Category: Psychiatry/Psychology

The chronic fatigue syndrome: a reappraisal and unifying hypothesis

Abstract:

The chronic fatigue syndrome is one of the most common medical problems in Western countries. Research work in virology, immunology, metabolic medicine and psychiatry in this area is reviewed and a disease model proposed. The chronic fatigue syndrome can be considered as a continuum ranging from cases with chronic viraemia on the one hand to instances of frank psychiatric illness on the other. In the majority of patients the fully evolved syndrome may involve an interaction of premorbid factors (psychological, immunological), environmental trigger factors (virus) and enhancing factors (emotional response to illness). A Venn diagram is a convenient way of expressing this concept.

 

Source: Byrne E. The chronic fatigue syndrome: a reappraisal and unifying hypothesis. Clin Exp Neurol. 1991;28:128-38. http://www.ncbi.nlm.nih.gov/pubmed/1821821

 

Life insurance MDs sceptical when chronic fatigue syndrome diagnosed

Comment on: Life insurance MDs sceptical when chronic fatigue syndrome diagnosed. [CMAJ. 1990]

 

As a physician with chronic fatigue syndrome (CFS) since the early days of the Lake Tahoe, Calif., outbreak, in 1984, I read Olga Lechky’s report (Can MedAssoc J 1990; 143: 413- 415) with particular interest. It was refreshing to hear Dr. Richard Proschek, assistant medical director of Mutual Life of Canada, admit that the industry’s attitude to CFS is one of hostility. Unfortunately for the thousands of severely debilitated patients with the condition this scepticism and hostility are not restricted to that industry, which in many instances has behaved with compassion and responsibility toward its clients. The hostile viewpoint is also widely prevalent in the medical profession and is often freely communicated to patients.

To hold that CFS is not a real disease it is necessary to imagine that in 1984 people of all ages began to manufacture a condition with clearly defined symptoms that begins as a flu-like illness, persists and evolves. How many diseases fit this description? When, before 1984, did depression present so? Can it be true that thousands of our brightest citizens, including children, Olympic aspirants, several members of some families, alarming numbers of teachers, 50% of a symphony orchestra and 10% of the population of Incline Village, Nev., abruptly and concurrently elected to drop out of life, then continued to complain in the face of widespread scepticism, hostility, marital breakdown and, frequently, isolation? What, other than an infectious agent, could cause this?

Proschek’s bias arises from his position. Physicians in practice, however, see many CFS patients who have no insurance or are quite wealthy. The degree to which imagination must extend to accommodate a diagnosis of secondary gain in these people is beyond belief. Many physicians lament the lack of a blood test for CFS. What, pray, is the test for malingering, a diagnosis we seem to have no difficulty making?

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1452931/pdf/cmaj00229-0013.pdf

 

Source: Sean J. O’Sullivan, MD. Life insurance MDs sceptical when chronic fatigue syndrome diagnosed. CMAJ. 1990 Dec 15;143(12):1283-6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1452931/

 

Hyperventilation disorders

Hyperventilation syndrome falls into the shadowy hinterland between physiology, psychiatry, psychology and medicine. In this respect it joins a long list of syndromes from the past of which effort syndrome is just one example. Myalgic encephalomyelitis (ME) and postviral fatigue syndrome are recent attempts to impose a unitary definition on what is probably a complex interaction between many different organic and psychological factors. The recent introduction of terms such as somatization disorder recognize this aetiological heterogeneity (1).

The symptoms of hypocapnia induced by voluntary overbreathing were first described by Haldane in 1908, the first case of spontaneous hyperventilation by Goldman in 1922 (2), and the term Hyperventilation Syndrome was first used by Dalton, Kerr and Gliebe in 1937 to describe patients with symptoms both of hypocapnia and anxiety (3). Since then, many different interpretations of this term have appeared in the literature encompassing patients with widely different aetiologies. Much research in this area is bedevilled by failure to define clearly the detailed characteristics of the patients studied; by the assumption of definitions for which there is no universal agreement; and by the presentation of scientifically unsound data lacking in rigorous quantitative proof and with perpetuation of circular arguments. The papers in this issue of the journal make a commendable attempt to reintroduce the reader to the historical perspectives of this subject and to clarify some of the issues, but unfortunately also have some of the shortcomings common to so many of the studies in this very difficult field.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292944/pdf/jrsocmed00129-0005.pdf

 

Source: Gardner W. Hyperventilation disorders. J R Soc Med. 1990 Dec;83(12):755-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292944/

 

Chronic fatigue syndrome and the psychiatrist

Abstract:

The number of patients who are identified as having chronic fatigue syndrome (CFS) has increased, and as a result, chronic fatigue syndrome has received widespread attention. Research has demonstrated that cognitive, affective and behavioural symptoms are prominent in CFS. Psychiatrists are therefore being asked to participate in the assessment and management of patients with this syndrome. This paper will provide an overview of the clinical characteristics of CFS and the current empirical findings related to its pathology, and will conclude with a discussion of the management of these patients.

 

Source:  Abbey SE, Garfinkel PE. Chronic fatigue syndrome and the psychiatrist. Can J Psychiatry. 1990 Oct;35(7):625-33. http://www.ncbi.nlm.nih.gov/pubmed/2268845

 

Postviral syndrome

Note: This letter appeared in the Journal of the Royal Society of Medicine, Volume 83, July 1990.

 

We read with interest the paper by Bowman (December 1989 JRSM, p 712) which suggests that the positive monospot test may only be present within the first four weeks of the illness. They also questioned the specificity of V P-I antigen, a view recently supported by Lynch and Seth. (1)

We are, however, interested in their comment that the General Health Questionnaire (GHQ) is having a limited usefulness in the context, of postviral syndrome. They have used an older version of the GHQ which includes 60 questions. There is a 30 item GHQ which was derived from the GHQ-60 by excluding symptoms that were commonly present in subjects with entirely physical illness thus the GHQ-30 could be regarded as a measure of more purely psychological or psychosocial symptoms (2). Another difficulty with postviral syndrome patients is that by definition they suffer from chronic symptoms. By using the GHQ as a screening instrument, it is likely that there will be a number of cases that will not be detected by GHQ (false negatives). It has been suggested that false negatives largely result from the relative insensitivity of the GHQ for chronic disorders (3,4). To overcome this problem Goodchild and Duncan-Jones have proposed a new scoring procedure (C-GHQ) to eliminate the insensitivity of the GHQ for chronic complaints (5).

Further investigation on this showed that the new scoring method was better with regard to both the GHQ at the measure of severity and GHQ with the screening instrument (6,7). We therefore suggest that in future investigation of the psychological well being of patients with postviral syndrome the shorter version of the GHQ with the revised scoring methods is to be used.

~B T FARID Consultant Psychiatrist

~A CHANDRA Registrar in Psychiatry New Cross Hospital Wolverhampton WV10 0QP

References

1 Lynch S, Seth R. Postviral fatigue syndrome and the V P-I antigen. Lancet 1989;ii.1160-1

2 Huppert FA, et al. The factor structure of the General Health Questionnaire (GHQ-30). Br J Psychiatry 1989; 155:178-85

3 BenJamin S, elm P, Haran D. Community screening for mental illness: A validity study of the General Health Questionnaire. Br J Psychiatry 1982;140:174-80

4 Finlay-Jones RA, Murphy E. Severity of psychiatric disorder and the 30-item GHQ. Br J Psychiatry 1979; 134:609-16

5 Goodchild ME, Duncan-Jones P. Chronicity and the General Health Questionnaire. Br J Psychiatry 1985; 146:55-62

6 Koetar MWJ, Van Den Brink W, Ormel J. Chronic psychiatric complaints and the General Health Questionnaire. Br J Psychiary 1989;155:186-90.

7 Surtees PG. Psychiatric disorder in the community and the General Health Questionnaire. Br J Psychiatry 1987;150:828-35

 

Source:  B T Farid and A Chandra. Postviral syndrome. J R Soc Med. 1990 Jul; 83(7): 476. PMCID: PMC1292747 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292747/

 

Depression and myalgic encephalomyelitis

This comment, published in the Journal of the Royal Society of Medicine in May 1990, was written in response to a letter by Dr. Lev. You can read the letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292388/

 

We read the letter from Lev (November 1989 JRSM, p 693) with interest, but see a danger in using assumptions as to aetiology in definition of study groups. Operational definitions not making this assumption will produce replicable findings and progress towards better definitions and understanding of aetiology.

Definitions of depressed control groups are difficult, for example the following need to be controlled:

(1) Demographic variables

(2) Severity of depression symptoms: inappropriate control groups for ME patients would be severely depressed inpatients. Outpatient depressives are not too dissimilar in severity.

(3) Psychotropic medication: this is less likely to be given to ME patients where treatment is not agreed and could modify symptoms to be compared.

(4) Psychiatric history: in possible ME patients a previous significant psychiatric illness prior to fatigue symptoms leads to difficulty in studying this symptom and produces too much overlap with depressed controls.

(5) History of febrile illness: to minimize overlap, one must also control for preceding febrile illness in otherwise typical depressive illness.

Comparison of control groups should be serial, not cross-sectional as physical symptoms and markers may fluctuate, as may fatigue and depression.

Assessment of depressive symptoms is difficult, as Lev points out, due to non-specific ‘biological’ symptoms of depression. However, psychic ones such as pessimism should not overlap and could be assessed.

The concept of fatigue is poorly understood, as is its assessment. The paradigm of pain research has much to offer, where ‘dichotomization’ of physical and psychological components is not thought useful, but assessment emphasizes all components of the experience of pain. Thus, psychometric assessment of fatigue, for example, its severity, frequency, and pattern may be a future research area. Using such a paradigm, our initial findings of differences in fatigue in the two groups are because depressed patients are predominantly anergic, but ‘ME’ patients have more variability and unpredictable onset of fatigue relative to the severity of exercise attempted. Lack of motivation overlaps in both groups, explicable in Lev’s own terms as due to a reaction to a chronic illness.

~SEAN LYNCH Lecturer and Honorary Senior Registrar in Psychiatry

~RAM SETH Senior Registrar in Psychiatry St Charles Hospital, London

 

Source: S Lynch and R Seth. Depression and myalgic encephalomyelitis. J R Soc Med. 1990 May; 83(5): 341. PMCID: PMC1292666. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292666/pdf/jrsocmed00136-0073a.pdf

 

The psychiatric status of patients with the chronic fatigue syndrome

Abstract:

The prevalence of psychiatric disorder in 48 patients with chronic fatigue syndrome (CFS) was determined. Twenty-two had had a major depressive (non-endogenous) episode during the course of their illness, while seven had a current major (non-endogenous) depression.

The pre-morbid prevalence of major depression (12.5%) and of total psychiatric disorder (24.5%) was no higher than general community estimates. The pattern of psychiatric symptoms in the CFS patients was significantly different to that of 48 patients with non-endogenous depression, but was comparable with that observed in other medical disorders. Patients with CFS were not excessively hypochondriacal.

We conclude that psychological disturbance is likely to be a consequence of, rather than an antecedent risk factor to the syndrome.

 

Source: Hickie I, Lloyd A, Wakefield D, Parker G. The psychiatric status of patients with the chronic fatigue syndrome. Br J Psychiatry. 1990 Apr;156:534-40. http://www.ncbi.nlm.nih.gov/pubmed/2386862

 

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