variation or change. We might bring the most powerful and most modern appliances to our aid, and yet as far as human research is concerned, we should be unable to reveal any ultimate difference, which could enable us to arrive at a conclusive estimate as to the reason, why we should suffer from diseases which never existed in the body of primitive man. (Dowse, 1880, p. 17)
More than a century after physician Thomas Stretch Dowse wrote these words, we still grapple with the same question: Why should we be seeing diseases today for which there are no precursors, despite the physiological similarities between modern and primitive man? Perhaps similar symptom presentations are interpreted differently and disease categorization schemas are changing more than physiology. Unlike nineteenth- century physicians like Dowse who had nothing but subjective patient accounts of symptoms on which to base disease legitimization (Theriot, 2001), contemporary physicians require an objective, demonstrable link between symptoms and organic pathology before granting disease status. In fact, physical symptoms may not be indicative of disease at all, but rather of illness. This distinction between disease and illness (Feinstein, 1967) is reflected in medical textbooks in the following way: "disease is an objectively verified disorder of bodily functions or systems, characterized by a recognizable cause and by an identifiable group of signs and symptoms. Illness, by contrast, is used inside medicine to indicate the patient's subjective experience, which may or may not indicate the presence of disease" (Morris, 1998, p. 37).
1 Biomedical technology has forced this disease-illness distinction as we have become able to "see" into the body in ways that were unavailable to Victorian physicians.
It is now possible to be diseased - one can have high blood pressure, cancer, osteoporosis - devoid of any subjective experience or report of illness (Theriot, 2001).
We can also be ill without being diseased. Psychosomatic illness is defined, in fact, as the presence of symptoms in the absence of disease (Shorter, 1994), or symptoms that cannot be scientifically explained. While some disease categories like neurasthenia, insanity of adolescence, and hysteria have disappeared from the diagnostic nomenclature
(Theriot, 2001), certain symptoms - like fatigue and pain - have transcended historical boundaries and have changed little quantitatively or qualitatively (Shorter, 1992). Time and place, however, have changed the meaning of these symptoms (Aronowitz, 1992).
The meaning that accrues to symptoms is a sociocultural product expressed in the form of illness scripts which grant approval to some symptom forms in certain places and times while discouraging others (Horowitz, 2002). There is an inherent reflexivity between biology and culture that shapes the interpretation of physical sensations and occurs beyond the awareness of individuals. Historian of medicine Edward Shorter
(1994) points to both social and medical models of behavior as shaping symptom presentation. For example, upper class nineteenth-century women, who were encouraged to be passive, could present with paralysis because it was not only an accurate reflection of women's social and gender role status, but because it also fit the prevailing medical model inspired by Charcot's (1825-1893) conceptualization of hysteria. Symptoms like paralysis and hysterical fits would, today, be socially unacceptable given current cultural
2 expectations of women to work outside the home, raise children, take care of aging parents, and more. Ware and Kleinman's (1992) "sociosomatic" approach describes the interaction between culture and biology as the way in which "events and processes in the social world influence symptoms; (and) symptoms themselves shape and structure the social world" (p. 548). This interaction, and the relative status of culture and biology in the interaction, is open to various interpretations. Had Dowse been alive a century later, he may have rephrased his question the way Shorter does: "When symptoms change, is it because life has become more stressful, because the biological basis of illness has altered, or because the culture enveloping us has started sending different messages?" (p. viii).
Rosenberg (1989) argues that disease, while consisting of a biological event, requires consensus in order for it to be named as such. Shorter (1994), emphasizing the biological, hypothesizes that perhaps some individuals are genetically predisposed to becoming ill in the absence of disease. Kleinman (in Ware, 1993) offers the pathoplastic- pathogenic model in which "biology provides the structure of the disorder; culture shapes the symptoms..." (p. 80).
Regardless of where one falls on the biology-culture spectrum, the relative influence of each on the shaping of disease is value-laden. Nowhere is this more apparent than in the often contested arena of diagnosis. In the current diagnostic hierarchy, diseases (sets of symptoms with clear organic etiology) are accorded top spot
(Zavestoski et al., 2004). As etiology becomes less clear, symptom clusters may be granted lower status as psychogenic factors are considered in the absence of clear biological markers. That diagnosis is an integral part of illness and is a negotiation
3 between sufferers and physicians is entrenched in human history (Rosenberg, 1989).
Diagnosis of disease has typically conferred legitimacy to sufferers (Brown, 1995;
Cathebras, 1994), thus the negotiation can become highly charged when conditions are ill-defined and when "the logical and the biological...fail to coincide" (Morris, 1998, p.
39). Battles over diagnosis are often representative of broader social conflicts and can be the catalyst for social movements in health (Zavestoski et al., 2004). Ill individuals with a disease diagnosis are granted social support and an understanding that they are not to blame for their illness. Other ill individuals, who are arguably no less sick than those whose symptoms fall into a recognized disease category, are often stigmatized and held accountable for their illness.
Neurasthenia and Chronic Fatigue Syndrome: The Case for a Comparison
Neurasthenia embodied a set of symptoms that in the late nineteenth- and early twentieth-centuries granted sufferers a disease diagnosis, allowing them to escape the stigma of psychosomatic illness (Ware & Weiss, 1994). More than a century later, chronic fatigue syndrome (CFS) sufferers present with remarkably similar symptoms yet have not been granted disease status. In this project I use neurasthenia and CFS as case studies to explore the meanings of symptoms, the construction of disease, and the experience of illness in the modern (neurasthenia) and postmodern (CFS) contexts. By situating each within its historical and cultural context, I address a body of work that has suggested that CFS is, in fact, neurasthenia revisited. My position is that whether or not the two disease categories could ever be shown to share the same underlying, organic cause (and it would be impossible, at this point, to prove this), the way these albeit
4 similar categories have been experienced medically makes a direct comparison not only perilous, but impossible. But from an interpretive standpoint their similarities illustrate an enduring need to define symptoms as either biogenic or psychogenic, thereby resulting in an illness experience that, despite the passage of time, is congruent in many ways.
My research extends beyond symptom presentation to evaluate similarities and differences in etiological theories and treatment strategies, while also considering the impact of the illness-disease distinction on self-concept, the doctor-patient relationship, and on the broader cultural interpretation of symptoms in search of disease. I argue that the question of whether CFS is neurasthenia revisited is the wrong question to ask for a couple of reasons. First, my interest is not medical, hence the controversy over etiology is relevant only insofar as it relates to the social construction of illness and disease. The fact that both the neurasthenia and CFS discourses are illustrative of the biogenic versus psychogenic debate is what makes them worthy of comparison, not whether they do, in fact, share the same etiology. Second, neurasthenia affords us an historical perspective we do not as yet have with respect to CFS, thereby making a comparison possibly illuminating of the way a more contemporary illness versus disease negotiation may proceed. Contemporary critics argue that comparing neurasthenia and CFS is problematic because of changing uses and contexts of diagnosis; misdiagnosis; dissimilar case definitions; gaps in records; data skewed by gender, class, and race; and even the mutability of pathogens (Shorter, 1993; Wall, 2005). These are limitations in making a direct comparison, however, that does not preclude engaging in an interpretive analysis
5 comparing cultural patterns, one not subject to the same criteria as analysis within the medical science model (Ware, 1993).
My comparison of neurasthenia and CFS is not without precedent, however the current literature tends to take a literal, essentialist view of these disease categories instead of focusing on how they have been socially constructed and negotiated, thus allowing both similarities and differences to emerge. Greenberg (1990) labels CFS the
1980s version of neurasthenia; Ware and Kleinman (1992) assert that both neurasthenia and CFS represent the body's way of signaling interpersonal distress and initiating change; Sharpe (1998) claims the medical writings of more than 100 years ago are relevant to modern illnesses like chronic fatigue; Luthra and Wessely (2004) argue that clinical descriptions of both neurasthenia and CFS indicate they are the same illness; and
Abbey and Garfinkel (1991) cite cultural parallels leading to the rise of both illnesses, such as the fixation on business and monetary success and the changing role of women. I believe there is value in comparing the two disorders by looking at each grounded within its own historical and cultural contexts to understand where there are similarities, and where, by contrast, there are differences.
Comparisons between neurasthenia and CFS begin, on the most superficial level, with symptom presentation. While a much more detailed history and comparison of both will follow in subsequent chapters, a brief discussion of their respective symptoms, starting with neurasthenia, will begin to set the stage for a more comprehensive comparison.
6 Neurasthenia and CFS: An Overview of Symptoms
From around the mid-nineteenth century patients began presenting with a mix of physical and psychological symptoms doctors were to term neurasthenia (Theriot, 2001).
The first to write about neurasthenia was Michigan physician E. Van Deusen (1828-
1909). Writing in the Journal of Insanity in 1869, he referred to neurasthenia as an old term, but a better descriptor of the disorder than "nervous prostration" (p. 449). In describing the symptomatology of neurasthenia, he listed the leading symptoms as,
"general malaise, impaired nutrition and assimilation; muscular atonicity, changing the expression of the countenance; uterine displacements, with consequent results, and neuralgias of debility, cerebral anaemia, with accompanying tendency to hyperaesthesia, irritability, mental depression, impaired intellection, melancholia and mania" (p. 445).
However, it is neurologist George M. Beard (1839-1883) of New York who is credited with popularizing and describing neurasthenia as a clinical syndrome (Bunker, 1930), with his contemporaries referring to him as the father of neurasthenia (Gijswijt-Hofstra,
2001). The subsequent cultural acceptance of neurasthenia cannot be understated. In his
1913 book, Neurasthenia, Ballet stated, "The fortunes of the word Neurasthenia have been remarkable; not only did it quickly take a place in the medical vocabulary, but it soon became popular. Everybody knows it and makes use of it..." (p. 105). Like Van
Deusen, Beard also published his first work on neurasthenia in 1869 in the Boston
Medical and Surgical Journal, defining it as "a want of strength in the nerve" (p. 217), and describing symptoms such as "general malaise, debility of all the functions, poor appetite, abiding weakness in the back and spine, fugitive neuralgic pains, hysteria,
7 insomnia, hypochondriases, disinclination for consecutive mental labor, severe and weakening attacks of sick headache..." (p. 218). Overtime, Beard was to expand the list of symptoms to include:
Tenderness of the scalp (cerebral irritation, cerebrasthenia); tenderness of the spine
(spinal irritation, myelasthenia); tenderness of the teeth and gums; tenderness of the
whole body (general hyperaesthesia); general or local itching; abnormalities of the
secretions; vague pains and flying neuralgias; flushing and fidgetiness; tremulous
and variable pulse with palpitation; sudden giving way of general or special
functions; special idiosyncrasies in regard to food, medicine, and external irritants;
sensitiveness to changes in the weather; a feeling of profound exhaustion
unaccompanied by pain; ticklishness; desire for stimulants and narcotics; insomnia;
nervous dyspepsia; partial failure of memory; deficient mental control; seminal
emissions; spermatorrhea; partial or complete impotence; changes in the expression
of the eyes and countenance; mental depression, with general timidity; morbid fear
of special kinds, as agoraphobia (far of places); astraphobia (fear of lightning); sick
headache and various forms of headache; disturbances of the nerves and organs of
special sense; localized peripheral numbness and hyperaesthesia; general and local
chills and flashes of heat; local spasms of muscles. (Beard, 1879, p. 246)
By the time he had published his clinical text, American Nervousness, in 1881,
Beard had listed more than 75 neurasthenic symptoms. With a list that extensive it is not surprising that no organ or bodily function was considered safe from the disease (Beard,
1879). Nor is it surprising that neurasthenia was characterized as a late nineteenth
8 century social problem of mammoth proportions by no less than fellow physicians
Sigmund Freud (1856-1939), Richard von Krafft-Ebing (1840-1902), and Paul J. Mobius
(1853-1907) (Slijkhuis, 2001).
Acceptance of neurasthenia as a disease entity was certainly not universal, but
detractors were in the minority and Beard's ideas quickly spread to Europe where his
books enjoyed extraordinary success (Rosenberg, 1962). However, by the end of the first
decade of the twentieth century, the vagueness of neurasthenic symptoms and the catch
all nature of the disease itself had become problematic. An undiscovered organic
etiology, in conjunction with the ideas of thinkers like Freud (1856-1939) and Janet
(1859-1947) led, by the nineteen teens, to an alternative label for patients exhibiting
neurasthenic symptoms. "Nervousness found a new name in neurosis" (Cayleff, 1988).
The emergence of psychosomatic medicine on the heels of neurasthenia's decline and a
series of epidemics of neurasthenia-like symptoms subsequently labeled as cases of mass
hysteria, set the stage for the emergence of chronic fatigue syndrome in the early 1980s.
CFS was identified and named after a number of published cases described a
possible epidemic of what appeared to be lingering flu-like symptoms speculated to be
associated with the Epstein-Barr virus (EBV) (Aronowitz, 1992). The first case
definition of CFS was published by researchers in the Annals of Internal Medicine in
1988 (Holmes et al.). CFS was described as "a syndrome of unknown cause
characterized primarily by fatigue" (p. 387). To be diagnosed with CFS, a patient had to have persistent or relapsing fatigue for no less than six months; other clinical conditions that could account for the symptoms had to be ruled out; and have eight or more of
9 eleven symptom criteria: mild fever, sore throat, painful lymph nodes, muscle weakness,
muscle discomfort or myalgia, prolonged fatigue after activity that would have been
easily tolerated prior to the onset of symptoms, headaches, migratory arthralgia,
neuropsychological complaints (some of which include forgetfulness, excessive
irritability, confusion, depression, difficulty concentrating); sleep disturbance; and
description of the main symptom complex as initially developing over a few hours to a
few days. The case definition was updated in 1994 (Fukuda et al.), primarily to facilitate
systematic data collection. There was a decrease in the number of symptoms from eight
to four, and a decrease in the list of symptoms from eleven to eight. From a lay
perspective, CFS is best described by the Centers for Disease Control and Prevention
(CDC) as:
.. .an illness characterized by profound, debilitating fatigue lasting at least six
months that results in substantial reduction in occupational, personal, social, or
educational activities. The fatigue is not improved by rest, may be worsened by
physical or mental activities, and is accompanied by characteristic symptoms.
These symptoms include problems with memory and concentration, unrefreshing
sleep, muscle and joint pain, headaches, tender cervical or axillary lymph nodes,
recurrent sore throat, and an increase in fatigue and in patient-specific symptoms
persisting longer than 24 hours following mental or physical exertion. (CFS
Toolkit)
With nowhere near the 75 symptoms described by Beard, one researcher reports
28 symptoms with frequency estimates (Komaroff, 1993), almost all of which can be
10 found in Beard's writings. Abbey and Garfinkel (1991) draw a similar conclusion, noting that the only CFS symptom in the case definition not listed by Beard is painful lymph nodes. They further argue that both neurasthenia and CFS share a similar function - giving name to a disparate set of physical symptoms.
On the basis of symptomatology alone, neurasthenia and CFS could be granted equivalent standing. That neurasthenics were accorded disease status for some three decades and CFS sufferers are still bitterly embroiled in a battle to be upgraded from syndrome, is evident not only of a sociohistorical shift but of the cultural shaping of health and illness perceptions. One of the questions I explore in this project is how the blue chip symptoms of the late nineteenth century tumbled to penny stock value by the end of the twentieth.
The Theoretical Underpinnings of Health and Illness Perceptions
I suggest the distinction between illness and disease is rooted in the Western ideological embrace of Cartesian dualism. Our understanding of symptoms as either psychogenic or biogenic in nature is simply a reflection of the centuries-old mind-body problem, a dualism that is both epistemological and ontological. Epistemologically, the patient's subjective report of symptoms is contrasted with the objective tests and instruments of biomedicine, and ontologically the duality is expressed as either psychological disturbance or real physical disease (Kirmayer & Young, 1998). The epistemological and ontological dualism has spawned an ethical conundrum - ill individuals are held responsible for their so-called imaginary or psychosomatic illness, while the diseased are absolved from blame for their biologically-based, real suffering.
11 Despite frequent claims that dualism is dead, it lives on in the controversies surrounding
CFS (Wessely, 1991).
The mind-body split was a precondition of the modern period, which took hold in
Europe from around the seventeenth century (Giddens, 1990). Science and technology were Enlightenment heroes in a battle against religion for the legitimate claim to knowledge, and in the arena of psychiatry, which became known as a distinct sub- discipline of medicine in the mid-1800s, three philosophic themes emerged: "the quest for objective truth, faith in method, and a telos of emancipation from mental illness through progress" (Lewis, 2000, p. 74-75). Progress and emancipation could be attained by the application of rationality, thereby ensuring a truth that was objective and fixed
(Charlton, 1993). Medical knowledge was objective knowledge. Traditionally, physicians would train and then build on that training over the course of their careers via scientific journals, books, professional associations, conferences, and libraries which, until fairly recently, were inaccessible to the lay public (Muir Gray, 1999). Their knowledge was privileged and their authority was strengthened by the discovery of new organisms and disease processes, treatments, and cures. With each new advance, medicine's claim to objective, scientific knowledge was further legitimized, thus making it more resistant to criticism from those on the outside (Salmon & Hall, 2003).
Charlton (1993) calls medicine "modernity in action" (p. 497), its purpose to alleviate symptoms and eradicate disease - goals which can be objectively measured. So, when physicians are faced with patients exhibiting symptoms for which no underlying disease can be found, the mind-body separation is breached and controversy is sure to
12 follow (Aceves-Avila, Ferrari, & Ramos-Remus, 2004). Biomedicine is not particularly
accepting of conditions requiring the integration of mind and body or of understanding
such conditions within a sociocultural context (Kleinman & Straus, 1993). At issue are
patients' subjective accounts of their physical sensations and the objective products of
scientific testing. Morris (1998) categorizes patient accounts as "untrustworthy and
trivial," and lab reports as "truthful and serious" (p. 37-8). Thus, as Shorter (1992)
argues, patients unconsciously present with symptoms physicians are likely to recognize
and categorize as indicative of disease. There is a cultural shaping of symptoms which
not only accounts for the rise and fall of particular symptoms historically, but also
acceptance and rejection of disease categories. This is not a unidirectional process -
some unexplained symptoms are explained when causes are discovered, and other
previously assumed causes of symptoms have subsequently been discredited (Sharpe &
Carson, 2001). Thus dualism forces the distinction between symptoms as indicative of
bodily disease and symptoms as the product of mental disorganization - a distinction that
is the cornerstone of the theory and practice of modern medicine (Ware, 1993).
Psychosomatic symptoms are not only the result of cultural shaping, but are also
rooted in the psychogenic and neurogenic traditions (Shorter, 1994). Psychogenesis, of which there are three versions, places the origin of symptoms in the mind. The three ways this can occur are: as a response to the stresses of everyday life situations; the
Freudian-influenced idea of early childhood trauma; or by suggestion, an idea popularized by the Nancy physician Hippolyte Bernheim (1840-1919). In the neurogenic tradition, psychosomatic symptoms are the product of chemical changes in the brain,
13 which in effect, "reduce the complexity of the mind to the biology of the brain" (Shorter,
1994, p. 202) but nonetheless establish a connection between mind and brain. However,
Shorter points out that even this form of biological reductionism neither accounts for how
symptoms are chosen nor for the timing or length of illness. Modern medicine assumes
that disease is progressive - either symptoms intensify and physical signs corroborate a
disease diagnosis, or symptoms resolve and health is restored. Either way, the possibility
of diagnostic error is reduced (Macy & Allen, 1933-34). The longer symptoms persist
with no identified organic etiology, the greater the likelihood they will be labeled
psychosomatic.
The critique of modernism's dualistic underpinnings arose with postmodernism, a
Western intellectual movement beginning around the 1950s with the work of theorists
like Jacques Derrida (1930-2004), Michel Foucault (1926-1984), and Jean-Francois
Lyotard (1924-1998) (Lewis, 2000). The postmodern critique questions the legitimacy of
modernist knowledge claims, arguing that science is just one world view seeking to
answer fundamental questions about human existence (Lewis, 2000). Postmodernism
advances the ideas of multiple realities, embracing ambiguity, and rejecting the modernist
assumption of objective truth. Dualistic binaries, themselves culturally constructed, become continuums. Postmodernism in medicine, therefore, reconceptualizes health and
illness not as discrete entities, but rather as a health-illness continuum on which individuals are neither healthy nor ill, but are characterized by varying degrees of both.
Scheurich (2000) describes postmodern medicine as "a contemporary medicine in which illness, diagnosis, and treatment are no longer objective and scientific, but rather
14 strongly shaped by individual viewpoints as well as social and cultural trends..." (p. 461).
The illness experience gives patients a voice in the discourse such that the right to speak does not lie solely with physician "experts" (Lewis, 2000). Health and illness discourses become more inclusive, more of a co-construction than merely the reflection of the modernist preference for one type of discourse, the scientific discourse. Such a shift would emphasize "care" over "cure" (Scheurich, 2000) or, in other words, replace the modernist goal of eradicating disease with the postmodern goal of helping patients cope with and adjust to disease, given that disease is an ever-present element of our everyday lives (Lewis, 2000).
Postmodern medicine has also brought changes to the doctor-patient relationship, as evidenced by the loss of faith in physicians, with patients becoming medical experts in their own right (Zavestoski et al., 2004). Technologies such as the Internet, have, as Muir
Gray (1999) suggests, done a better job than dynamite in opening the doors to knowledge that was previously privileged and inaccessible to lay people. The worldwide web has leveled the playing field, and it is not just physicians and patients engaging in discourse: the postmodern challenge to the "physician as expert" has created a space for alternative and complementary healers to help shape cultural understandings of health and illness.
There are many actors taking part in the cultural construction of postmodern illness, and the recognition of our intersubjective culture accepts that objectivity is open to different interpretations (Morris, 1998). Neither the "objective" judgment of the physician nor the
"subjective" experience of the patient is privileged in a postmodern dialogue.
15 Postmodern medicine challenges many modernist-inspired dichotomies - health-
illness, biogenic-psychogenic, real-imagined, culture-biology, physician expertise-patient
narrative. While neurasthenia has been characterized as a disorder of modernity (Porter,
2001), CFS is being characterized as a postmodern illness (Ware, 1999; Zavestoski et al.,
2004; Morris, 1998). This is not an entirely incorrect characterization but, I will argue, is
certainly an oversimplification. In fact, such either-or characterizations are themselves
part of the modernist paradigm. My argument is that neurasthenia was, and CFS is,
constructed in eras marked by specific cultural transitions: in the case of neurasthenia,
between pre-modernity and modernity, and in the case of CFS, between modernism and
post-modernism.
Neurasthenia was the product of pre-modern Victorian medicine with modernist
aspirations, making it a disorder that bridged both pre-modernity and modernity. The
understanding of neurasthenia was not influenced by the mind-body dualism so
fundamental to modern medicine. The concern of Victorian physicians was treating
symptoms and mitigating suffering, not on determining whether a mental or bodily
ailment was responsible for the symptoms (Aceves-Avila et al., 2004). "Diagnosis was
based on patients' subjective reports of symptoms because that was the only information
available - symptoms of illness became distinct diseases" (Theriot, 2001, p. 352).
Neurasthenia remained relatively uncontested for as long as physicians and patients believed in the reality of its physical symptoms and did not frame it as being either biogenic or psychogenic (Wessely, Hotopf, & Sharpe, 1998). The mind-body problem was acknowledged but, based on Beard's own writings, handled in a way that sounds
16 presciently like the biological psychiatry of today: "Whatever our philosophy of the relation of mind to body may be, practically we are compelled to study the mental as well as the physical side of the nervous system both in health and disease. Psychology may be but physiology out of sight..." (Beard, 1881/1972, p. 2).
While reports of fatigue are nothing new, the complaint of chronic fatigue was all but unheard of prior to the late nineteenth century (Shorter, 1993). In fact, chronicity is unique to our more contemporary illnesses (Mechanic, 1995), less likely to result in death or remission but rendering sufferers disabled on a relative scale (Scheurich, 2000).
Whereas neurasthenics did often recover, CFS sufferers currently have a poor prognosis
(Cho, Hotopf, & Wessely, 2005) though it is unclear what form the recovery discourse will ultimately take. Somatization is increasing, not by way of psychiatric diagnoses like somatization and conversion disorder but via the presentation of ambiguous, unexplained somatic symptoms (Scheurich, 2000). Fatigue and headache are the two symptoms battling it out for the top spot in surveys (Wessely et al., 1998). In part, it is the lack of specificity, a reductionist requirement of our current diagnostic model that prevents CFS from being granted legitimacy and its sufferers from garnering sympathy (Rosenberg,
1989). Social sanction of symptoms is tied to disability compensation, therefore the controversy over diagnosis has an enormous impact on CFS sufferers (Aceves-Avila et al., 2004). The biogenic-psychogenic etiological debate, so low key during the glory days of neurasthenia, is at the forefront of controversies over the chronic, poorly understood postmodern illnesses of today.
17 Where Beard's neurasthenia was perceived as physical and was diagnosed instead
of hypochondria, malingering, or insanity (Wessely, 1990), today the line between
physical and mental illness is less distinct. In Psychology Today, James F. Jones, M.D., a
chronic fatigue expert with the U.S. Centers for Disease Control and Prevention says,
"Anybody who has a chronic illness has alterations in biological and psychological
mechanisms. You really can't separate the brain and the body, because psychology is
biology - everything that takes place in the brain is chemical or electrical. You can't
have one without the other" (Schorr, 2005). Herein lies the problem: the very same
culture that wishes to reduce psychology to biology is, nonetheless, still apt to judge
sufferers of contested illnesses as weak-minded or perhaps even morally deficient.
Theoretically, the reductionist model should provide sufferers with the same support -
both social and financial - as currently accorded only to those with "real" or uncontested
diseases (Ware, 1992). The very dualism responsible for great advances in disease treatment and eradication by treating the body mechanistically and separate from the
mind, has become restrictive and limited in response to postmodern illnesses like chronic
fatigue syndrome for which mind-body separation is impossible (Eisenberg, 1977). The
Victorian physician's goal of alleviating suffering by treating both mind and body has been overshadowed by the search for cause and cure. Diagnostic precision has not only
shifted the focus away from the whole person, but has become ever more granular - from noting changes in organs to alterations at the molecular level (Aceves-Avila et al., 2004).
The passing of neurasthenia from disease to illness re-cast perceptions of similar
18 symptoms, such that today CFS sufferers continue fighting the battle to achieve the disease status from which neurasthenics benefited for so long.
Overview of the Current Project
In Chapter One, I document the rise and fall of neurasthenia, the emergence of psychosomatic medicine, and the outbreaks of neurasthenia-like illnesses that led to the recognition of CFS in the early 1980s. The focus of Chapter Two is on how the modernist biogenic/psychogenic framework similarly shaped the etiological theories and treatments of both neurasthenia and CFS, and in Chapter Three, I explore the illness experiences of neurasthenics and CFS sufferers - the meaning ascribed to symptoms by the sufferers themselves, by the doctors on whom they have depended for diagnosis, and by the the respective cultures which have alternately granted disease legitimacy or illness stigmatization on sufferers. While we cannot, as yet, benefit from the historical perspective we can apply to the study of neurasthenia, there are aspects of the neurasthenia story that facilitate our understanding of contemporary illnesses like chronic fatigue syndrome.
19 Chapter 1
Neurasthenia and CFS - An Historical Timeline
Neurasthenia—What it Was and What it Wasn 't
"The symptoms of neurasthenia are legion. It is easier to tell what they are not
than what they are," wrote physician and neurasthenic Margaret Cleaves in the late 1880s
(Cleaves, 1886, p. 167). Beard (1881/1972) himself defined neurasthenia by what it
wasn't - it was not emotional, indicative of intellectual inferiority, or a sign of mental
disorganization. He was quick to caution against confusing unbalanced mental states
with nervousness, likening such confounding to the relationship between idiocy and
insanity. Idiocy, he argued, arose from mental disorganization and a deficient brain,
whereas insanity was actually a disease of the brain; nervousness, for Beard, lay
somewhere between emotional excess and organic disease.
No part of the body was immune from the effects of neurasthenia. The prevailing
late eighteenth-century model that best explains the panoply of neurasthenic symptoms is
reflex theory, which effectively accounted for the connection between mind and body:
"According to reflex theory, each organ system of the body could influence or be
influenced by any other through the medium of the nervous system. Similarly, mental
and physical states were connected via the nerves" (Theriot, 2001). The regulation of body systems, as well as the brain, was through nervous connections running through the
spine - none of which was controllable on a conscious level (Shorter, 1992). As an explanatory model, it suited both physicians and patients - physicians understood how
20 multiple systems could be implicated in disease, and patients could make sense of
symptoms that were otherwise puzzling.
Beard, and most physicians of the time believed that all disease was somatically
based (Rosenberg, 1962; Gosling, 1985) using the term 'functional,' in lieu of organic, to
describe diseases like neurasthenia for which no physical correlate, like a lesion, could be
found: "This term did not carry any of its modern undertones of'psychological' or even
'factitious,' but meant a condition in which no anatomical abnormality of the nervous
system had been detected, that is, the disturbance was one of function" (Taylor, 2001, p.
552). The appearance of a physical disease with an unidentified cause was not problematic for Victorian physicians, who believed scientific techniques would advance
and that organic defect would eventually become detectable (Bassuk, 1986). In the
meantime, using economic metaphors like over-drawn nerve force and likening it to an
electric battery low on reserve force, Beard was able to fashion a disease by drawing on
such timely scientific theories as conservation of energy (Sicherman, 1977). Other neurologists took up Beard's mechanical analogies and incorporated batteries and light bulbs in the growing number papers expounding on the theory of neurasthenia
(Fullinwider, 1974).
In keeping to the realm of the mechanical and physical, Beard and his colleagues adequately distinguished neurasthenia from insanity and were able to steer patients away from the stigmatization of other mental diseases and labels like 'malingerer' (Gosling,
1985). In fact, it was generally agreed that the nervous system was comprised of both higher and lower centers and that neurasthenia was exhaustion of these higher centers, 21 thus affording sufferers a sense of moral superiority (Fullinwider, 1974). Hard work and the over taxing of brain power were to blame for depleted nerve force and the dizzying array of neurasthenic symptoms. "Beard had a gift for expressing social concerns in a scientific idiom, striking a balance between the language of the current scientific discourse, and the concerns and language that were meaningful to the lay reader"
(Wessely, 1994, p. 193-94).
In spite of symptoms that included both the physical and the psychological, it was neurologists who frequently treated neurasthenia, not psychiatrists. Psychiatry confined itself almost exclusively to the management of the insane, leaving the budding specialty of neurology to treat the emotional and somatic symptoms of neurasthenia - an arrangement that suited both patients, who might otherwise have been dismissed, and physicians, who prospered financially and professionally from their new clientele
(Sicherman, 1977). But for neurasthenia to maintain its credibility as a functional disease it had to be delineated from mental disorders with which it shared many symptoms, such as hysteria, hypochondria, and melancholia/depression. Logical inconsistencies, like
Beard's inclusion of hysteria as a feature of neurasthenia, made this difficult, but many nonetheless made the attempt (Wessely, 1990). In an 1894 journal article, Deale and
Adams stated that many writers confuse hysteria and neurasthenia. They made clear the distinction by characterizing hysterics as emotionally excitable with warped intellect, but in excellent physical health, while neurasthenics were intelligent but had been physically and intellectually compromised by their lack of nerve force. Almost a decade later,
Ballet wrote in the 1913 edition of Neurasthenia that its essential feature, exhaustion,
22 made it a somatic disease, while hysteria was a psychical disease characterized by a fixation on certain images or suggestions. However, Ballet did not dismiss the relationship between the mental and the physical, arguing that the neurasthenic state of exhaustion is a predisposing factor in the development of pathological mental states. In
1915, Angell (1915) called hysteria "that half-sister of neurasthenia," (p. 368) characterizing it as the nervous system run amok, in contrast to neurasthenia which was simply a loss of energy. The moral implications were evident in his pronouncement,
"The neurasthenic would, but cannot. The hysteric could, but will not" (p. 368).
Sicherman (1977) also echoed the lack of moral attunement seemingly characteristic of the hysteric and contrasts this with the neurasthenic's more refined nature. Hysteria, long associated with women, incorporated theatric-like fits, choking, paralysis, and trances which led to a great deal of antipathy toward such patients. No doubt physicians' empathy, or lack thereof, influenced diagnosis: "Where neurasthenics seemed deeply concerned about their condition and eager to cooperate, hysterics were accused of evasiveness - la belle indifference - and even intentional deception" (Sicherman, 1977, p.
41). It is unclear whether hysteria and neurasthenia were describing the same set of symptoms and that gender alone was the basis for diagnosing one over the other, as some historians have suggested (Shorter, 1992; Showalter, 1987). That symptoms of other illnesses might overlap with neurasthenia is not surprising given its broad scope, but many physicians of the time nonetheless attempted to maintain its distinctiveness.
Another diagnosis neurasthenics were in danger of attracting was hypochondria.
Van Deusen (1869), who preceded Beard, claimed that hypochondriasis had not been
23 seen in a single case of neurasthenia. Deale and Adams (1894) cautioned against
confusing the neurasthenic with the hypochondriac, stating that the neurasthenic truly had
a disease whereas the hypochondriac simply fears disease: "In the neurasthenic there is
usually evidence of a nerve impoverishment, while the hypochondriac appears healthy
and robust" (p. 193). The hypochondriac not only had imaginary ailments but also had
no desire to get well (Gosling, 1987). Ballet (1913) characterized hypochondria as a
symptom or complication of neurasthenia but acknowledged a time when the two were
confused. His claim that this was beginning to happen again - that neurasthenia was
being characterized as a disease of the imagination - foreshadowed the demise of
neurasthenia.
The mental disorder overlapping with neurasthenia that becomes fascinatingly
similar in the CFS story is melancholia or depression. Nervous exhaustion and
depression were often used interchangeably in early twentieth-century diagnostics
(Shorter, 1992). While in North America melancholia and neurasthenia were compared
on the basis of similar symptom presentation, in Germany they were conceptually linked
with an overlapping diagnosis of neurasthenic melancholia (Misbach & Stam, 2006).
Wessely (1990) cites early descriptions of neurasthenia that incorporated depression, but
by 1893 depression was considered a 'first order' symptom of neurasthenia, although
others maintained that affective changes were the result of organic pathology. Van
Deusen (1869) recognized the association between neurasthenia and melancholia, but
argued that proper medical management could prevent the onset of melancholia in neurasthenics. Ballet (1913) went to considerable pains to argue that melancholia was
24 very distinct from neurasthenia and that any resemblances were but superficial. Stressing the emotional or affective nature of melancholia, he linked it with the emotional side of the mind and related it to lack of will and sluggishness in intellect. Again, the thinly- veiled moral judgments implicit in the diagnosis of psychiatric maladjustments were evident.
Whether or not neurasthenia was delineated from mental disorders like hysteria and hypochondria, together they represented end-of-century problems that were of a non- psychotic nature (Chatel & Peele, 1970-71, p. 36-37). Well known physician Charles C.
Dana (1904) classified neurasthenia as a non-insane psychosis, or a possible pre-cursor to insanity if not properly managed. Despite attempts at maintaining neurasthenia's distinctiveness from psychiatric maladjustment, change was afoot. While Dana did not dismiss neurasthenia out of hand, he argued for a consideration of psychological factors:
I specially urge that the mental state of these patients be carefully examined. The
neurologist needs the help of the psychiatrist here, and I hope it will be given. I
doubt if neurologists, as a rule, know enough of psychiatrical methods to make
always the proper diagnosis of neurasthenia. This ignorance, however, will not last
long and then there will develop a readjustment of our neurasthenic states with a
knowledge of the psyche as a basis as well as of the soma. (p. 341)
The varieties of neurasthenia.
Since reflex theory explained how various body or organ systems could be implicated in disease, different varieties of neurasthenia corresponded to the different body systems. Initially Beard subdivided neurasthenia into cerebrasthenia, exhaustion of
25 the brain, and myelasthenia, exhaustion of the spinal cord (Dowse, 1880). Dowse
expressed doubt that neurasthenia of the brain could exist independently of neurasthenia
of the spinal cord, but expounded on some of the differences in presentation. Brain
exhaustion, he argued, was characterized by symptoms such as memory and perceptual
impairment, lack of purpose, confusion, headache, irritability, cravings, sleep
disturbances, dry mouth, and palpitations. Neurasthenia of the spinal cord was expressed
in the form of weakness in the upper and lower limbs, a burning sensation down the spine,
numbness, muscle pain and stiffness, and fatigue after minimal exertion.
Over time, neurasthenia became further subdivided by grouping certain symptoms
together. Ballet (1913) distinguished four forms of neurasthenia: cerebro-spinal,
neurasthenia of women, genital neurasthenia, and traumatic neurasthenia. Cerebro-spinal
neurasthenia was the most common form, characterized by "persistent headache, vertigo,
insomnia, emotionalism, inaptitude for brain work, rapid fatigue of vision, muscular
feebleness, rachialgia, various neuralgic pains, and gastro-intestinal atony, with or
without precordial anxiety" (p. 93). Within cerebro-spinal neurasthenia, Ballet
recognized Beard's early distinction between cerebrasthenia and myelesthenia, stating
that when cerebral symptoms predominate there is said to be cerebrasthenia, but when
spinal symptoms like back pain, burning in the spine, and loss of motor power are present,
it is a case of myelesthenia.
Neurasthenia of women shared many of the same symptoms as cerebro-spinal neurasthenia, but etiology was linked to the utero-ovarian apparatus, making this type
somewhat distinct. Dowse (1880) also referenced the pressure women faced as a result
26 of their caretaking responsibilities, which could lead to exhaustion: "The dominant
feature of this neurasthenic state is profound discouragement, powerlessness to exert the
will, in one word aboulia, joined to a degree of muscular asthenia that is hardly ever seen
except in this form. The patients tire on the slightest effort, and finally they no longer
dare walk.. .all activity is painful to them" (p. 95).
Genital neurasthenia was the male form of the disease resulting from sexual
excesses like masturbation during adolescence, excessive coitus, and possibly physical
effects of gonorrhoea. Dowse (1880) characterized these neurasthenics as already
mentally unstable prior to becoming neurasthenic and described their symptoms as
"frequent and exhausting nocturnal pollutions, priapism, and speedy ejaculation on
contact.. .real impotence (at a more advanced stage) which however is more psychical
than spinal" (p. 98-99). Disorders of erection and ejaculation carried with them
unpleasant symptoms such as pains in the thighs and loins, burning in the urethra, as well
as other symptoms characteristic of cerebro-spinal neurasthenia.
Traumatic neurasthenia evolved from another nervous illness called railway spine.
Victims of railway accidents presented with nervous symptoms initially explained as
lesions on the brain or spinal cord, but later explained as traumatic neuroses. A link was made to the symptoms of hysteria by Charcot, who recognized the symptoms in men and
women who had been in other types of accidents as well, like falling from a horse or
carriage, or sustaining a blow to the head. What became clear is that their symptoms were not consistent with the degree of injury, leading to the conclusion that their
symptoms had less to do with the injury or shock itself and more to do with the fear
27 associated with the accident: "Traumatic neurasthenia owes its characteristic
physiognomy chiefly to the psychical disorders, which are, at least in typical cases, much
more marked than in the other forms of neurasthenia" (Dowse, 1880, p. 102-103). The
clinical picture of traumatic neurasthenia, however, matched that of the other forms of
neurasthenia. The link between traumatic neurasthenia and the post-traumatic group of
syndromes, which also included Da Costa's syndrome and war neurosis, has been
subsequently noted in the psychiatric literature (Berger, 1973).
Who became neurasthenic?
The gender component of the neurasthenia/hysteria diagnosis problem described
previously is important to address in the broader context of who suffered from
neurasthenia. That both men and women were diagnosed with neurasthenia is clear from
Ballet's (1913) delineation of neurasthenia of women and genital neurasthenia.
Nonetheless, the question of gender distribution was and continues to be contentious.
Abbey and Garfinkel (1991) claim that women were overrepresented, and Showaiter
(1987) asserts that the majority of American neurasthenics were female. Margaret
Cleaves' (1886) early statement supports these contentions: "My object is to consider
neurasthenia as a disease of women. While in no sense peculiar to them, it occurs with
greater frequency among women than among men" (p. 165). Beard believed there were
greater numbers of female neurasthenics, though males presented as the more difficult
cases (Gosling, 1987). To confuse the issue further, claims of gender representation by physicians were confounded by their particular specialty - with gynecologists claiming
greater vulnerability among their female patients (Gosling & Ray, 1986), genitourinary
28 specialists reporting a preponderance of male neurasthenics, and other specialists reporting equal numbers of sufferers (Gosling, 1987).
Other writings of the time present a very different picture. Ballet (1913) stated that neurasthenia was more common in men than in women, but did accord more muscular neurasthenia to women due to their comparative physical weakness and more cerebro-neurasthenia to men. The German literature represents both men and women; the
British picture is more confusing but still does not support the claim that the majority of neurasthenics were women (Gijswift-Hofstra, 2001). Forth (2001) characterizes neurasthenia as first and foremost a condition of men while not denying that many women were also diagnosed. In a late nineteenth-century study by Collins and Phillips
(1899), of the 333 neurasthenics identified, males comprised 55 percent of the sample.
Even as late as 1920, some still ascribed the diagnosis to slightly more men than women
(Cobb, 1920). Perhaps, as many historians suggest, neurasthenia was the male alternative to hysteria (Shorter, 1992; Showalter, 1987; Thomson, 2001; Cayleff, 1988). Jelliffe's
1905 statistics from the Department of Nervous Diseases in the Vanderbilt Clinic partly support this claim. Of the 326 patients with neurasthenia, 194 were male and 132 were female, but of the 77 patients diagnosed with hysteria, 69 were female and only eight were male. Granted, the fewer than one percent of males diagnosed with hysteria supports a clear gender bias, but the 60/40 split in the diagnosis of neurasthenia still suggests that neurasthenia was a disease of both genders.
In addition to gender, class was another predisposing factor in the diagnosis of neurasthenia. Whether true or not, there was an enshrined belief that neurasthenia was a
29 disease of the educated, middle to upper classes (Gosling & Ray, 1986; Rockwell; 1892,
Ballet, 1913; Cayleff; 1988; Wessely, 1990). The literature is rife with examples of the
characterization of neurasthenia as a fashionable disease of the upper classes. Beard, in his first paper on neurasthenia in 1869, labeled neurasthenia as a disease of brain workers.
Rockwell (1892) wrote that the alarming number of intellectuals and professionals in the upper echelons of society with neurasthenia was not reflected among the poor, and Ballet
(1913) stated that neurasthenia was limited to the cultivated classes and was rare among
labourers. However, as with gender, class representation is also contentious. The same
gender bias in the hysteria/neurasthenia diagnosis translated into a class bias such that a member of the lower class would receive a diagnosis of insanity for the same symptom presentation as an upper class neurasthenic patient (Sicherman, 1977). There is evidence, however, that during the 1890s, with growth of public dispensaries and hospitals, physicians were also observing symptoms of neurasthenia in the poor. In Gosling and
Ray's (1986) examination of 232 case studies appearing in the medical literature between
1885 and 1910, 167 of the cases were identified by class. Of that number, 107 were lower class (56 male, 51 female), though it is important to note that the causes of neurasthenia in working-class men were more likely to be ascribed to sexual excess and drug abuse than overwork.
As early as 1899, Charcot began a lecture by saying, "Whenever one speaks of neurasthenia, it seems one is almost exclusively talking about a man from the privileged classes, but it is not the exclusive right of the good and the great, but has extended its empire to the laboring classes" (as cited in Wessely, 1990). Charcot is an example of a 30 physician who, due to both his private practice and work in charity hospitals, was treating men and women of both classes. Physicians like Beard were treating and writing exclusively about members of the upper classes, hence their tunnel vision regarding class distribution. As more physicians began working with working-class and poor patients, there were greater opportunities to recognize neurasthenic symptoms in these groups
(Gosling, 1985). In fact, the medical literature reflected a much greater diversity of patients by class than historians have acknowledged (Gosling, 1987). Nonetheless, causes for neurasthenia were ascribed based on class and empathy for sufferers reflected these attributional biases. Interestingly, gender and class overlapped in that the greatest amount of empathy was reserved for those perceived to be afflicted due to overwork - a group comprised of middle-class men and lower-class women, and the least amount of empathy was shown to those assumed to be afflicted due to bad habits or vices - usually lower-class men (Gosling & Ray, 1987). The plight, and resulting powerlessness, of lower-class women was recognized by physicians, and once both class and gender biases were exposed, the democratization of neurasthenia set the stage for its demise (Gosling,
1987).
The Beginning of the End
Neurasthenia began its meteoric rise at a time of intense rivalry between medical specialties, helping fledgling neurologists establish their practices and earning for them both professional recognition and financial success (Sicherman, 1977). A "made in
America" disease, neurasthenia was exported to Europe where it also became extraordinarily popular, however it was never without its detractors. Its popularity 31 differed across time, regions, and countries, but it was universally viewed as a serious
social problem even though statistics are scarce and the actual incidence rate cannot be determined (Gijswift-Hofstra, 2001). Indicative, though not conclusive, is research by
Taylor (2001), who studied the annual reports of Queen Square Hospital in London from
1870 to 1947:
The diagnosis makes its first appearance in 1886, after which it follows a steep and
almost linear increase, peaking in 1906 at 11% of all discharges. There is a sharp
fall from this peak in 1908, the diagnosis averaging 7.4% of all discharges until
another sharp peak in 1920, and a further peak of 11% in 1928. This is followed by
an abrupt decline down to only 3% in 1930, and 1% in 1935 after which it vanishes,
(p. 552)
In a less empirical attempt but one that supports Taylor's work, Lutz (2001) tracked the frequency of diagnosis against published cases in major journals, concluding that neurasthenia was on the increase in America in every decade and peaked in the 10-year period 1900-1910. While neurasthenia rose very quickly, its decline came much more
slowly and was due to a number of factors.
I suggest the democratization of neurasthenia was instrumental in its decline.
While its social exclusivity made it a rather attractive diagnosis in the beginning (Porter,
2001), it became increasingly clear that neurasthenia was just as likely to be found among members of the lower classes. More significant, however, was its reclassification from a neurological to a psychological entity. Two interconnected factors contributed to this shift: medicine's inability to find an organic cause of neurasthenia as the search for
32 organicity became more central to diagnosis, and the gradual acceptance of Freud's views
of neuroses and psychoses (Gosling, 1987).
The discovery of more sophisticated diagnostic tools like blood tests and
urinalysis were making it possible to diagnose diseases like diabetes (Gosling, 1985), thus creating a demand for the identification of a pathological basis for neurasthenia amid
growing physician skepticism (Gosling, 1987). Neurasthenia, the diagnosis covering a
raft of non-specific emotional, psychological, and nervous symptoms, had become
overinclusive at a time when medicine was searching for specificity in its disease
categories. Even before the turn-of-the-century, Emil Kraepelin (1856-1926) eliminated
neurasthenia as a discrete entity in the fifth edition of his Textbook (1896), though he had
granted it status as a "functional neurosis" in the Compendium of 1883 (Roelcke, 1997).
Increasingly, Kraepelin was searching for discrete somatic causes for disease entities and was among the first psychiatrists to move in the direction of seeking biological causes without consideration of social factors. For decades though, neurasthenia served a useful
function in that it represented a legitimate means of coping with the stresses of late nineteenth-century life (Luthra & Wessely, 2004) and was an outlet for emotional distress that was not actual insanity (Gosling & Ray, 1986). But stressors were changing and
cumbersome diseases that did not lend themselves to the demands of diagnostic
specificity were no longer medically useful. The absence of an identifiable biogenic cause for neurasthenia opened the door to a competing explanatory model, and Beard's nervousness became Freud's neurosis: "Narrow, somaticism had failed, but in its place came 'belligerent Freudianism'" (Wessely et al., 1998, p. 102).
33 Freud was aware of Beard's work as it was cited in the writings of Charcot that
Freud translated in 1886 (MacMillan, 1976). Just one year later Freud himself referred to neurasthenia as "the commonest of all diseases in our society" (Freud, 1887, p. 35) and counted himself among neurasthenic sufferers in letters to Fliess, with symptoms that included tiredness, weakness, and sadness; paraesthesias, sensations of pressure on the head, sensations of drawing or pressing on the muscles; loss of appetite and weight; attacks of weakness, giddiness, indigestion, dyspepsia, and constipation; neuralgias of all kinds; loss of male potency (Freud, 1888). Gradually Freud and others began questioning
Beard's formulation of neurasthenia as a single clinical entity and sought to narrow its definition and, in doing so, take into account the shifting perception that psychological factors could be the cause of neurasthenic symptoms, not the necessarily the result
(Wessely et al., 1998). Thus began the tug-of-war between biogenic and psychogenic explanations of neurasthenia and the gradual unraveling of the neurasthenic symptom complex.
In 1894 Freud attempted to separate neurasthenia from other neuroses, specifically from anxiety neurosis:
In my opinion, it can be nothing but a gain to neuropathology if we make an
attempt to separate from neurasthenia proper all those neurotic disturbances in
which, on the one hand, the symptoms are more firmly linked to one another than
to the typical symptoms of neurasthenia (such as intracranial pressure, spinal
irritation, and dyspepsia with flatulence and constipation); and which, on the other
34 hand, exhibit essential differences in their aetiology and mechanism from the
typical neurasthenic neurosis, (p. 90)
He did not, however, abandon somatic explanations entirely, asserting that both anxiety neurosis and neurasthenia share, as their source, a somatic disturbance rather than the psychical disturbance more characteristic of hysteria and obsessional neurosis. The source of neurasthenia, Freud proposed, was sexual. MacMillan (1976) suggests that neurasthenia may have been the first disorder for which Freud proposed a sexual cause, leading eventually to his theory of sexual etiology of neuroses in general. In the final analysis, neurasthenia was due either to masturbation or interrupted coitus - when normal sexual release was replaced by inadequate release. And, while both anxiety neurosis and neurasthenia were caused by sexual difficulties, anxiety neurosis differed in that it could also be the result of overexertion and exhaustion. In this way, Freud distinguished between neurasthenia and anxiety neurosis, even though symptoms of anxiety could co- occur not only with symptoms of neurasthenia, but also with hysteria, obsessions, or melancholia. Thus neurasthenia became a relatively rare occurrence, placed by Freud in the category of the actual neuroses rather than the psychoneuroses because of its characterization as a disturbance of the physical - not the psychical - component of sexuality (Bunker, 1930). Symptoms of neurasthenia became limited to headaches, spinal irritation, and dyspepsia with flatulence and constipation (Wessely, 1990); symptoms of anxiety neurosis included general irritability, anxious expectation, anxiety attacks, disturbances of the heart action and respiration, sweating, tremors, ravenous hunger, vertigo, and sleep disturbances (Freud, 1894/1956), all of which were formerly
35 among the panoply of neurasthenic symptoms. The separation of anxiety neurosis and
neurasthenia was not complete - there was still overlap between them. Freud referred to
'mixed neuroses' as encompassing both neurasthenia and anxiety neurosis, citing as an
example a masturbating neurasthenic man who becomes engaged and finds himself
sexually excited by his fiancee, thereby adding anxiety neurosis to his neurasthenia.
Freud and Beard differed in their views on the role of sexual factors in
neurasthenia. For Beard, sexual factors were but one of many possible contributors to
neurasthenia; for Freud there were no other factors.
The central mechanism proposed by both Beard and Freud was very similar:
Freud's neurasthenics had been drained of somatic sexual excitation, Beard's of
nerve force. Both theories implied that the loss affected a multiplicity of the
organism's processes. In this respect, Beard's theory was superior to Freud's, for
the reflex model appeared to provide an immediate explanation of the multiplicity
of symptoms. (MacMillan, 1976, p. 389)
However, once the multiplicity of symptoms and their somatic causes were challenged,
the clinical entity that was neurasthenia split apart.
French physician Pierre Janet (1859-1947) also contributed to the dismantling of
neurasthenia. In contrast to Freud, Janet regarded neurasthenia as a psychological
disorder, a neurosis from which obsessions and phobias sprung. Janet coined the term psychasthenia and introduced the concept to the United States (Greenberg, 1990).
Psychiatrist Adolph Meyer (1903) ascribed the term psychasthenia to Janet and
distinguished it from neurasthenia, describing it as "a group of psychopathic and neurotic
36 conditions which comprehends obsessions, impulsions, manias, phobias, scruples, tics, states of anxiety, etc." (p. 363). While acknowledging some overlap with neurasthenia,
Meyer distinguished neurasthenia as a state of exhaustibility and irritability, focusing on physical symptoms like head pressure, heart palpitations, gastric disturbances, and abnormal sexual responsiveness, particularly in men. Williams (1909) similarly distinguished between neurasthenia and psychasthenia, citing disruption of the nerve centers in neurasthenia, in contrast to the "psychical vagaries" (p. 33) inherent in psychasthenia. Donley (1906) too, was clear that obsessions characteristic of psychasthenia were psychogenic in origin, based on previous experience which was either forgotten or not related by the patient to his or her obsession. So while Janet's psychasthenia became part of the larger discourse on nervous disorders, it did not quickly or easily displace neurasthenia. But as the first decade of the twentieth century passed, neurasthenia was losing momentum. In a 1912 book by James J. Walsh, he cautioned against confusing neurasthenia and psychasthenia. Of Janet's psychasthenia Walsh stated,
"It is formed on the model of the word neurasthenia and unless it is used with discretion will have all the objections that attach to that other term.. .Much more can be said in defense of psychasthenia, however than of neurasthenia..." (p. 597).
Gradually neurasthenia was dismembered - Freud removed anxiety neurosis,
Janet detached obsessive-compulsive states and phobias, and others like Jaspers and
Bleuler, postulated that neurasthenia was really depression or anxious melancholia
(Wessely et al., 1998). Eventually, very little was left of the formerly robust syndrome:
"Neurasthenia shifted from a somatic into a psychic diagnosis.. .eventually resulting in 37 the replacement of the language of nerves by the language of neuroses and psycho- neuroses, neurasthenia being reduced to just one psycho-neurotic symptom, namely abnormal fatigue" (Gijswift-Hofstra, 2001, p. 21).
Somatization in a Post-Neurasthenia World
The controversy over neurasthenia as a physiological or psychological disorder not only contributed to its decline, but created a psychiatric culture that became defined by the split (Lutz, 2001). If there was any doubt left that the mind was powerful enough to wreak havoc with the physical body, World War I and the rafts of neurotic, "shell shocked" soldiers left little room to doubt the strength of the psychogenic argument.
With respect to fatigue, the one symptom left to neurasthenia, the psychodynamic interpretation was that fatigue was not a lack of energy, but was misdirected energy resulting from psychic conflict (Greenberg, 1990), psychotherapy being the treatment of choice. And while patients eventually realized that neurasthenia was no longer a free pass to medical treatment (Luthra & Wessely, 2004), they were by no means ready to embrace psychogenic explanations for their physical ailments. Shorter (1992) states the opposite was true: patients insisted their symptoms were somatically based and continued to seek the help of neurologists and internists, not psychiatrists. An unspoken truce, of sorts, was reached between physicians and patients. Physicians, unable to find evidence of organic disease, would nonetheless perform futile operations to appease their patients.
In his paper, "What is Wrong With the Patient Who Feels Tired, Weak and Toxic? "
Alvarez (1935) expressed incredulity at the number of patients coming to his clinic seeking surgery. He stated that many of these types of patients were undergoing
38 unnecessary operations, citing a man who had had eight operations on his colon and
another man who had had ten abdominal operations in nine years. Admitting to having
engaged in the practice himself, Alvarez pleaded with his colleagues to have the strength
to ".. .recognize the nervous breakdown when we see it, and then we must have 'the
confidence and the courage to tell the patient what he has; we must have the sense not to
tinker at teeth or tonsils or hernias or any other little thing we have found wrong..." (p.
98). Analyzing the accuracy of the diagnosis "chronic nervous exhaustion," Macy and
Allen (1933-34) supported the claims made by Alvarez in their examination of the case
records of 235 patients of the Mayo Clinic an average of six years after their diagnosis.
They divided their sample into three groups: the first group never had an organic disease;
the second group had an organic disease but the disease was not responsible for the
original symptoms; and the third group had an organic disease which explained their
chronic nervous exhaustion. This first group, representing 200 patients or 85 per cent of
all patients in the study, had undergone a total of 289 separate operations, with failure to
obtain relief of symptoms in most cases. Alvarez blamed the state of medical training,
which taught medical students to expect organic disease. The emphasis was on the
presentation of rare disease entities, with few if any examples of the neurotic patients
physicians were seeing every day in practice.
As is often the case when the pendulum swings too far in one direction, a reactionary movement surfaces to restore balance. Psychosomatic medicine emerged as a neutralizing force, not by reemphasizing the psychogenic at the expense of the biogenic, but by challenging the very distinction between mind and body. With a long history
39 going back to Hippocrates' link between the humors and personality types (Gottschalk,
1975), the relationship of mind to body has been intuitively understood and applied to the practice of medicine. The mind-body dichotomy is an artificial one that was created to keep religion in control of the soul, philosophy in charge of the mind, and physicians in command of bodily functions (Kaplan & Kaplan, 1956). The separation of mind and body became even more entrenched as nineteenth-century medicine began making scientific progress, with the laboratory serving to de-emphasize the psychological components of sickness and disease. It was in this context that neurasthenia emerged, challenged at the turn of the century by Freud's theory of psychogenic neuroses and the psychoanalytic technique that would re-unify mind and body (Kaplan & Kaplan, 1956).
The concept of psychosomatic medicine challenged the logic of a mind-body distinction and brought together the mental and physical by seeking to discover the relationship between psychological tension and bodily malfunction (Kaplan & Kaplan, 1956).
Dunbar (1934) argued that it".. .is not a matter of "either or".. .there are psychic and somatic components in all illness not merely coexistent but interdependent... What this means is that as the concept of disease is changing, clinicians like exact scientists are entering the period of "both and" in their thinking" (p. 550). Dunbar, too, cited the large number of unnecessary surgeries being performed due to the single-mindedness of physicians. The claim of psychosomatic medicine was that".. .psychic and somatic phenomena take place in the same biological system and are probably two aspects of the same process" (Kaplan & Kaplan, 1956, p. 546), thus some of these surgeries could have been avoided had psychotherapy been done in conjunction with diagnostic testing
40 (Dunbar, 1934). In some deference to psychosomatic medicine, physicians during the interwar years did consider the patient's environment in the clinical context, taking a more holistic, "patient as person" approach (Shorter, 1994). Alvarez (1935) demonstrated this in his presentation of a case in which he criticized the patient's former physicians for depending on laboratory tests to make a diagnosis. "I don't depend on these things.. .1 like to sit down and become acquainted with my patient. I want to know something about her life and I want to know all of the details about how her disease began and what seems to keep it up" (p. 103). Psychosomatic medicine emphasized the importance of the doctor-patient relationship, of listening to patients and making connections between the physical disorder and possible psychological and social factors
(Gottschalk, 1975). It was in this context that the journal Psychosomatic Medicine was sponsored in 1939. But in spite of the movement to break down the barriers between mind and body and recognize the psychological contributors to physical illness, there was still an underlying value judgment or understanding that implied physical cause was preferable to psychological. Even Dr. Alvarez said about his nervous patients:
I seldom have much difficulty with the people because I first try to convince them
of my sympathy for them and my understanding of the problem. I always try to
make them see that I do not question for a moment the reality or the seriousness or
the annoying nature of their symptoms. I tell them I would rather have a broken leg
than go through what they are experiencing, (p. 104)
They resent, he said, the characterization of their symptoms as "nervous" because they felt they were being judged negatively, as silly or hysterical. Patients were clearly not
41 ready to give up their beliefs about the organic nature of their illnesses. And neither were
all physicians, some of whom agreed that psychological factors could lead to lesions or
the disruption of body systems, but that the nature of the tensions was not important
(Gottschalk, 1975). Some individuals were predisposed to physical weakness in the wake
of psychological tension, but this predisposition was somatically rooted. The holistic,
kinder medicine being practiced by many physicians would, once again, be usurped by a
more quantitative, scientific approach by 1950 (Gottschalk, 1975).
The Bridge Between Neurasthenia and CFS
One line of descent from neurasthenia was psychosomatic medicine, which
interpreted excessive fatigue in the context of patients' psychological and social lives.
But there was a second line of descent characterized by a series of illnesses related to
fatigue, seemingly due to biogenic factors - though they, too, became subject to
psychological interpretation (Wessely, 1994). Fatigue-like illnesses were not prevalent
again in the medical literature until 1934, when one of a number of cluster outbreaks was
reported that would emerge periodically until the mid-1950s (Luthra & Wessely, 2004).
Infection was the explanation of choice, and despite lack of evidence researchers
maintained a belief, for the most part, in the organic etiology of these outbreaks and
designated to them names like neuromyasthenia or myalgic encephalomyelitis (Wessely
et al., 1998). These outbreaks represent the link between neurasthenia and chronic
fatigue syndrome.
Chronic brucellosis was often mislabeled as neurasthenia (Imboden, Canter, Cluff,
& Trever, 1959). Acute brucellosis, a genuine bacterial infection spread from animals to
42 humans, emerged in the late nineteenth century and peaked in 1947 (Sauret & Vilissova,
2002). The disease is self-limiting, but some patients continue to experience symptoms in the absence of any physical abnormalities and have been diagnosed with "chronic brucellosis" (Imboden et al., 1959). Chronic brucellosis is characterized by fatigue and weakness, among other subjective symptoms. "As in the neurotic patient, there is hardly a subjective symptom that may not be attributable to brucellosis" (Harris & Kemple,
1954, p. 414-415) and its resemblance to psychoneurosis ensured dispute among clinicians as to its diagnosis. Imboden, et al. conducted a study comparing three groups of brucellosis patients: chronic recovered, acute recovered, and chronic symptomatic.
They reported a significantly higher hypochondriasis score in the chronic symptomatic group; higher depression and psychasthenia scores, as well as high neuroticism and low morale in both chronic groups; and a resistance to discussing personal issues in the chronic symptomatic group. They concluded that chronic brucellosis was effectively an emotional disorder. Harris and Kemple drew a similar conclusion, asserting that patients with a history of acute brucellosis with no evidence of lasting infection exhibit"... a prevailing psychological pattern of hysteria with anxiety, depression, frustrated ambition, suppressed aggression, and sexual inadequacy; and often confusion and difficulty in thinking, suggesting a possible relationship between brucellosis and interference with rational processes" (p. 424). Chronic brucellosis never gained traction as a disease attribution perhaps, as Shorter (1992) suggests, because it could never become fashionable given its association with animals and rural life.
43 Poliomyelitis was another infectious disease that became associated with a series
of cluster outbreaks later linked with CFS. The Los Angeles County General Hospital
experienced an outbreak of "atypical poliomyelitis" among health care workers, mostly
nurses, in 1934 during a polio epidemic, however, it became apparent that the illness they
seemed to have contracted was not polio (McEvedy & Beard, 1970b). They exhibited the
motor and sensory symptoms typical of polio, however their laboratory results were
negative for polio and muscular atrophy was rare. Of the almost 200 cases, no deaths
were reported and complete recovery was the rule (Acheson, 1959).
Another major outbreak occurred at London's Royal Free Hospital in early July of
1955 characterized by headache, sore throat, malaise, vertigo, pain, and stiffness
(McEvedy & Beard, 1970a). From fewer than five cases initially, the number increased
to 100 within two weeks. The hospital was closed on July 25 until early October, with
the total number of cases reaching more than 300. Initially glandular fever was suspected,
but laboratory tests did not support this diagnosis. Polio was then suspected, but as in the
Los Angeles outbreak, there was no diagnostic support. "A new syndrome was defined,
most commonly called 'benign myalgic encephalitis.' This label has been most durable
and was so named because no one died (benign), diffuse muscle pains (myalgia) were prominent, and subjective symptoms were thought to be secondary to brain infection
(encephalitis)" (Aronowitz, 1992, p. 160). Other cluster outbreaks included Akureyri in
Iceland (1948), Middlesex in England (1952), and Punta Gorda in Florida (1956), with almost a dozen more referenced in Acheson's (1959) paper as far afield as South Africa and Australia, and both in and out of hospital settings. Some shared characteristics of the
44 outbreaks included symptoms like headache, myalgia, paresis, mental symptoms, low or
no fever, no deaths, relapses in most outbreaks, and a disproportionate number of women
sufferers. Acheson also noted that in addition to relapses, a chronic state of ill health
developed - which certainly strengthens the link to chronic fatigue syndrome. He also
made a case both for and against classifying these outbreaks as hysterical epidemics,
settling on this summary statement:
The diagnosis (of benign myalgic encephalomyelitis) should therefore be reserved,
in isolated instances, for patients with evidence of acute damage to the brain or cord,
including the characteristic paresis. If not, the syndrome will become a convenient
dumping ground for non-specific illnesses characterized by fluctuating aches and
pains, fatigue, and depression, (p. 591)
The most influential study of the cluster outbreaks came from McEvedy & Beard (1970a
and 1970b) who, retrospectively, questioned an article that appeared in the Lancet one year after the Royal Free epidemic which effectively dismissed hysteria as a possible
explanation. By re-analyzing the case notes, McEvedy & Beard (1970a) concluded that there was no evidence to support organic disease and the most likely explanation for the
outbreaks was epidemic hysteria. A key characteristic cited to support their hypothesis was the high attack rate among females compared with males, as well as the absence of
significant findings - no high temperature, no deaths, no inflammatory response in the blood or cerebrospinal fluid, and no dysfunction of the central nervous system. The onus was on the organicists to prove the outbreaks were biogenic, and they failed to do so. In the final analysis, McEvedy and Beard (1970b) described these cluster outbreaks as
45 "...psychosocial phenomena caused by one of two mechanisms, either mass hysteria on
the part of the patients or altered medical perception of the community. We suggest that
the name "myalgia nervosa" should be used for any future cases of functional disorder
which present the same clinical picture" (p. 11). That some of the patients did, indeed,
have viral illnesses is certain, however, as evidence was compiled it became clear that not
everyone presenting with symptoms was involved in the epidemics (Shorter, 1992).
There was no widespread medical awareness, let alone acceptance, of these
disease entities as was the case with neurasthenia, which may account for why they never
spread (Wessely et al., 1998). That these epidemics can be linked to CFS not only
historically but also medically is questionable, however, in Britain the name did provide
continuity insofar as CFS is still referred to as myalgic encephalomyelitis or ME (the
'benign' was dropped) and supporters continue to argue that these original outbreaks
were organic.
A Mysterious Illness Emerges
Other illness themes emerged from the 1960s on - like candidiasis, food allergies,
and temporomandibular joint (TMJ) syndrome - but none reached epidemic status until
CFS (Shorter, 1992). A given symptom can mushroom into an epidemic by
"appropriating a genuine organic disease - whose cause is difficult to detect or
substantiate - as a template" (p. 305). Shorter cites four separate organic diagnoses,
some with disease status, sharing similar symptoms and appropriated by individuals with psychosomatic illness: neuromyasthenia, the diagnosis of the 1934 Los Angeles County
General Hospital outbreak linked to polio; infectious mononucleosis, which was
46 displaced by its discovered cause, the Epstein-Barr virus; the British myalgic encephalomyelitis; and fibrositis, or fibromyalgia. Fatigue and muscle pain are the two key symptoms common to all, the main difference between the U.S. and British versions is the emphasis on fatigue as the presenting symptom in the U.S. outbreak and muscle pain in the case of the Royal Free outbreak in London. Fibromyalgia was taken on by rheumatologists and has its own controversial history, but debate has been more restrained and limited to the professional arena (Wessely et al., 1998). Similarities between CFS and fibromyalgia exist, however differences in emphasis are apparent - the
CFS focus is on fatigue and the virological and immunological correlates, while the fibromyalgia focus is on muscle pain and inflammation of tender points.
CFS is historically linked with neuromyasthenia and myalgic encephalomyelitis, but became medically linked with the Epstein-Barr virus (EBV). The story, best chronicled by journalist and CFS sufferer Hilary Johnson (1996), begins in Incline
Village, a small town near Lake Tahoe, Nevada, in 1984. Internists and partners Daniel
Peterson and Paul Cheney began seeing a seemingly large number of patients complaining of sudden and intense fatigue, as well as other flu-like symptoms including sore throat, fever, night sweats, swollen lymph nodes, and headaches. The doctors noticed that patients described their illnesses in similar terms and, in spite of running many tests, came up with nothing to explain these patients' illnesses. Peterson began to suspect Epstein-Barr, the easily-transmissible virus responsible for mononucleosis, as well as HIV given the swollen lymph nodes and viral-like symptoms. HIV tests were negative, but patients did have high EBV antibodies. At the same time as Peterson and
47 Cheney began to notice their particular symptom pattern, a number of influential papers
were published linking 'chronic Epstein-Barr virus syndrome' to chronic fatigue. The
confluence of these two events sparked media interest, and an epidemic was born
(Wesselyetal., 1998).
Cheney and Peterson notified the Centers for Disease Control (CDC) when the
number of symptomatic patients reached 120, a number that climbed to 160 by the
outbreak's end (Showalter, 1997). Increasingly diverse complaints were emerging - loss
of sensation in the fingers, numbness in the face, swelling, allergies, cold sores,
mysterious rashes, gastrointestinal complaints, rapid heartbeat, blurred vision, light
sensitivity, ringing in the ears, and loss of libido (Johnson, 1996) - the number and
variety of symptoms appearing remarkably close to Beard's list of neurasthenic
symptoms. Epidemiologists Jon Kaplan and Gary Holmes of the CDC arrived in Incline
Village in September of 1985 to investigate the outbreak. They reviewed 150 patient
charts, examined around ten patients, and attempted to identify a homogeneous group.
Due to the non-specificity of the syndrome, the researchers eliminated all patients with
other medical problems - a controversial move - leaving them with 15 cases for which
no other cause for illness could be ascertained. Of the 15, all were white and 13 were
women.
CDC investigators were bound to draw media attention. A story appeared in the
Sacramento Bee on October 11, 1985, with press coverage growing nationally and even
internationally. The Incline Village doctors received 200 calls in three days from people
all over North America claiming to have the mystery illness: "For those who had been
48 suffering in isolation, particularly those who had been written off by their doctors and
families as hypochondriacs or malingerers or lunatics, the news of the Nevada outbreak
crystallized the nature of their problem. An uncounted population of sufferers
experienced the news as a powerful epiphany: they weren't crazy" (Johnson, 1996, p. 65-
66). Johnson cites other cluster outbreaks, among them Los Angeles, a year before
Incline Village; Yerington, Nevada (1985); Raleigh, North Carolina (1984); Lyndonville,
New York (1985-6); among others.
In May 1986, the first public report on the Tahoe epidemic was released,
concluding that the diagnosis of chronic Epstein-Barr virus (CEBV) should be made only
after excluding other diseases. The report pointed out the overlap in antibody levels
between patients and the general population and also questioned the reliability of the EB
virus test. However, like neurasthenia, in the beginning the etiology of CFS was
presumably organic, hence its initial name, chronic Epstein-Barr infection: "Popular journals reported the results widely, private laboratories promoted EBV blood tests, and
patients began arriving at doctors' doors. During the next three years interest in chronic
EBV infection spread among clinicians, and medical journals generally treated it as a
credible entity" (Aronowitz, 1.992, p. 162). A patient group, the National CEBV
Association, formed in Portland, Oregon in 1986 and, in less than two years, had become
a national group with more than 10,000 members (Johnson, 1996). Support groups
quickly formed in 30 states, and a free national hotline set up in Incline Village was,
within a year, taking 250 calls per day.
49 The CDC skepticism around whether or not CEBV was a credible disease entity persisted. In 1988, Gary Holmes and Jonathan Kaplan, the original CDC investigators,
along with more than a dozen other researchers from across the country, published the
first case definition for the illness known, up to that point, as CEBV. Designed to
facilitate epidemiological studies and clinical research into the illness, the paper also
proposed a name change: "We propose a new name for the chronic Epstein-Barr virus
syndrome - the chronic fatigue syndrome - that more accurately describes this symptom
complex as a syndrome of unknown cause characterized primarily by chronic fatigue" (p.
387). The organic link to EBV was effectively severed. The similar levels of antibodies
found in healthy controls made it near impossible to establish a causal connection between the virus and chronic fatigue syndrome (Koo, 1989). "This semantic vagrancy
had a devastating impact on patients, shifting the illness from one of viral origin, CEBV
(read, organic), to an unknown origin, CFS (read, raised eyebrows)" (Wall, 2005). Initial
medical publications did not explicitly link CEBV with psychiatric problems, but as the
viral link became weaker and weaker, it was inevitable that questions would be raised
(Aronowitz, 1992).
What's in a name?
The history of CFS is almost inseparable from the history of the names ascribed to the illness. The naming issue is not only indicative of certain milestones, but also representative of the controversy that has defined CFS. As different etiological theories have been considered, name changes have been proposed. In 1988, Seymour Grufferman, a cancer epidemiologist who became interested in a virus/cancer link, told sufferers at a
50 conference in Portland, Oregon, "You are not going to get a fair shake if you call yourself the Chronic Fatigue Syndrome Association, because that carries with it a judgment. Your
group should be renamed as well as the disease" (as cited in Wall, 2005, p. 48). His
suggestion for a CFS replacement was chronic fatigue and immune dysfunction
syndrome (CFIDS), which implies an immune disorder as the cause of the illness. The
name was adopted by some groups and individual sufferers and it is still common for
patients to refer to their illness as CFIDS.
Many hoped the CDC revised case definition in 1994 would include a name
change to reflect what the patient advocacy groups considered the more important
symptoms of the illness: cognitive impairment, muscle and joint pain, swollen lymph
nodes, and sore throat (Wall, 2005). However, the Fukuda, et al. (1994) revised case
definition did not include a name change:
We sympathize with those who are concerned that this name may trivialize this
illness. The impairments associated with chronic fatigue syndrome are not trivial.
However, we believe that changing the name without adequate scientific
justification will lead to confusion.. .We support changing the name when more is
known about the underlying pathophysiologic process or processes associated
with the chronic fatigue syndrome and chronic fatigue, (p. 958)
The naming controversy is inexorably linked with the difficulty in diagnosis. A CFS diagnosis is invariably a diagnosis of exclusion: "The absence of other conditions results in a diagnosis of CFS, rather than an affirmation of clinical certainty" (Zavestoski et al.,
2004, p. 167). In both case definitions CFS is identified solely based on symptoms, 51 degree of disability, and the elimination of other possible causes (Prins, van der Meer, &
Bleijenberg, 2006). While there has been no further attempt at updating the case definition, there was one more push for a name change in 1998 (Wall, 2005). A workgroup within the Department of Health and Human Services was tasked with setting criteria against which a new name could be judged. The group presented its proposal in
2001, recommending a new name for CFS: chronic neuroendocrineimmune dysfunction syndrome (CNDS). While it did not imply a causal agent, it pleased patient groups insofar as it better reflected key symptoms. The research community was not as pleased and remained opposed to a name change, resulting in the eventual refusal of the committee to adopt the name change in 2003. In a decidedly postmodern move, patient activists are adopting all kinds of names to describe their illness, some of which reflect newer etiological theories or areas of research: "One woman says she has RNase-L enzyme dysfunction disorder, or REDD. Others use the name postinfectious fatigue syndrome, PIFS. Some say they have atypical multiple sclerosis. Many use ME or
CFS/ME or ME/CFS" (Wall, 2005, p. 194-195). And the turf war over naming crossed the Atlantic. ME and CFS may refer to the same condition, but ME's more medical- sounding label implies an organic etiology, even in the absence of empirical evidence
(Huibers & Wessely, 2006).
There are other cross-cultural differences worthy of note. While neurasthenia is no longer a diagnosis in the North American context after DSM-III (American
Psychiatric Association, 1980) removed neurosis as a category, it is still included in the
World Health Organization's International Classification of Diseases (ICD-10) under
52 'Other neurotic disorders', with a specific exclusion of postviral fatigue syndrome. The category 'Postviral fatigue syndrome' includes benign myalgic encephalomyelitis (ME) under the broader category of 'Other disorders of the brain.' So it is not surprising that
British ME advocates have fought against the U.S. adoption of the ME label for fear that it would negatively impact on their own battle for legitimacy, since ME focuses more on the neurocognitive component than CFS (Wall, 2005). As Showalter (1997) points out, the name does not change the disorder regardless of how medical sounding. "ME is no more life-threatening or lethal than CFS" (p. 124). And, according to Farmer et al.
(1995): "The ICD-10 'neurasthenia' definition identifies almost all subjects with CDC- defined CFS" (p. 503).
Who are CFS sufferers?
Historians can excuse the lack of epidemiological data for neurasthenia. We look at hospital reports, patient records, medical journals, and popular cultural references to paint a picture of how widespread neurasthenia was and who the sufferers were. Some of the problems comparing neurasthenia and CFS cited in the Introduction implied that the same data lacking for neurasthenia would, 100 years later, be available for CFS.
Unfortunately, this is not the case. Valid and reliable epidemiological data on CFS is unavailable (Prins et al., 2006); prevalence rates change based on the diagnostic criteria used (Moss-Morris, 1997); and studies are subject to physician referral bias and differences in health-seeking behavior (Luthra & Wessely, 2004). My comparison of neurasthenia and CFS is interpretive, not medical, however it is interesting to note the
53 similarity in determining the 'who' and 'how many' plaguing them both - a difficulty
common to any protean illness presentation with a questionable etiology.
The initial report of class distribution is common to neurasthenia and CFS. In the
early years of the CFS epidemic fatigue was associated with higher social status, hence
the moniker "yuppie flu" that took hold in the popular press (Wessely et al., 1998). Like
neurasthenia, however, the assumed relationship between high socio-economic class and
CFS was illusory, most likely due to selection bias in published studies (Wessely, 1990).
Incline Village internist Paul Cheney acknowledged the seeming connection between the
professional class and CFS, but questioned the logic of an illness distinguishing whether
or not someone is a yuppie. His explanation was that, "Only people from higher
socioeconomic groups, and highly educated people, have the ability to get through the roadblocks that exit to this diagnosis. It requires persistence, an ability to challenge
medical authority" (as cited in Johnson, 1987a). People with money, he believed,
eventually get a diagnosis. The same class bias factored into the diagnosis of
neurasthenia insofar as the physicians publishing in the medical journals were treating a
clientele who could afford their services. When public hospital records were examined, the prevalence of neurasthenia among the lower classes became readily apparent.
Similarly, when community-based CFS studies were conducted, prevalence rates were
higher among people with less education and lower occupational status (Jason, Richman,
Rademaker, et al., 1999; Reyes, Nisenbaum, Hoaglin, et al., 2003). Earlier studies were based on non-random, medical facility-based populations, which no doubt left out low-
income patients with little or no access to health care (Jason et al., 1999).
54 Overall prevalence estimates based on both studies suggest a rate somewhere
between .142 percent and .56 percent of the U.S. population (Solomon & Reeves, 2004).
However, the most recent study (Reeves et al., 2007) measuring the prevalence of CFS in
Georgia estimates that 2.54 percent of people between the ages of 18 and 59 suffer from
CFS, a rate six to ten times higher than previous population-based studies. Lead author,
Reeves, says that it's not that the incidence rate is rising, but rather that the ability to
identify those with CFS has improved. The CDC estimates that at least one million
Americans have CFS, but claim that fewer than 20 percent of Americans with CFS have
been diagnosed (CFS Toolkit). In a key difference between neurasthenia and CFS,
women - in virtually all CFS studies - are overrepresented (Reyes et al., 2003). Prins, et
al. (2006) report that in most studies, women comprise 75 percent or more of patients,
and in studies depending on physician referrals, more than 80 percent of CFS sufferers
are women, and most are white (Ware, 1999). The 2007 Reeves et al., study reports a
ratio of females to males of 11.2:1. While the neurasthenia literature is certainly
controversial with respect to whether more men or women were sufferers, neurasthenia
was never purported to be a "women's disease." The fact that there were different
varieties of neurasthenia based on gender paints a very different picture from that of CFS.
Some of the same explanations have been cited to explain both neurasthenia and CFS in
women. Shorter (1994) suggests that women's misery is a common theme and that psychosomatic illness transcends time and place. Abbey and Garfinkel (1991) cite a parallel gender dynamic in which women struggle with conflicts around ambition, social roles, and family life, with a retreat into illness a perceived sanction to withdraw from
55 such difficult situations. Other explanations for the preponderance of women suffering
from CFS may or may not apply equally to neurasthenia. Some gender difference is
ascribed to biological variables that seem to predispose women to other diseases such as
lupus, multiple sclerosis, thyroiditis, and rheumatoid arthritis (Komaroff, 1993). Other
explanations suggest that perhaps men and women become fatigued at the same rate but
that women remain tired longer, or that excessive fatigue in women may be explained by
depression (Wessely et al., 1998). Health-seeking behavior is another bias used to
explain gender differences in many areas relating to health and illness (Ware, 1999;
Komaroff, 1993) - women are simply more likely to seek medical care than men.
Conclusion
In this chapter I have set the stage for a more in-depth analysis of neurasthenia
and CFS. Their histories have some commonalities and differences. Both were
presumed to be biogenic in the initial stages; their symptom presentation is remarkably
similar; they were believed to be diseases of the upper classes, a claim subsequently
disproved; and both have been shrouded in controversy stemming from questions
surrounding etiology. Disease attribution was granted to neurasthenia; CFS is still
classified as a syndrome despite activist sufferers' attempts at name changes and their
fight for legitimization. Where neurasthenia was a disease that was demoted when it fell
into disrepute, the CFS history is still being written, thus there is the potential for it to
follow the opposite course and be promoted to disease status. Neurasthenia was not
subject to the same naming problems as CFS. Rather than being renamed, it was dismantled and subsumed by other entities like psychasthenia, the psychoneuroses, and
56 depression. The gender distribution is, I believe, an interesting difference. While some historians have classified neurasthenia as a disease primarily afflicting females - making the comparison between neurasthenia and CFS stronger - that claim has not gone uncontested. Such is not the case with CFS, which has always been characterized as an illness afflicting women in far greater numbers than men. However, a National Institute of Allergy and Infectious Diseases pamphlet (Fact Sheet, 2000) suggests that a more diverse patient group is likely to emerge as more doctors accept CFS as a real disorder.
Having provided a history of the rise and fall of neurasthenia and a bridge linking it to CFS more than 100 years later, in the next chapter I will turn to an analysis of etiological theories and treatments.
57 Chapter 2
Neurasthenia and CFS - Etiology and Treatment
Etiological Theories: The Biological, Psychological, and Social
When dealing with an illness of uncertain etiology, many explanatory theories inevitably emerge. This was as true for neurasthenia as it is for CFS. Many of their etiological theories are remarkably similar and some are different due, in large part, to advances in biomedicine. The modernist approach to understanding disease favored by biomedicine is to identify the somatic processes responsible for symptoms, but the postmodern approach is to at least pay lip service to the more inclusive 'biopsychosocial' framework (Engel, 1977) in which all three classes of factors are presumed to interact to produce disease. Victorian medicine did not overtly adopt a biopsychosocial approach to understanding neurasthenia but, as Engel points out, the identification of psychological and social factors influencing disease transcends sociohistorical boundaries. George
Beard was particularly astute in his consideration of psychosocial variables, along with the biological, in his etiological theorizing. His historical significance is due, in large part, to his psychosomatic understanding of neurasthenia and elaboration of its social and cultural causes (Wiener, 1956). As a postmodern illness, the social construction of CFS has more naturally adopted a biopsychosocial approach. However both the neurasthenia and CFS discourses reference clearly distinguishable biological, psychological, and social factors, some of which are transhistorical, and others of which are contextual.
58 Biological theories.
Beard was influenced by a number of scientific advances and was known to draw upon metaphors from the sciences, like Edison's electric light and the steam engine, to explain neurasthenia:
The nervous system of man is the centre of the nerve-force supplying all the organs
of the body. Like the steam engine, its force is limited, although it cannot be
mathematically measured - and, unlike the steam engine, varies in amount of force
with the food, the state of health and external conditions, varies with age, nutrition,
occupation, and numberless factors. The force in this nervous system can, therefore,
be increased or diminished by good or evil influences, medical or hygienic, or by
the natural evolutions - growth, disease and decline; but none the less is
limited.. .there comes a period, sooner or later, varying in different individuals, and
at different times of life, when the amount of force is insufficient to keep all the
lamps actively burning... this is the philosophy of modern nervousness. (Beard,
1881/1972, p. 98-99)
Rosenberg (1962) describes Beard's conception of the nervous system as a "closed and continuous channel" (p. 249) that could deal with a limited amount of nerve force, which took the form of electrical energy. Consistent with reflex theory, nerve force carried messages to and from different organ systems, and the idea of conservation of energy dictated that nerve force was limited - that energy expended in one area could not be expended elsewhere. Those with inadequate amounts of nerve force were victims of neurasthenia. Silas Weir Mitchell, a physician and colleague of Beard's and well known
59 for his treatment of neurasthenic women, described the physiology of neurasthenia: "In
all probability incessant use of a part flushes with blood the nerve-centers which furnish
it with motor energy, so that excessive work may bring about a state of congestion, owing to which the nerve-center becomes badly nourished..." (Mitchell, 1871, p. 69).
The differing amount of nerve force between individuals was accounted for in a
number of ways. And while Beard is known for his multifactorial approach to the
etiology of neurasthenia he was, like the culture in which he lived, influenced by the
interpretive framework provided by evolutionary theory. That social life was understood
in terms of Darwinian biology was certainly not unique to this time (Roelcke, 1997), thus
neurasthenia was characterized as either congenital/hereditary or acute/acquired. The
former type was based on the assumption that nerve force was inherited, passed on to
offspring by parents. Ballet (1913) called it neuro-arthritic heredity and considered it a
predisposing cause of neurasthenia, above all other possible causes: "the first bough of
the genealogical tree, with its many and busy branches, that represents the neuropathic
family" (p. 36). Iconic physician, William Osier (1912), cited parents who overindulged
themselves in various ways and led irrational lives as possibly transmitting to their
children an inadequacy of nerve force. The late nineteenth-century Collins and Phillips
(1899) study of more than 300 nervous cases stated that more than half of patients
reported nervous disease in their immediate or collateral family, and Deale and Adams
(1894) insisted that heredity as a primary cause of neurasthenia could not be doubted.
The idea that nervous energy was both limited and inherited was an important part of the
neurasthenic model.
60 Today we are much more likely to talk of genetic predisposition than heredity, genes being the mechanism through which heredity expresses itself. Victorian medicine could not elaborate on the "how" of hereditary neurasthenia, but CFS researchers are working at much more finite level to determine genetic factors as possible causes. The most significant CFS study to date has taken a multi-disciplinary approach, leading to a series of papers co-authored by experts in medicine, molecular biology, epidemiology, genomics, mathematics, engineering, and physics, who analyzed data collected from CFS sufferers and healthy controls. Part of the study included an assessment of the activity of
20,000 genes. In lay terms, a press release issued by the CDC (Genetic and environmental factors, 2006) stated, "People who suffer from chronic fatigue syndrome
(CFS) have a genetic make up that affects the body's ability to adapt to change..." One of the physicians involved in the study, Dr. Susanne Vernon of the CDC, stated, "There is a clear biologic basis for CFS, and knowing the molecular damage involved will help us devise effective therapeutic intervention and control strategies." However, in one journal article reporting on the same set of data (Rajeevan et al., 2007), the researchers review past studies associating CFS with Cortisol levels, stating that previous studies found both high and low levels of Cortisol, the stress hormone, not only in CFS subjects, but also in subjects with conditions like CFS and which share similar risk factors, like fibromyalgia, sleep disorders, anxiety, and depression. The conclusion of the researchers was that the study uncovered a potential genetic mediator of chronic fatigue.
A number of media, however, picked up on the CDC studies, with Newsday stating that CFS "is caused by genetic mutations that inhibit the body's ability to respond
61 to stress...Findings from the largest chronic fatigue study to date reveal that certain clusters of genes underlie the syndrome, which scientists now say is indisputably real"
(Ricks, 2006). In O, The Oprah Magazine, readers were told that those accused of being hypochondriacs or depressed now had scientific validation for their illnesses: "People with chronic fatigue syndrome have a genetic quirk that causes them to overrespond to physical and emotional stress" (Fischer, 2006). The article went on to explain that while the healthy immune system is capable of fighting and healing the body, the abnormal gene pattern in CFS sufferers accounts for why certain triggers overload their immune systems and cause symptoms.
A closer reading of the research suggests, as the CDC web site states, "A number of biologic abnormalities have been identified in people with CFS, but how they contribute to the illness is still unclear" (CFS Toolkit). Research continues, but the etiology and pathophysiology of CFS remains unknown, the difficulties being that it
"involves multiple body systems and results from the combined actions of many genes, environmental factors, and risk-conferring behavior" (Vernon & Reeves, 2006, p. 341) and remains "recalcitrant to diagnostic biomarker discovery" (Vernon, Whistler,
Aslakson, et al, 2006, p. 211). With more than a century's worth of advances we are still not able to state that the cause of CFS is biogenic, and we will never know whether the biologic abnormalities found in today's CFS sufferers would, with today's technology, have been equally apparent in Beard's neurasthenics. Nonetheless, heredity as a possible biological cause is implicated in both the neurasthenia and the CFS literature.
62 The other proposed biological cause for both neurasthenia and CFS is infection.
In the early years of the epidemic, CFS was known as chronic Epstein-Barr virus (CEBV) because the etiology was presumed to be this particular viral infection. Even after no causal link between CEBV and CFS symptoms could be established the search for a viral cause continued, the belief being that perhaps a new, as yet unidentified virus was at the root of CFS (Abbey & Garfinkel, 1991). An inciting virus or a reactivated virus was believed to cause the symptoms sufferers were reporting, many of whom claimed their illnesses began with a virus or flu from which they simply did not recover. Scientists searched for a virus similar to that which causes AIDS and a particular type of hepatitis
(Winslow, 1990), but to date no virus has been isolated as the cause of CFS.
Wessely (1990) suggests that in the early years of neurasthenia infection was not considered as a cause, but that advances in bacteriology between 1870 and the turn of the century focused attention on the potential for an infectious origin. Ballet (1913) wrote that influenza was frequently found to be the origin of neurasthenia, that infection reduced resistance and rendered one vulnerable: "It is well-known how capable infective diseases are of deranging.. .the nutrition of the brain, spinal cord, and nerves.. .Thus the majority of the authors who have written on neurasthenia have ranked infective states among its most efficacious causes..." (p. 32). Angell (1915) also cited influenza as a direct cause of neurasthenia, and later editions of Dowse's (1880) book added influenza as a cause (Neve, 2001). In Taylor's (2001) review of the Queen Square Hospital records, references to etiology are very much in line with modern ideas relating to CFS. For example, in the report of 1894: "The recent epidemics of influenza have not only been
63 directly responsible for many of the cases under the head 'neurasthenia' and 'functional paralysis,' but also indirectly by weakening the nervous system, have made patients liable to many other forms of nervous disease, which, but for the antecedent influenza they would probably have escaped" (p. 552). Taylor even suggests that we ought not discount the possibility that neurasthenia's sudden appearance and rather sudden disappearance after 1930 might be consistent with an infectious disease during an epidemic. Post-viral fatigue is very definitely common to descriptions of both neurasthenia and CFS. Even
Beard, in 1869, wrote that, "Acute neurasthenia resulting from acute disease usually recovers rapidly; but sometimes becomes chronic, especially when the previous disease has been long and exhausting" (p. 218).
Immunological considerations are specific to advances in biomedicine and, therefore, to the CFS story. When viral and infectious etiologies were not found, researchers began focusing on the idea that immune system activation resulting in lasting physiological changes was perhaps the result of an acute infection or virus (Demitrack &
Greden, 1991). The patient-inspired name change to Chronic Fatigue and Immune
Dysfunction Syndrome (CFIDS) reflects this idea of an immune system disruption, but represents "a pseudobiological link between inciting virus, life events, and disease"
(Aronowitz, 1992, p. 165). Prins et al. (2006) state that more than half of CFS research between 1980 and 1995 was dedicated to uncovering biological causes for CFS, including but not limited to, viral infections, immune dysfunction, neuroendocrine responses, and central nervous system dysfunction.
64 Physicians treating neurasthenia also pointed to non-viral, external triggers like poisons and toxins (Knapp, 1896; Angell, 1915) including lead, mercury, and copper
(Donley, 1906). While these are less popular and certainly less medically acceptable potential causes for CFS, external triggers that have been hypothesized include dental
amalgam (Luthra & Wessely, 1994), environmental pollutants and allergens (Chronic
fatigue syndrome, 1989), and a host of possibilities cited by Dr. Chris Meletis, chief
medical officer and dean of Clinical Education of the National College of Naturopathic
Medicine in Portland, Oregon which include brucella, giardia lamblia (a bug found in
water close to camp sites or other areas close to human fecal waste), and even certain prescription medications (Brown, 2001). Wessely (1990) points to another biological
correlate common to neurasthenia and CFS - the idea of autointoxication in which
decayed or poisonous substances leak out from the colon and cause disease in other parts
of the body. Alvarez (1935) referred to his nervous patients experiencing a feeling of
autointoxication, treating them with enemas to keep the colon clean, a practice similar to today's colonic irrigation.
Biological correlates that reflect historical discontinuities between neurasthenia
and CFS include the Victorian preoccupation with reproduction and the reproductive
organs. To account for neurasthenia in women Angell (1915) included excessive childbearing or prolonged lactation among the many direct or indirect causes of neurasthenia and Ballet (1913) referred to certain genital disorders and "utero-ovarian affections" as the starting point or first cause of neurasthenia. But while CFS researchers would not link the illness to pregnancy, lactation, or disorders of the reproductive organs,
65 the preponderance of female CFS sufferers suggests some commonality to the illness experience. Shorter (1994) suggests that women's greater unhappiness transcends historical boundaries and that women have always been more apt to express unhappiness through their bodies. Whether this is biological or cultural or some combination of both is unclear - somehow gender becomes part of the social construction of illness, seemingly irrespective of sociohistorical shifts. The rate of psychosomatic illness,
Shorter points out, has remained stable even though women's lives have changed dramatically. The Victorian view that the seat of women's problems was the reproductive organs was open to scientific refutation (Theriot, 1993), thus CFS researchers have had to shift their focus to other possible biological explanations for the overrepresentation of women sufferers.
Psychological theories.
When the search for a biological basis for neurasthenia dead ended, the emphasis shifted to psychological theories. There was also a move away from earlier hereditarian explanations as evidenced by AngelPs writings in 1915 in which he claimed a curious lack of patients predisposed to neurasthenia based on family history. As discussed in the last chapter, there was some debate over whether or not neurasthenia was really just melancholia or depression, and when neurasthenia as a disease complex was dismantled, depression subsumed a number of sufferers who would previously have been diagnosed as neurasthenic. From the standpoint of psychological theories, the strongest link between neurasthenia and CFS is this confounding with depression. In a foreshadowing of the psychosomatic vs. somatopsychic debate plaguing CFS and depression - is chronic
66 fatigue simply a function of depression or do the debilitating physical symptoms of CFS lead to depression - Dowse wrote in 1880 that,
the action of mind upon body, and body upon mind, is co-existent. And if I
maintain, that the healthy mind or individual character can be, and is influenced
by constitutional causes, on the other hand I am quite inclined to hold that a
previously healthy body, evincing no especial tendency to any functional
derangement can, by excessive mental strain, be so acted upon as to become
functionally diseased; then the enfeebled and disorganized body reacts upon the
previously diseased mind, leading to the worst form of obscure, and even of
readily recognized, nervous diseases, (p. 38)
Dowse did link mental derangement with some kind of molecular derangement of the brain cells thus giving it a somatic interpretation, claiming that despite the relationship between mind and body there was a distinction between what he called psychic force and nerve force. Ballet (1913) also made this link when he stated that exhaustion could equally affect the psychical functions and the nervous functions.
With CFS, as the idea of lingering infection was increasingly called into question, some researchers claimed that a very high percentage of CFS sufferers also met the criteria for a psychiatric disorder (Moss-Morris, 1997; Greenberg, 1990). Given that fatigue has long been associated with depression, it is not surprising that these researchers reinforced this association (Wessely et al., 1998). To confound things further, "many of the epidemiological features of the common psychiatric disorders resemble those of fatigue - the over-representation of women, the particular risk for younger adults and the 67 negative socio-economic gradient, and the associations with demographic factors such as
divorce, unemployment, and having young children at home" (p. 84). The absence of a
diagnostic marker for CFS leads to this circularity because fatigue is a key symptom in so many psychiatric disorders (Demitrack & Greden, 1991). As Greenberg (1990) points
out, neurasthenia played a role in our current psychiatric classification of depression - not
surprising given that chronic fatigue was a key symptom and no organic etiology for neurasthenia was ever uncovered. Depression is not the only psychological symptom associated with fatigue; fatigue is a component of other psychiatric presentations as well
(Wesselyetal., 1998).
Other research challenges the link between CFS and depression. Studies comparing CFS sufferers and control groups found that depressive disorders were present in a minority of the CFS groups (Wessely et al., 1998). The confounding of CFS with psychiatric disorders can be attributed, in part, to differences in case definitions, settings in which patients are seen, and the instruments used to detect psychiatric disorders, leading to both over- and under-diagnosis of psychiatric disorders (Prins et al., 2006).
There is also no consensus on the role of somatization in CFS. On the one hand, fatigue and weakness are key features of somatization disorder - somatizers present with physical symptoms and are resistant to explanations linking their symptoms with psychological stress - but on the other hand, somatizers are less depressed than those presenting with psychological complaints (Wessely et al., 1998).
Since the pharmacological revolution that began in the late 1950s, biomedicine is increasingly open to the idea that psychological disorders have biological roots. In this
68 case, then, whether depression is psychosomatic or somatopsychic becomes irrelevant - depression as an organically based disease allows for an organic reframing of CFS (Ware,
1992). However, the CFS literature consistently demonstrates that sufferers share an attribution bias; an insistence that their illness is physically based, and as a rule are highly resistant to any hint of psychiatric involvement (Moss-Morris, 1997). Sufferers interpret their depression as either a part of the syndrome itself, a symptom like any other, or as the understandable result of coping with years of debilitating illness (Ware, 1992).
Depression is an effect, not a cause. Researchers don't deny that an acute illness may have triggered symptoms, but argue that psychological response may perpetuate the illness, turning it from acute to chronic (Wessely et al., 1998). Sufferers then begin a vicious cycle in which physical deconditioning becomes confused with ongoing disease -
sufferers rest in order to recover from the illness, but too much rest results in deconditioning, which leads to more physical symptoms. Prins et al. (2006) cite other illness perpetuating factors like "strong belief in a physical cause of the illness; strong focus on bodily sensations; poor sense of control over complaints; social processes like solicitous behavior, (and) lack of social support" (p. 349). Increasingly, CFS is being understood as 'multifactorial' - neither physical nor psychological, but arising from a complex interaction between mind, body, and social factors (Banks & Prior, 2001).
Personality as a predisposing or perpetuating factor in neurasthenia and CFS is another shared theme. Donley (1906) contended that unstable personality, or the inability to synthesize conscious states was, in its mildest form, neurasthenia. As personality disintegrated further, more serious forms of psychopathology resulted such as hysteria
69 and dissociated or multiple personality. Meyer (1903) cited emotional weakness and lack of emotional control as constitutional factors leading to nervousness, Angell (1915) contended that overreaction to impressions and undue irritability led to the weakening of nervous energy characteristic of neurasthenia, and Fullinwider (1974) refers to "morbid introspection" (p. 7) as a cause or a symptom of neurasthenia. Anxiety as a common factor predisposing one to neurasthenia was cited in Van Deusen's writings as early as
1869. The overlap between CFS and generalized anxiety disorder (GAD) and episodic anxiety is also common to the CFS literature (Wessely et al., 1998), suggesting that those prone to panic attacks or anxiety are more likely to express themselves somatically. Here again the line between biological and psychological become blurred. Are the personality factors common to sufferers of chronic illnesses based in biology?
A recent twin study (Kato, Sullivan, Evengard, & Pedersen, 2006) suggests certain personality traits relating to emotional instability and the ability to manage stress may increase risk of developing CFS. "Elevated pre-morbid stress is a significant risk factor for chronic fatigue-like illness, the effect of which may be buffered by genetic influences. Emotional instability.. .is associated with chronic fatigue through genetic mechanisms contributing to both personality style and expression of the disorder" (p.
1267). To further confuse, stress can change cellular immunity thus predisposing one to viral assault and further stress (Teague, 2007).
Another recently published study (Heim et al., 2006) claims a key risk factor for
CFS is childhood trauma, with two-thirds of the CFS group reporting childhood experiences of emotional, physical, or sexual abuse or emotional or physical neglect
70 compared with one-third of the non-fatigued group. However, the researchers implicate biology in prevention recommendations by suggesting future research examine not only the psychological, but also the neurobiological mechanisms linking adversity in childhood to CFS. This message is making its way to lay audiences as well. The Oprah magazine article on CFS (Fischer, 2006) quotes CDC researcher Suzanne Vernon as saying, "Early life adverse events - abuse, neglect, longterm malnutrition - can really mess us up and change the architecture of the brain."
What is common to the illness experiences of neurasthenics and CFS sufferers when psychological factors are believed to be implicated is that they are in some sense responsible for either the onset or the perpetuation of the illness. If neurasthenics could assert control of their mental states and CFS sufferers could alter their illness attributions and better cope with stress, then perhaps distress would not be expressed somatically.
Social theories.
George Beard wrote a great deal about the particularities of late nineteenth- century life and how aspects of social organization contributed to nervous exhaustion. In this oft-quoted passage from Beard's American Nervousness (1881/1972), he distinguished what made modern civilization so different: "The modern differ from the ancient civilizations mainly in these five elements - steam power, the periodical press, the telegraph, the sciences, and the mental activity of women. When civilization, plus these five factors, invades any nation, it must carry nervousness and nervous disease along with it" (p. 96). Changing ideas around work, the role of women, scientific advancement, and the perception that life was moving at a much faster pace led to the 71 impoverishment of nerve force and, thus, enhanced nervousness. That the pressures of modernity increased the stresses of daily life were reflected in the culture:
The man finds his work no easier, but rather multiplied, by the assistance of
telegraphs, telephones, and railways, and the racket and noise which accompany
his labours are infinitely increased. Add to this the tension which comes of
attending to too many interests at the same time, and it is not difficult to believe
that the nerves of modern men are often put to a heavier strain than nature
intended them to bear. (Nerves and nervousness, 1894, p. 11)
By replacing the telegraph, telephone, and railway with the fax machine, computers, and jet travel, this passage could just as easily been written about the late twentieth century.
Perhaps it is transhistorical to believe that the present is necessarily more stressful and fast-paced than the past. In referring to the advances of the nineteenth century, Beard claimed they "made it possible to transact a hundred-fold more business in a limited time than even in the eighteenth century" (p. 116), a claim as true then as now if one compares the late twentieth century with Beard's time.
It became part of the cultural narrative to accept increasing nervousness as a price to be paid for progress - not that progress was considered wholly beneficial. With progress came upheaval and existence had become more of a struggle due to changing social, political, and economic conditions. Social critics questioned the ability of increasingly weak men and women to cope with the stresses of urban life in particular, while also recognizing the link between the pace of life in big cities and the benefits of progress (Bresnahan, 2003). The question was whether humans would evolve to better 72 cope with the nervous exhaustion that had become so characteristic of the times. Beard believed they would. His prediction was that by the turn of the century, neurasthenia would have peaked and begun its decline as people adapted to the demands of what would eventually lead to a better society (Rosenberg, 1962). He was only partly right - neurasthenia did decline, but not for the reasons Beard predicted.
The emergence of CFS could be construed as contradicting Beard's prediction.
There wasn't anything particular to the late nineteenth century that didn't manifest similarly in the late twentieth, and evolution does not appear to have improved our ability to adapt to rapid social change. Wessely (1990) points out that other than the problematic mental activity of women, all the other social factors Beard believed contributed to neurasthenia can be found in the CFS/ME literature, citing descriptions of the illness as
'particular to the twentieth century' (Maclntyre, 1989) and 'an overload disease unique to this century' (Steincamp, 1989). Because of their numbers, baby boomers ("yuppies") were forced to work longer and harder in order to successfully compete in the labor market, which only served to ratchet up the pace of life (Ware & Kleinman, 1992). And, similar to the questions around gender roles in the late nineteenth century, women from around the 1970s were being encouraged to combine family and career in an attempt to
"have it all," which also served to fuel the treadmill-like existence that characterized the
1980s and still continues. The invalidism that became a way of life for many middle- to upper-class women of the late nineteenth century, which historians have attributed to issues like taking on too much in a man's world (Haller, 1970), the strain of nursing sick relatives (Gosling & Ray, 1986), and demands for education and fulfilling work
73 (Showalter, 1987), echo more recent claims that overcommitted women struggling with social-role confusion have unconsciously sought relief by assuming the sick role
(Richman & Jason, 2001). Not surprising, the most at-risk population for CFS is young to middle-aged women juggling the demands of home, work, and community (Ware,
1999). The overlap between the social and psychological is evidenced by the psychiatric interpretation of CFS as the unconscious attempt to disengage from the overcommitted, overburdened life sanctioned by the culture in which we live. Slow down by taking on a different culturally sanctioned role: the role of a person with a chronic disease.
Certain lifestyle concerns are common to both the neurasthenia and CFS discourses. The number of bad habits that could lead to neurasthenia were legion.
Rockwell (1892) cited indolent habits and overeating and suggested exercise and activity instead of rest. An article in the popular magazine, The Spectator, goes so far as to say about the neurasthenic, "His discomforts are not those of the well-bread racehorse that has been overtrained, but of the stalled-pig that has been overfed" (Nerves and nervousness, 1894, p. 12). In contrast, Beard (1869) mentions as a cause "civilized starvation, such as is sometimes observed even among the wealthy order of society" (p.
218). Bad habits and substance abuse were very prevalent in the literature as contributors to neurasthenia. Beard (1869) referred to abuse of stimulants and narcotics; Collins and
Phillips (1899) to indulgence in alcohol, tobacco, tea, coffee, narcotics and other intoxicants; and Weir Mitchell (1871), listed a number of habits which could overexcite the nervous system like eating unwholesome foods, eating and sleeping irregularly, and overindulging in smoking and late-night amusements.
74 A notable difference between neurasthenia and CFS is the focus of the former on the bad habits and excesses of individuals, the moralistic implications clearly apparent.
The CFS literature is focused much less on individual culpability and much more on environmental factors like overuse of antibiotics, foods manufactured with yeast and refined sugars, allergens, as well as pollutants of all kinds (Abbey & Garfinkel, 1991).
As a group, CFS sufferers are less likely to look at the effects of their own behavior, rather focusing on external agents like a virus or pollution (Moss-Morris, 1997). Perhaps the difference is due to the modernist focus on individual morality and culpability, in contrast to the postmodern critique of rampant individualism and the resulting consideration of how social and environmental factors impinge upon the health of individuals.
One final area of difference was Beard's (1879) contention that climate was a predisposing etiological factor in neurasthenia, especially in regions subject to both extremes of temperature: "The rapid evaporation in our dry, out-door air and in our overheated rooms.. .heightens the rapidity of the processes of waste and repair in the brain and nervous system, and the exhausting stimulation of alternations of torrid heat and polar cold" (p. 722). These conditions, he believed, were particularly prevalent in the northeastern United States. Collins and Phillips (1899) wrote of a nervous system
"bombarded by impulses far more intense than that of other people" (p. 473) due to the dry atmosphere in North America which, in combination with the vicissitudes of urban life, overstimulated neural circulation.
75 Clearly the recognition of biological, psychological, and social factors implicated in both neurasthenia and CFS led to certain commonalities in etiological theories proposed for both illnesses. The Collins and Phillips study (1899) was a perfect example.
Of the 123 cases of neurasthenia for which a cause could be listed, the biological, psychological, and social were all represented. Attributed causes, in order of prevalence, were: overwork, masturbation, worry, fright, childbirth, sorrow, traumatism, previous disease, and alcohol. The CFS story began with the presumption of a biological cause but, in the absence of any clear biological marker, included psychological and social considerations. The more recent research suggests that the etiology and pathogenesis are multifactorial (Prins et al., 2006), which turns the question of etiology on its head. If legitimacy is conferred on a set of symptoms such that they form a recognized disease entity, uncertainty as to the source of the symptoms can only lead to controversy.
Neurasthenia did not survive intact; CFS might benefit from the tendency to reduce even the psychological and social to biology.
Treatment Strategies: Biological, Psychological, and Social
Since etiological theories encompassed the biological, psychological, and social, so do treatment strategies. When illnesses are defined by symptoms and causes are indeterminate, as is the case with both neurasthenia and CFS, medical treatments are generally aimed at the alleviation of symptoms. Psychological treatments become mired in the cause/effect conundrum and are somewhat more contentious, and treatments aimed at the social contributors to illness are necessarily more difficult to effect and sustain,
76 having more to do with personal lifestyle changes than systemic modifications to social structures.
Biological treatments.
Perhaps because Victorian medicine presumed an organic etiology for neurasthenia - whether or not it could be conclusively revealed - there were a wide range of treatment options available relative to CFS. Linked to the proposed etiologies relating to the sexual and reproductive organs, neurasthenics were often treated surgically. Reflex theory provided justification for these surgeries and localized treatments - with women being the recipients more often than men. It is historically inaccurate, however, that only women were subjected to what now appear to be unnecessary, dangerous procedures
(Parsons, 1977). Sexual excess in men, especially frequent masturbation, was believed to re-direct nerve force to the sexual organs at the expense of the brain and spinal cord.
Parsons lists many treatments to which men were subjected in order to restore balance, including plaster casts, leeching, acupuncture needles in the testes, blistering, electricity applied to the genitals, internal electrodes in the rectum and urethra, cauterization, internal chemical injections, and in the most extreme cases, castration. The most drastic operations performed on women were ovariotomies and clitoridectomies, but local treatments using caustics, leeches, and cautery irons were also common (Shorter, 1992).
Gosling and Ray (1986) suggest that doctors and patients were co-conspirators - doctors were able to specialize and believed they were adding scientific credibility to neurasthenia by treating it surgically, while patients demanded that doctors acknowledge the veracity of their symptoms and do something to effect relief.
77 As barbaric and unnecessary as many of these procedures seem in retrospect, treatment of this type served a legitimating role. Sufferers were taken seriously, though whether these treatments actually relieved symptoms was a matter of debate. According to Shorter (1992), women accepted the premise of reflex irritation and often demanded procedures that would remove the source of their problems, and Theriot (1993) goes further in suggesting that some women feigned nervous symptoms in order to justify operations to render them sterile, thus knowingly preventing further pregnancies.
However, as competing psychological theories arose to explain neurasthenia, the wisdom of surgical procedures in its treatment was questioned. Reynolds (1910) called these operations "disastrous" because patients were subjected to great harm, with no change in their neurotic tendencies. But Reynolds did not call for a wholesale abandonment of gynecological surgeries:
The radical removal of the pelvic organs is, in my experience, of benefit to
neurasthenic symptoms only in women who are past the menopause.. .In young
women our effort should be to remove the disease without injuring the
organs.. .we must never forget that the operative treatment of the local lesion by
itself rarely dissipates neurasthenia of any considerable degree, (p. 115)
The focus on surgical treatments for neurasthenia, and especially on procedures aimed at both the male and female sexual anatomy, was specific to neurasthenia. Women justifiably viewed their reproductive responsibilities as troublesome, however, refutation of the connection between the reproductive organs and neurasthenic symptoms led to what Theriot (1993) describes as "a neurological/psychiatric theory of invisible
78 femininity" (p. 24) predicated on the male notion of repression, which blatantly disregarded women's own perceptions of symptoms and causes. As pointed out in the first chapter, surgeries were still very common among both males and females well into the 1930s. The rise of the psychological paradigm rendered certain somatic symptoms no longer amenable to surgical interventions, thus it is not surprising that no surgical treatments for CFS have ever been proposed.
More common to neurasthenia and CFS is the use of drugs to alleviate symptoms.
For neurasthenics, drugs were most often used to either stimulate the central nervous system or to treat pain (Gosling, 1987). Dowse (1880) listed quite an assortment of medicines and supplements to treat nervous exhaustion: opium to excite brain cells; arsenic; phosphorous; strychnine; salts of bromine, zinc and iron; quinine; chloroform; sulphur; and nitrate of silver, among others. Deale and Adams (1894) cautioned against the overuse or misuse of drugs, wanting "to avoid transforming the unhappy neurasthenic into a hopeless inebriate" (p. 195). They cited dubious results with such elements as arsenic, cannabis, caffeine, cocoa, zinc, the bromides, opium, alcohol, the mineral acids and the phosphates.
Similarly, drugs used to treat the symptoms of CFS include anti-inflammatory medications and pain relievers for muscular discomfort (Coulter, 1988) and tricyclic antidepressants for both pain and sleep problems (CDC Toolkit). A physician contributor to the The National CFIDS Foundation web site (Goudsmit, 2000) advises sufferers not to believe media reports on antidepressants, citing their potentially beneficial effect on the immune system and their ability to help with pain, sleep problems, and mental 79 disorganization. Another patient support group, CFIDS Association of America
(Treatment: medical), includes in their section on medical treatment, over-the-counter pain relievers like aspirin, Ibuprofen, and acetaminophen.
Beard's (1869) neurasthenia treatment strategies centered on the use of electricity and he described its effects as twofold: "First, the electric current may directly improve the quantity and quality of the vital force, in accordance with the theory of the correlation and conservation of forces. Secondly, the violent and repeated muscular contractions that are produced during the operations of general electrization greatly increase the processes of waste and repair" (p. 219). The use of electricity had a dual purpose - it satisfied the patient that the physician was actually doing something to relieve symptoms, and it enabled physicians to incorporate modern technology into treatment (Gosling, 1987).
Different types of current were used to stimulate the nervous system as well as aid in sleep and digestion, but the use of electricity was in decline by 1910. CFS sufferers complain equally of loss of energy, so it is not surprising that similar versions of Beard's electrization have emerged - replacing energy with energy makes a certain amount of sense and there are reports of some doctors using electromagnetic therapy and galvanic currents in treatment (Wessely et al., 1998).
The use of water was another popular treatment for neurasthenia, with some physicians arguing its superiority over electricity. Hydriatic procedures included cold ablutions, the dripping sheet, the spray, and the simple douche (Collins & Phillips, 1899).
Hydrotherapy was thought to have a relaxing effect, calming the mind and facilitating sleep, with water also being applied via enemas and sponge baths (Gosling, 1987). 80 Neurasthenics were advised to bathe often to "stimulate the skin to renewed activity"
(Deale & Adams, 1894, p. 194), while Beard (1884) combined electricity and water in a
treatment called a faradic bath in which the patient sat in water through which an electric
current was run.
Though medical in nature, cures were never promised. One male neurasthenic
writing anonymously (The autobiography of a neurasthenic, 1896) summed up the
problems in treating contested illnesses with no known cure:
I tried them all, from medicines, to electric belts, crayons inserted in urethra,
medication by rectum, etc., and steadily got worse.. .nearly two months with
magnetism.. .one month with galvanism.. .three months taking animal extracts.. .1
have tried self application of electricity, both magnetism and galvanism... I have
also tried preparations of phosphourus, strychnia, damiana, saw palmetto, etc., but
these never did me any good.. .(p. 369)
Psychological treatments.
Our current understanding of psychotherapy is an outgrowth of the response to late
nineteenth-century theories of the psychoneuroses, or non-organic mental disorders
(Gosling, 1985). After the turn of the century, skepticism with respect to the organic
origins of neurasthenia was building and, in turn, treatment strategies shifted toward the
psychological. This shift was subtle in terms of patient perceptions - physicians allowed patients to believe they were receiving organic therapy but took advantage of the doctor- patient relationship to engage in gentle persuasion or suggestion (Shorter, 1992). It was not untoward at that time for physicians to "re-educate" their neurasthenic patients as part
81 of a treatment program, doing so with both patience and empathy and the belief that individuals could direct their thoughts toward improving their health (Gosling, 1987). By
1913, Ballet wrote: "All authors agree nowadays in recognizing the importance of psychotherapy in the treatment of nervous asthenia" (p. 178) and described it as a re education designed to help "the mind to correct certain erroneous perceptions" (p. 181).
However, Ballet was not willing to subscribe to the idea that psychotherapy was the only treatment for the psychoneuroses as he still maintained that there was both a physical and psychical component to the disease.
On the leading edge of psychotherapeutic techniques were European physicians like
Dubois (1848-1918) of Berne, Dejerine (1849-1917) of Paris, and Bernheim (1840-1919) of Nancy. Dubois (1906) named his approach "rational persuasion" and believed neurasthenia, hysteria, hysterical neurasthenia, hypochondria, and melancholia - the pure psychoneuroses - were all amenable to this type of psychotherapy. Suggestibility, he believed, was exaggerated in these patients, so therapy relied on reason to stop unhealthy suggestions and replace them with thoughts of self-mastery. Through the moral influence of the physician, patients could heal themselves through the application of reason.
The psychotherapeutic techniques of Dejerine and Bernheim are described by New
York physician, Evelyn Garrigue, who visited their clinics in Paris and Nancy and wrote of her experiences in the Woman's MedicalJournal in 1909. Dejerine, who succeeded
Charcot at the Salpetriere in Paris, was a friend of and very much influenced by Dubois.
Garrigue described how Dejerine examined patients, ensuring the absence of organic lesion, and used his persuasive powers without the use of drugs or hypnotism. In 82 describing Dejerine's treatment, Garrigue wrote: "The patients are taught to exert self- control and that many symptoms they believed outside of their control are entirely within it" (p. 28). In contrast, Bernheim was described as using hypnotism, as well as drugs to treat pain, fever, and to stimulate the heart. He countered the criticisms of Dubois and
Dejerine, who claimed he was putting his thoughts into his patients, by arguing he was taking away their fears and making them use their own powers. What Dubois and
Dejerine described as their use of suggestion, Bernheim called re-education. The themes common to both approaches were the belief that patients, with the help of physicians, could direct their thoughts toward achieving self-control and that there was a moral imperative to do so. Garrigue described it as a matter of will power: "The physician can and must point out the road and be guide and director to the goal of health, but the moral responsibility of getting there and remaining there lies with the patient" (p. 30).
Cognitive behavioral therapy (CBT) is one of the few treatments for CFS that has been demonstrated to have some positive effects. Remarkably similar in theory to rational persuasion, CBT is one of the mainstays of CFS treatment. Not unlike neurasthenics, CFS sufferers are encouraged to challenge illness perceptions and coping responses which can perpetuate symptoms (Moss-Morris, 1997). A somatic attribution bias and the ensuing belief that activity is harmful are two key illness perceptions CBT is aimed at altering. Two trials of CBT have demonstrated a marked improvement in symptoms and functioning, especially when the belief that activity is harmful is altered
(Sharpe et al., 1996; Deale, Chalder, Marks, & Wessely, 1997). CBT has enabled patients to gain some control over their symptoms and there is also evidence suggesting 83 that neuroendocrine abnormalities may be corrected after successful CBT (Prins et al.,
2006). Some researchers have been careful to point out that treatment can be effective even when a cause is unknown, however, the use of anti-depressants and anti-anxiety drugs, coupled with CBT, can easily be construed as framing CFS in psychiatric terms
(Richman & Jason, 2001). CFS patients have been resistant to CBT as they still adhere to the belief that the success of CBT necessarily infers a psychogenic cause of CFS (Prins et al., 2006). Accepting psychiatric treatment is perceived as stigmatizing, however, the dismissal of psychiatric treatments may be a factor in the poor prognosis of CFS
(Wessely, 1994).
One question that has been raised in relation to the use of psychological treatments for CFS is whether improvement is due to a placebo response. Physicians treating neurasthenia may not have had a name for it, but became increasingly aware of the psychical benefits of physical treatments and of the power of standalone psychological treatments (Gosling, 1987). More contemporary research suggests placebos are ideally suited to conditions consisting of very subjective symptoms for which no biological cause can be found, like CFS, headaches, allergies, digestive disorders, depression, and anxiety for example (Cho, Hotopf, & Wessely, 2005). In a study comparing CFS with other medical conditions, Cho et al. hypothesized that placebo response in the CFS group would be unusually high given the subjective and fluctuating symptom presentation and unknown etiology. In fact, in a systematic review of published studies, the pooled placebo response was lower than the projected one-third. The interesting result of the study was that placebo response differed based on type of intervention. Given the
84 somatic bias of CFS sufferers, it is not surprising that the highest placebo response rates were to infectious-immunological and alternative-complementary interventions and the lowest placebo response rate was to psychological-psychiatric interventions. The interpretation of the results suggest that low placebo response could be related to low expectation. Given that CFS is very difficult to treat, sufferers may have lower expectations of treatment success than sufferers of other illnesses. As well, the strained relationships between CFS sufferers and medical professionals due to different illness interpretations may play a role because a more collaborative patient-clinician relationship is related to placebo response.
Some of the issues raised by this study are being addressed. In the CDC's CFS
Toolkit aimed at medical professionals, there is a stress on how important it is for patients to believe the therapy can be beneficial. Physicians need to counter the public misperception that CFS is "all in the head," which makes patients resist interventions like
CBT. The CDC recommendation to physicians includes:
Assuring patients that you are aware that research indicates that there is an organic,
biologic basis for chronic fatigue syndrome and educating them about the role CBT
plays in other illnesses can help overcome this reluctance. When patients realize
that CBT is used as an adjunct therapy for cardiovascular disease, diabetes, cancer,
orthopedic injuries, and other medical conditions, and that CBT may help CFS
symptoms, they are more likely to be receptive to this therapy.
85 Social or lifestyle treatments.
Perhaps the most extreme of the treatments for neurasthenia designed to address social roles and lifestyle was Silas Weir Mitchell's rest cure. Because of its attention to all facets of the neurasthenia symptom complex, there were elements of the treatment related to the biological and psychological, but I've chosen to categorize the rest cure as a social/lifestyle treatment because of its focus on diet, rest, and seclusion. Mitchell
(1877/1907), who treated women almost exclusively, also proposed a modified rest cure for men. He felt it was of the utmost importance to separate neurasthenics from their surroundings, household duties, habits, and "from contact with those who have been the willing slaves of their caprices" (p. 50). He argued that the mere removal of neurasthenics from their moral and physical surroundings was curative in itself, though this was not always financially possible. Lutz (1991) describes the differences between this type of treatment for women and men: "The rest cure for women and its enforced infantilization and isolation.. .and the exercise cure for men, with its rugged outdoor sports and other public activity, are clear indications that cure was designed in response not to a specific pathology but in response to ideas of man's or woman's place" (p. 20).
The cornerstones of Mitchell's (1908) treatment were seclusion, rest, massage, full feeding, and electricity. In extreme cases, the patient was to stay in bed anywhere from six to eight weeks: "At first, and in some cases for four or five weeks, I do not permit the patient to sit up, or to sew or write or read, or to use the hands in any active way except to clean the teeth" (Mitchell, 1877, p. 66). In order to keep muscles stimulated he relied on the use of massage as a form of passive exercise, which also
86 increased the flow of blood to the tissues and, he believed, increased the production of red corpuscles. He also used faradic electricity to exercise the muscles, recommending slowly interrupted currents as more easily tolerated by the patient. The medical rationale for the rest cure was to build up the patient's supply of fat and blood (Showaiter, 1987), thus Mitchell's reliance on the milk diet. Ballet (1913) described the dietary overfeeding recommended by Mitchell as beginning with a milk diet:
The patient drinks four or five pints of milk daily, taking half a pint at a time
every two hours. After seven or eight days of milk diet she takes a light lunch at
noon, consisting of a cutlet. Then, at the end of three or four days more, the
amount of food is progressively increased by adding a slice of bread and butter
two to three times a day. About the tenth or fifteenth day the invalid takes three
complete meals, but still drinks three or four pints of milk. (p. 358)
Rest cure patients were under the care of a private nurse and were visited regularly by their doctors. Important characteristics for physicians implementing the rest cure were "an eye for detail, earnestness, firmness, tact, patience, persistence, and an ability to determine and implement the sick room" (Bassuk, 1986, p. 143). Once physical vigor was restored, advice and talks with the physician would help patients achieve control over their emotions (Mitchell, 1908). That such treatment would be expensive and inaccessible for anyone of the lower classes is clear. However, a modified rest cure in hospital, aimed at the lower classes, included tonics, bromides, massage, and a special diet which included milk, cream toast, eggnogs, and alcoholic beverages; many patients reported having enjoyed their hospital stays (Sicherman, 1977).
87 The success of Mitchell's rest cure is debatable. Therapeutic effects were reported but many patients remained ill after taking the rest cure (King, 1989), however,
British physician, William Playfair, successfully restored many invalid women to full health using the rest cure (Showalter, 1987). It was generally accepted that the rest cure was successful for around 30 years, until psychotherapy became the treatment of choice, thereby calling into question the need for and advisability of excessive rest for a condition whose biological basis was in question (Wessely, 1991).
The amount of rest necessary, balanced with a suitable amount of exercise, was considered in the treatment of neurasthenia. Collins and Phillips (1899) recommended exploring hilly or mountainous areas by walking, climbing, or donkey riding, but acknowledged the difficulty in determining which forms of exercise were most suitable to women. Ballet (1913) cited the need to introduce activity slowly when treating invalids who were extremely feeble, but that activity should be progressively increased. It was this idea of graduated exercise that was proposed to overcome the extreme fatigue that threatened the recovery of neurasthenics (Wessely, 1990). Wessely cites Fernand
Lagrange as being associated with this graded, but steady increase in activity: "physical exercise, gentle and not excessive, but progressive in nature, provides the best method of treatment" (author's translation, p. 46).
Other treatments for neurasthenia included visits to spas, the seaside, or the mountains which, not only offered a rest from the vicissitudes of daily life, but addressed some of Beard's concerns relating to climactic factors influencing neurasthenia. Dowse
(1880) wrote that "change of air and scene and diet, if not carried out to excess or fatigue,
88 is one of the most important aids to the cure of neurasthenia which we have at our command" (p. 57). Deale and Adams (1894) concurred with the advice to travel, but questioned whether the change of scenery or the change in meteorological conditions was more beneficial.
In terms of addressing the social conditions which were thought to be causing this rise in nervous disease, Garrigue (1909) wrote of prevention: "Our practical work in prophylaxis to stem the tide of increasing insanities and neuroses goes still further in this age of rapid pace with soul-destroying competition and unsatisfied personal ambition. As
Prof. William James expresses it, "It is no small matter to inoculate seventy millions of people with new standards; yet if there is to be any relief, that will have to be done"" (p.
33). That CFS has also been linked with the social pressures relating to the rapid pace of life and competition, suggests James's advice was not heeded.
No comprehensive treatment protocol reminiscent of Weir Mitchell's rest cure has ever been proposed for CFS but there are, nevertheless, many overlapping treatment strategies, primarily with respect to diet, rest, and exercise. Veering into the realm of alternative or complementary therapies, dietary adjustments purported to relieve CFS symptoms include megavitamins and mineral supplements; elimination, avoidance, and rotation diets - none of which has been supported by evidence (Morris & Stare, 1993).
CFS sufferers have been encouraged to avoid yeast and sugar to combat Candida overgrowth, as well as food additives and preservatives. Morris & Stare suggest that the popularity of dietary therapies is that diet is a lifestyle element over which people feel like they have some control. Other suggestions are found in the popular press and from 89 patient advocacy groups. In the Nutrition Health Review (Stoff, 1990) a low-fat diet is recommended which is purported to strengthen the immune system, and vitamins and supplements are also encouraged, somewhat reminiscent of the regimen suggested for neurasthenics. The National CFIDS Foundation also supports limiting sugar and fat, but also adds alcohol, red meat, and anything fried (Goudsmit, 2000).
Rest is another treatment strategy common to neurasthenia and CFS, the theme of supply and demand of energy running through both discourses (Wessely, 1994). Citing an American self-help book with a section entitled, 'Rest, Rest and More Rest,' and its focus on aggressive rest therapy (Feiden, 1990), Wessely points to the parallels with the
Weir Mitchell rest cure. And Ware (1993) refers to a restful state common to CFS sufferers who, after becoming ill, have given up the stress of their frantic pace of life and limited their activity in a way reminiscent of the late nineteenth-century rest cure. In a book describing her experience as a CFS sufferer, Dorothy Wall (2005) says: "It's maddening to think I've become the enforcer of Dr. Mitchell's stultifying regime... with my regulated routine of healthy meals and rest" (p. 90). Her description of a typical day is remarkably similar to that of a female neurasthenic a century earlier.
And while some CFS sufferers have become permanent invalids, the form of therapy believed to prevent this and improve function is also similar to that which was proposed for neuarasthenia: Graded Exercise Therapy (GET). GET is a personalized exercise program in which intensity of activity is increased based on individual ability.
With treatment options so limited, the most efficacious treatments thus far studied are
CBT and GET (Whiting et al., 2001). GET is a purely physiological treatment designed 90 to prevent muscular deconditioning, while CBT, which always has a graded exercise component, also focuses on shifting cognitions relating to illness interpretation and optimal activity levels which may account for the higher rates of improvement reported in CBT studies (Prins et al, 2006).
Conclusion
The etiological theories of and treatments for neurasthenia and CFS reflect similar frameworks for understanding and treating illnesses for which no discernable biogenic cause can be established. The initial presentation of somatic symptoms led to a biogenic etiological assumption in both cases - presumed in the case of neurasthenia for upwards of three decades, and initially linked to the Epstein-Barr virus in CFS. The modernist search for certainty and truth through science has driven the categorization of symptoms as either biogenic or psychogenic in both neurasthenia and CFS. It is not surprising, then, that in the absence of biological proof, both became subject to psychosocial etiological interpretations. If, as Dowse (1880) suggests, humans have not changed much physiologically over the centuries, somatic expressions of distress should share certain fundamental characteristics. As paradigms like reflex theory are abandoned and replaced by the psychological paradigm, differences in etiological theories and treatments are inevitable. But given the overlapping symptomatology of neurasthenia and CFS, their similarities are more apparent than their differences.
Etiologically, discourses focusing on heredity and genes, the overlap with depression, and the social changes contributing to the stresses of living a fast-paced, competitive existence were invoked for neurasthenia and are seen again in CFS. There
91 are also similarities in some of the treatment strategies, such as medications to treat symptoms; psychotherapy; and diet, rest, and exercise. Based on my reading of the literature, it appears the prognosis or recovery rate for neurasthenia was more positive than is currently the case for CFS, which may be due to what Theriot (2001) argues was the success of placebo-related cures in the nineteenth century, like having ovaries removed and taking the rest cure.
I alluded to illness representations in the context of both the somatic attribution bias of CFS sufferers and in relation to the use of CBT to challenge illness perceptions.
Illness representations is the theme of the next chapter, which will analyze the effect of diagnosis on the experience of illness, the legitimization of disease and stigmatization of illness, changes in the doctor-patient relationship and how those changes have impacted the social construction of illness, and the relationship between the chronically ill and the broader culture.
92 Chapter 3
The Socio-cultural Shaping of Illness Representations
For any disease, diagnosis begins with both patients and physicians, which necessarily makes it a co-construction. The balance of power in this co-construction has not been static. Neurasthenia and CFS stories exemplify a shift in this balance of power and, hence, a very real change in doctor-patient dynamics. Diagnosis not only names a symptom complex for medical purposes, but also influences its interpretation in the wider socio-cultural context and the degree to which sufferers are either legitimized or stigmatized.
While the case for CFS as neurasthenia revived may be substantiated by their similar symptom presentation, and may even hold up based on etiological theories and treatments, the similarities between the neurasthenia and CFS narratives, or the lived experiences of the neurasthenic and CFS sufferer, are not as congruent. It is true of many other illnesses and diseases that time, as an intervening variable, will always change the sufferers' experience even when etiology is uncontested. The interesting question is how illnesses that share so many symptoms take on diverse meanings in different sociohistorical contexts.
Negotiating Diagnosis
In a modernist context the power distribution in the doctor-patient relationship clearly favored the doctor: "One knows, the other feels; one prescribes, the other complies; one is paid, the other pays" (Morris, 1998, p. 38). In the postmodern world,
Morris argues that the sources of medical knowledge, like laboratory tests and research 93 studies, do not tell the whole story. The subjective experience of illness, or the illness narrative, ought to be a resource for physicians as well. In the case of neurasthenia, illness narratives constituted the basis for diagnosis - doctors and patients worked collaboratively in order to diagnose and treat the disease. Nineteenth-century medical knowledge was gleaned from patients' self-reported symptoms and input from family and friends; diagnosis was a social interaction of sorts (Theriot, 1993). Definitions of health and illness were co-constructed and physicians and lay people learned from each other.
In order for the diagnosis and treatment of neurasthenia to move forward, however, certain conditions had to be met. As a diagnosis, the neurasthenia label was acceptable to both physicians and patients (Sicherman, 1977) but for treatment to be effective there had to be some give and take on both sides: "It is absolutely necessary that the physician be able to gain the confidence of his patient and assume an uncontested authority over him. For this purpose he must at the very first interview listen patiently and with apparent interest to the sometimes very long recital of the troubles experienced by the neurasthenic..." (Ballet, 1913, p. 200). The right degree of firmness, almost severity, was necessary for the patient to accept the doctor's superior judgment. Patients' authority was in the telling of their stories, which was key to the diagnostic process, then patient compliance with the prescribed treatment was the expectation of the physician:
"Nineteenth-century case histories and reports of cases indicate that physicians and patients constructed a "modern" form of interaction that served both parties' interests, an interactive style based on physicians' authority and sympathy and on patients' honest and thorough report of their problems" (Theriot, 2001, p. 356).
94 Patient compliance was especially evident in Weir Mitchell's rest cure in which the doctor assumed a paternal role and required complete acquiescence from patients such that a trust was built; the doctor-patient rapport itself became integral to the cure
(Bassuk, 1986; Marland, 2001). Doctors' writings were full of references to the importance of sympathetic listening, especially in cases where etiology was unclear and there was both a physical and mental component to the illness (Theriot, 2001).
Compliance was not granted in all cases. One of the most well-known rest cure failures was social critic Charlotte Perkins Gilman (1860-1935) who, after almost succumbing to a nervous breakdown as a result of Mitchell's 'cure,' wrote the short story, "The Yellow
Wallpaper," which first appeared in the 1892 issue of The New England Magazine and described the fall into madness of the female protagonist. In a later piece entitled, "Why I
Wrote The Yellow Wallpaper" (1913), Gilman recounted how she followed the advice to live a domestic life, limit intellectual activity, and not write again. For three months she complied and came near to madness. It was only when she ignored the advice and went back to work that she regained both her sanity and her power. She sent a copy of The
Yellow Wallpaper to Weir Mitchell, who apparently never acknowledged it. However,
Gilman was later told that he had, in fact, altered his treatment of neurasthenia after reading The Yellow Wallpaper.
The compliance of patients was also evident in their apparent rush to be operated on in order to relieve symptoms. Shorter (1994) uses stronger language, describing it as a collusion between doctors - who sought scientific validity and monetary gain - and patients - who prided themselves on their "modish" diagnosis and the socioeconomic 95 status necessary to pay for their operations. In the interests of both attracting a biological disease diagnosis and avoiding the label hypochondriacal, neurasthenics were desperate for treatment and a restoration of mental health (Gosling & Ray, 1986). Beard understood the effect of the mind on the body but preferred somatic treatments to psychical or moral treatments, believing it important to assure patients their symptoms were very real and that they were in no way were malingerers, thereby engaging the patient's trust and acceptance of traditional therapies (Rosenberg, 1962). Other physicians of the time, like Collins and Phillips (1899), were well aware that if the doctor-patient relationship was not solid patients would seek so-called cures by Christian scientists and other fakers. To prevent this, they were clear in how neurasthenics were to be treated:
As a rule, it may be said that a patient with neurasthenia should be examined and
treated with the same attention to detail as a patient with typhoid fever or
endocarditis. That such careful examination and methodical treatment encompass a
cure, in part or largely through their appeal to the mind of the individual, in no way
detracts from them as tangible therapeutic measures. On the contrary, there is all
the more reason for their utilization, (p. 421)
The co-construction of the neurasthenia diagnosis and its treatment worked for both physicians and patients and was evident in the overlap between lay and medical views of health and illness during the Victorian era (Davis, 1989). After the turn-of-the-century and the emergence of the biomedical illness model, however, a shift began: "The importance of the patient's interpretation began to diminish. The bedside medicine
96 model... with its emphasis on patients' explanations and interpretations of their symptoms, was superseded by the hospital and laboratory models" (Lupton, 1994, p. 84).
The doctor-patient dialogue of the late twentieth-century has taken on a very different form. Laboratory results and clinical examinations have largely usurped the role of patient narratives in the diagnosis of disease, changing the very nature of the doctor-patient relationship (Theriot, 2001). Where nineteenth-century physicians were encouraged to take the time to listen to the patient's story, to have patience and empathy, physicians treating CFS patients are charged with accurately diagnosing symptoms in a comparatively short period of time. The patient narrative has come to be viewed as a digression, an interruption, and possibly even irrelevant (Mechanic, 1995). Physicians, in large part, still practice with a modernist mindset, seeking to maintain the assumed superiority of medical knowledge and authority over patients. From the standpoint of patients, however, their idolization of physicians gave way to mistrust with the consumer movement of the 1960s (Shorter, 1992).
While the neurasthenia diagnosis served the interests of both physicians and patients, no such accommodation has been reached between CFS patients and their physicians. The fight over the name has been representative of the conflict between the two factions - physicians have sought to retain their authority over naming disease entities, arguing that the name given to the symptom complex must not imply etiology, while patient-advocates have fought for a name change, in the absence of which they have taken to adopting whichever name best suits, for example, the name of a leading advocacy group which calls itself the Chronic Fatigue and Immune Dysfunction
97 Syndrome (CFIDS) Association of America. In the CFS documentary film, I Remember
Me (Snyder, 2001), sufferer and soccer star Michelle Akers says about the name: "The name chronic fatigue syndrome, I think sucks. I think there could be a better name.
Chronic fatigue, I mean like I've read in a book, you know would you name cancer 'big tumor in your body,' or pneumonia 'coughing disease'? I mean, it's like naming an illness after one of its symptoms, it doesn't, it doesn't give the disease or the illness credibility" (29:14-29:45).
The battle between patients and the biomedical establishment is very much centered around the authority to define disease (Aronowitz, 1992). Sharpe (1998) suggests that physicians are unwilling to capitulate to patient demands for a biological diagnosis in the absence of a biological cause because they are reluctant to give up their power in the relationship, they wish to maintain medical integrity, and are fearful of both worsening symptoms and standing in the way of potentially helpful non-biological treatments. The reality of CFS is disputed within the medical profession, which is also well illustrated in the film I Remember Me (Snyder, 2001). Dr. Peter Manu, psychiatrist at Hillside
Psychiatric Hospital, says to director Kim Snyder of the controversy surrounding CFS:
"The syndrome is controversial, and it's controversial for a relatively simple reason Kim, that is, it's a syndrome that has no cause that has been defined, has no abnormalities on physical examination, and has no specific set of laboratory abnormalities either" (26:27 -
26:44). In response, Nancy Klimas, an Immunologist/AIDS researcher at the University of Miami says: "Doesn't it make you crazy that we're 10 years into this and we've published 855 articles on the Medline when I checked last week and, to say there's no
98 physiologic abnormality? I'm sorry, the problem is which physiologic abnormality do you feel like focusing on?" (26:45 - 26:59).
CFS patients have fought for a diagnosis - but not just any diagnosis. The absence of a biological marker and the inevitable shift toward psychosomatic explanations for
CFS created a battleground, with patients much more likely to accept a biomedical diagnosis than a psychiatric one (Sharpe, 1998). The frustration of CFS sufferers is illustrated in a story related by Hilary Johnson, herself afflicted with CFS, in her 1987a
Rolling Stone article. She describes a conversation with a fellow sufferer who was subsequently diagnosed with cancer:
After the months spent in what she described as the "fog" of CEB V, a cancer
diagnosis came as a relief, she said. Finally her suffering was "validated," her
doctor would take swift and serious action. Having endured surgery and
chemotherapy, she said that she is more afraid of a recurrence of CEBV - which
seems to have gone into remission - than of cancer, (p. 58)
Johnson describes the medical ignorance and frequent misdiagnosis of CEBV, claiming she began to understand her strange array of symptoms after undertaking her own research.
This theme of patients becoming "lay experts" is common and is illustrated in a study by Clarke (2000) reporting that two-thirds of sufferers have relied on their own research to better understand their disease, its symptoms, and treatment options. The maxim 'nature abhors a vacuum,' could not apply better to the rise of lay expertise in the absence of clear medical consensus. CFS patients will either seek out physicians who
99 share their illness beliefs or will self-diagnose, which only serves to exacerbate the hostility between physicians and patients (Huibers & Wessely, 2006). Illness attribution by patients is not new, but in the past they have been open to competing medical interpretations (Shorter, 1995). What is historically unprecedented, according to Shorter, is the fixity of patient belief, an unwavering certainty that they know what they have.
That certainty emphasizes the somatic: "Patients often construct narratives of physical aetiology. References to earlier fevers, infections, and thyroid problems are frequent.. .it is in the virus theory of infection that we truly meet the nub of the contest between patients and physicians" (Banks & Prior, 2001, p. 16). Illustrative of the breakdown in the doctor-patient relationship is this story of a CFS sufferer: "I've been fired by doctors," said Arlene Rubb, a 58-year-old Rocklin woman who believes her illness was triggered by an aerobics class and made worse after a car accident in 1982. "We are too hard to treat. We don't fit into a box" (Griffith, 2006).
This strain in doctor-patient relations has taken a postmodern turn. While a diagnosis of neurasthenia often resulted from a doctor-patient collaboration, the self- diagnosis of CFS and patient constructions of etiology have created rifts between patients and medical professionals, with each side arguing for knowledge superiority. Patients perceive their subjective experience of symptoms as privileged knowledge doctors cannot access, and have interpreted the inability to uncover a biological etiology for CFS as a clear failure of biomedicine (Peters, Stanley, Rose, & Salmon, 1998). A CFS sufferer since late-1979, Pat McCloud describes the experience of going from doctor to doctor looking for answers. They all agreed that something was wrong, but they did not know
100 what: "If they don't understand what it is, they will say you're stressed out; maybe you're working too hard. And I'm going, this is a bunch of garbage. There is something wrong with me. I mean who knows your body better than yourself?" (Snyder, 2001, 48:43-
48:56).
A co-construction seems possible, so long as both parties are searching for biomedical causes - a preoccupation of patients who fear disease but are seeking an explanation for their somatic symptoms, and of physicians who are trained to search for somatic causes and fear the legal consequences of missing a medical diagnosis (Bensing
& Verhaak, 2006). Taking on the role of patient is to submit, and this submission requires inherent trust in the doctor-patient relationship (Hadler, 1996). This was understood by neurasthenic patients, who submitted to the doctor's authority because the relationship was mutually respectful, based in no small part on the physician's willingness to consider the primacy of the patient narrative. The message sent by physicians to CFS patients is that their illness narratives are unreliable. CFS sufferer,
Dorothy Wall (2005), sums it up nicely: "There are two stories of illness, that of the patient and that of the doctor, and both deserve thoughtful attention. They remind us that medicine is an interpretive art, not always a science, and that a physician's interpretive act can have damaging as well as helpful consequences" (p. 128).
There was a give and take in the doctor-patient relationship characteristic of neurasthenia that is missing in CFS. An unspoken exchange of sorts, such that patient compliance was assured once trust between doctor and patient was established - the building of trust coming not only as the result of the relatively uncontested nature of 101 neurasthenia, but also due to the patience and empathy exhibited by the physician in listening to the patient's narrative. It is the contested nature of CFS that challenges the doctor-patient relationship. Nancy Klimas, MD, works with both AIDS patients and CFS patients and describes the difference: "My AIDS days are uplifting compared to my chronic fatigue days. And that's saying a lot, I have to tell you. My AIDS patients walk in and I know what's wrong with them; I know what the intervention should be; I know exactly where I stand with the patients and so do they" (Snyder, 2001, 47:05 - 47:25).
Even the most devastating of illnesses, if etiologically uncontested, make for better doctor-patient relationships than those that are also devastating but contested.
The distinct absence of diagnostic tests for neurasthenia prevented the battle for etiological and diagnostic authority that typifies CFS doctor-patient exchanges and makes a co-construction of CFS very difficult. Clarke (2000) describes the search for a diagnosis and the propensity of CFS patients to label doctors good or bad: "The "good" doctor may not be able to diagnose the disease but still believed the patient. The "bad" doctor is the one who doesn't take the symptoms seriously, doesn't believe the lay person or suggests that it is "all in his/her head"" (p. 83). Some patients find a doctor who is at least open to learning from them, while other will travel hundreds of miles just to find a doctor willing to give them a CFS diagnosis (Clarke & James, 2003).
The Importance of Diagnosis: Legitimacy or Stigmatization
The importance of diagnosis is that it confers legitimacy on a set of symptoms, ends patient uncertainty, and can itself be considered an active intervention leading to treatment (Huibers & Wessely, 2006). The absence of a diagnosis, or a psychosomatic
102 diagnosis, calls into question the patients' suffering and symptoms, leading to the stigmatization that results from the inference that the symptoms are not real and/or that patients are to blame for their illnesses (Wessely, 1994). Diagnosed with CFS at age twelve, Heidi Pask questioned her own perceptions: "When you feel that bad for so long you think that some of this has got to be in my head because it's just, it's too bad.
There's no way; nobody can feel this bad and still be alive" (Snyder, 2001, 17:03-17:11).
When describing why she embarked on the CFS documentary, I Remember Me (2001), filmmaker and sufferer Kim Snyder says: "I took on this project because of my own need for answers and because I was hearing about so many people that were suffering from the physicality of the illness, but they were suffering almost as much from ignorance and from the treatment by society" (51:33-51:52).
Neurasthenia, when it was accepted as a pathological condition, conferred on its sufferers a legitimate right to be sick - especially when it was believed to be linked with overwork (Gosling & Ray, 1986). Thomson (2001) suggests market forces were at work to legitimize neurasthenia in that upper class patients would not accept a stigmatizing diagnosis. From the physician standpoint there were remedies at hand to treat neurasthenia - diet, drugs, rest - that in actuality were psychological but carried no patient-blaming implications: "The great strength of neurasthenia in the late-nineteenth century had been that it satisfied the interests of both doctors and medical consumers" (p.
84). However, it would be inaccurate to suggest there was no stigmatization associated with a neurasthenia diagnosis. Because they looked healthy, neurasthenics were often treated unsympathetically (Beard, 1880), though always less so than hysterics and those
103 perceived to have acquired neurasthenia from less-than-praiseworthy means (Gosling &
Ray, 1986). A popular press editorial from 1894, for example, was rather harsh in its critique of neurasthenia: "Doctors would be well advised if they could invent some other term for the genuine cases of nervous-breakdown through overwork and mental worry, and leave the word "nerves" to be discredited and gradually grow disgraceful in the mouths of these weaklings. If only nerves were looked upon as something shameful to confess, much fewer people would suffer from them" (Nerves and nervousness, p. 12).
Examples from popular fiction were often critical of neurasthenia and its relationship to modern society (Lutz, 1991). Lutz cites many examples of the nervous breakdowns and the deaths of characters in books like Fran Norris's The Pit (1903), Edith
Wharton's House of Mirth (1905), and Theodore Dreiser's Genius (1915). Interestingly, in Silas Weir Mitchell's many works of fiction, a number of his female characters were unsympathetically portrayed as nervous, manipulating invalids (Wood, 1973). Wood points out that Mitchell did not doubt the veracity of their illnesses, however, he believed women would become ill when they did not act in ways befitting their feminine role.
Neurasthenic writers were not uncommon and fiction "was a major forum for the articulation, dissemination, and elaboration of neurasthenic discourse..." (Lutz, 1991, p.
29). Neurasthenia was not just common to writers; neurasthenics traveled in intellectual circles that included the likes of William and Alice James, Jane Addams, George Eliot,
Herbert Spencer, and Charles Darwin (Haller, 1970). One could, as a neurasthenic, hold one's head high in society (Gosling, 1987). And, in addition to fiction, non-fiction works on neurasthenia garnered popular appeal - both Beard and Mitchell were extraordinarily 104 successful with their books, some of which became best sellers (Wessely, 1989). The ubiquity of neurasthenia was evidenced by representations in magazines, fiction, poetry, newspapers, medical and scholarly journals, as well as in advertisements for cures, nostrums, and spas (Lutz, 1991), and its cultural consequences cannot be underestimated:
"The people who were central to the production and reproduction of the discourses and practices of sociology, politics, charities, history, education and other fields were very often themselves neurasthenic, and had a view of nervous energy and civilization very similar to Beard's..." (p. 7).
The legitimacy conferred on neurasthenia began to wane as turn-of-the-century changes in the doctor-patient relationship began favoring the doctor (Lupton, 1994).
Thomson (2001) suggests the "neurasthenic contract" was broken when
"psychologically-inclined doctors and somatically-resilient patients" began to clash (p.
84). Sufferers encountered less sympathy and more stigmatization as neurasthenia became categorized as a neurosis, putting it virtually on par with hysteria (Wessely,
1990). Hence the similarities between neurasthenic and CFS narratives become more congruent when their etiological theories are based in psychology rather than biology.
Without legitimization from the powerful medical profession, the self-representations of
CFS sufferers are de-legitimized (Clarke & James, 2003). Wessely (1994) suggests that long-standing anti-psychiatry prejudices within the medical profession itself contribute to the stigmatization of CFS - when other medical specialties malign psychiatry's treatment of "non-existent" diseases it is not surprising that condescending physician attitudes are so often described in CFS self-help literature. One young sufferer describes her
105 experience: "Nobody knew what was wrong with me. In fact, one of my doctors called me a hypochondriac and told me that I just didn't like school" (Snyder, 2001, 5:01-5:06).
CFS sufferers' somatic attribution bias and quest for biomedical legitimacy is in direct response to the perceived illegitimacy our society accords to psychological factors
(Davison & Pennebaker, 1997). In her qualitative research, Ware (1992) describes the delegitimization of CFS sufferers as devastating and humiliating, the result of having their illness labeled psychosomatic. They feel shame at being told they are not really ill and that their perceptions of reality are suspect. To illustrate this point, in a 1985
Chicago Tribune article, the opening sentence reads: "The day Nomi Antelman learned she had an incurable disease, she rejoiced" (Ames, 1985). The relief was in the diagnosis and the fact that, finally, a doctor believed her. Even twenty years later, Carole Howard says she has been subjected to very derogatory comments and still runs up against skeptics, one of whom was a woman hired to help her around the house who told her she didn't look sick (Schorr, 2005). The modernist mind-body duality that implies physical illness is out of the control of the patient, but psychological illness is not only within the patient's control but may even be due to some personal characteristic, is still very much a part of the cultural narrative in which CFS is situated.
The quest for a medical diagnosis goes beyond the need for legitimacy. There are practical considerations like the ability to reduce workload and home responsibilities and entitlement to financial aid from government, insurers, and employers (Sharpe, 1998;
Clarke, 2000). A psychiatric diagnosis not only carries with it all of the inferences relating to malingering and blame, but also the likelihood of lower financial benefits or 106 none at all. The social and financial repercussions of a contested illness like CFS highlights the power struggle between physicians and patients: "The authority of scientific medicine to validate or invalidate our experience, to alienate us from what we experience in our bodies, and to give or deny a diagnosis that will bring or undermine social support constitutes too great a concentration of power" (Wall, 2005, p. 195).
Guggenbuhl-Craig and Micklem (1988) suggest that the way in which physicians maintain their legitimacy and control over diagnosis based on medical knowledge and experience is to construct a narrative that assigns low accountability to physicians and high accountability to patients - the narrative best fitting this need is a psychosomatic one.
Illustrative of this position is Dr. Peter Manu, who states: "I think that chronic fatigue syndrome is a way of expressing a sense of ill being that has been medicalized, that has been transformed by a relatively small group of activists, both physicians and patients, into a proposal for a new disease" (Snyder, 2001, 27:34 - 28:04).
The CFS Counter-narrative
Alternative or counter-narratives are common when diagnoses are contested
(Clarke & James, 2003). A characteristic of many CFS narratives is the mind-body dualism typical of their focus on CFS as a disease of the physical body (Tucker, 2004).
In Tucker's discursive analysis of CFS stories, sufferers focus on the physical effects of the illness on their bodies and link the onset of illness with an external event like a bacteria or virus. Suggestions from the medical establishment that CFS might be a psychological disorder are countered by the claim that these health professionals are clearly not knowledgeable about CFS. 107 Some of the factors fueling the counter-narrative are the media, the rise of patient advocacy and support groups, and technology - all of which are reflexively interconnected. Morris (1998) says "the concept of a media-generated hyperreal world is crucial.. .for an understanding of postmodern illness" (p. 25) and clinical experience suggests that patient awareness of the CFS diagnosis has come from media coverage
(Abbey, 1993). The erosion of prestige plaguing the medical profession since the 1960s has made way for the rise of the media as perhaps the more trusted source of medical information for patients (Shorter, 1995). In the genesis of CFS, patient awareness was raised with Hilary Johnson's account of her own experience in Rolling Stone (1987a,
1987b), the first major magazine article to cover the then-named CEBV. The idea that
CFS was linked to upwardly mobile young professionals, however inaccurate, was perpetuated by the media who created the headline-grabbing, popular term "yuppie flu" to describe the illness (Aronowitz, 1992). MacLean and Wessely (1994) suggest that the media interest in CFS has been due, in part, to the fact that there is no accepted etiology, leaving the door open for journalists to pick and choose from competing professional opinions. In their review of professional and popular views of CFS, they found that the
British media favored an organic etiology, positioned CFS as reacting to paternalism in medicine, and also contributed to the belief in the higher value accorded to physical versus psychological illnesses. Wessely et al. (1998) found that research articles showed a slight bias toward psychosocial explanations for CFS, in contrast to the popular emphasis on organic etiology, with the media supporting the consumer agenda and the subjective experience of patients over the view of the doctor as expert.
108 In contrast to sufferers who were proud to move in neurasthenic circles, few celebrities have been willing to go public with their CFS battles. In the early years,
CEBV was also known as 'screenwriter's disease' or the 'Hollywood blahs,' but only a few in the community, like Gore Vidal and Blake Edwards, were willing to go on record
(Johnson, 1987a). Johnson said CFS came almost as close as AIDS to being bad for one's career in Hollywood. And comparisons to AIDS are common among CFS sufferers like Pat McCloud: "There's a parallel, to the, to when the AIDS outbreak started. The lack of belief, the lack of credibility. They parallel each other so closely, and here we are, over a decade into this illness, and we are still fighting for some sort of recognition whatsoever" (Snyder, 2001, 51:53 - 52:10).
Unlike the popularity of nervous illness and invalidism in Victorian popular culture, Morris (1998) says of popular culture today: "Chronic illness has almost no place in popular self-representations of the postmodern world. It is nearly absent from network television, which prefers to focus on acute illness that is curable, curable especially by handsome, heroic, young doctors using drugs, technology, and the resources of biomedicine" (p. 220-221). O'Brien (2000) concurs, pointing out the preference for recovery stories akin to the Puritan conversion narrative (I was blind, but now I can see), as opposed to stories of long-term suffering. However, ordinary people have authored books on their experiences living with chronic illness in an emerging sub-genre termed
'pathography' (Morris, 1998).
The self-diagnosis so common to CFS sufferers can be traced to the counter- narrative constructed by patient support groups, as patients disillusioned with their
109 physicians began comparing symptoms (Clarke & James, 2003). Wessely et al. (1998) point out that such support and advocacy groups are not unique to CFS, but are indicative of the growth of consumerism within medicine and patient dissatisfaction with physicians.
Technology has fueled the growth and power of such groups, with web sites, e-mail lists, and the like creating forums for sufferers to share their stories and discuss treatment strategies (Fox & Ward, 2006). One sufferer, after being diagnosed, almost immediately searched the Internet: "I found a whole community of support groups, one located right in my own neighborhood. There were tips on treatment options, possible causes, and how to get disability benefits.. .1 was able to help my doctor with diagnosing the multiple problems that turned out to be causing my fatigue and pain, and to recommend drug therapies that worked" (Floyd, 2000). After experiencing the powerlessness that can come with illness, technology was credited with offering empowerment and facilitating an understanding of what was wrong and how best to fix it. Guise, Widdicombe, &
McKinlay (2007) suggest that researchers, too, should engage with the new forms of communication patients have at their disposal.
Support groups have endured criticism by researchers, who have suggested that such groups are biased against recovery, thus pessimistic illness perceptions of those who believe they will never recover from CFS can, in effect, spread to others (Huibers &
Wessely, 2006). Shorter (1995) suggests illnesses that would have run their natural course, having been labeled psychosomatic by mainstream medicine, live on within patient support groups depicting doctors as ignorant and heartless. Chronic sufferers are over-represented in support groups, which can also be virulently anti-psychiatry (Huibers
110 & Wessely, 2006), a virulence Shorter (1992) suggests is out of proportion compared with sufferers of other illnesses and is, in fact, a characteristic of CFS. Doctors, he suggests, are evaluated not on the basis of sound clinical judgment, but on how favorable they are to a CFS diagnosis. In contrast, Wall (2005) characterizes sufferers like herself as experts on CFS who must endure physicians who are less knowledgeable.
In a study examining the online activities of various patient support groups,
Davison and Pennebaker (1997) characterize the communications of CFS sufferers as affected and reactive compared with those suffering from other illnesses like arthritis, breast and prostate cancer, heart disease, and diabetes. The participation of CFS sufferers was very high, with more posts in a two-week period than by all the other support groups combined. Their posts were often punctuated with an abundance of exclamation points and catastrophic conclusions, while demonstrating a familiarity with recent research and a disdain for any research suggesting psychological or psychosocial etiology or treatment.
The authors not only illustrate the recalcitrance of CFS sufferers, but that of the research community in their statements:
How is it that individuals who are too tired to function or make their children's
lunches can write hundreds of words and spend hours at the computer reading the
posts by others and comparing symptoms of exhaustion?...One can only speculate
that this group's suffering evokes little sympathy in the doctor's office. Moreover,
of all the groups, they have the most rigidly defined boundaries about illness
prototypes. This seems ironic in view of its status as a diagnostic exclusion, (p.
479)
111 The power struggle has been very public, with advocacy groups employing some controversial tactics. Psychiatric research and researchers have been insulted and/or discredited, while some activists have lobbied research bodies, journals, and government institutions to prevent the funding and publication of research believed to be detrimental to the CFS cause (Wessely, et al., 1998). In 1996, activist Hillary Johnson sparked controversy when promoting her book on national television, claiming that CFIDS was a very contagious brain disease (Wall, 2005). Academic Elaine Showalter, whose book
Hystories: Hysterical Epidemics and Modern Media (1997) labeled CFS an hysterical epidemic, had to abandon a book signing due to the menacing nature of CFS activists who had been dogging her book tour as well as attempting to discredit her by questioning her academic competency and mental health (Herbert, 1997). And in 2001, an anonymous group called No Time to Lose, planned to very publicly announce that a large number of CFIDS patients would donate blood on May 12, their position being that an outcry by public officials would be indicative of their acceptance of CFS as a communicable disease (Wall, 2005).
Patients are also known to attend academic meetings on chronic fatigue, the effect of which, according to Shorter (1995), has been to minimize the information shared by the researchers during the meeting, with the more meaningful exchange of information taking place during after-meeting-hours social gatherings. More recently, at the 2007
International Association for Chronic Fatigue Conference, the two-day session focused on patient needs was attended by 350 patients and 220 professionals (Teague, 2007). The subsequent three-day professional session was attended by 169 patients - further
112 confirmation that, as a group, CFS sufferers are very well educated and informed about their illness. They have successfully driven professional and institutional action by courting sympathetic physicians, medical societies, and philanthropies (Brown, 1995).
In spite of some questionable tactics, patient activism has had an effect. After twenty years of contentiousness between doctors and patients, the CDC acknowledges the public health impact of CFS, especially on women. William Reeves, chief virologist at the CDC says:
Putting it in terms of magnitude of public health problems, if one is looking at just
pure prevalence rates, chronic fatigue syndrome is in the range of HIV infection
in women, slightly more, and in terms of existing cases, there are considerably
more existing cases of chronic fatigue syndrome in women than there are of either
breast cancer or cervical cancer. So it really is a much larger public health
problem in terms of cases than we'd thought before. (Snyder, 2001,47:35 - 48:07)
Wall (2005) has noted the increasing credibility of CFS; "yuppie flu" has been replaced with portrayals of CFS as widespread, real, and organically based. In part, Wall says, this is due to an increasing number of high-profile sufferers going public with their illness. In 2001, Laura Hillenbrand, author of the best-selling book Seabiscuit: An
American Legend, chronicled her struggle to write the book while battling CFS in more than 300 media interviews.
Most recently, in late 2006, the CDC launched a national public awareness and education campaign called 'Get Informed. Get Diagnosed. Get Help' (CDC launches,
2006). The popular press cites the campaign as helping Americans move past skepticism
113 about CFS (Stobbe, 2007) and for contributing to more funding for research dedicated to finding both a cause and a cure for the illness (Griffith, 2006). The CDC press release
(CDC launches, 2006) claims the need for such a campaign because 80 percent of
Americans with CFS may not even be aware they have it. As of the end of January, 2007 the spot had aired 4,425 times in 122 markets on 180 television stations (Stobbe, 2007).
Conclusion
What is common to the understanding of neurasthenia and CFS is the importance of the interactions between doctors and patients, lay and medical attitudes, and how these interactions and attitudes contribute to the cultural shaping of illness and disease. When neurasthenia met the needs of both physicians and patients, the equilibrium of a co- construction was maintained. As an uncontested disease entity with converging lay and medical narratives, as well as doctor-patient relations that were based on mutual respect and patient compliance, neurasthenics skirted stigmatization for upwards of three decades.
Legitimacy, in the case of both neurasthenia and CFS, has been predicated on a somatic illness narrative and resulting disease status. The mere suggestion of a psychogenic etiology injects a degree of skepticism, thus shifting the narrative away from 'legitimate disease entity' and toward 'questionable illness,' with the accompanying stigmatization of such a shift. The co-construction between physicians and patients so characteristic of neurasthenia was replaced by a different kind of CFS construction - a patient-constructed understanding of the illness based on information gleaned and exchanged via support and advocacy groups, as well as the technological advances that enabled patients to educate themselves by accessing the latest research about their illness.
114 After 20 years of stigmatization it appears that CFS is gradually being upgraded and accorded the legitimacy and status of a real disease. The cultural narrative is changing, less because of advances in research and more due to political pressure.
According to the CFIDSLink E-newsletter reporting on the CDC awareness campaign
(CDC and press validate CFS, 2006):
The CFIDS Association has been working for more than three years to bring this
$4.5 million public awareness campaign to fruition, not only securing the
government contract to implement the campaign, but organizing the press
conference and managing the development of campaign materials including the
television, radio and print PSAs, print ad, patient brochure and CFS toolkit for
healthcare professionals..
Tucker (2004) suggests the CFS controversy has been maintained due to competing narratives and the absence of a single unifying discourse. And while there is still no diagnostic test for CFS, few advances in treatment management, and a rather poor prognosis for CFS sufferers, Dr. Anthony Komaroff, a CFS physician and researcher at
Harvard Medical School told reporters at the November 2006 press conference (Press conference, 2006):
While we still don't understand the cause or causes of the illness, the good news
is that literature from over 4,000 published research studies has revealed a number
of physical or biological abnormalities in CFS. The illness is not simply a set of
symptoms people imagine they have, and it is not a psychological illness. In my
115 view, that debate - which has raged for the past two decades in the United States
and abroad - should finally be over.
It appears as if a unifying discourse has emerged and the somatic co-construction reminiscent of the early decades of neurasthenia may heal the rift between doctors and patients that has characterized the competing CFS narratives of the past 20 years.
What is most interesting about neurasthenia and CFS are the ways in which modernist cultural assumptions have produced similar interpretations of symptoms in the absence of disease. The propensity to make meaning of symptoms by categorizing them as either biogenic or psychogenic in origin and granting legitimacy to the former over the latter, seems indicative of a transhistorical need to frame our understanding of illness in a mind-body/subjective-objective dualistic way. I believe this is changing and that the postmodern critique is reflected in the very recent shifts in the perception of CFS as a legitimate disease in spite of the continuing uncertainty with respect to etiology.
116 Conclusion
Perhaps the best way to characterize the relationship between neurasthenia and
CFS is as Wall (2005) does: distant cousins. As a CFS sufferer herself, she acknowledges the connection historians have made between them as well as the interesting conversations possible when neurasthenia and CFS are considered together.
From an interpretive standpoint, neurasthenia and CFS serve as excellent case studies for better understanding the cultural meanings ascribed to symptoms in the social construction of illness and disease categories. There is little evidence to suggest that levels of fatigue, aches, and pains have changed much historically; what has changed is the meaning of these symptoms, their attributions, and their categorization as diseases
(Shorter, 1992).
The meaning of symptoms
Symptoms in the absence of disease are commonly understood as expressions of interpersonal distress, spurring sufferers to negotiate life changes in a culturally acceptable way (Ware & Kleinman, 1992; Wessely, 1994; Horowitz, 2002). Historically, neurasthenia and CFS have been linked as 'fin-de-siecle' illnesses evolving from difficulties adapting to rapid, and often unwelcome, changes in social life (Wessely et al.,
1998). Neurasthenia was, for around three decades, a culturally acceptable way to navigate the upheavals in social life (Lutz, 1991) and the doctors treating it offered more than just medical relief- their advice crossed into the social and moral arenas as well
(Wessely, 1994). The functional nervous paradigm within which physicians worked acknowledged the interplay between somatic symptoms and psychological factors: 117 "Symptoms were seen as a manifestation of a reversible functional disturbance rather than as fixed pathology of a purely psychological nature" (Sharpe & Carson, 2001, p.
929). Change was believed to be possible and neurasthenics appeared to recover to a far greater degree than CFS sufferers do. By contrast, there is a hopeless, defeatist attitude apparent in my reading of CFS narratives. The tension between patients and medical professionals is a pervasive theme, and yet the relationship is an ambivalent one: "As disenfranchised patients, we want access to the realm of scientific cures. We believe that with enough focus and resources the biological mechanism behind CFIDS will be duly revealed and all of us who have suffered the ignominy of disbelief will be granted legitimate standing in the halls of medicine" (Wall, 2005, p. 28). The very same doctors and researchers who have been accused of being ignorant of CFS and of turning their backs on the plight of sufferers are, ultimately, expected to discover a diagnostic test for
CFS, a biogenic cause, and hopefully a cure. The conundrum facing CFS sufferers is best summed up by Charlton (1993) who says, "A sick person wants the certainties of modernity. Only when we are feeling well are we inclined to gamble on the glamorous relativities of post-modernity" (p. 498).
The less ambivalent and more intimate doctor-patient relationship of the nineteenth century, which is described by Ehrenreich & English (1971) as "little more than a historical curiosity" (p. 78), is seen today as one physicians would do well to emulate. Dr. David Bell, a physician who treated a cluster of CFS patients in
Lyndonville, New York has said: "If I were to make any suggestions for changes in
American medical schools it would be that they train doctors to be more like doctors in
118 the nineteenth century. They were great clinicians, and I think they would have handled chronic fatigue syndrome quite nicely" (as cited in Johnson, 1996, p. 368). Physicians like Dubois, who weaved psychological interventions into the medical consultation, understood the importance of the doctor-patient alliance and its relationship to treatment outcome (Sharpe & Carson, 2001). Eisenberg (1977) suggests that, culturally, we have been far too dismissive of the potential 'placebo effect' of psychotherapy and benefits obtained by patients due to the social component of the doctor-patient encounter, stating that, "placebo has become almost an epithet suggesting charlatanism rather than a marker for an extraordinary and quite fundamental characteristic of good medical care" (p. 20).
Just as pure psychogenic theories were unwelcome to neurasthenics, they are equally untenable to the CFS patients of today (Wessely et al., 1998) who, understandably, do not take kindly to the dismissal of their somatic symptoms. The same dualism that facilitated the study of the body as a machine and contributed to so many beneficial advances in biomedicine, has become limited in its ability to make sense of chronic, multifactorial, postmodern illnesses (Eisenberg, 1977). Dualism links neurasthenia and CFS together in that the search for a biogenic or psychogenic cause, in both cases, has aroused controversy and dissent. Neurasthenia was accepted as biogenically based, not because there was evidence that this was so, but because of the view that psychological illnesses were not real or due to malingering: "Neurasthenia provided a haven for those uncomfortable with the psychological aspects of illness, who either insisted on its solely organic basis, or saw it as a refuge for the mentally infirm"
(Wessely et al., 1998). The old tension between biogenic and psychogenic etiologies re-
119 emerged as doctors and patients battled over the legitimacy of virtually the same symptoms a century later. The co-construction of an organic diagnosis within a modernist biomedical paradigm confers legitimacy and social benefits on sufferers, thus cultural acceptance of disease, in effect, determines its existence as a social phenomenon
(Rosenberg, 1989). The disputes between physicians and patients around diagnosis and disease legitimacy are reflective of social conflicts relating to medical and health issues
(Zavestoski et al., 2004).
Most notably, the conflict has taken shape in the form of social sanctions granting
CFS patients economic compensation due to the debility of their illness (Aceves-Avila,
Ferrari, & Ramos-Remus, 2004). Disease specificity has been a precondition of social and economic sanctions - no disease diagnosis means no sympathy and no reimbursement (Rosenberg, 1989). The simplicity of the modernist disease model is simply inadequate as we come to terms with the fact that, as Morris (1998) points out,
"Patients who suffer from an unverified illness are no less sick than patients whose disease matches the textbook. Sometimes they are worse: not only ill but also frustrated, disabled, worried, out of work, and out of hope" (p. 39).
Postmodern medicine: Hope for the future?
If, as CFS researchers like Dr. Anthony Komaroff suggest, the debate is over and a biogenic etiology is no longer necessary for symptoms to be granted disease status, what theoretical shifts are occurring that are conferring new meaning on old symptoms?
I see evidence that the postmodern critique of medicine is having an effect. It has taken a number of different, but complementary, forms. Ware & Kleinman (1992) have put
120 forward a 'sociosomatic' approach to the study of illness, one that fosters an understanding of how biological and psychological processes are influenced by social context. Morris (1998) calls his model a biocultural model of medicine, one designed not only to question the assumptions of Cartesian dualism but also to encourage dialogue across specialties because postmodern illness cannot be adequately addressed by monologues of single specialties. A comprehensive biospsychosocial approach is advocated by Bensing & Verhaak (2006), who argue that medically unexplained symptoms can only be understood as both biomedical and psychosocial. Their approach to treatment is to follow a dual track, whereby patients' biomedical needs are addressed at the same time as they are being engaged in discussions of psychosocial issues. Patients are more willing to discuss psychosocial variables when they feel their somatic complaints are being taken seriously and explored, but not when they are engaged in a psychosocial dialogue only after all medical avenues have been explored and no conclusive results have been produced. This more integrative approach rises above the simplistic body-mind distinction to study the interactions between the biological and psychological (Sharpe & Carson, 2001).
The postmodern critique of biomedicine is that it has become so specialized due to its preoccupation with disease specificity that it has inadequately dealt with the chronic, multi-causal illnesses that have been characterized as postmodern. The role of culture in the shaping of symptoms has been all but ignored in favor of biomedical initiatives like gene mapping and increasingly high-tech ways of 'seeing' into the body causing, in effect, a collision between the modern and postmodern, clinical practice and
121 patient expectations. Postmodern illness, says Morris (1998) "encompasses both the patient's experience and whatever biological condition initiates or accompanies it. In effect, it conflates two concepts that medicine normally prefers to keep separate" (p. 40).
A postmodern theoretical shift requires not only an abandonment of dualism, but the acceptance of ambiguity - recognition of the reality of suffering in the absence of etiological certainty.
The theoretical challenges of postmodern medicine are not just to researchers and clinicians, but also to patients, who may even be more resistant to conceptualizing their somatic symptoms in a sociosomatic, biocultural, or biopsychosocial framework. Like
Alice James, the invalid sister of William James, and the CFS sufferer described by
Hillary Johnson in Rolling Stone (1987a), both were relieved by a firm, organic cancer diagnosis (Morris, 1998). Culturally, letting go of dualism will prove difficult as long as our social institutions operate within the modernist model, sanctioning 'real' disease and equating etiologically uncertain symptoms with imagined or psychogenic illness. Hadler
(1996) illustrates the problem perfectly in the title of his paper, "If you have to prove you are ill, you can't get well." The disease-illness distinction contributes to a vicious circle characterized by increasing debility as the veracity of patients' stories is questioned. In this scenario, to get well is to abandon your truth.
But what of the social and economic consequences of a wholesale abandonment of modernist ideals? There are clear costs to postmodern subjectivity becoming the rule and patient narratives being granted the same legitimacy as the specificity of a medical diagnosis, yet we currently apportion benefits based on causation to recognized diseases 122 even when lifestyle choices contribute to onset. Two-pack-a-day smokers may not garner much sympathy for their lung cancer, but disability benefits are, nonetheless, forthcoming. The comforting aspect to the objective/subjective and mind/body distinctions was the simplicity they afforded us in attributing blame to those with psychogenic illnesses and absolution to those with biogenic diseases. And even though we are situated somewhere between modernism and postmodernism, it is common today to think of disease in a much more holistic, biopsychosocial way. Messages about disease prevention focus on individual agency and the lifestyle contributors to disease, like obesity to diabetes, heart disease, and many forms of cancer; the association between stress and high blood pressure; and smoking to cancer. The list is long and getting longer, but the cultural narrative is confusing and inconsistent. On the one hand, a disease diagnosis may not be a free ticket to social legitimacy if one's lifestyle choices contribute to the onset and perpetuation of disease. On the other hand, behaviors previously conceptualized as being within individuals' control - like addictions to drugs, alcohol, the Internet, and gambling - are being repositioned as diseases to which individuals are genetically predisposed. The cultural narratives are confusing - sufferers of 'real' diseases may be increasingly stigmatized due to bad lifestyle choices correlated with their diseases, while addicts may be increasingly legitimized as sufferers of 'real' disease as genetic factors are correlated with their addictive behaviors.
CFS is illustrative of a new postmodern narrative but, as Morris (1998) suggests,
"represents for us the confusing historical moment we are living through when the biomedical model has begun to reveal its inherent limitations but when a biocultural
123 model (or whatever we come to call it) has not yet proven its power to constitute a satisfying and coherent replacement" (p. 278). The neurasthenia story also unfolded as old models were making way for new and ways of knowing were being challenged.
Ambiguity was tolerated in the late nineteenth century because there was no alternative.
Subjective reports of symptoms and the doctor-patient interaction gave meaning to symptoms until they were re-shaped by the emergence of laboratory medicine in the early twentieth century. Neurasthenia, when viewed under this new lens, was dismantled as a disease category and its symptoms de-legitimized as their meaning was re-framed as psychoneurotic in origin. In a way we've come full circle as the modernist biomedical narrative creates a space for an alternative, multi-causal, biopsychosocial understanding of medically unexplained symptoms. If, as Morris suggests, a coherent replacement of the biomedical model can evolve into a new cultural narrative, CFS may be spared the same historical fate as neurasthenia.
124 References
Abbey, S. E. (1993). Somatization, illness attribution, and the sociocultural psychiatry of
chronic fatigue syndrome. In G. R. Bock & J. Whelan (Eds.), Chronic fatigue
syndrome: Ciba Foundation Symposium 173, pp. 238-261. Chichester, U.K.: John
Wiley & Sons.
Abbey, S. E. & Garfinkel, P. E. (1991). Neurasthenia and chronic fatigue syndrome: The
role of culture in the making of a diagnosis. The American Journal of Psychiatry,
148(12), 1638-1646.
Aceves-Avila, F. J., Ferrari, R., & Ramos-Remus, C. (2004). New insights into culture
driven disorders. Best Practice & Research Clinical Rheumatology, 18(2), 155-171.
Acheson, E. (1959). The clinical syndrome variously called benign myalgic
encephalomyelitis, Icelandic disease and epidemic neuromyasthenia. American
Journal of Medicine, 26, 569-595.
Alvarez, W. (1935). What is wrong with the patient who feels tired, weak and toxic? New
England Journal of Medicine, 212, 96-104.
American Psychiatric Association (1980). Diagnostic and statistical manual of mental
disorders (3rd ed.). Washington, DC: APA.
Ames, M. (1985, June 9). Learning to live with incurable virus doctors' doubts add to
burden of hard-to-diagnose disease. The Chicago Tribune, retrieved May 23, 2007,
http://pqasb.pqarchiver.com/chicagotribune.
Angell, E. B. (1915). Neurasthenia. The American Journal of Nursing, 15, 364-371.
125 Aronowitz, R. A. (1992). From myaligic encephalitis to yuppie flu: A history of chronic
fatigue syndromes. In C. E. Rosenberg & J. Golden (Eds.), Framing disease:
Studies in cultural history (pp. 155-181). New Brunswick, NJ: Rutgers University
Press.
Ballet, G. (1913). Neurasthenia (3rd ed.). Toronto: Macmillan.
Banks, J., & Prior, L. (2001). Doing things with illness: The micro politics of the CFS
clinic. Social Science and Medicine, 52, 11-23.
Bassuk, E. L. (1986). The rest cure: Repetition or resolution of Victorian women's
conflicts. In S. R. Suleiman (Ed.), The female body in western culture:
Contemporary perspectives (pp. 139-151). Cambridge: Harvard University Press.
Beard, G. M. (1869). Neurasthenia or nervous exhaustion. Boston Medical & Surgical
Journal, 80, 217.
Beard, G. M. (1879). Other symptoms of neurasthenia (nervous exhaustion). Journal of
Nervous and Mental Disease, 6, 246-261.
Beard, G. M. (1881/1972). American nervousness: Its causes and consequences. New
York: Arno Press Inc.
Beard, G. M. (1884). Sexual neurasthenia (nervous exhaustion). New York: E. B. Treat.
Bensing, J. M., & Verhaak, P. F. M. (2006). Somatization: A joint responsibility of
doctor and patient. The Lancet, 367, 452-454.
Berger, D. M. (1973). The return of neurasthenia. Comprehensive Psychiatry, 14(6), 557-
62.
126 Bresnahan, K. (2003). Neurasthenic subjects and the bourgeois interior. Space and
Culture, 6, 169-177.
Brown, L. (2001, February). Breaking free - chronic fatigue syndrome. Better Nutrition.
Retrieved April 14, 2007,
http://www.findarticles.eom/p/articles/mi mOFKA/is 2 63/ai 78476726.
Brown, P. (1995). Naming and framing: The social construction of diagnosis and illness.
Journal of Health and Social Behavior, 35, Extra issue: Forty years of medical
sociology: The state of the art and directions for the future, 34-52.
Bunker, H. A. (1930). From Beard to Freud: A brief history of the concept of
neurasthenia. Medical Review of Reviews, 36, 109-114.
Cathebras, P. (1994). Neurasthenia, spasmophilia, and chronic fatigue syndrome in
France. Transcultural Psychiatric Research Review, 31, 259-270.
Cayleff, S. E. (1988). 'Prisoners of their own feebleness': Women, nevers and Western
medicine - A historical overview. Social Science and Medicine, 26{\2), 1199-1208.
CDC and press validate CFS. (2006, November). CFIDSLink E-newsletter. Retrieved
September 2, 2007, http://www.cfids.org/cfidslink/2006/press-coverage.asp
CDC launches 'Get informed. Get Diagnosed. Get Help' campaign. (1996, November 3).
PRNewswire. Retrieved April 14, 2007,
http://www.keepmedia.eom/pubs/PRNewsiwre/2006/l 1 /03/1944881.
CFS Toolkit for Health Care Professionals: Basic CFS Overview. Centers for Disease
Control and Prevention web site at www.cdc.gov/cfs/pdf/Basic_Overview.pdf.
127 Charlton, B. G. (1993). Medicine and post-modernity. Journal of the Royal Society of
Medicine, 86, 497-499.
Chatel, J. C, & Peele, R. (1970-1). The concept of neurasthenia. Inter nationalJour nal of
Psychiatry, 9, 36-49.
Cho, H. J., Hotopf, M., & Wessely, S. (2005). The placebo response in the treatment of
chronic fatigue syndrome: A systematic review and meta-analysis. Psychosomatic
Medicine, 67, 301-313.
Chronic fatigue syndrome: "Yuppie" flu reassessed. (1989, February). Health News.
Retrieved April 14, 2007,
http://w\\rvv.findarticles.com/p/articles/mi m0857/is_nl_v7/ai 7410539.
Clarke, J. N. (2000). The search for legitimacy and the "expertization" of the lay person:
The case of chronic fatigue syndrome. Social Work in Health Care, 30, 73-93.
Clarke, J. N., & James, S. (2003). The radicalized self: The impact on the self of the
contested nature of the diagnosis of chronic fatigue syndrome. Social Science and
Medicine, 57, 1387-1395.
Cleaves, M. (1886). Neurasthenia and its relation to diseases of woman. Transactions of
the Iowa State Medical Society, 7, 164-179.
Cobb, I. G. (1920). A manual of neurasthenia-Nervous exhaustion. London: Balliere &
Co.
Collins, J., & Phillips, C. (1899). The etiology and treatment of neurasthenia: An analysis
of three hundred and thirty-three cases. Medical Record, 55, 413-422.
128 Coulter, P. (1988). Chronic fatigue syndrome: An old virus with a new diagnosis. Journal
of Community Health Nursing, 5(2), 87-95.
Dana, C. L. (1904). The partial passing of neurasthenia. The Boston Medical and Surgical
Journal, 60, 339-344.
Davis, D. L. (1989). George Beard and Lydia Pinkham: Gender, class and nerves in late
19* -century America. Health Care for Women International, 10(2-3), 93-114.
Davison, K. P., & Pennebaker, J. W. (1997). Virtual narratives: Illness representations in
online support groups. In K. Petrie, & J. Wienman (Eds.), Perceptions of health and
illness: Current research and applications (pp. 463-486). London: Harwood
Academic Publishers.
Deale, A., Chalder, T., Marks, I., & Wessely, S. (1997). Cognitive behavior therapy for
chronic fatigue syndrome: A randomized controlled trial. American Journal of
Psychiatry, 154(3), 408-414.
Deale, H. & Adams, S. (1894). Neurasthenia in young women. American Journal of
Obstetrics, 29,190-195, 256-258.
Demitrack, M. A., & Greden, J. F. (1991). Chronic fatigue syndrome: The need for an
integrative approach. Biological Psychiatry, 30, 747-752.
Donley, J. E. (1906). Obsessions and associated conditions in so-called psychasthenia.
The Journal of Abnormal Psychology, 4(2), 172-181.
Dowse, T. S. (1880). On brain and nervous exhaustion. London: Baillere, Tindall, and
Cox.
129 Dubois, P. (1906). The psychic treatment of nervous disorders. New York: Funk &
Wagnalls.
Dunbar, H. F. (1934). Physical mental relationships in illness: Trends in modern
medicine and research as related to psychiatry. The American Journal of Psychiatry,
91, 541-562.
Ehrenreich, B, & English, D. (1973). Complaints and disorders: The sexual politics of
sickness. New York: The Feminist Press.
Eisenberg, L. (1977). Disease and illness: Distinction between professional and popular
ideas of sickness. Culture, Medicine and Psychiatry, 1, 9-23.
Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine.
Science, 196, 129-136.
Fact Sheet - Chronic Fatigue Syndrome - Pamphlet (December 1, 2000). Prepared by the
Office of Communications and Public Liaison for the National Institute of Allergy
and Infectious Diseases. Retrieved April 17, 2007,
http://findarticles.eom/p/articles/mi m0660/is 2000 Dec 1/ai 73579307.
Farmer, A., Jones, I., Hillier, J., Llewelyn, M., Borysiewicz, L., & Smith, A. (1995).
Neurasthenia revisited: ICD-10 and DSM-II1-R psychiatric syndromes in chronic
fatigue patients and comparison subjects. The British Journal of Psychiatry, 167,
503-506.
Feiden, K. (1990). Hope and help for chronic fatigue syndrome: The official guide of the
CFS/CFIDS network. New York: Prentice Hall.
Feinstein, A. R. (1967). Clinical judgment. Huntingdon: UK Krieger.
130 Fischer, M. A. (2006, September). You think you're tired? O, The Oprah Magazine.
Retrieved April 9, 2007, http://www.accessmylibrarvxom/coms2/summarv__0286-
20825566 ITM.
Floyd, J. (2000, Spring). Internet plugged in - Internet use by chronic fatigue syndrome
patient. Accent on Living. Retrieved April 14, 2007.
http://www.findarticles.eom/p/articles/mi_m0803/is_4_44/ai_61860203.
Forth, C. E. (2001). Neurasthenia and manhood in fin-de-siecle France. In M. Gijswijt-
Hofstra, & R. Porter (Eds.), Cultures of neurasthenia: From Beard to the first world
war (pp. 329-361). Amsterdam/New York: Rodopi.
Fox, N., & Ward, K. (2006). Health identities: From expert patient to resisting consumer.
health: An Interdisciplinary Journal for the Social Study of Health, Illness and
Medicine, 10(4), 461 -479.
Freud, S. (1887). Review of Averbeck's Die Akute Neurasthenia. In J. Strachey (Ed.),
The Standard Edition of the Complete Psychological Works ofSigmund Freud
(1955-1974). London: Hogarth Press.
Freud, S. (1888). Letters to Wilhelm Fliess, Drafts and Notes: 1887-1902 (Letter 3,4
February 1888). In M. Bonaparte, A. Freud, & E. Kris (Eds.) The Origins of
Psychoanalysis (1954). London: Imago.
Freud, S. (1894/1956). On the grounds for detaching a particular syndrome from
neurasthenia under the description 'anxiety neuroses.' In J. Strachey (Ed.), The
standard edition of the complete psychological works ofSigmund Freud volume III
(1893-1899) (pp. 87-117). London: Hogarth Press.
131 Fukuda, K., Straus, S. E., Hickie, I., Sharpe, M. C. Dobbins, J. G., & Komaroff, A.
(1994). The chronic fatigue syndrome: A comprehensive approach to its definition
and study. Annals of Internal Medicine, 121, 953-959.
Fullinwider, S. P. (1974, April). Neurasthenia: The genteel caste's journey inward. The
Rocky Mountain Social Science Journal, 11, 1-9.
Garrigue, E. (1909). Psychotherapy and re-education: Some observations after visiting
clinics in Paris and Nancy. The Woman's Medical Journal, 19, 28-33.
Genetic and environmental factors impact CFS patients (2006, April 20). Press Release
issued by the Centers for Disease Control. Retrieved July 4,2007,
http://wwvv.cdc.gov/od/oc/media/pressrel/r060420.htm.
Giddens, A. (1990). The consequences of modernity. Stanford, CA: Stanford University
Press.
Gijswijt-Hofstra, M. (2001). Introduction. In M. Gijswijt-Hofstra, & R. Porter (Eds.),
Cultures of neurasthenia: From Beard to the first world war (pp. 1-30).
Amsterdam/New York: Rodopi.
Gilman, C. P. (1892, January). The Yellow Wallpaper. The New England Magazine,
11(5), 647-657.
Gilman, C. P. (1913, October). Why I wrote The Yellow Wallpaper. The Forerunner
Retrieved June 22, 2007,
www.library.csi.cuny.edu/dept/history/lavender/whyyw.html.
Gosling, F. G. (1985). Neurasthenia in Pennsylvania. Journal of the History of Medicine
and Allied Sciences, 40(2), p. 188-206.
132 Gosling, F. G. (1987). Before Freud: Neurasthenia and the American medical community,
1870-1910. Urbana: University of Illinois Press.
Gosling, F. G., & Ray, J. M. (1986). The right to be sick: American physicians and
nervous patients, 1885-1910. Journal of Social History, 20,251-268.
Gottschalk, L. A. (1975). Psychosomatic medicine - Past, present, and future. Psychiatry,
38, 334-345.
Goudsmit, E. (2000). Chronic fatigue syndromes: A different approach. Retrieved August
19, 2007 from The National CFIDS Foundation web site, http://www.ncf-
net.org/library/goudsmit.html.
Griffith, D. (2006, December 11). Tired all the time. Sacramento Bee. Retrieved April 9,
2007, www.accessmylibrary.com/coms2/summary_0286-28883501_ITM.
Greenberg, D. B. (1990). Neurasthenia in the 1980s: Chronic mononucleosis, chronic
fatigue syndrome, and anxiety and depressive disorders. Psychosomatics, 31(2),
129-137.
Guggenbuhl-Craig, A. & Micklem, N. (1988). No answer to Job: Reflections on the
limitations of meaning in illness. In M. Kidel and S Rowe-Leete (Eds.), The
meaning of illness (pp. 141-153). London: Routledge.
Guise, J., Widdicombe, S., & McKinlay, A. (2007). 'What is it like to have ME?': The
discursive construction of ME in computer-mediated communication and face-to-
face interaction. Interdisciplinary Journal for the Social Study of Health, Illness,
and Medicine, 11, 87-108.
133 Hadler, N. M. (1996). If you have to prove you are ill, you can't get well: The object
lesson of fibromyalgia. Spine, 21(20), 2397-2400.
Haller, J. S. (1970). Neurasthenia: The medical profession and the and the urban 'blahs.'
New York State Journal of Medicine, 70, 2489-2497.
Harris, H. & Kemple, C. (1954). Chronic brucellosis & psychoneurosis. Psychosomatic
Medicine, 16, 414-425.
Heim, C, Wagner, D., Maloney, E., Papanicolaou, D. A., Solomon, L., Jones, J. F., et al.
(2006). Early adverse experience and risk for chronic fatigue syndrome: Results
from a population-based study. Archives of General Psychiatry, 63, 1258-1266.
Herbert, W. (1997, May 19). The hysteria over 'Hystories.' U. S. News & World Report.
Retrieved April 3, 2007,
http://www.usnews.com/usnews/culture/articles/970519/archive_006959.htm
Holmes, G. P., Kaplan, J. E., Gantz, N. M., Komaroff, A. L., Schonberger, L. B., Straus,
S. E., et al. (1988). Chronic fatigue syndrome: A working case definition. Annals of
Internal Medicine, 108,387-389.
Horowitz, A. V. (2002). Creating mental illness. Chicago: University of Chicago Press.
Huibers, M. J. H., & Wessely, S. (2006). The act of diagnosis: Pros and cons of labeling
chronic fatigue syndrome. Psychological Medicine, 36, 895-900.
Imboden, J., Canter, A., & Cluff, L. (1959). Brucellosis: Psychologic aspects of delayed
convalescence. Archives of Internal Medicine, 103, 406-414.
134 Jason, L. A., Richman, J. A., Rademaker, A. W., Jordan, K. M., Plioplys, A. V., Taylor,
R. R., McCready, W., Huang, C. F., & Plioplys, S. (1999). A community-based
study of chronic fatigue syndrome. Archives of Internal Medicine, 159, 2129-2137.
Jelliffe, S. E. (1905). Dispensary work in nervous diseases. Journal of Nervous and
Mental Disease, 32, 449-453.
Johnson, H. (1987a, July 16 - July 30). Journey into fear: The growing nightmare of
Epstein-Barr virus (Part I). Rolling Stone, 56-58, 60, 62-63,139, 141.
Johnson, H. (1987b, August 13). Journey into fear: The growing nightmare of Epstein-
Barr virus (Part II). Rolling Stone, 42, 44, 56-57.
Johnson, H. (1996). Osier's web: Inside the labyrinth of the chronic fatigue syndrome
epidemic. New York: Penguin Books.
Kaplan, H. I. & Kaplan, H. S. (1956). An historical survey of psychosomatic medicine.
The Journal of Nervous and Mental Disease, 124(6), 546-568.
Kato, K., Sullivan, P. F., Evengard, B., & Pederson, N. L. (2006). Premorbid predictors
of chronic fatigue. Archives of General Psychiatry, 63, 1267-1272.
King, C. R. (1989). Parallels between neurasthenia and PMS. Women & Health, 15(4), 1-
23.
Kirmayer, L. J., & Young, A. (1998). Culture and somatization: Clinical, epidemiological,
and ethnographic perspectives. Psychosomatic Medicine, 60, 420-430.
Kleinman, A., & Straus, S. E. (1993). Introduction. In G. R. Bock, & J. Whelan (Eds.),
Chronic fatigue syndrome: Ciba Foundation Symposium 173 (pp. 1-5). Chichester,
U.K.: John Wiley & Sons. 135 Knapp, P. C. (1896). Are nervous diseases increasing? Century Magazine, 30, 146.
Komaroff, A. L. (1993). Clinical presentation of chronic fatigue syndrome. In G. R. Bock,
& J. Whelan (Eds.), Chronic fatigue syndrome: Ciba Foundation Symposium 173
(pp. 43-61). Chichester, U.K.: John Wiley & Sons.
Koo, D. (1989). Chronic fatigue syndrome; a critical appraisal of the role of Epstein-Barr
virus. The Western Journal of Medicine, 150, 590-597.
Lewis, B. (2000). Psychiatry and postmodern theory. Journal of Medical Humanities, 21,
71-84.
Lupton, D. (1994). Medicine as culture: Illness, disease, and the body in Western
societies. London: Sage Publications.
Luthra, A. & Wessely, S. (2004). Unloading the trunk: Neurasthenia, CFS and race.
Social Science & Medicine, 58, 2362-2369.
Lutz, T. (1991). American nervousness, 1903: An anecdotal history. Ithaca, NY: Cornell
University Press.
Lutz, T. (2001). Varieties of medical experience: Doctors and patients, psyche and soma
in America. In M. Gijswijt-Hofstra, & R. Porter (Eds.), Cultures of neurasthenia:
From Beard to the first world war (pp. 51-76). Amsterdam/New York: Rodopi.
Maclntyre, A. (1989). ME: Post-viral fatigue syndrome: How to live with it. London:
Unwin.
MacLean, G., & Wessely, S. (1994). Professional and popular views of chronic fatigue
syndrome. British Medical Journal, 308, 776-777.
136 MacMillan, M. B. (1976). Beard's concept of neurasthenia and Freud's concept of the
actual neuroses. Journal of the History of the Behavioral Sciences, 12(4), 376-390.
Macy, J., & Allen, E. (1933-34). Justification of the diagnosis of chronic nervous
exhaustion. Annals of Internal Medicine, 7, 861-867.
Marland, H. (2001). 'Uterine mischief: W. S. Playfair and his neurasthenic patients. In
M. Gijswijt-Hofstra, & R. Porter (Eds.), Cultures of neurasthenia: From Beard to
the first world war (pp. 117-139). Amsterdam/New York: Rodopi.
McEvedy, C. P., & Beard, A. W. (1970a). Royal Free epidemic of 1955: A
reconsideration. British MedicalJournal, 7(5687), 7-11.
McEvedy, C. P., & Beard, A. W. (1970b). Concept of benign myalgic encephalomyelitis.
British MedicalJournal, 7(5687), 11-15.
Mechanic, D. (1995). Sociological dimensions of illness behavior. Social Science and
Medicine, 41, 1207-1216.
Meyer, A. (1903). An attempt at analysis of the neurotic constitution. American Journal
of Psychology, 14(3-4), 354-367.
Misbach, J. & Stam, H. J. (2006). Medicalizing melancholia: Exploring profiles of
psychiatric professionalization. Journal of the History of the Behavioral Sciences,
42(1), 41-59.
Mitchell, S. W. (1871). Wear and tear, or hints for the overworked. Philadelphia: J. B.
Lippincott Company.
Mitchell, S. W. (1877/1907, 8th edition). Fat and blood: An essay on the treatment of
certain forms of neurasthenia and hysteria. Philadelphia: J. B. Lippincott Company.
137 Mitchell, S. W. (1908). The treatment by rest, seclusion, etc. in relation to psychotherapy.
Journal of the American Medical Association, 25, 2033-2037.
Morris, D. B. (1998). Illness and culture in the postmodern age. Berkeley: University of
California Press.
Morris, D., & Stare, F. (1993). Unproven diet therapies in the treatment of chronic fatigue
syndrome. Archives of Family Medicine, 2, 181-186.
Moss-Morris, R. (1997). The role of illness cognitions and coping in the aetiology and
maintenance of the Chronic Fatigue Syndrome (CFS). In K. Petrie, & J. Weinman
(Eds.), Perceptions of health and illness: Current research and applications (pp.
411-439). London: Harwood Academic Publishers.
Muir Gray, J. A. (1999). Postmodern medicine. The Lancet, 554(9198), 1550-1553.
Nerves and nervousness. (1894, January 6). The Spectator, 72, 11-12.
Neve, M. (2001). Public views of neurasthenia: Britain, 1880-1930. In M. Gijswijt-
Hofstra, & R. Porter (Eds.), Cultures of neurasthenia: From Beard to the first world
war (pp. 141-159). Amsterdam/New York: Rodopi.
O'Brien, S. (2000). The country of the ill. American Quarterly, 52(4), 765-774.
Osier, W. (1912). The principles and practice of medicine (vol. 8). New York: Appleton
&Co.
Parsons, G. P. (1977). Equal treatment for all: American medical remedies for male
sexual problems: 1850-1900. Journal of the History of Medicine and Allied
Sciences, 32,55-71.
138 Peters, S., Stanley, I., Rose, M., & Salmon, P. (1998). Patients with medically
unexplained symptoms: Sources of patients' authority and implications for demands
on medical care. Social Science and Medicine, 46(4-5), 559-565.
Porter, R. (2001). Nervousness, eighteenth and nineteenth century style: From luxury to
labour. In M. Gijswijt-Hofstra, & R. Porter (Eds.), Cultures of neurasthenia: From
Beard to the first world war (pp. 31-48). Amsterdam/New York: Rodopi.
Press conference (2006, November). CFIDSLink E-newsletter. Retrieved September 3,
2007, http://www.cfids.org/sparkcfs/press-conference.asp
Prins, J. B., van der Meer, J. W. M., & Bleijenberg, G. (2006). Chronic fatigue syndrome
(research). The Lancet, 367.9507, 346-356.
Rajeevan, M. S., Smith, A. K., Dimulescu, I. Unger, E. R., Vernon, S. D., Heim, C, &
Reeves, W. C. (2007). Glucocorticoid receptor polymorphisms and haplotypes
associated with chronic fatigue syndrome. Genes, Brain and Behavior, 6,167-176.
Reeves, W. C, Jones, J. F., Maloney, E., Heim, C, Hoaglin, D. C, Boneva, R. S., et al.
(2007). Prevalence of chronic fatigue syndrome in metropolitan, urban, and rural
Georgia. Population Health Metrics, 5, (online journal, retrieved August 20, 2007,
www.pophealthmetrics.com/content/5/1/5.
Reyes, M., Nisenbaum, R., Hoaglin, D. C, Unger, E. R., Emmons, C, Randall, B.,
Stewart, J. A., Abbey, S., Jones, J. F., Gantz, N., Minden, S., & Reeves, W. C.
(2003). Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas.
Archives of Internal Medicine, 163, 1530-1536.
139 Reynolds, E. (1910). Gynecological operations on neurasthenics: Advantages,
disadvantages, selection of cases. Boston Medical & Surgical Journal, 163, 113-
118.
Richman, J. A., & Jason, L. A. (2001). Gender biases underlying the social construction
of illness states: The case of chronic fatigue syndrome. Current Sociology, 49(3),
15-29.
Ricks, D. (2006, April 21). Fatigue gene isolated: With discovery of mutation that
inhibits stress response and causes chronic syndrome, researchers hope to improve
patient care. Newsday. Retrieved April 10, 2007,
www.accessmylibrary.com/coms2/browse_JJ_N241
Rockwell, A. D. (1892). Nervous diseases and civilization. Science, 20, 373.
Roelcke, V. (1997). Biologizing social facts: An early 20th century debate on Kraepelin's
concepts of culture, neurasthenia, and degeneration. Culture, Medicine and
Psychiatry, 21(4), 383-403.
Rosenberg, C. E. (1962). The place of George M. Beard in nineteenth-century psychiatry.
Bulletin of the History of Medicine, 36, 245-259.
Rosenberg, C. E. (1989). Disease in history: Frames and framers. The Milbank Quarterly,
67, 1-15.
Salmon, P., & Hall, G. M. (2003). Patient empowerment and control: A psychological
discourse in the service of medicine. Social Science & Medicine, 57, 1969-1980.
Sauret, J. M, & Vilissova, N. (2002). Human brucellosis. Journal of the American Board
of Family Medicine, 15(5), 401-406. 140 Scheurich, N. (2000). Hysteria and the medical narrative. Perspectives in Biology and
Medicine, 43,461-474.
Schorr, M. (May - June 2005). Is it all in my head? Psychology Today. Retrieved April
10, 2007, vv^ww.psychologvtoday.com.
Sharpe, M. (1998). Doctors' diagnoses and patients' perceptions: Lessons from chronic
fatigue syndrome. General Hospital Psychiatry, 20, 335-338.
Sharpe, M. & Carson, A. (2001). "Unexplained" somatic symptoms, functional
syndromes, and somatization: Do we need a paradigm shift? Annals of Internal
Medicine, 134(9), 926-930.
Sharpe, M, Hawton, K., Simkin, S., Surawy, C, Hackmann, A., Klimes, I., et al. (1996).
Cognitive behaviour therapy for the chronic fatigue syndrome: A randomized
controlled trial. British Medical Journal, 312(7022), 22-26.
Shorter, E. (1992). From paralysis to fatigue: A history of psychosomatic illness in the
modern era. New York: The Free Press.
Shorter, E. (1993). Chronic fatigue in historical perspective. In G. R. Bock, & J. Whelan
(Eds.), Chronic fatigue syndrome: Ciba Foundation Symposium 173 (pp. 6-22).
Chichester, U.K.: John Wiley & Sons.
Shorter, E. (1994). From the mind into the body: The cultural origins of psychosomatic
symptoms. New York: Free Press.
Shorter, E. (1995). Sucker-punched again! Physicians meet the disease-of-the-month
syndrome. Journal of Psychosomatic Research, 39(2), 115-118.
141 Showalter, E. (1987). The female malady: Women, madness, and English culture, 1830-
1980. New York: Penguin Books.
Showalter, E. (1997). Hystories: Hysterical epidemics and modern media. New York:
Columbia University Press.
Sicherman, B. (1977, January). The uses of a diagnosis: Doctors, patients and
neurasthenia Journal of the History of Medicine and Allied Sciences, 32(1), 33-54.
Slijkhuis, J. (2001). Neurasthenia as Pandora's box? 'Zenuwachtigheid' and Dutch
psychiatry around 1900. In M. Gijswijt-Hofstra, & R. Porter (Eds.), Cultures of
neurasthenia: From Beard to the first world war (pp. 257-278). Amsterdam/New
York: Rodopi.
Snyder, K. (Producer/Director/Writer). (2001). I remember me [Motion picture]. United
States: Zeitgeist Films.
Solomon, L, & Reeves, W. C. (2004). Factors influencing the diagnosis of chronic
fatigue syndrome. Archives of Internal Medicine, 164, 2241-2245.
Steincamp, J. (1989). Overload: Beating ME. London: Fontana.
Stobbe, M. (2007, February 18). Funding for chronic fatigue study illustrates role politics
plays in research. Canadian Press, Retrieved from Yahoo! News Canada, February
18,2007.
Stoff, J. A. (1990, Summer). Chronic fatigue and immune dysfunction syndrome.
Nutrition Health Review. Retrieved April 14, 2007,
www.findarticles.com/p/articles/mi_m0876/is_n55/ai_9132130
142 Taylor, R. (2001). Death of neurasthenia and its psychological reincarnation: A study of
neurasthenia at the National Hospital for the Relief and Cure of the Paralysed and
Epileptic, Queen Square, London, 1870-1932. British Journal of Psychiatry, 179,
550-557.
Teague, V. (2007). A retrospective on the 8th IACFS Conference. Retrieved August 19,
2007 from the IACFS/ME (International Association for Chronic Fatigue Syndrome)
web site http://iacfs.net/p/L522.html
The autobiography of a neurasthenic (1896). The Post-Graduate, 9, 369-370.
Theriot, N. M. (1993). Women's voices in nineteenth-century medical discourse: A step
toward deconstructing science. Signs, 19,1-31.
Theriot, N. M. (2001). Negotiating illness: Doctors, patients, and families in the
nineteenth century. Journal of the History of the Behavioral Sciences, 37(4), 349-
368.
Thomson, M. (2001). Neurasthenia in Britain: An overview. In M. Gijswijt-Hofstra, & R.
Porter (Eds.), Cultures of neurasthenia: From Beard to the first world war (pp. 77-
95). Amsterdam/New York: Rodopi.
Treatment: medical, CFIDS Association of America web site. Retrieved August 20, 1997,
http^Vwww.cfids.org/about-cfids/medical.asp.
Tucker, I. (2004). 'Stories' of chronic fatigue syndrome: An exploratory discursive
psychological analysis. Qualitative Research in Psychology, 1, 153-167.
Van Deusen, E. H. (1869). Observations on a form of nervous prostration, (neurasthenia,)
culminating in insanity. American Journal of Insanity, 25, 445-461. 143 Vemon, S. D., & Reeves, W. C. (2006). The challenge of integrating disparate high-
content data: Epidemiological, clinical and laboratory data collected during an in-
hospital study of chronic fatigue syndrome. Pharmacogenomics, 7(3), 341-343.
Vernon, S. D., Whistler, T., Aslakson, E., Rajeevan, M, & Reeves, W. C. (2006).
Challenges for molecular profiling of chronic fatigue syndrome. Pharmacogenetics,
7(2), 211-218.
Wall, D. (2005). Encounters with the invisible: Unseen illness, controversy, and chronic
fatigue syndrome. Dallas: Southern Methodist University Press.
Walsh, J. J. (1912). Mental incapacity (psychasthenia). In Psychotherapy: Including the
history of the use of mental influence, directly and indirectly in healing and the
principles for the application of energies derived from the mind to the treatment of
disease (pp. 597-603). New York: D. Appleton & Company.
Ware, N. C. (1992). Suffering and the social construction of illness: The deligitimation of
illness experience in chronic fatigue syndrome. Medical Anthropology Quarterly,
6(4), 347-361.
Ware, N. C. (1993). Society, mind and body in chronic fatigue syndrome: An
anthropological view. In G. R. Bock, & J. Whelan (Eds.), Chronic fatigue syndrome:
Ciba Foundation Symposium 173 (pp. 62-82). Chichester, U.K.: John Wiley & Sons.
Ware, N. C. (1999). Toward a model of social course in chronic illness: The example of
chronic fatigue syndrome. Culture, Medicine and Psychiatry, 23, 303-331.
144 Ware, N. C. & Kleiman, A. (1992). Culture and somatic experience: The social course of
illness in neurasthenia and chronic fatigue syndrome. Psychosomatic Medicine, 54,
546-560.
Ware, N. C, & Weiss, M. G. (1994). Neurasthenia and the social construction of
psychiatric knowledge. Transcultural Psychiatry, 31(2), 101-123.
Wessely, S. (1990). Old wine in new bottles: Neurasthenia and 'ME'. Psychological
Medicine, 20,35-53.
Wessely, S. (1991). History of postviral fatigue syndrome. British Medical Bulletin, 47,
919-941.
Wessely, S. (1994). Neurasthenia and chronic fatigue: Theory and practice in Britain and
America. Transcultural Psychiatry, 31(2), 173-209.
Wessely, S., Hotopf, M., & Sharpe, M. (1998). Chronic fatigue and its syndromes.
Oxford: Oxford University Press.
Whiting, P., Bagnall, A., Sowden, A. J., Cornell, J. E., Mulrow, C. D., & Ramirez, G.
(2001). Interventions for the treatment and management of chronic fatigue
syndrome. The Journal of the American Medical Association, 286, 1360-1368.
Wiener, P. P. (1956). G. M. Beard and Freud on 'American nervousness.' Journal of the
History of Ideas, 17, 269-21 A.
Williams, T. A. (1909). The importance for research and treatment of distinguishing
clinical types among the psycho-neuroses. The Journal of Abnormal Psychology,
4(\), 32-35.
145 Winslow, R. (1990, November 19). CDC to study illness derided as 'yuppie flu.' Wall
Street Journal, B1.
Wood, A. D. (1973, Summer). "The fashionable diseases": Women's complaints and
their treatment in nineteenth-century America. Journal of Interdisciplinary History,
4(1), 25-52.
World Health Organization (1992). The ICD-10 classification of mental and behavioral
disorders. Clinical descriptions and diagnostic guidelines. Geneva: WHO.
Zavestoski, S., Brown, P., McCormick, S., Mayer, B., D'Ottavi, M., & Lucove, J. C.
(2004). Patient activism and the struggle for diagnosis: Gulf War illnesses and other
medically unexplained physical symptoms in the US. Social Science & Medicine,
58, 161-175.
146