Tag: comment

Cognitive behaviour therapy and chronic fatigue syndrome

Comment on: Chronic fatigue in general practice: is counselling as good as cognitive behaviour therapy? A UK randomised trial. [Br J Gen Pract. 2001]

 

Ridsdale and colleagues state that there is evidence that cognitive behaviour therapy (CBT) is effective for patients with chronic fatigue syndrome (CFS), but fail to point out that such evidence derives only from studies performed in the United Kingdom, where CFS is diagnosed on the basis of the Oxford criteria. There is no evidence that CBT is beneficial to patients fulfilling the Australian criteria for CFS or the American ones, namely, the original criteria of the Centers for Disease Control.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1313986/pdf/11458489.pdf

 

Source: Baschetti R. Cognitive behaviour therapy and chronic fatigue syndrome. Br J Gen Pract. 2001 Apr;51(465):316-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1313986/ (Full comment)

 

Toward a new definition of chronic fatigue syndrome

To the editor,

I agree with Lane when he writes that the operative criteria for diagnosing chronic fatigue syndrome (CFS) are unsatisfactory. Some patients who have been assigned this label may be better described as having depression or somatization, and this mislabeling prejudices the understanding of CFS in cross-sectional studies.1 Lane is presumably referring to the definition of the Centers for Disease Control and Prevention, with its concentration on physical symptoms.2 This definition also is not all that helpful in assigning a label to individuals for the purposes of estimating prognosis or deciding on treatment because the physical symptoms cited are nonspecific.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071345/

 

Source: Robertson-Ritchie H. Toward a new definition of chronic fatigue syndrome. West J Med. 2001 Apr;174(4):241. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071345/ (Full article)

 

Diagnose and be damned. Corroboration is important when children’s illnesses are diagnosed

EDITOR—Marcovitch’s arguments about treatment of the chronic fatigue syndrome (myalgic encephalomyelitis) in children are illogical.1 He writes of the “hatchet job” performed by Panorama in the programme of 8 November and refers to the Washington Post’s policy that news requires corroboration.

One of the responses to his article, by Wessely [published here, p 1005], states, “contrary to the message of the programme, the management of chronic fatigue syndrome in children is not contentious.”2 In referring to a case reported by Panorama Marcovitch states that “parents’ views and those of the local medical team were in conflict.” Yet the programme made clear that the dispute was between the parents supported by their own medical advisers and the local medical team, so perhaps there is greater disagreement than has been asserted.

Marcovitch discussed at length Munchausen’s syndrome by proxy; Panorama labelled one of the cases of myalgic encephalitis as being a case of this syndrome. No one likes receiving emotional, intemperate outbursts, even from people who think they have been wrongly accused. But what is sauce for the goose is surely sauce for the gander. Even doctors sometimes make mistakes, yet Marcovitch disregards the possibility that parents, knowing themselves innocent, may feel themselves to have been receiving exactly the same type of vituperative attack that he objects to when doctors are on the receiving end. Such allegations turn on fact rather than clinical opinion so should be subject to Marcovitch’s own test of corroboration.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1117876/

 

Source: Pheby D. Diagnose and be damned. Corroboration is important when children’s illnesses are diagnosed. BMJ. 2000 Apr 8;320(7240):1004. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1117876/ (Full article)

 

Chronic fatigue syndrome and depression

Comment on: Cerebral perfusion in chronic fatigue syndrome and depression. [Br J Psychiatry. 2000]

 

I found MacHale et al’s (2000) discussion of their results confusing. According to the abstract and methods, they screened their patients with chronic fatigue syndrome (CFS) to exclude those with depression. Then they examined this group further using a standardised psychiatric interview (Schedule for Affective Disorders and Schizophrenia), in order to “ exclude subjects with current psychiatric illness, with a particular emphasis on depression”. The data from the Hamilton Rating Scale for Depression are difficult to interpret given the number of illnessrated items, but the scores did not indicate a significant degree of depression either. So, having excluded “subjects with depression or anxiety”, why did the authors claim in their discussion that “the main limitation of the present study is that our CFS subjects had high levels of depression”?

You can read the rest of this comment here: http://bjp.rcpsych.org/content/177/5/470.long

 

Source: Goudsmit E. Chronic fatigue syndrome and depression. Br J Psychiatry. 2000 Nov;177:470. http://bjp.rcpsych.org/content/177/5/470.long

 

Chronic fatigue syndrome: is it physical?

Comment on: Strength and physiological response to exercise in patients with chronic fatigue syndrome. [J Neurol Neurosurg Psychiatry. 2000]

 

It is increasingly recognised that chronic fatigue syndrome (CFS) is heterogeneous. A significant proportion of patients fulfilling operative criteria for a diagnosis of CFS will also fulfill criteria for a psychiatric disorder, such as depression or somatisation. Failure to recognise this heterogeneity prejudices attempts to understand CFS in cross sectional studies. In this issue (pp 302–307) Fulcher et al report a study of muscle strength, aerobic exercise capacity, and functional incapacity in a group of patients with CFS without concurrent psychiatric disorder, compared with patients with major depression and a group of normal but sedentary subjects.1 In an incremental treadmill exercise test, patients with CFS and depressed patients had lower peak oxygen consumption rates, maximal heart rates, and plasma lactate concentrations than the sedentary controls; but this reflected the shorter duration of exercise tolerated by these patients. At submaximal work rates, patients with CFS and depressed patients experienced greater perception of eVort than sedentary controls at the same level of work. This is in keeping with the finding that such patients show greater sensitivity to bodily sensations than normal subjects. Overall, there was little difference between the patients with CFS and the depressed patients in exercise characteristics, yet the patients with CFS reported significantly greater degrees of physical fatigue and physical incapacity.

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1737076/pdf/v069p00289.pdf

 

Source: Lane R. Chronic fatigue syndrome: is it physical? J Neurol Neurosurg Psychiatry. 2000 Sep;69(3):289. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1737076/

 

Demonstration of borna disease virus nucleic acid in a patient with chronic fatigue syndrome

Comment on: Borna disease virus in human brains with a rare form of hippocampal degeneration but not in brains of patients with common neuropsychiatric disorders. [J Infect Dis. 1999]

 

To the Editor

Czygan et al. [1]reported the detection of Borna disease virus (BDV) nucleic acid in 3 cases of a rare form of hippocampal degeneration, whereas the brains of patients with other neuropsychiatric disorders tested negative for BDV. Chronic fatigue syndrome (CFS) is another, more frequently diagnosed neuropsychiatric disease that is associated with BDV infection. However, the published findings are highly controversial. Nakaya et al. [2, 3] and Kitani et al. [4] showed both BDV-specific antibodies and RNA in a high percentage of Japanese patients with CFS. Bode et al. [5]isolated BDV from peripheral blood mononuclear cells (PBMC) of an American patient with CFS; however, in an earlier publication, Bode et al. [6], as well as Evengård et al. [7] and Yamaguchi et al. [8] in recent publications, did not find serologie evidence for BDV in patients with CFS. A possible explanation for the controversial results is that the term “chronic fatigue syndrome” probably includes several similar clinical conditions that may have different etiologies. In the study by Czygan et al. [1], brain tissue samples from patients who had CFS were not included. Unfortunately, none of the BDV sequences of the CFS cases mentioned above are available in the GenBank database.

You can read the rest of this comment here: http://jid.oxfordjournals.org/content/181/5/1860.long

 

Source: Nowotny N, Kolodziejek J. Demonstration of borna disease virus nucleic acid in a patient with chronic fatigue syndrome. J Infect Dis. 2000 May;181(5):1860-2. http://jid.oxfordjournals.org/content/181/5/1860.long (Full article)

 

Benefits of exercise therapy

Comment on: Acute effects of thirty minutes of light-intensity, intermittent exercise on patients with chronic fatigue syndrome. [Phys Ther. 1999]

 

We were interested to read in the report by Clapp et al (August 1999) that 30 minutes of intermittent walking did not exacerbate symptoms or cause any abnormal physiological response to exercise in subjects with chronic fatigue syndrome (CFS). Clapp and colleagues go on to suggest that “some individuals with CFS may be able to use low-level, intermittent exercise without exacerbating their symptoms.” They also write that “there are no data suggesting that exercises are effective as a primary treatment for patients with CFS.”

These authors do not go far enough in their recommendation and are quite wrong in their assumption regarding exercise as a primary treatment. Our group has published a randomized controlled trial showing that graded aerobic exercise therapy, properly supervised, is a significantly more effective treatment than the same amount of therapist input using only stretching and relaxation exercises.
This study showed that 52 % of patients rated themselves as “much” or “very much” better after 3 months of treatment, analyzed by intention to treat, compared with 27% of those treated with a control treatment. At the 1-year follow-up, the proportion of those who rated themselves as “much” better increased to 63% by intention-to-treat analysis (74% by completed patients’ analysis). Only 1 patient out of 33 patients rated himself “worse” after treatment, the same proportion as in the control treatment. Four patients dropped out of exercise therapy, and 3 patients dropped out of the control treatment. We excluded patients with a comorbid psychiatric disorder. We concluded that “these findings support the use of appropriate prescribed graded aerobic exercise in the management of patients with chronic fatigue syndrome.”

You can read the rest of this comment here: http://ptjournal.apta.org/content/80/1/115.long

 

Source: White P, Fulcher K. Benefits of exercise therapy. Phys Ther. 2000 Jan;80(1):115. http://ptjournal.apta.org/content/80/1/115.long

 

Paraoxonase/MCS

Work in multiple laboratories on paraoxonase polymorphism has shown that this mammal enzyme protects against chlorpyrifos and other organophosphates differentially, depending on which inherited forms of the enzyme predominate. This variable ability to process pesticides exists in humans and is trackable ethnically (1), and very recent articles have suggested the polymorphism may be responsible for host susceptibility to Gulf War syndrome (2,3). Because my own interest is in multiple chemical sensitivity (MCS) mechanisms, I immediately searched Medline (National Library of Medicine, Bethesda, MD) for publications that included paraoxonase and MCS, fibromyalgia, or chronic fatigue syndrome (CFS), which have been suggested as being overlapping or identical with each other and with Gulf War syndrome (4,5). I found no other references at all.

You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566473/pdf/envhper00513-0015b.pdf

 

Source: Rowat SC. Paraoxonase/MCS. Environ Health Perspect. 1999 Aug;107(8):A395. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1566473/pdf/envhper00513-0015b.pdf

 

Single aetiological agent may not be feasible in CFS patients

Comment on: Cortisol deficiency may account for elevated apoptotic cell population in patients with chronic fatigue syndrome. [J Intern Med. 1999]

 

Dear Sir, I would like to thank Dr Baschetti for his very interesting letter. I hope clinicians and CFS patients will be able to benefit from its contents. We agree that chronic fatigue syndrome (CFS) is an illness with uncertain aetiology. Although it is true that no single infectious agent has been identified as a primary cause of CFS, a variety of pathogens, including HTLV-II, EBV, cytomegalovirus, herpes simplex viruses 1 and 2, and human herpes viruses 6, 7 and 8, have been identified in CFS patients [1–7]. In addition to the pathogens previously mentioned, a recent study by our laboratory has identified Mycoplasma fermentans in a statistically significant number of CFS patients over non-CFS control subjects [8]. Further investigation is necessary to determine whether these pathogens are occurring secondarily to some immunological disturbances, as some investigators believe, or whether they are involved as a primary cause of symptoms characteristic of CFS. As mentioned by Dr Baschetti, various measures of immune function have been reported to be altered in CFS subjects, thereby suggesting an association rather than demonstrating a causative link. Abnormalities that have been reported include increased circulating immune complexes, reduced CD4 and CD8 T-lymphocyte subsets, diminished natural killer cell activity, reduction in IgG subclasses, reduced mitogenic response of lymphocytes, altered cytokine production, elevated titres of antibodies to a number of viruses and abnormal production of IFN [9–15]. However, similar immune functional abnormalities have been reported in patients exposed to toxic chemicals without evidence of viral infection or reactivation [16, 17]. Moreover, the symptomatologies described in these patients overlap with CFS patients, thus making the differentiation between the two groups extremely difficult [18–21]. In these articles, the substantial overlap between chemical sensitivity, fibromyalgia and CFA was discussed. It was concluded that the latter two conditions may involve chemical sensitivity and may even be the same disorder. In fact, in a separate study strictly with CFS patients without evidence of viral reactivation but exposed to methyl tertiary-butyl ether (MTBE) and benzene, we showed that programmed cell death and cell cycle were abnormal in both groups [22]. Similarly, in our original article published in this journal, we reported elevated apoptosis and abnormal cell cycle in CFS patients without a history of exposure to toxic chemicals. The interferon-induced protein kinase RNA (PKR) was found to be elevated in these patients as well and was therefore proposed as a possible mechanism of induction of apoptosis and cell cycle abnormalities [23].

 

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.1999.00479.x/full

 

Source: Vojdani A. Single aetiological agent may not be feasible in CFS patients. J Intern Med. 1999 Apr;245(4):410-2. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.1999.00479.x/full

 

Cortisol deficiency may account for elevated apoptotic cell population in patients with chronic fatigue syndrome

Comment in: Single aetiological agent may not be feasible in CFS patients. [J Intern Med. 1999]

Comment on: Elevated apoptotic cell population in patients with chronic fatigue syndrome: the pivotal role of protein kinase RNA. [J Intern Med. 1997]

 

Dear Sir, Vojdani et al. [1] report that patients with chronic fatigue syndrome (CFS) display an increased apoptotic cell population. This abnormality, according to the authors, is due to the activation of protein kinase RNA pathway, which, in turn, ‘could result from disregulated immune system or chronic viral infection’[1].The latter explanation, however, seems unlikely, because no specific virus has been identified in CFS patients, despite extensive research [2]. Special attention, therefore, should mainly be paid to the immune system of CFS patients, because its repeatedly reported abnormalities may help reveal both the aetiology of CFS and an effective treatment against it.

As Vojdani et al. [1] point out, decreased natural killer (NK) cell activity and altered cytokine production characterize CFS patients. These immunological abnormalities, however, may simply reflect the hypocortisolism of CFS patients [3], because a mere lack of steroid restraint on the immune system may well account for its derangement [3]. In fact, since NK cell activity is directly associated with the circadian rhythm of cortisol [4], the decreased NK cell activity observed in CFS patients may simply be due to their cortisol deficiency [3]. The latter, additionally, may also explain why the release of the cytokines interleukin-lβ, interleukin-6, and tumour necrosis factor-α has been found to be increased in peripheral blood mononuclear cell cultures from patients with CFS [5]. All those cytokines, in fact, have been reported to rise during hypocortisolism [6]. This suggests, therefore, that the cortisol deficiency of CFS patients may play a central role in causing both their immunological abnormalities and, presumably, their elevated apoptotic cells.

In view of the role of hypocortisolism in CFS, Vojdani and coworkers might be interested in determining whether the enhanced apoptosis found in their subjects with CFS could be reduced by giving them small daily doses of hydrocortisone and fludrocortisone. The latter, notably, already has been reported to be of great benefit to CFS patients [7]. The rationale for treating CFS patients with the two steroids that are routinely administered to Addisonian patients [8] lies primarily in the fact that no medical condition, except Addison’s disease, shares 20 features with CFS [3]. Five additional symptoms (dizziness upon standing, orthostatic tachycardia, nausea, diarrhoea, and constipation) can be found in both CFS [9] and Addison’s disease [8, 10, 11]. Rather surprisingly, however, despite the staggering similarities between CFS and Addison’s disease, as yet no published attempt has been made to treat CFS patients with both hydrocortisone and fludrocortisone.

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.1999.00478.x/full

 

Source: Baschetti R. Cortisol deficiency may account for elevated apoptotic cell population in patients with chronic fatigue syndrome. J Intern Med. 1999 Apr;245(4):409-10. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.1999.00478.x/full