A personal encounter with a mystery illness

Abstract:

I urge all practitioners to accept that ‘chronic fatigue’ patients have genuine symptoms. This disease can cause depression, but for most patients it is not caused by depression. I acknowledge that a depressed patient can develop the chronic fatigue syndrome in the same way that they can contract any other disease. If you are unable to diagnose a patient with these symptoms please refer them to a centre specialising in this devastating and poorly understood disease.

 

Source: Lopis R. A personal encounter with a mystery illness. Aust Fam Physician. 1991 Mar;20(3):316-7.  http://www.ncbi.nlm.nih.gov/pubmed/2039419

 

A practical approach to chronic fatigue syndrome

Abstract:

Chronic fatigue may have several physical causes, but a psychiatric condition is often involved. A substantial minority of patients are not diagnosed by conventional tests and do not respond to antidepressant therapy. These patients should be referred for psychiatric opinion or observed for new developments. Extensive virologic testing and unorthodox treatment approaches have no scientific basis at present. Claims of dramatic new diagnostic tests or therapy should be treated with caution because of the long history of unsuccessful attempts to categorize chronic fatigue into one diagnosis and the strong placebo effect shown in controlled trials.

 

Source: Hayden SP. A practical approach to chronic fatigue syndrome. Cleve Clin J Med. 1991 Mar-Apr;58(2):116-20. http://www.ncbi.nlm.nih.gov/pubmed/2025913

 

Myalgic encephalomyelitis

Comment in: Myalgic encephalomyelitis. [J R Soc Med. 1991]

Comment on: Myalgic encephalomyelitis: an alternative theory. [J R Soc Med. 1990]

 

I am pleased that Dr Wilson (August 1990 JRSM, p481) has paid me the compliment of giving my article on the vexed topic of ‘myalgic encephalomyelitis’ (April 1989 JRSM, p 215) serious attention, and echoes our call’ for a ‘new approach’ to the problem, based on an absence of prejudice and a sound clinical and social history. He also notes the parallels between neurasthenia and ‘ME’, although the former was not, as he writes, first described in 18842. However, I only wish I could follow the rest of his arguments so clearly:

Dr Wilson states that I failed to realize that ‘about 100%’ of patients have an allergic diathesis and an allergic family history. I was indeed unaware of this remarkable finding. Unfortunately, I have been unable to trace the two sources cited for this observation, one an American paperback, the other a society newsletter. Similarly, I am afraid that neither I nor any of my colleagues have ever met anyone suffering from ‘Alternate Multiple Personality’. Perhaps this was because I was again unaware of the relevant literature. However, in my defence I would not otherwise have known that the two references quoted, namely Dr Wilson’s paper on allergic disease, multiple personality and dowsing, and his paper on possession and multiple personality, are actually about chronic fatigue syndrome. Similarly, I would not have known that an article in the Christian Parapsychologist called ‘Deliverance and dowsing’ is on the psychopathology of allergy and ME, nor that information on treatment of ME would be published in a series of titles beginning with ‘Current theological perspectives on possession. It is becoming harder to keep up with the relevant literature.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293160/pdf/jrsocmed00126-0074c.pdf

 

See the article “Myalgic encephalomyelitis: an alternative theory.” in volume 83 on page 481.

See letter “Myalgic encephalomyelitis.” on page 633.

See the reply “The author replies” on page 183a.

 

Source: Wessely S. Myalgic encephalomyelitis. J R Soc Med. 1991 Mar;84(3):182-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293160/

 

Nurse, is it ME? Understanding myalgic encephalomyelitis

Abstract:

Ignored or dismissed for years, myalgic encephalomyelitis (ME) is now recognised as a genuine illness, and sufferers are recommended strict rest until the symptoms of the virus subside. Public understanding of ME is still uncertain, and nurses are ideally placed to provide practical information and support.

 

Source: Dale S. Nurse, is it ME? Understanding myalgic encephalomyelitis. Prof Nurse. 1991 Mar;6(6):339-40. http://www.ncbi.nlm.nih.gov/pubmed/2000430

 

A comprehensive immunological analysis in chronic fatigue syndrome

Abstract:

A detailed analysis of cell-mediated and antibody-mediated immunity was performed in 20 CDC-defined patients with chronic fatigue syndrome (CFS) and 20 age- and sex-matched healthy controls.

CD3+, CD4+, CD8+, and CD20+ lymphocytes were comparable in two groups. Natural killer cells as defined by CD16, CD56 and CD57 antigens were significantly reduced in CFS. A significant increase in the proportions of CD4+ ICAM 1+ T cells was observed in CFS. Monocytes from CFS displayed increased density (as determined by mean fluorescence channel numbers) of intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function associated antigen 1 (LFA-1), but showed decreased enhancing response to recombinant interferon-gamma in vitro.

The lymphocyte DNA synthesis in response to phytohaemoglobulin (PHA), Concanavalin A (Con A) and pokeweed mitogen (PWM) was normal but the response to soluble antigens was significantly reduced. Serum IgM, IgG, IgA, and IgG subclasses were normal. In vivo specific antibody response to pneumococcus vaccine was depressed in CFS.

Forty percent of patients showed titres of anti-human herpes virus 6 (anti-HHV-6) antibody higher than that in the controls (greater than or equal to 1/80). These data suggest immunological dysfunction in patients with chronic fatigue syndrome. The significance of these observations is discussed.

 

Source: Gupta S, Vayuvegula B. A comprehensive immunological analysis in chronic fatigue syndrome. Scand J Immunol. 1991 Mar;33(3):319-27. http://www.ncbi.nlm.nih.gov/pubmed/1849315

 

Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome

Abstract:

We analysed peripheral blood CD56+ natural killer (NK) cell subsets in 23 carefully characterized patients with post-viral fatigue syndrome (PFS), compared with 19 healthy controls, using fluorochrome-conjugated, specific monoclonal antibodies and the FACScan.

We found significantly increased percentages of CD56+, and especially CD56bright+ NK cells in PFS patients. We also found significantly increased percentages of CD56+ high affinity interleukin-2 (IL-2) receptor (CD25)+ and CD56+ transferrin receptor (CD71+) subsets of cells, most of which also stained brightly for CD56.

Also, we found an increased percentage of CD56+ CD3+ cells, many of which stained brightly for CD56, although there was no increase in the percentage of CD56- CD3+ T cells in these patients. These observations, in conjunction with very low percentage of CD56- CD25+ cells, suggest that there is a preferential involvement of this minor subset of CD56+ CD3+ T cells in PFS.

Finally, a decreased percentage of CD56+ Fc gamma receptor (CD16)+ NK cells was identified, which suggests a reduced capacity of antibody-dependent cellular cytotoxicity in PFS patients. Subsets of CD56+ NK cells co-expressing CD2, CD4 or CD8 did not show any significant difference between PFS patients and healthy controls.

These phenotypic changes provide laboratory evidence of immunological abnormalities in this syndrome, and, we suggest, may be consistent with persistent viral infection.

 

Source: Morrison LJ, Behan WH, Behan PO. Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome. Clin Exp Immunol. 1991 Mar;83(3):441-6. http://www.ncbi.nlm.nih.gov/pubmed/1706238

You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1535328/

 

Chronic fatigue syndrome: I. Epstein-Barr virus immune response and molecular epidemiology

Abstract:

Patients with chronic fatigue syndrome were compared to healthy seropositive control subjects in an open study and a case-control study analyzing spontaneous transformation rates of peripheral blood lymphocytes, EBV viral genome characteristics as determined by DNA restriction fragment polymorphisms, and antibody production by Western blot analysis.

Thirty percent of patients versus 8% of control subjects underwent spontaneous transformation in the two studies. Viral genome patterns were overall similar to one another, with polymorphisms frequently present in BamHI B’, K, H, and Y fragments. Only one line was found with the EBNA-2B genotype.

Nineteen lines were found to contain viral DNA in the linear form suggesting active lytic replication. Western blot studies suggested that ill subjects made antibodies to lytic proteins more frequently than did healthy control subjects. Lack of control of EBV outgrowth in vitro is correlated with antibody evidence of active infection in vivo in some patients with chronic fatigue syndrome.

 

Source: Jones JF, Streib J, Baker S, Herberger M. Chronic fatigue syndrome: I. Epstein-Barr virus immune response and molecular epidemiology. J Med Virol. 1991 Mar;33(3):151-8. http://www.ncbi.nlm.nih.gov/pubmed/1679118

 

Cognitive behaviour therapy in chronic fatigue syndrome

Abstract:

Fifty patients fulfilling operational criteria for the chronic fatigue syndrome (CFS), and who had been ill for a mean of five years, were offered cognitive behaviour therapy in an open trial. Those fulfilling operational criteria for depressive illness were also offered tricyclic antidepressants. The rationale was that a distinction be drawn between factors that precipitate the illness and those that perpetuate it.

Among the latter are cognitive factors such as the belief that physical symptoms always imply tissue damage, and behavioural factors such as persistent avoidance of activities associated with an increase in symptoms. Therapy led to substantial improvements in overall disability, fatigue, somatic and psychiatric symptoms. The principal problems encountered were a high refusal rate and difficulties in treating affective disorders. Outcome depended more on the strength of the initial attribution of symptoms to exclusively physical causes, and was not influenced by length of illness.

These results suggest that current views on both treatment and prognosis in CFS are unnecessarily pessimistic. It is also suggested that advice currently offered to chronic patients, to avoid physical and mental activity, is counterproductive.

 

Source: Butler S, Chalder T, Ron M, Wessely S. Cognitive behaviour therapy in chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1991 Feb;54(2):153-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1014351/

 

A report–chronic fatigue syndrome: guidelines for research

Introduction:

Patients who present with a principal complaint of disabling fatigue of uncertain cause have received much attention in recent years. Correspondingly there has been an increasing amount of research into this problem. The findings have however often been contradictory. Resolution of these contradictions depends on the ability to compare research studies, but such constructive comparison has rarely been possible. This is largely because research has been carried out by investigators trained in different disciplines, using different criteria to define the condition. Whilst such an eclectic approach is to be welcomed, agreement on case definition, and assessment methods is necessary if progress is to be made.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293107/pdf/jrsocmed00127-0072.pdf

 

Source: Sharpe MC, Archard LC, Banatvala JE, Borysiewicz LK, Clare AW, David A, Edwards RH, Hawton KE, Lambert HP, Lane RJ, et al. A report–chronic fatigue syndrome: guidelines for research. J R Soc Med. 1991 Feb;84(2):118-21. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293107/

 

Muscle performance, voluntary activation, twitch properties and perceived effort in normal subjects and patients with the chronic fatigue syndrome

Abstract:

The decrease in maximal force-generating capacity, the degree of central activation of the muscle, and the subjective perception of effort were measured during prolonged submaximal isometric exercise in 12 male patients suffering from the ‘chronic fatigue syndrome’ and 13 naive, healthy male subjects.

Maximal voluntary isometric torque generated by the elbow flexors was measured before, and at 5 min intervals during an endurance sequence of 45 min of repetitive isometric contractions (6 s duration, 4 s rest interval) producing 30% of the initial maximal voluntary torque. Electrical stimuli were also delivered to the elbow flexors to measure the contractile force in the intervals between voluntary contractions. The degree of central motor activation during maximal voluntary contractions was assessed using a sensitive method of twitch interpolation.

In addition, the perceived effort required to achieve the target submaximal contractions was recorded using a standardized self-report scale. A high degree of central activation was achieved in maximal contractions during the endurance sequence both in the patients (mean of maximal force 93.6%; SD 7.8%), and in the control subjects (mean 90.9%; SD 9.5%).

The relative torque produced by either voluntary or electrically stimulated contractions was not significantly different between patients and control subjects throughout the test. There was no significant difference in the perceived exertion between the patients and control subjects.

These findings support the concept that neither poor motivation, nor muscle contractile failure is important in the pathogenesis of ‘fatigue’ in patients with the chronic fatigue syndrome.

 

Source: Lloyd AR, Gandevia SC, Hales JP. Muscle performance, voluntary activation, twitch properties and perceived effort in normal subjects and patients with the chronic fatigue syndrome. Brain. 1991 Feb;114 ( Pt 1A):85-98. http://www.ncbi.nlm.nih.gov/pubmed/1998892