Old wine in new bottles: neurasthenia and ‘ME’

Abstract:

The history of  is discussed in the light of current interest in chronic fatigue, and in particular the illness called myalgic encephalomyelitis (‘ME’). A comparison is made of the symptoms, presumed aetiologies and treatment of both illnesses, as well as their social setting.

It is shown that neurasthenia remained popular as long as it was viewed as a non-psychiatric, neurological illness caused by environmental factors which affected successful people and for which the cure was rest. The decline in neurasthenia was related to the changes which occurred in each of these views. It is argued that similar factors are associated with the current interest in myalgic encephalomyelitis.

It is further argued that neither neurasthenia nor ‘ME’ can be fully understood within a single medical or psychiatric model. Instead both have arisen in the context of contemporary explanations and attitudes involving mental illness. Future understanding, treatment and prevention of these and related illnesses will depend upon both psychosocial and neurobiological explanations of physical and mental fatigability.

 

Source:  Wessely S. Old wine in new bottles: neurasthenia and ‘ME’. Psychol Med. 1990 Feb;20(1):35-53.  http://www.ncbi.nlm.nih.gov/pubmed/2181519

 

Management of post-viral fatigue syndrome

Note: This letter appeared in the February 1990 issue of the British Journal of General Practice. The letter was written in response to an article, “Patient management of post-viral fatigue syndrome,” written by Dr. Ho-Yen, in which he advised that patients rest. You can read the article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371214/

 

Management of the post-viral fatigue syndrome Sir, We read with interest Dr Ho-Yen’s thoughtful paper on the management of the post-viral fatigue syndrome (January Journal, p.37) and welcome the renewed interest in practical management. Dr HoYen’s article is written in response to our previous paper on the subject, (1) and although there are differences between the two approaches, we must first point out the considerable areas of agreement between us, perhaps no more so than the emphasis on the role of the general practitioner, and of the crucial importance of a healthy doctor-patient relationship.

Many of the apparent differences between our approach and that of Dr HoYen are, as he states, due to sample differences. Our experience is based on patients with chronic illness seen in specialist neurological settings with a mean illness duration of five years.(2 )Dr Ho-Yen is familiar with patients with shorter illness durations, referred for a microbiological opinion. Many of the strategies advocated by Dr Ho-Yen are therefore designed for those in whom spontaneous recovery can still be anticipated. However, what about when such recovery has not occurred? In the two largest samples to date others have noted ‘an alarming tendency to chronicity (1,3) and it has been alleged that ‘most of the cases seen do not improve, give up their work and become permanent invalids’.(4) The current therapeutic approach for these patients is obviously unsatisfactory.

How does such chronicity develop? Dr Ho-Yen criticizes the first stage of the model we proposed to explain such chronicity, and points out that far from initially adopting forced inactivity after a viral infection, many chronic sufferers did the opposite, and tried to exercise away the fatigue. We accept his observation. Dr HoYen’s comments do indeed coincide with our own clinical impressions: many patients report initially adopting such strategies, and find that these are unsatisfactory, leading to a rapid recurrence of symptoms. However, we suggest this is an even more convincing explanation of the remainder of the model we propose Simple operant conditioning suggests that such a powerful experience of failure will lead to persistent avoidance, perhaps when the original need for it is no longer present. We also suggest that early and repeated exposure to uncontrollable, aversive and mysterious symptoms, such as the profound muscle pain that characterizes the syndrome, is another potent cause of the demoralization and helplessness so frequently found (Powell R, Wessely S, manuscript submitted for publication) and may in turn explain the high rates of mood disorder that have been observed in several studies.

We do, however, disagree that the management we advocate is to ‘get out and exercise’. This is a common misconception. Cognitive behavioural therapy is not exercise therapy, and we are not physiotherapists. It is true that in the later stages of treatment patients are encouraged to increase their activity (which must ultimately be the aim of any treatment) but therapy does not involve the simple prescription of set amounts of exercise. Instead, treatment is based on mutually agreed targets, which are themselves jointly chosen as being some activity that the patient wishes to undertake, but has avoided. In practice this may simply be brushing one’s teeth, or sitting out of bed to eat a meal. The behaviour is chosen solely on the basis of avoidance; the physiological and ergonomic consequences of such activity are irrelevant. The aim is to introduce predictability, and the return of self-control and self efficacy, not to restore muscle power. Furthermore, the other important component of our approach to management is an awareness of emotional disorders, and a recognition that these may need treatment in their own right.

We agree that the management we advocate is neither new nor unique. Almost identical management is now the treatment of choice for chronic pain (5) and fibromyalgia. (6) The latter is particularly relevant, since it is increasingly accepted that fibromyalgia may indeed be the same condition as post-viral fatigue.(7) Furthermore, it is difficult to think of a pathological mechanism by which gradual increased activity could be harmful, (8’9) even in the minority of patients with clear cut neuromuscular pathology.

The final decision must be based on evidence. We have already announced preliminary details of a pilot evaluation of cognitive behavioural therapy (Wessely S, et al, abstract presented at the scientific meeting of the Royal College of Psychiatrists, London, 25 September 1989). Our conclusion was that the advice currently offered to these patients may not be accurate, and that the current therapeutic nihilism in this condition may be unduly pessimistic.

In summary, the differences between our approach and that of Dr Ho-Yen may be less marked than at first sight. Given the difference in our samples and clinical experience, one might summarize by saying that whereas Dr Ho-Yen correctly emphasizes the dangers of doing too much, too early in the natural history of the condition, we emphasize the equally damaging consequences of doing too little, too late. The most appropriate strategy depends upon the stage of the illness reached by the patient.

~SIMON WESSELY , ANTHONY DAVID Institute of Psychiatry De Crespigny Park London SE5 8AF

~SUE BUTLER, TRUDIE CHALDER National Hospital for Nervous Diseases Queen Square London WC1N 3BG

References

  1. Wessely S, David A, Butler S, Chalder T. The management of chronic post-viral fatigue syndrome. J R Coll Gen Pract 1989; 39: 26-29.
  2. Wessely S, Powell R. Fatigue syndromes: a comparison of chronic ‘postviral’ fatigue with neuromuscular and affective disorders. J Neurol Neurosurg Psychiatry 1989; 52: 940-948.
  3. Smith D. Myalgic encephalomyelitis. In: 1989 Members’ reference book. London: Sabrecrown Publishing, 1989: 247-250.
  4. Behan P, Behan W. The postviral fatigue syndrome. CRC Crit Rev Neurobiol 1988; 42: 157-158.
  5. Pither C. Treatment of persistent pain. Br Med J 1989; 299: 1239.
  6. Yunus M. Diagnosis, etiology and management of fibromyalgia syndrome: an update. Comp Ther 1988; 14: 8-20.
  7. Goldenberg D. Fibromyalgia and other chronic fatigue syndromes: is there evidence for chronic viral disease? Semin Arthritis Rheum 1988; 18: 111-120.
  8. Vignos P. Physical models of rehabilitation in neuromuscular disease. Muscle Nerve 1981; 6: 323-338.
  9. Milner-Brown S, Miller R. Muscle strengthening through high-resistance weight training in patients with neuromuscular disorders. Arch Phys Med Rehabil 1988; 69; 14-19

 

Source: Wessely S, David A, Butler S, Chalder T. Management of post-viral fatigue syndrome. Br J Gen Pract. 1990 Feb;40(331):82-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371151/pdf/brjgenprac00083-0040.pdf

 

Objective measurement of personality variables in epidemic neuromyasthenia patients

Abstract:

The psychological symptoms of patients diagnosed as having epidemic neuromyasthenia were investigated using the Minnesota Multiphasic Personality Inventory, the Social Readjustment Rating Scale, the Mehrabian Achieving Tendency Scale for Females, a personal data questionnaire, and a subjective anxiety rating.

Twenty-five women with epidemic neuromyasthenia were compared with 25 women who were not ill. Multivariate analysis using the Hotelling T-test on the group data indicated that the patient and non-patient groups differed significantly (P less than 0.001) in respect of psychological characteristics. Stress as a possible predisposing factor in the illness was supported (P less than 0.001).

The data do not support the concept of epidemic neuromyasthenia as being ‘mass hysteria’ as mentioned by McEvedy and Beard, but rather seem to support the suggestion that diagnosis can be made by use of a combination of logical, objective medical and physiological measures. The use of biofeedback as a possible treatment is also proposed.

 

Source: Stricklin A, Sewell M, Austad C. Objective measurement of personality variables in epidemic neuromyasthenia patients. S Afr Med J. 1990 Jan 6;77(1):31-4. http://www.ncbi.nlm.nih.gov/pubmed/2294610

 

The neuropsychological dimensions of postinfectious neuromyasthenia (chronic fatigue syndrome): a preliminary report

Abstract:

Postinfectious neuromyasthenia (PIN) is a clinical syndrome of protracted and incomplete recovery after an apparent viral-like illness. Medical investigation yields few abnormalities which might account for the symptomatology. A substantial number of PIN patients complain of cognitive changes.

Specific complaints include impaired attention, concentration and abstraction skills. This study was designed to systematically investigate whether the aforementioned subjective complaints could be quantified objectively using standard neuropsychological instruments. Results indicated that on all tests but one, the subjects’ performances were significantly higher than those of their age matched groups in the normative data.

Specifically, PIN patients scored significantly better than their age matched norms on tests of concentration, attention and abstraction. What is most striking is the discrepancy between the subjective complaints of cognitive impairment and the objective results of the subjects’ performances on all tests.

These findings suggest that psychological factors may play an important role in the cognitive functioning of individuals diagnosed with postinfectious neuromyasthenia.

 

Source: Altay HT, Toner BB, Brooker H, Abbey SE, Salit IE, Garfinkel PE. The neuropsychological dimensions of postinfectious neuromyasthenia (chronic fatigue syndrome): a preliminary report. http://www.ncbi.nlm.nih.gov/pubmed/2394541

 

Attributions and self-esteem in depression and chronic fatigue syndromes

Abstract:

There is considerable overlap in symptomatology between chronic fatigue syndrome (CFS) and affective disorder.

We report a comparison of depressive phenomenology and attributional style between a group of CFS subjects seen in a specialized medical setting, which included a high proportion with depression diagnosed by Research Diagnostic Criteria (RDC), and depressed controls seen in a specialized psychiatric setting.

Significant symptomatic differences between the depressed CFS group and depressed controls were observed for features such as self-esteem and guilt as well as attribution of illness. All the CFS groups tended to attribute their symptoms to external causes whereas the depressed controls experienced inward attribution.

This may have resulted from differences in the severity of mood disorder between the samples, but it is also suggested that an outward style of attribution protects the depressed CFS patients from cognitive changes associated with low mood but at the expense of greater vulnerability towards somatic symptoms such as fatigue.

 

Source: Powell R, Dolan R, Wessely S. Attributions and self-esteem in depression and chronic fatigue syndromes. J Psychosom Res. 1990;34(6):665-73.  http://www.ncbi.nlm.nih.gov/pubmed/2290139

 

Neurasthenia in the 1980s: chronic mononucleosis, chronic fatigue syndrome, and anxiety and depressive disorders

Abstract:

In the 1980s, patients suffering from unexplained fatigue and what seemed like a prolonged attack of acute mononucleosis were given the diagnosis of chronic mononucleosis or chronic infection with the Epstein-Barr virus.

Although the diagnosis has great appeal, the Epstein-Barr virus does not cause the syndrome (CFS) of chronic fatigue, which has been renamed and redefined chronic fatigue syndrome to remove the inference that the virus is its cause.

From a historical perspective, both syndromes represent the 1980s equivalent of neurasthenia, a disease of fatigue that influenced the development of psychiatric nosology. Because patients with depression and anxiety also have chronic fatigue and because most patients with CFS have an affective disorder, the assessment of organic causes of this syndrome requires careful psychiatric diagnosis and treatment.

Defining chronic fatigue syndrome as a medical disorder may deprive patients of competent treatment of their affective disorder.

 

Source: Greenberg DB. Neurasthenia in the 1980s: chronic mononucleosis, chronic fatigue syndrome, and anxiety and depressive disorders. Psychosomatics. 1990 Spring;31(2):129-37. http://www.ncbi.nlm.nih.gov/pubmed/2184452

 

Isolation of human herpesvirus-6 from clinical specimens using human fibroblast cultures

Abstract:

The isolation and characterization of human herpesvirus-6 (HHV-6) has been hindered by the lack of cell lines useful for its rapid propagation. Recently, we have reported that the MRC-5 cell line (human diploid lung fibroblasts) was susceptible for HHV-6 infection.

In this study, we report on the isolation of HHV-6 from the peripheral blood or buffy coat of three chronic fatigue syndrome patients, one post-liver transplant patient, and one severe chronic active Epstein-Barr virus syndrome patient using the MRC-5 cell line.

Additionally, it was observed by Southern blot hybridization studies that four of five isolates had different restriction enzyme fragment patterns than the isolate obtained from the National Institutes of Health with Eco RI.

These data suggest the usefulness of the MRC-5 cell line in the isolation and characterization of HHV-6 from various patients.

 

Source: Luka J, Okano M, Thiele G. Isolation of human herpesvirus-6 from clinical specimens using human fibroblast cultures. J Clin Lab Anal. 1990;4(6):483-6. http://www.ncbi.nlm.nih.gov/pubmed/2178187

 

Severe chronic active Epstein-Barr virus infection syndrome and adenovirus type-2 infection

Abstract:

Four patients from 4 to 24 years of age (3 males, 1 female) with generalized lymphadenopathy, hepatosplenomegaly, and intermittent fever associated with chronic active Epstein-Barr virus (EBV) infection were investigated.

Laboratory data showed polyclonal gammopathy and a tendency for bone marrow suppression. Noteworthy were the extremely elevated immunoglobulin G (IgG) antibody titers to Epstein-Barr viral capsid antigen (VCA) (range, 10,240-81,920) and early antigen (EA) (range, 1,280-40,960). All patients had IgA antibodies to VCA and EA. Subtle, heterogeneous immune functional defects were observed in all four patients. Another unusual feature was our inability to establish spontaneous or B95-8 EBV-immortalized lymphoblastoid cell lines (LCLs) due to a marked cytopathic effect (CPE). Thus, we investigated for other viruses.

Both IgG and IgM antibodies to adenovirus type-2 (Ad-2) were positive by enzyme-linked immunosorbent assay (ELISA) and immunofluorescence (IF) test, suggesting recent or activated Ad-2 infection had occurred. Dual active EBV and Ad-2 infections were likely etiologic in this severe chronic active EBV infection syndrome.

 

Source: Okano M, Thiele GM, Purtilo DT. Severe chronic active Epstein-Barr virus infection syndrome and adenovirus type-2 infection. Am J Pediatr Hematol Oncol. 1990 Summer;12(2):168-73. http://www.ncbi.nlm.nih.gov/pubmed/2165745

 

Patient management of post-viral fatigue syndrome

Abstract:

A case definition for post-viral fatigue syndrome is proposed within which various subgroups of patients exist. Any one treatment may not apply to all the subgroups. In particular, patients’ experiences do not show that avoidance of exercise is maladaptive. It is proposed that the recently ill often try to exercise to fitness whereas the chronically ill have learnt to avoid exercise. Recovery is more likely to be achieved if patients learn about their illness and do not exhaust their available energy.

 

Source: Ho-Yen DO. Patient management of post-viral fatigue syndrome. Br J Gen Pract. 1990 Jan;40(330):37-9. http://www.ncbi.nlm.nih.gov/pubmed/2107839

Note: You may read the full article here:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371214/

 

Usefulness of a standard battery of laboratory tests in investigating chronic fatigue in adults

Abstract:

Twenty-two adults with chronic fatigue were studied to determine the clinical usefulness of commonly applied laboratory tests. Subjects with the chief complaint of fatigue persisting for more than one year were followed for an average of seven months at a university family health centre.

During this time a group of commonly recommended tests were carried out and the patients had repeated physical examinations. Physical diseases and laboratory abnormalities were few, and patients with abnormal values and active problems were followed until their fatigue resolved or their abnormalities reverted to normal following therapy. The study demonstrated that the presence of an abnormal laboratory result in a fatigued individual does not necessarily indicate the cause of fatigue.

A psychiatric history was also performed and patients were tested with the symptom check list 90-R (SCL-90-R), a 90-item psychological symptom check list. Seven patients were receiving psychotherapy when they enrolled in the study. Two additional subjects entered therapy after the start of the study. Results on the symptom check list for the study group were largely abnormal, with a majority scoring in the highest quartile for depression, paranoid ideation and psychoticism.

It is concluded that the investigation of patients with fatigue which has lasted for longer than one year should focus on psychological causes. In this group of patients laboratory abnormalities are not useful in guiding evaluation or treatment for their fatigue.

 

Source: Valdini A, Steinhardt S, Feldman E. Usefulness of a standard battery of laboratory tests in investigating chronic fatigue in adults. Fam Pract. 1989 Dec;6(4):286-91. http://www.ncbi.nlm.nih.gov/pubmed/2632306