Tag: post-viral fatigue syndrome

Myth of the chronic fatigue syndrome

THE CHRONIC FATIGUE SYNDROME is a symptom complex characterized by fatigue, myalgias, arthralgias, neurologic symptoms-headaches, paresthesias, dizziness-lymph node swelling or tenderness, cognitive dysfunction, sleep disorders, and depression. The symptoms are similar to those seen in inflammatory illnesses and can be induced by the systemic administration of interferon beta. Severe fatigue is a perplexing and constant complaint in many patients with multiple sclerosis. This indicates that the perception of energy level has a sensitive physiologic basis that is dependent on the homeostasis of other body systems.

The chronic fatigue syndrome has gained popularity among the lay public and has stimulated considerable scientific debate about its existence. Many investigators and practitioners have attributed the disorder to chronic depression. Difficulty arises from the diverse symptoms associated with fatigue states; fatigue is a prominent feature of many systemic, neurologic, and psychiatric disorders. Also, fatigue is a subjective complaint without a quantifiable measure. This interweaving of many symptoms and diagnoses with disabling fatigue makes it difficult to compare patient groups. Terms applied to disorders that probably represent chronic fatigue syndrome are chronic infectious mononucleosis, myalgic encephalomyelitis, idiopathic chronic fatigue and myalgia syndrome, epidemic neuromyasthenia, postviral fatigue syndrome, and fibrositis-fibromyalgia.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1002920/pdf/westjmed00095-0070a.pdf

 

Source: Murray RS. Myth of the chronic fatigue syndrome. West J Med. 1991 Jul;155(1):68. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1002920/

 

Antibody to Coxsackie B virus in diagnosing postviral fatigue syndrome

Abstract:

OBJECTIVE: To study the association between coxsackie B virus infection and the postviral fatigue syndrome and to assess the immunological abnormalities associated with the syndrome.

DESIGN: Case-control study of patients with the postviral fatigue syndrome referred by local general practitioners over one year.

SETTING: General practitioner referrals in Dunbartonshire, Scotland.

PATIENTS: 254 Patients referred with the postviral fatigue syndrome (exhaustion, myalgia, and other symptoms referable to postviral fatigue syndrome of fairly recent onset–that is, several months) and age and sex matched controls obtained from same general practitioner; 11 patients were rejected because of wrong diagnoses, resolution of symptoms, and refusal to participate, leaving 243 patients and matched controls.

MAIN OUTCOME MEASURES: Detailed questionnaire (patients and controls) and clinical examination (patients) and blind analysis of blood sample at entry and after six months for determination of coxsackie B virus IgM and IgG antibodies and other variables (including lymphocyte protein synthesis, lymphocyte subsets, and immune complexes).

RESULTS: Percentage positive rates for coxsackie B virus IgM at entry were 24.4% for patients and 22.6% for controls and for coxsackie B virus IgG 56.2% and 55.3% respectively; there were no significant differences between different categories of patients according to clinical likelihood of the syndrome nor any predictive value in a fourfold rise or fall in the coxsackie B virus IgG titre in patients between entry and review at six months. The rates of positive antibody test results in patients and controls showed a strong seasonal variation. Of the numerous immunological tests performed, only a few detected significant abnormalities; in particular the mean value for immune complex concentration was much higher in 35 patients and 35 controls compared with the normal range and mean value for total IgM was also raised in 227 patients and 35 controls compared with the normal range.

CONCLUSIONS: Serological tests available for detecting coxsackie B virus antibodies do not help diagnose the postviral fatigue syndrome. Percentage positive rates of the antibodies in patients simply reflect the background in the population as probably do the raised concentrations of total IgM and immune complexes.

 

Source: Miller NA, Carmichael HA, Calder BD, Behan PO, Bell EJ, McCartney RA, Hall FC. Antibody to Coxsackie B virus in diagnosing postviral fatigue syndrome. BMJ. 1991 Jan 19;302(6769):140-3. http://www.ncbi.nlm.nih.gov/pubmed/1847316

 

Natural killer cells and the post viral fatigue syndrome

Abstract:

60 patients were referred with a diagnosis of post viral fatigue syndrome (PVFS), but only 50 fulfilled strict criteria for this illness. Many lymphocyte subpopulations were normal, but there was a spectrum of natural killer (NK) cell results: 20/50 (40%) were raised; 8/50 (16%) were low;, 5/50 (10%) were low initially but normal on repeat testing; 17/50 (34%) were normal.

When patients were categorised on their NK cell results, there were significant differences in the two groups with raised or low NK cells compared to the “Not PVFS” group: the CD8 cells were increased (p less than 0.001, p less than 0.02) and the CD4/CD8 ratio was reduced (p less than 0.05) but the CD4 cells were normal.

Clinical data showed that the “Not PVFS” group were older, with less severe illness, less muscle pain and less virological evidence of infection. It is postulated that patients have low NK cells initially and then progress to normal or raised levels dependent on factors such as stress, other infections and behaviour.

 

Source: Ho-Yen DO, Billington RW, Urquhart J. Natural killer cells and the post viral fatigue syndrome. Scand J Infect Dis. 1991;23(6):711-6. http://www.ncbi.nlm.nih.gov/pubmed/1815333

 

Postviral fatigue syndrome

This is a syndrome that may or may not follow what appears to be an acute infectious illness, and may occur in epidemic or sporadic forms consisting of persisting or relapsing ‘fatigue’ or easy fatiguability of at least six months’ duration, for which no other cause is apparent. It is associated with a number of other variable features including mild fever, sore throat, painful lymph nodes, headaches, muscle pain, migratory arthralgia, photophobia, forgetfulness, irritability, concentration difficulties, depression, and sleep disturbance. It has been recognised since the early 1930s and known by a wide variety of names including Iceland disease, Royal Free disease, epidemic neuromyasthenia, myalgic encephalomyelitis, postviral syndrome, and more recently chronic fatigue syndrome.( 1 )

Although predominantly a disorder of young adults, it has been recognised in children with either an acute or insidious onset. At least 10-15 cases of the sporadic form are seen each year at the Hospital for Sick Children, Great Ormond Street, with lethargy, headache, abdominal pain, and subjective muscular weakness being the most common manifestations. Abnormal physical findings are usually conspicuous by their absence but occasionally pharyngeal injection, tender cervical lymph nodes, and muscle tenderness are present. A proportion of patients have an ‘atypical’ lymphocytosis, increased plasma creatine phosphokinase activity, circulating immune complexes, minor changes on electroencephalography and electromyelography, increased serum Epstein-Barr and Coxsackie B antibody titres, and VPI antigen in serum. Some workers have demonstrated enteroviral RNA in muscle biopsy material.(2 )Although an infective aetiology has been invoked, however, the full nature of the illness remains obscure and is probably a mixture of an initial infective insult followed by or associated with an important psychological component.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1792622/pdf/archdisch00656-0012.pdf

 

Source:  Lask B, Dillon MJ. Postviral fatigue syndrome. Arch Dis Child. 1990 Nov;65(11):1198. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1792622/

 

Effect of high doses of essential fatty acids on the postviral fatigue syndrome

Abstract:

Sixty-three adults with the diagnosis of the postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study of essential fatty acid therapy. The patients had been ill for from one to three years after an apparently viral infection, suffering from severe fatigue, myalgia and a variety of psychiatric symptoms.

The preparation given contained linoleic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acids and either it, or the placebo, was given as 8 x 500 mg capsules per day over a 3-month period. The trial was parallel in design and patients were evaluated at entry, one month and three months. In consultation with the patient the doctors assessed overall condition, fatigue, myalgia, dizziness, poor concentration and depression on a 3-point scale. The essential fatty acid composition of their red cell membrane phospholipids was analysed at the first and last visits.

At 1 month, 74% of patients on active treatment and 23% of those on placebo assessed themselves as improved over the baseline, with the improvement being much greater in the former. At 3 months the corresponding figures were 85% and 17% (p less than 0.0001) since the placebo group had reverted towards the baseline state while those in the active group showed continued improvement.

The essential fatty acid levels were abnormal at the baseline and corrected by active treatment. There were no adverse events. We conclude that essential fatty acids provide a rational, safe and effective treatment for patients with the post-viral fatigue syndrome.

 

Source:  Behan PO, Behan WM, Horrobin D. Effect of high doses of essential fatty acids on the postviral fatigue syndrome. Acta Neurol Scand. 1990 Sep;82(3):209-16. http://www.ncbi.nlm.nih.gov/pubmed/2270749

 

Chronic fatigue syndrome

Abstract:

Reports on conditions of chronic fatigue associated with other somatopsychic symptoms after acute viral infections have led to the hypothesis of a “chronic fatigue syndrome” (CFS). Historical disease descriptions, like e.g. “myalgic encephalomyelitits”, were updated by means of modern virological diagnostic techniques and data analysis.

Several viral agents like enteroviruses, Epstein-Barr virus, Human-Herpesvirus 6 and other herpesviruses have been implicated for possible underlying infections. A preliminary disease definition by the Center for Disease Control (CDC) seeks to provide a rational basis for further etiological studies. In fact, there is growing consensus that the syndrome comprises various separate disease entities and causative agents.

Today we can tentatively differentiate a “chronic mononucleosis” after infection with Epstein-Barr virus, an etiologically undetermined “postviral fatigue syndrome” and a fatigue syndrome of the myalgic type after Coxsackie-B virus infection. Furthermore, a valid diagnosis of CFS must be based on the exclusion of defined other diseases and the awareness of dealing with a hypothetical concept. As a result, current knowledge does not yet allow specific therapeutic recommendations.

 

Source: Ewig S, Dengler HJ. Chronic fatigue syndrome. Klin Wochenschr. 1990 Aug 17;68(16):789-96. [Article in German] http://www.ncbi.nlm.nih.gov/pubmed/2170741

 

Myalgic encephalomyelitis: an alternative theory

Note: in this editorial published in the Journal of the Royal Society of Medicine ,Volume 83, August 1990, Dr. Wilson discusses the role allergy plays in the development of post-viral fatigue syndromes.

 

In his discussion paper on myalgic encephalomyelitis (April 1989 JRSM, p 215), Wessley drew attention to the destruction of body and mind, and subsequent suicidal despair, and torment, of patients suffering from myalgic encephalomyelitis (ME) or the postviral fatigue syndrome (PVFS). He referred to the reported relationship between identification of the VPI antigen and the presence of disease symptoms. He stated that more attention requires to be paid to methodological detail which he defined as population sample definition, and adoption of operational criteria. He suggested that a new term should be used to describe the observed symptoms: chronic fatigue syndrome (CFS), and enquired what constitutes the syndrome? Unfortunately he did not refer to the necessity for taking a complete clinical and family history in all patients. In his definition of CFS, he did not refer to any of the somatic symptoms which are always present. Yet, he stated that cases of this disease can only be selected by the (presumably holistic) clinical history. It appears that a new kind of approach based on absence of prejudice, more exhaustive and thorough clinical history taking, a wider approach to clinical examination of the patients, and a critical assessment of the origin of this psychosomatic disease would be of value in our investigations.

You can read the rest of the article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292769/pdf/jrsocmed00133-0005b.pdf

 

Source: Wilson CW. Myalgic encephalomyelitis: an alternative theory. J R Soc Med. 1990 Aug;83(8):481-483. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292769/

 

Post-viral fatigue syndrome, viral infections in atopic eczema, and essential fatty acids

Abstract:

Three clinical observations relating to viral infections are well-known but poorly understood. These are: the susceptibility of people with atopic eczema to viral infections; the occasional precipitation of an atopic syndrome by viral infections; the occurrence of a fatigue syndrome following viral infections.

A unifying hypothesis is presented which explains these observations in terms of the interactions between viral infections and essential fatty acid (EFA) metabolism. Key elements of the hypothesis are the facts that interferon requires 6-desaturated EFAs in order to exert its anti-viral effects, that people with atopic eczema have low levels of 6-desaturated EFAs, and that viruses, as part of their attack strategy, may reduce the ability of cells to make 6-desaturated EFAs.

The hypothesis has practical implications for the treatment of patients with viral infections.

 

Source: Horrobin DF. Post-viral fatigue syndrome, viral infections in atopic eczema, and essential fatty acids.  Med Hypotheses. 1990 Jul;32(3):211-7.  http://www.ncbi.nlm.nih.gov/pubmed/2204789

 

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

 

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/