CFS/M.E. and Neuresthenia Retasted
Jock Millenson (1993)
In two independent articles, psychiatrists from Britain and the USA have advanced the thesis that Chronic Fatigue Syndrome (CFS) is identical to neurasthenia, a Victorian syndrome characterized by severe chronic fatigue, depression and a host of other somatic symptoms2. The argument is of more than academic interest to CFS sufferers, for neurasthenia is generally regarded as a psychiatric disorder and its treatment would presumably be a variation of the treatments given for any other psychoneurotic depressive disorder: antidepressants, minor and major tranquilizers, perhaps electro-convulsive and insulin shock in severe cases, along with a psychotherapy that encourages activity.
Besides such inappropriate treatments the psychiatrization of CFS, if sustained by the medical establishment, would also have grave consequences for the status of CFS as an authentic disease. It is unlikely, for instance, that state disability benefits would be made available for a psychoneurotic CFS, and the stigmatization with which our society views such disorders would naturally fall upon sufferers. Since as late as 1991 two thirds of family practitioners stated that they did not believe there is any such disease as CFS,3 there is a real concern that doctors especially are likely to be prone to the suggestion that CFS is a psychoneurotic syndrome. Hence the arguments marshaled by Simon Wessely at the Institute of Psychiatry in London and Donna Greenberg in Massachusetts must be taken very seriously.
Fortunately, although there is an important germ of truth in their position, their conclusion that CFS is a psychoneurotic disorder follows only if neurasthenia itself is. But is that so?
When I first learned that CFS was being equated to neurasthenia, I was quick to condemn this as a misleading analogy based on a superficial comparison of the two syndromes confined principally to the two symptoms of depression and fatigue4. I was well aware both as a sufferer and a psychologist that the etiologies are different, and that the depression of CFS is in part viral induced and in part a secondary consequence of the reduction in one’s ability to lead a normal life. I also knew that CFS involves as its keynote symptom a sense of constantly feeling ill with flu-like symptoms. None of these attributes fitted a syndrome of fatigue, listlessness, and depression arising out of disappointment in love, financial failure, death of spouse, chronic unfulfilled creative potential and other problems of living.
But when I went back to read the original literature on neurasthenia I was startled to discover that the symptoms first described by the American neurologist G. M. Beard in 1869 fitted virtually point-for-point all the weird and bizarre symptoms which by now we are all familiar with as CFS. Beard recognized that neurasthenia was worsened by exercise, that it struck industrious people hitherto without depressive histories, and that it had a long course with uncertain prognosis. I began to wonder if perhaps Wessely and Greenberg had, after all, made an important discovery, yet because they came from a psychiatric frame of reference missed its implications. Was neurasthenia of Victorian times an early epidemic of CFS? Aside from the striking similarity in symptomatology, there were two additional provocative hints. Firstly, it was recognized very early that a significant group of neurasthenic patients were post-infective. Secondly, Beard himself suffered from his own disease. He knew it first hand, and was absolutely certain that it was an organic disease whose pathology would in due course be discovered. One hundred and twenty years ago viruses were of course unknown. The symptomatology led Beard naturally to assume that the disease pathology would be found in the nerves—today we would say the central nervous system—hence the name he gave the disease, neurasthenia = nerve weakness.
Fatigue is a symptom of many illnesses and disorders with a wide variety of etiologies
There are other important correspondences between nerve weakness of the 1880/1890s and CFS of the 1980/1990s. First of all the principle effective treatment was the “rest cure” formulated by Beard’s colleague S. Weir Mitchell which consisted of absolute bed rest for many weeks. Although the rest cure was later discredited for reasons that we shall shortly see, in its day it was widely hailed as the principle effective therapy. There is also a connection between the presumed etiologies. Neurasthenia was regarded as an exhaustion disease, what we would today call “burn out”. When an individual “who is driven to think, to work to strive for success presses himself and his life force to the limit, he eventually exhausts his currents like an overloaded battery.”5 I have pointed out elsewhere that what little there is of value in the odious term “Yuppie Flu” refers to exactly this predisposing factor in CFS.6
Depression was a common side effect of neurasthenia too, but the Victorians were clear that this depression was not the same as that seen in major psychiatric depression disorders then called melancholia.
The depression of neurasthenia is attimes mistaken for that of melancholia, but this should not occur as the whole history is different and even the nature of the depression varies.7
This passage, written 80 years ago in an authoritative textbook of clinical psychiatry, is still valid, and has recently been re-emphasized. Colette Ray (1991) writing in response to Simon Wessely’s article has cautioned against the facile incorporation of CFS into the category of a psychoneurotic disorder on the basis of the observed depression in both cases.8 As she notes, the psychological tests used to assess degree of depression invariably include in them items relating to fatigue, loss of libido, sleep disruption and loss of appetite, all of which are frequent primary results, not causes, of CFS.
It is thus one thing to agree with the psychiatrists that “nerve weakness” of Victorian times is CFS of today, but something quite different to say that therefore they are both psychoneurotic depressive disorders with all that that implies for disease authenticity and treatment.9 To see that more clearly we must trace the development and psychiatrization of the term neurasthenia itself, which began as a well-defined syndrome with a specific etiology and ended as a dumping ground for chronic fatigues of any sort for which no organic cause (read disease) could be found.
Because fatigue is a symptom of many illnesses and disorders with a wide variety of etiologies and varying degrees of psychogenesis, this symptom, however prominent, can never in itself be diagnostic. The cases of fatigue with organic bases could be appropriately assigned to particular disease categories, but for others in which medical diagnostics could reveal neither pathology nor physiological dysfunction there was an obvious inclination to consider them inauthentic, that is to say “psychological”. Thus the failure of any actual nerve pathology to be discovered in neurasthenia proved not only highly embarrassing to its status asdisease, it eventually facilitated the transition of neurasthenia to a diagnostic wastebasket lumped together with psychoneurotic fatigue. This confusion of different syndromes helps explain why Weir Mitchell’s rest cure lost its effectiveness. Resting would have been quite useless for psychoneurotic depression fatigue, which does indeed require a very different kind of therapy.
Knowing what we now do about the tendency of CFS to occur in epidemic-like episodes, it appears that gradually the Victorian episode, still unexplained, subsided after some years. Wessely says that the term neurasthenia fell out of fashion and attributes its decline to the reduced social value of the illness behaviour of neurasthenia once the working classes began to complain of it. This view of course assumes that neurasthenia/CFS is an example of somatisation: complaints of physical symptoms that either lack demonstrable organic basis or are judged to be grossly in excess of what would be expected on the grounds of objective medicalfindings. It seems to me much more likely that the demise of neurasthenia occurred because for nearly a century the disease was relatively quiescent, save for the occasional limited outbreaks in Los Angeles in 1939, Iceland in 1944, and the Royal Free Hospital London in l955.
It is the failure to find an organic basis for this illness that creates an explanatory vacuum into which psychiatrization rushes. The tendency to psychologize illnesses that are poorly understood is a well-known phenomenon. For instance, prior to the discovery of the tuberculosis bacillus, tuberculosis was considered a psychosomatic disease.10 Thus the search for a viral pathogen to explain CFS is rightly regarded as a top priority. But I sometimes wonder if this emphasis on organic pathogenesis, certainly worthy, does not deflect us from the fundamental nature of the illness experience and its psychosocial causal nexus. People with tuberculosis were sick and died long before the microbe associated with the disease was discovered. Of course the discovery of the specific germ not only discredited once and for all the idea that tuberculosis was due to an oversensitive soul, it led to appropriate and effective treatment. We wish for the same in CFS. But whether that happens in the near future or not, we remain ill and we do not require laboratory tests to tell us that.
We have, I think, to be prepared for the possibility that just as the theory of nerve weakness proved illusory, so too the search for a specific viral pathogen for CFS could also prove equally futile. Medical science is limited not only by its current knowledge base and technology, but even more by its prevailing concepts of disease.
The search for a specific viral pathogen for CFS could prove futile
It might well turn out, for instance, that CFS/neurasthenia is not due to any special new virus that remains yet undiscovered. It could perhaps be the consequences of any common garden variety influenza, cold, mononucleosis, glandular fever virus that somehow breaches the individual’s primary defenses in the upper respiratory and lymph tissue and for reasons we do not fully understand makes its way deeper into the body, e.g., the gut. From that focus it eludes the immune system and radiates its effects throughout the body. The conditions under which such an extraordinary progression occurs may have something to do with the virulence of the infective agent (hence the tendency for the disease to appear in episodic epidemic-like outbreaks), but also something to do with an individual’s own personality that exhibits a reluctance to rest and restore energy when a viral illness strikes. In a broad-based holistic system of medicine that looks at influences beyond the body of the host, refusing to rest when ill with a cold or influenza or glandular fever could in fact be the effective pathogen. Of course, not all M.E./CFS sufferers are post-infective, but those individuals' who can find no viral illness preceding their CFS may in fact have been sub-clinically infected.
In summary, Victorian neurasthenia was indeed an early epidemic of CFS. Its symptomatology, etiology and effective treatment were clearly identified as early as 1880. As the episode passed with no organic basis having been discovered with the diagnostic tools available to 19th century medicine, it soon faded from view as a true disease category, being eventually incorporated into psychiatry along with psychoneurotic fatigue states of widely differing origins. In particular the confusion with depressive disorders may have led then, as it has today11, to quite inappropriate treatments. Although the term neurasthenia lingered on well beyond the end of the Victorian epidemic as a diagnostic category, by mid-20th century it was rarely invoked and its original meaning virtually lost. CFS is potentially susceptible to the same fate of psychiatrization that neurasthenia suffered so long as its organic pathogenesis eludes medical science, which it may well do for some time to come. This fate, which has quite severe consequences for sufferers, can best be avoided by firstly holding fast to the primary observable illness experience which clearly distinguishes this unique syndrome; and secondly, by endeavoring to substantiate the etiological (“burn out”) and therapeutic (complete rest) hints first proposed over a century ago.
3 November 1993
1 Jock Millenson is associate professor of psychological medicine at the National College of Naturopathic Medicine in Portland, Oregon, USA, and also practices as a medical herbalist at the Prometheus Clinic in South London. He has had CFS/post-infective neurasthenia since the winter of 1987-88.
2 Greenberg, D.B. (1990) Neurasthenia in the 1980s: chronic mononucleosis, chronic fatigue syndrome and anxiety and depressive disorders. Psychosomatics, 31, 129-137; Wessely, S. (1990) Old wine in new bottles: neurasthenia and ‘ME’. Psychological Medicine, 20, 35-53. The title of the present paper is based on Wessely’s title.
3 Hooge, J. (l992) Chronic fatigue syndrome: cause, con-troversy, and care. British Journal of Nursing, 1, 440-446.
4 Millenson, J. (1992) M.E.: An alternative view. Interaction, Jan/Feb.
5 Drinka, G.F. (1984) The birth of neurosis : myth, malady, and the Victorians , New York : Simon and Schuster.
6 Millenson (1992), op. cit.
7 Craig, M. (l912) Psychological medicine. London: J. & A. Churchill.
8 Ray, C. (l991) Editorial: Chronic fatigue syndrome and depression: conceptual and methodological ambiguities. Psychological Medicine, 21, 1-9.
9 Psychogenic depression is of course a serious and often intractable malady; but it is not a disease. See T. Szasz (1974), The myth of mental illness, New York: Harper & Row.
10 Sontag, S. (l977) Illness as a metaphor. New York: Farrar, Straus, Giroux.
11 Butler, S., Chalder, T., Ron, W., Wessely, S. (l991) Cognitive behavior therapy in CFS. Journal of Neurology and Neurosurgery in Psychiatry, 54, 153-158. The therapy involved encouraging patients to carry out normal activities in spite of symptoms. It is difficult to imagine a more lethal prescription for CFS patients.