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Volume 1, Number 2 |
1st June 1998 |
Visser, J., Blauw, B., Hinloopen, B., Brommer, E., de Kloet, ER., Kluft, C and Nagelkerken, L. CD4 T lymphocytes from patients with chronic fatigue syndrome have decreased interferon-g production and increased sensitivity to dexamethasone. Journal of Infectious Diseases, 1998, 177, 2, 451-454
A disturbed hypothalamus-pituitary-adrenal gland axis and alterations at the immune system level have been observed in patients with CFS. Glucocorticoids are known to modulate T cell responses; therefore, purified CD4 T cells from CFS patients were studied to determine whether they have an altered sensitivity to dexamethasone (DEX).
CD4 T cells from 18 patients with CFS (CDC criteria '94) produced less interferon-g than did cells from healthy, sex and race matched controls; by contrast, interleukin-4 production and cell proliferation were comparable. With CD4 T cells from CFS patients (compared with cells from controls), a 10- to 20-fold lower DEX concentration was needed to achieve 50% inhibition of interleukin-4 production and proliferation, indicating an increased sensitivity to DEX in CFS patients. Surprisingly, interferon-g production in patients and controls was equally sensitive to DEX.
The reduced interferon-g production may reflect a selective reduction in activity of Th1 cells, rather than a shift from Th1 to Th2. The authors also state that a differential sensitivity of cytokines or CD4 T cell subsets to glucocorticoids might explain an altered immunologic function in CFS patients.
Duprez, DA., De Buyzere, ML., Drieghe, B., Vanhaverbeke, F., Taes, Y., Michielsen, W and Clement, DL. Long- and short-term blood pressure and RR-interval variability and psychosomatic distress in chronic fatigue syndrome. Clinical Science, 1998, 94, 1, 57-63.
Chronic low blood pressure has been associated with fatigue and low mood. However, in patients with CFS, the blood pressure (BP) and heart rate profile and their variabilities have not been characterised as yet.
The researchers performed office and 24h ambulatory BP recordings as well as short-term beat-to-beat BP and RR-interval recordings for 10 minutes in supine and standing position, and calculated spectral indices. The samples were 38 patients with CFS (CDC criteria '88) and 38 healthy control subjects.
In the CFS group, the office BP of 123(+/-19)/70(+/-12) mmHg as well as 24-h, day- and night-time BP values of 116(+/-11.1)/71 (+/-11.1), 121(+/- 9.2)/77(+/-8.0) and 110(+/- 10.5)/65(+/-9.2) mmHg respectively were within reference limits.
Heart rate was consistently higher (p<0.01) in CFS patients, based on both office rates of 77(+/-12) compared with 68(+/-12) beats min-1) and 24-h ambulatory recordings of 77(+/-12) compared with 67(+/- 15) beats min-1.
In the supine position, spectral indices of BP variability (total, low-frequency and high-frequency variances) were all significantly (p<0.01) lower in the CFS group. In the standing position the differences disappeared. The analysis of RR-interval variability could not detect major alterations in autonomic function in CFS. There was no significant relationship between severity of fatigue, low BP and low mood.
Lane, RJM., Barrett, MC., Woodrow, D., Moss, J., Fletcher, R and Archard, LC. Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome. Journal of Neurology, Neurosurgery and Psychiatry, 1998, 64, 3, 362-367.
The aim of this study was to examine the proportions of type 1 and type 2 muscle fibres and the degree of muscle fibre atrophy and hypertrophy in patients with CFS in relation to lactate responses to exercise, and to determine to what extent any abnormalities found might be due to inactivity.
Quadriceps needle muscle biopsies were obtained from 105 patients with CFS (Oxford criteria) and the proportions of type 1 and 2 fibres and fibre atrophy and hypertrophy factors were determined from histochemical preparations, using a semiautomated image analysis system. Forty one randomly selected biopsies were also examined by electron microscopy. Lactate responses to exercise were measured in the subanaerobic threshold exercise test (SATET).
Inactivity would be expected to result in a shift to type 2 fibre predominance and fibre atrophy, but type 1 predominance (23%) was more common than type 2 predominance (3%), and fibre atrophy was found in only 10.4% of cases. Of the total sample, 37% had abnormal lactate responses to exercise. Patients with increased lactate responses to exercise had significantly fewer type 1 muscle fibres (p<0.043 males, p<0.0003 females), but there was no evidence that this group was less active than the patients with normal lactate responses. No significant ultrastructural abnormalities were found.
The researchers conclude that muscle histometry in patients with CFS generally did not show the changes expected as a result of inactivity. Patients with abnormal lactate responses to exercise had a significantly lower proportion of mitochondria rich type 1 muscle fibres.
Scott LC and Dinan, TG. Urinary free cortisol excretion in chronic fatigue syndrome, major depression and in healthy volunteers. Journal of Affective Disorders, 1998, 47, 1-3, 49-54.
Urinary free cortisol excretion (UFC) was measured in 21 patients with CFS (CDC criteria, 5 had comorbid depression), in 10 melancholic depressives and in 15 healthy controls.
Patients with depression had UFC values which were significantly higher than healthy comparison subjects, whereas UFC excretion of CFS patients was significantly lower than the comparison group. These findings are in keeping with currently held hypotheses of hyperactivity and hypoactivity of the hypothalamic-pituitary-adrenal (HPA) axis in depression and CFS. The subgroup of CFS patients with depression retained the profile of UFC excretion of those with CFS alone, suggesting a different pathophysiological basis for depressive symptoms in CFS.
Strickland P., Morriss R., Wearden A and Deakin B. A comparison of salivary cortisol in chronic fatigue syndrome, community depression and healthy controls. Journal of Affective Disorders, 1998, 47, 191-194.
Previous studies reporting cortisol hyposecretion in CFS may have been confounded by venepuncture, fasting and hospitalisation. In this study, morning and evening salivary cortisol were obtained on consecutive days during the first 3 days of the menstrual cycle and compared to those of 3 samples of women taking no medication and matched for age: 14 patients with CFS (Oxford criteria, 10 of whom also met criteria for mild/moderate depression); 26 community cases with current depression and 131 healthy community controls.
The mean evening cortisol was significantly lower in the CFS patients compared to the people with depression (p=0.02) and healthy controls (p=0.005). CFS patients without psychiatric disorder had significantly lower morning salivary cortisol compared to controls (p=0.009). The levels were not related to sleep disturbance or fitness.
The researchers conclude that CFS patients display cortisol hyposecretion in saliva compared to patients with depression and healthy controls. There was no assessment of chronic anxiety.
"Chronic fatigue syndrome is biochemically distinct from community depression".
Young, AH., Sharpe, M., Clements, A., Dowling, B., Hawton, KE and Cowen, PJ. Basal activity of the hypothalamic-pituitary-adrenal axis in patients with the chronic fatigue syndrome (neurasthenia) Biological Psychiatry, 1998, 43, 236-237
Basal activity of the HPA was assessed using salivary and urinary cortisol collection over a 24-hour period in 22 patients with CFS (CDC criteria '94, mean duration 2.5 years) and neurasthenia (ICD-10). None suffered from a current depressive or anxiety disorder. Their results were compared with those from 22 sedentary, healthy controls.
The findings showed that salivary and urinary cortisol measures did not differ between CFS patients and controls. Thus basal activity of the HPA was not reduced in CFS patients.
Christodoulou, C., DeLuca, J., Lange, G., Johnson, SK., Sisto, SA., Korn, L and Natelson, BH. Relation between neuropsychological impairment and functional disability in patients with chronic fatigue syndrome. Journal of Neurology, Neurosurgery and Psychiatry, 1998, 64, 431-434.
This study examined the relationship between neuropsychological impairment and functional disability in 53 patients with CFS (CDC criteria '88 and '92, plus additional requirements) and 32 healthy controls who did not take regular exercise. Measures included the Beck Depression Inventory (BDI), the Functional Status Questionnaire (assessing activity) and tests of verbal memory (CVLT), attention and concentration (PASAT) and visual memory (ROCF). A test score was defined as failing when it was >2 SD below the mean of the healthy controls after controlling for demographic factors. Subjects were also interviewed (Q-DIS).
Those patients with CFS with higher numbers of failing neuropsychological test scores reported significantly more days of general inactivity in the past month than those with fewer failing scores. This result remained significant even after partialling out the contribution of the presence of a comorbid axis I psychiatric episode and total BDI score. Patients with failing verbal memory scores were particularly functionally disabled compared with those with passing scores. There was no significant relationship between cognitive test results and either daily living or social activities.
The researchers conclude that the relationship between cognitive impairment and functional disability could not be explained entirely on the basis of psychiatric factors.
The associated editorial by Lambert and David (p. 430) regards cognitive impairment as mental fatigue and is largely focused on those findings which are consistent with the CBT model of CFS.
Garcia-Borreguero, D., Dale, JK., Rosenthal, NE., Chiara, A., O'Fallon, A., Bartko, JJ and Straus, SE. Lack of seasonal variation of symptoms in patients with chronic fatigue syndrome. Psychiatry Research, 1998, 77, 2, 71-77.
Since several of the symptoms involved in CFS such as fatigue, hypersomnia, hyperphagia, weight gain and mood show seasonal variations in the general population, the researchers investigated whether patients with CFS experience seasonal fluctuations in these symptoms as well.
Seasonal variation of symptoms was assessed in a group of 41 patients with CFS (CDC criteria '94) and 41 controls matched for age, gender, and city of residence. Participants were recruited from the entire US and were asked to complete the Seasonal Pattern Assessment Questionnaire (SPAQ) and the Profile of Mood States (POMS).
The CFS patients had significantly lower scores on SPAQ-derived measures as compared with controls. These included seasonal variation in energy, mood, appetite, weight and sleep length. Patients also reported a significantly reduced sensitivity toward sunny, dry and long days than the controls. No association was noted between intensity of seasonal changes and severity of depressive symptoms. "Patients with CFS exhibit an abnormally reduced seasonal variation in mood and behaviour and would not be expected to benefit from light therapy".
[Ed. note: these results are inconsistent with anecdotal reports from people with CFS, many of whom have noted an exacerbation of symptoms during humid periods and during the Autumn and Spring.]
Ray, C., Jefferies, S., Weir, W., Hayes, K., Simon, S., Akingbade, F and Marriott, P. Making sense of chronic fatigue syndrome: patients' accounts of onset. Psychology & Health, 1998, 13, 99-109.
Sixty patients with CFS (Oxford criteria plus post-exertional fatigue) were interviewed about the onset of their illness, and the factors which they felt had contributed to that onset.
Common themes in these qualitative data were episodes of infection, "doing too much" and stressful circumstances; in two-thirds of cases, accounts encompassed physical, behavioural and psychological factors. Patients described a gradual, sharp or phased onset, the latter involving a sharp onset but with a short term lifting of symptoms before worsening into chronic illness. A gradual onset was associated with longer duration of illness.
Particular themes played a different role in patients' accounts, depending upon onset pattern. With a sharp or phased onset the most common perceived trigger for the abrupt change in health status was an episode of infection, but preceding factors were often invoked to explain the effect that this had had. With a phased onset, subsequent compounding factors (typically overdoing things) were similarly cited to explain worsening and the long term effect of the trigger. Thus, patients provided complex and dynamic accounts of illness onset, incorporating interacting factors.
Streeten, DHP and Bell, DS. Circulating blood volume in chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome, 1998, 4, 1, 3-11.
A study of 19 patients with severe CFS (CDC criteria '94) revealed that the RBC mass was significantly reduced (p<.001) and below the normal range in 16 of the subjects. Plasma volume was subnormal in 10 of the 15 female subjects, while the total blood volume was below normal in 12 of the 19 subjects.
According to the researchers, the subnormal RBC mass or decreased circulatory blood volume may result in a diminished cerebral blood flow with subnormal oxygen-carrying capacity. However, since the abnormalities were not found in everyone, they cannot account for all cases of CFS.
Perrin, RN., Edwards, J and Hartley, P. An evaluation of the effec-tiveness of osteopathic treatment on symptoms associated with Myalgic Encephalomyelitis. A preliminary report. Journal of Medical Engineering & Technology, 1998, 22, 1, 1-13.
This study assessed 58 patients with ME (London criteria) who also fulfilled the CDC ('88) criteria for CFS. Of these, 33 completed osteopathic treatment while 24 acted as controls. Measures assessed fatigue, weakness, perceived exertion (Borg scale), spinal mobility as well as depression (BDI), anxiety, CFS symptoms (PFRS), back pain, cognitive function, sleep problems and general symptoms. Treatment included general advice, contrast bathing, soft tissue massage, high and low manipulation of the thoracic and upper lumbar spinal segments using supine and side-lying combined leverage and thrust techniques, gentle articulation of thoracic and upper lumbar spine plus the ribs, stimulation of the cranio-sacral rhythm by functional-cranial techniques, and exercises to improve the mobility of the thoracic spine and to improve physical co-ordination. As they improved, patients were advised to increase their walking activity levels and to do backstroke swimming. They had a minimum of 20 sessions, for which they had to pay. Follow-up assessments were completed at regular intervals for a period of one year.
There was a 40% improvement in the level of symptoms in the patient group but no overall reduction in the controls. The lab tests showed an improvement in exercise-induced fatigue but no change in thoracic mobility.
According to the authors, the reduction in symptoms is due to the stabilising of afferent sympathetic flow as a result of the relaxation of soft tissue and an improvement in visceral function plus increased blood and lymph circulation.
White, PD and Cleary, KJ. An open study of the efficacy and ad-verse effects of moclobemide in patients with chronic fatigue syndrome. International Clinical Psychopharmacology, 1997, 12, 1, 47-52.
This study assessed the efficacy of the antidepressant moclobemide in 49 patients with CFS (Oxford criteria), of whom 16 also suffered from major depression. The dose was 150 mg bd for two weeks, then 300 mg bd if tolerated. Outcome was determined using measures for sleep disturbance, fatigue, depression (HDRS and HAD), somatisation and a clinical global impression. Patients were also evaluated using a standardised clinical interview.
Eight per cent dropped out of the 6 week trial. After 4 weeks, 24% rated themselves as much or very much better. By six weeks, 29% rated themselves as better. The improvement was more noticeable among the depressed where 50% rated themselves as better versus 19% of the non-depressed. There was little between-group difference in terms of symptoms.
"These results do not support moclobemide as an effective treatment of CFS in the absence of major depression".
Albrecht, F and Wallace, M. Detecting chronic fatigue syndrome: The role of counsellors. Journal of Counselling and Development, 1998, 76, 2, 183-188.
Short, balanced and realistic review of CFS from a psychologist's perspective.
Clauw, DJ; Chrousos, GP. Chronic pain and fatigue syndromes: Overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation, 1997, 4, 3, 134-153.
A hypothesis is presented to demonstrate how genetic and environmental factors (e.g. stress) may interact to cause the development of CFS and fibromyalgia, which the authors postulate are caused by central nervous system dysfunction, particularly 'hypofunction of the stress system'. Various components of the central nervous system appear to be involved, including the hypothalamic pituitary axes, pain-processing pathways, and autonomic nervous system. These central nervous system changes lead to corresponding changes in immune function, which they postulate are epiphenomena rather than the cause of the illnesses.
Fuller, NS and Morrison, RE. Chronic fatigue syndrome. Helping patients cope with this enigmatic illness. Postgraduate Medicine, 1998, 103, 1, 175-176, 179-182, 184.
Short, biased review.
Ambrogetti, A., Olson, LG., Sutherland, DC., Malcolm, JA., Bliss, D and Gyulay, SG. Daytime sleepiness and REM sleep abnormalities in chronic fatigue: a case series. Journal of Chronic Fatigue Syndrome, 1998, 4, 1, 23-35.
This study assessed 56 patients with chronic fatigue, of whom 41 had CFS (own criteria), using overnight polysomnography and multiple sleep latency tests.
The results revealed that a subgroup had sleep disorders including narcolepsy, daytime sleepiness and/or REM sleep abnormalities. Twenty-nine were treated with either dexamphetamine or methylphenidate with good results in about half.
Baraniuk, JN., Clauw, D., MacDowell-Carneiro, A-L., Bellanti, J., Pandiri, P., Foong, S and Ali, M. IgE concentrations in chronic fatigue Syndrome. Journal of Chronic Fatigue Syndrome, 1998, 4, 1, 13-21.
This study reviewed the records from patients with allergic rhinitis (AR, n=51), CFS (n=113) with and without symptoms of allergic rhinitis and healthy controls (n=76), to ascertain their symptoms and levels of serum IgE.
Amongst those with AR, 98% had a raised serum IgE compared with 9.2% of the controls and 31% of the patients with CFS. Fatigued patients without AR had IgE levels which were no different from those of the normal controls.
Although 60% of the CFS patients with AR had high IgE levels, there was no evidence that true IgE mediated allergies were at an increased prevalence in CFS or that allergies played a role in the pathogenesis of CFS. CFS and atopy appear to be common independent conditions which may coexist in some subjects.
Costello, NL., Antoni, MH., Baldewicz, T., Lutgendorf, S., Klimas, N and Schneiderman, N. Coping and emotional expression effects upon distress, illness burden, and cytokines in CFS patients after Hurricane Andrew. Psychosomatic Medicine, 1998, 60, 1, 121-122. Abstract.
A study of 42 CFS patients in the aftermath of Hurricane Andrew found a relationship between avoidance coping and higher IL-6 levels. Path analysis revealed that expression of negative feelings mediated the avoidance coping effect on IL-6. Insight predicted less depression and total illness burden, while the reduced use of behavioural disengagement mediated the relationship between insight and lower illness burden. These findings show that coping and emotional expression are important mediators of the mental and physical response to a significant stressor.
Gregg, VH. Hypnosis in chronic fatigue syndrome. Journal of the Royal Society of Medicine, 1997, 90, 12, 682-683.
Three case histories to illustrate the value of hypnosis to reduce feelings of fatigue and myalgia in CFS.
Jason, LA., Tryon, WW., Frankenberry, E and King, C. Chronic fatigue syndrome: relationships of self-ratings and actigraphy. Psychological Reports, 1997, 81, 1223-1226
Case study of one person with CFS (CDC criteria '94) who was assessed for six days using a waist actigraph to measure activity, plus hourly subjective measures (from 6.00 am to 9.00 pm) for fatigue, physical and mental exertion, positive and negative affect plus perceived and expended energy.
Correlations between the hourly measures included significant relationships between actigraphy on the one hand and expended energy, physical exertion, mental exertion and negative affect but not with fatigue, perceived energy or positive affect.
This study suggests that activity and fatigue may not be as closely related as was previously thought.
Hyman, H and Wasser, TE. Gastrointestinal manifestations of chronic fatigue syndrome (CFS): symptom perceptions and quality of life. Journal of Chronic Fatigue Syndrome, 1998, 4, 1, 43-52.
A small study suggesting that patients with CFS have more symptoms and a lower quality of life than patients with functional bowel disease.
Miller, BJ., Whiting, JL and Clouston, AD. Coincidental splenectomy in chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome, 1998, 4, 1, 37-42.
This is a case report of a 27 year-old woman with CFS (CDC criteria '92). A splenectomy which was performed following a car crash revealed abnormalities suggestive of a chronic inflammatory process. The patient made a full recovery.
[Ed. note: One of our consultants considers this paper to be of interest because it describes the infiltration of CD45RO memory T cells into the spleen unconnected with the injury at the time of the car crash. He notes that one would not expect to find CD45RO cells congregating in the spleen unless they were signalled by the presence of some foreign protein such as a virus, infection etc.]
Pemberton, S. Getting the measure of chronic fatigue syndrome. British Journal of Therapy and Rehabilitation, 1997, 12, 663-666.
Short article describing a study of 33 patients with CFS (CDC criteria '94), assessed using questionnaires. All experienced post-exertional fatigue. The author found that the level of symptoms was not significantly correlated with functioning.
Sensky, T. Causal attributions in physical illness. Journal of Psychosomatic Research, 1997, 43, 6, 565-573.
Editorial which notes that "from research evidence to date, there is little support for a direct relationship between specific attributions and either particular emotions or particular behaviours..."
Sharpe, M and Wessely, S. Putting the rest cure to rest - again. British Medical Journal, 1998, 316, 796.
Editorial which suggests that rest has no place in treating chronic fatigue. The impression is given that CFS is a single entity with a single common pathway and that a single treatment is appropriate - and safe - for everyone with unexplained chronic fatigue. It is also implied that the main problem underlying CFS is excessive inactivity and that books, magazines and some doctors still emphasise the "need to avoid exercise" (no reference is given).
Sharpe and Wessely currently advocate planned and predictable rest periods plus gradual, individually tailored activity, starting at an easily tolerable level and increased only at a manageable pace.
[Ed. note: there is only one study which supports the view that some people with CFS rest excessively. This was the Sharpe et al trial of CBT where modestly disabled patients (Karnofsky score above 60, mean 71) spent about 3 days a week in bed. There is no other published evidence which supports the notion of total rest and complete avoidance of activity throughout the illness. There is plenty of data which supports a different view, not least the many studies which show that a substantial minority of patients still manage to work].
Sung, B., Golden, L., Garg, V and Wilson, MF. Hemodynamic mechanisms of syncope in chronic fatigue syndrome during head-up tilt test. Psychosomatic Medicine, 1998, 60, 1, 104. Abstract.
This study compared 26 patients with syncope, 11 of whom fulfilled criteria for CFS. All underwent a 80' head-up tilt (HUT) test for 30 minutes.
Six of the CFS patients and 6 of the 15 non-CFS patients had a positive HUT test. These showed a significant decrease in blood pressure, but while the CFS patients recorded an increase in heart rate at the time of syncope, HR of the non-CFS group fell after an initial rise. The patients with CFS showed a pure vasodepressor response to HUT with adequate HR compensation while the non-CFS group had mixed vasodepression and cardioinhibition.
Wessely, S., Hotopf, M and Sharpe, M. Chronic fatigue and its syndromes. Oxford University Press. 1998. Hb. 416pp. £65.00
This is a comprehensive reference text on all aspects of fatigue. It covers the nature and extent of fatigue, the history of chronic fatigue, the main research on CFS as well as the assessment and management of various fatigue states. However, this is not an entirely objective account; the authors' interest in inactivity and deconditioning as a major source of CFS is very clear and this reviewer was reminded as early as page 55 that the book was written by three male psychiatrists who do not believe what their CFS patients say.
There is a surprising lack of respect for the experiences of patients and I saw no evidence that the authors have realised, like most of their colleagues, that the F word is totally inappropriate to describe the exhaustion and weakness experienced by people with CFS. I also noted an underlying sense of hostility towards patients and patient groups. Indeed, the authors continue to perpetuate the myths that sufferers tend to be stupid, weird and wacky and that every patient responds to fatigue in pretty much the same, maladaptive way. There are certainly no descriptions of courageous individuals, coping bravely and sensibly with a disorder which is highly disabling and much misunderstood.
As far as the aetiology is concerned, these psychiatrists seem to blame the victims, as evidenced by their obsession with the idea that attributions and excessive inactivity are the major determinants of ongoing fatigue.
To those unfamiliar with the literature on CFS, the text must appear authoritative and reliable. And while there are undeniably some sections which give a reasonably fair picture of the research on particular topics (immune status, neurasthenia etc), the discussion on other subjects (the nature of CFS, the views of the patients and the value of CBT) is as one-sided and reliable as a party political broadcast. Biological variables are of course acknowledged, though they get just one cross (denoting a possible role) in a grid of perpetuating factors, compared with three crosses (signifying an important role) for attitudes, inactivity, illness beliefs, avoidance behaviour, iatrogenesis, misinformation and occupational issues.
Although extremely well written, the text mixes the findings on chronic fatigue and CFS which not only simplifies an extremely complex subject, but also introduces errors and ends up trivialising and psychologising the latter. As for the account of the alternative view, i.e. that CFS is a mixed bag of entities (Straus); that some of these are closely linked to ongoing pathology (Bennett et al, McGarry et al, Lerner et al, Schwartz et al,) and that all require individually tailored advice (Jason et al), the discussion is largely dismissive, giving readers the impression that it has little going for it. Similarly, there's virtually nothing about the most common coping strategy (pacing), nor an indication that it's probably as good as CBT and graded exercise combined.
I found the book desperately depressing because it gives such a distorted picture of CFS, the lives of the majority who suffer from it and the work of the doctors and researchers from other schools of thought. For instance, I recall advice given by the President of the ME Association in 1989 to the effect that patients should try and remain as active as they can. I also know that none of the medical advisors of the British support groups have ever recommended total rest or the avoidance of all activities to treat ME. What doctors have debated since 1989 is not whether patients should exercise or rest but how much activity they should do and when. Basically, the CBT school advised patients to keep to a predetermined plan irrespective of how they felt while ME specialists proposed a more flexible approach, taking into account current energy levels and symptoms such as post-exertional malaise.
The book doesn't acknowledge this. Instead, it promotes the all-or-nothing myth, suggesting that all patients interpret their doctor's advice to rest as meaning they should do nothing else. This is then followed by a discussion on the dangers of bed rest, reinforcing the view that this is a major source of CFS.
I know that's not true, and I believe, so do the authors. As research has shown, the majority of patients with CFS remain ambulant, and although they reduce their activity levels, few suffer from muscle wasting and other common signs of deconditioning. In fact, there isn't a single study supporting the view that the majority of people with CFS take 'excessive rest' and the authors do not provide any references from research on ME or CFS to back up their claim. Studies showing that patients spend less than 17% of daytime resting (Packer et al) or that this population are no more inactive than people with mild MS (Vercoulen et al) are not mentioned. So much for evidence-based medicine!
Elsewhere, the authors argue that all studies to date which have assessed the influence of physical attributions on outcome have shown them to be "indicators of a poor prognosis" (p. 370). Yet, I know of several good studies which show no such relationship (e.g. Lawrie et al, Ray et al). Of course, people have a right to their opinion, but as scientists, shouldn't we expect a more balanced and fair representation of the research? Moreover, since they've been told by other experts that many patients do not conform to the stereotype of the frightened sufferer with maladaptive beliefs, why can't they at least acknowledge that these patients exist?
Finally, as in other writings from this school of thought, there are a number of factual inaccuracies, e.g. that the D in CFIDS stands for deficiency. If nothing else, it serves as a good illustration of the lack of attention to detail which I have criticised before. Incidentally, the authors must also have known that Peter Nixon's research on hyperventilation has now been totally discredited. However, the description of his work does not mention this (p. 217).
Those wishing to know more about the CBT model should read the Royal Colleges Report which is both much shorter and cheaper. People like myself, who are acquainted with the research and can separate the valuable scholarly sections from the political propaganda, will appreciate the massive amount of information on the subject of fatigue and the fascinating account of neurasthenia. However, I cannot recommend it to colleagues, unless they don't mind reading highly unbalanced text books which mislead readers, foster an antagonistic attitude towards patients and contribute to the stigmatisation of the latter in the process. Most importantly, this is not a book on the illness ME, and will not increase a doctor's understanding of the condition. As the authors say on page 137, "CFS is more... than just fatigue". Unfortunately, the rest of the text failed to communicate just how much more.
Copyright EM. Goudsmit 1998.
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This issue was compiled by Dr. E.M. Goudsmit, Dr. A. Macintyre and Mrs S. Howes. We gratefully acknowledge the help and support from Dr. C. Shepherd and Mr. D. Axford.
