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CO-CURE Medical & Research Posts Only Digest - 16 Oct 2006 to 23 Oct 2006 (#2006-48)

There are 19 messages totalling 2632 lines in this issue. Topics of the week:

[Return to digest index] --------------------------------------------- This is a special digest of Co-Cure Research & Medical posts only Problems? Write to mailto:mods@co-cure.org --------------------------------------------- ---------------------------------------------------------------------- Date: Tue, 17 Oct 2006 09:15:55 -0400 From: Fred Springfield <fredspringfield@xxxxxx.xxx> Subject: RES: Cognitive behavioural therapy in chronic fatigue syndrome: a randomised controlled trial of an outpatient group programme Cognitive behavioural therapy in chronic fatigue syndrome: a randomised controlled trial of an outpatient group programme Journal: Health Technology Assessment 2006; Vol 10: number 37 Authors: H O'Dowd [1,*], P Gladwell [1], CA Rogers [2], S Hollinghurst [3], and A Gregory [1] Affiliations: [1] Pain Management Centre, Frenchay Hospital, Bristol, UK [2] Bristol Heart Institute, Bristol Royal Infirmary, UK [3] Department of Community Based Medicine, University of Bristol, UK [*] Corresponding author Executive Summary: Background and objectives This report describes the conduct and results of a double-blind randomised controlled trial to compare group cognitive behavioural therapy (CBT) with education and support (EAS) and with standard medical care (SMC) for the treatment of patients with chronic fatigue syndrome/myalgic encephalopathy (CFS/ME). The research hypothesis was that group CBT would provide an effective and cost-effective management strategy for patients in primary care with CFS/ME and that treatment gains in these areas would be found even when controlling for the non-specific effects of therapist exposure. Methods Design A double-blind, randomised controlled trial was adopted with three arms. Outcomes were assessed at baseline and 6 and 12 months after first assessment and results were analysed on an intention-to-treat basis. Setting The study was set in a health psychology department for the management of chronic illness in a general hospital in Bristol, UK. Participants Adults with a diagnosis of CFS/ME were referred by their GP. Over a 2-year period (August 2000July 2002), 153 eligible patients were recruited and consented to participate; 52 were randomised to receive CBT, 50 to EAS and 51 to SMC. The target sample size for the trial, set at 43 per condition, was met. Seven patients did not receive the treatment assigned for clinical or ethical reasons and fear of contamination but all analyses were carried out on an intention-to-treat basis. Twelve patients failed to attend for the 12-month follow-up and 19 patients attended one follow-up, but not both. The sample was found to be representative of the patient group and the characteristics of the three groups were similar at baseline. Interventions The primary analyses compared the outcome scores between the three treatment interventions. Differences between the treatment cohorts are reported with 95% confidence intervals (CIs). For the primary outcome measures, the SF-36 physical and mental summary scales, the numbers of patients reporting a 15% increase over the baseline score (defined as a successful outcome) and the numbers returning to the normal range are also reported. Outcome measures A range of generic outcome measures were used as validated disease-specific outcome measures were not available for this condition. The primary outcome measure was the Short Form with 36 Items (SF-36) physical and mental health summary scales. Other outcome measures included the Chalder fatigue scale, Hospital Anxiety and Depression Scale (HADS), General Health Questionnaire, measures of physical function (shuttles walked, walking speed and perceived fatigue), health utilities index, cognitive function (mood, recall and reaction times) and resource use. Outcomes were measured as baseline (before randomisation) and at 6 and 12 months after the initial assessment. Results Three outcome measures, SF-36 mental health score, Chalder fatigue scale and walking speed, showed statistically significant differences between the groups. The CBT group had significantly higher SF-36 mental health scores (difference +4.35, 95% CI +0.72 to +7.97, p = 0.019), less fatigue (difference 2.61, 95% CI 4.92 to 0.30, p = 0.027) and was able to walk faster (difference +2.83 shuttles, 95% CI +1.12 to +5.53, p = 0.0013) than patients in the SMC group. CBT patients also walked faster and were less fatigued than those randomised to EAS (walking speed, difference +1.77, 95% CI +0.025 to +3.51, p = 0.047; fatigues, difference 3.16, 95% CI 5.59 to 0.74, p= 0.011). Overall, no other statistically significant difference across the groups was found, although for many measures a trend towards an improved outcome with CBT was seen. Excepting for walking speed, which, on average, increased by +0.87 shuttles (95% CI +0.09 to +1.65, p = 0.029) between the 6- and 12-month follow-ups, the scores were similar at 6 and 12 months. At baseline, 30% of patients had an SF-36 physical score within the normal range and 52% had an SF-36 mental health score in the normal range. At 12 months, the physical score was in the normal range for 46% of the CBT group, 26% of the EAS group and 44% of SMC patients. For mental health score, the percentages were CBT 74%, EAS 67% and SMC 70%. Of the CBT group, 32% showed at least a 15% increase in physical function and 64% achieved a similar improvement in their mental health. For the EAS and SMC groups, this improvement in physical and mental health was achieved for 40 and 60% (EAS) and 49 and 53% (SMC), respectively, but these changes were not statistically significant. There were multiple difficulties in completing the economic evaluation. A costutility (or cost-effectiveness) analysis was planned, but the quality of the data prevented this objective being realised. The intention was to use data from participating primary and secondary care centres and patient questionnaires. However, owing to the unexpected departure of the health economist early in the trial, the study was almost complete before it was realised that patient records would need to be scrutinised for resource use data. This meant that limited resources were available for this exercise, and minimal data were obtained. Also, the patient questionnaire was inadequate. It asked patients about treatments and medication use but failed to ascertain the cost involved. Data on direct patient costs and indirect societal costs was sought but the response was too poor for the data to be of much value, with a great deal of missing data. As a result, the quality of the health economic data was poor; the evaluation was limited to the perspective of the healthcare provider (NHS) and the reporting of results was descriptive only. The descriptive data tentatively suggest that most of the cost of CFS/ME is borne by family and friends. The economic impact appears substantial, with over 60% of patients citing the onset of CFS/ME as the main reason why they cannot work. Limitations The trial had a number of limitations: patients were referred from the GP, without a specialist diagnosis, and the individuals' suitability for group treatment was not assessed prior to randomisation. One patient was withdrawn because an alternative diagnosis was made and several patients would not, in clinical practice, have been considered psychologically appropriate for group treatment. Also, some subjects were already using good management techniques and could not, therefore, be expected to show a significant improvement. On average, the patients in the study population were more fatigued, had been ill for longer and were more distressed than samples used in previous research, although they were able to attend an outpatient programme, which implies a certain level of ability. It is not possible to assess from this trial whether the interventions investigated would be effective, ineffective or even hazardous for more severely disabled individuals. Conclusions Group CBT did not significantly improve cognitive function, quality of life, employment status or healthcare utility measures, although such changes have been demonstrated in the literature for individual CBT. The increased measures of mood and fitness and decreased symptoms of fatigue seen with CBT are comparable to the changes seen in the individual research literature. The similarity of the Borg perceived fatigue scores across each condition, both initially and at follow-up, indicates that each cohort reported exercising to a similar level of fatigue. This indicates that the significant increase in shuttle walking found in the CBT group was not an artificial gain achieved by 'pushing through' fatigue. It appears to be more substantial. These subjects reported increases in their normal walking pace. It seems that the gain is for both speed and endurance. This is of great functional significance for CFS/ME sufferers. This study is unable to shed any light on the mechanism underlying this change, and it may be possible that patients are feeling more confident and able to manage the condition. Recommendations for future research Further research is needed to develop better outcome measures, assessments of the broader costs of the illness and a clearer picture of the characteristics best fitted to this type of intervention. Publication O'Dowd H, Gladwell P, Rogers CA, Hollinghurst S, Gregory A. Cognitive behavioural therapy in chronic fatigue syndrome: a randomised controlled trial of an outpatient group programme. Health Technol Assess 2006;10(37). NHS R&D HTA Programme The research findings from the NHS R&D Health Technology Assessment (HTA) Programme directly influence key decision-making bodies such as the National Institute for Health and Clinical Excellence (NICE) and the National Screening Committee (NSC) who rely on HTA outputs to help raise standards of care. HTA findings also help to improve the quality of the service in the NHS indirectly in that they form a key component of the 'National Knowledge Service' that is being developed to improve the evidence of clinical practice throughout the NHS. The HTA Programme was set up in 1993. Its role is to ensure that high-quality research information on the costs, effectiveness and broader impact of health technologies is produced in the most efficient way for those who use, manage and provide care in the NHS. 'Health technologies' are broadly defined to include all interventions used to promote health, prevent and treat disease, and improve rehabilitation and long-term care, rather than settings of care. The HTA Programme commissions research only on topics where it has identified key gaps in the evidence needed by the NHS. Suggestions for topics are actively sought from people working in the NHS, the public, service-users groups and professional bodies such as Royal Colleges and NHS Trusts. Research suggestions are carefully considered by panels of independent experts (including service users) whose advice results in a ranked list of recommended research priorities. The HTA Programme then commissions the research team best suited to undertake the work, in the manner most appropriate to find the relevant answers. Some projects may take only months, others need several years to answer the research questions adequately. They may involve synthesising existing evidence or conducting a trial to produce new evidence where none currently exists. Additionally, through its Technology Assessment Report (TAR) call-off contract, the HTA Programme is able to commission bespoke reports, principally for NICE, but also for other policy customers, such as a National Clinical Director. TARs bring together evidence on key aspects of the use of specific technologies and usually have to be completed within a short time period. Criteria for inclusion in the HTA monograph series Reports are published in the HTA monograph series if (1) they have resulted from work commissioned for the HTA Programme, and (2) they are of a sufficiently high scientific quality as assessed by the referees and editors. Reviews in Health Technology Assessment are termed 'systematic' when the account of the search, appraisal and synthesis methods (to minimise biases and random errors) would, in theory, permit the replication of the review by others. The research reported in this monograph was commissioned by the HTA Programme as project number 97/41/08. The contractual start date was in August 2000. The draft report began editorial review in October 2004 and was accepted for publication in February 2006. As the funder, by devising a commissioning brief, the HTA Programme specified the research question and study design. The authors have been wholly responsible for all data collection, analysis and interpretation, and for writing up their work. The HTA editors and publisher have tried to ensure the accuracy of the authors' report and would like to thank the referees for their constructive comments on the draft document. However, they do not accept liability for damages or losses arising from material published in this report. The views expressed in this publication are those of the authors and not necessarily those of the HTA Programme or the Department of Health. Editor-in-Chief: Professor Tom Walley Series Editors: Dr Aileen Clarke, Dr Peter Davidson, Dr Chris Hyde, Dr John Powell, Dr Rob Riemsma and Dr Ken Stein Managing Editors: Sally Bailey and Sarah Llewellyn Lloyd © 2006 Crown Copyright [Note: The full text of this monograph is available in PDF for free at http://www.hta.ac.uk/fullmono/mon1037.pdf ] [Return to top] ------------------------------ Date: Tue, 17 Oct 2006 14:20:18 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxxx.xxx> Subject: RES: Fibromyalgia Pain and Substance P Decrease and Sleep Improves After Massage Therapy Fibromyalgia Pain and Substance P Decrease and Sleep Improves After Massage Therapy. J Clin Rheumatol. 2002 Apr;8(2):72-76. Field T, Diego M, Cullen C, Hernandez-Reif M, Sunshine W, Douglas S. Touch Research Institutes (TF, MD, CC, MH-R, WS), University of Miami School of Medicine, Miami, Florida; Children's Hospital of Philadelphia (SD), Philadelphia, Pennsylvania. PMID: 17041326 Massage therapy has been observed to be helpful in some patients with fibromyalgia. This study was designed to examine the effects of massage therapy versus relaxation therapy on sleep, substance P, and pain in fibromyalgia patients. Twenty-four adult fibromyalgia patients were assigned randomly to a massage therapy or relaxation therapy group. They received 30-minute treatments twice weekly for 5 weeks. Both groups showed a decrease in anxiety and depressed mood immediately after the first and last therapy sessions. However, across the course of the study, only the massage therapy group reported an increase in the number of sleep hours and a decrease in their sleep movements. In addition, substance P levels decreased, and the patients' physicians assigned lower disease and pain ratings and rated fewer tender points in the massage therapy group. [Return to top] ------------------------------ Date: Tue, 17 Oct 2006 14:24:46 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xx> Subject: RES: Cognitive and Dissociative Manifestations in Fibromyalgia Cognitive and Dissociative Manifestations in Fibromyalgia. J Clin Rheumatol. 2002 Apr;8(2):77-84. Leavitt F, Katz RS, Mills M, Heard AR. Department of Psychology (FL, MM) and Section of Rheumatology, Department of Internal Medicine (RSK), Rush Medical Center, Chicago, Illinois, and Department of Psychiatry and Behavioral Sciences (ARH), University of Washington Medical Center, Seattle, Washington. PMID: 17041327 Memory decline and mental confusion frequently complicate the clinical presentation of fibromyalgia; however, formal cognitive examination often does not support deterioration. This paradox was examined in the context of dissociation, a condition with many cognitive similarities. Dissociation refers to the separation of parts of experience from the mainstream of consciousness. A common example is highway hypnosis. Eighty-nine fibromyalgia (FM) patients and 64 other rheumatic disease patients were screened for memory decline and mental confusion using a questionnaire format. Pain, dissociation, affective distress, fatigue, sleep difficulty, and mental confusion were also assessed. Cognitive complaints (76.4%-43.8%) and dissociative symptoms (37.1%-1.9%) were overrepresented in patients with FM. Among FM patients with high dissociation, cognitive difficulties were reported by 95%; 100% of these cases reported that both memory and mental clarity were affected, a condition referred to as fibrofog. Dissociation in combination with fibrofog was associated with higher levels of FM symptom intensity and decreased mental well being. These findings suggest that dissociation may play a role in FM symptom amplification and may aid in comprehending the regularity of cognitive symptoms. Separating cases of fibrofog from cognitive conditions with actual brain damage is important. It may be prudent to add a test of dissociation as an adjunct to the evaluation of FM patients in cases of suspected fibrofog. Otherwise, test results may prove normal even in patients with disabling cognitive symptoms. [Return to top] ------------------------------ Date: Tue, 17 Oct 2006 23:08:21 -0400 From: "CF-Alliance <cf_alliance@xxxxx.xxx> (via Co-Cure Moderators" Subject: RES,MED:Antibiotic May Aid IBS Antibiotic May Aid Irritable Bowel Xifaxan Reduces Bloating, May Attack Main IBS Cause http://www.webmd.com/content/article/128/117134 [Return to top] ------------------------------ Date: Wed, 18 Oct 2006 11:03:00 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx> Subject: RES: Drug treatment for fibromyalgia Drug treatment for fibromyalgia. Musculoskeletal Care. 2004 May;2(2):90-100. Bird HA. University of Leeds, Leeds, UK. PMID: 17041973 The term 'fibromyalgia' probably covers a variety of diagnoses for which we have no formal diagnostic tests. Nevertheless, it remains a cause of discomfort and disability, often amenable to non-drug treatment that should always be tried first. This article reviews the different drug treatments available that are of interest to the rheumatology community because the drugs that often procure pain relief are not always the same as those that are conventionally used for degenerative or inflammatory polyarthritis. This, in turn, may provide a clue to causation. Copyright (c) 2004 Whurr Publishers Ltd. [Return to top] ------------------------------ Date: Wed, 18 Oct 2006 11:00:29 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx> Subject: RES: Pain mechanisms and the rheumatic diseases Pain mechanisms and the rheumatic diseases. Musculoskeletal Care. 2004 May;2(2):75-89. McCabe CS. Royal National Hospital for Rheumatic Diseases and School for Health, University of Bath, UK. PMID: 17041972 Pain is the predominant complaint of those with a rheumatological condition. This paper provides a broad overview of the current theories on the mechanisms of pain, the structure of the nervous system, and how these may relate to the sometimes seemingly incomprehensible symptoms of pain and other sensory disturbances that some rheumatology patients describe. Three case histories relating to rheumatoid arthritis, osteoarthritis and fibromyalgia are used to illustrate how this knowledge can be applied to clinical practice. Copyright (c) 2004 Whurr Publishers Ltd. [Return to top] ------------------------------ Date: Wed, 18 Oct 2006 11:11:47 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx> Subject: RES: Long-term effects of a shared decision-making intervention on physician-patient interaction and outcome in fibromyalgia A qualitative and quantitative 1 year follow-up of a randomized controlled trial Long-term effects of a shared decision-making intervention on physician-patient interaction and outcome in fibromyalgia A qualitative and quantitative 1 year follow-up of a randomized controlled trial. Patient Educ Couns. 2006 Nov;63(3):357-66. Epub 2006 Jul 26. Bieber C, Muller KG, Blumenstiel K, Schneider A, Richter A, Wilke S, Hartmann M, Eich W. University of Heidelberg, Medical Hospital, Department of Psychosomatic and General Internal Medicine, Heidelberg, Germany. PMID: 16872795 OBJECTIVE: Fibromyalgia syndrome (FMS) patients and their doctors frequently complain on interaction difficulties. We investigated the effects of a shared decision-making (SDM) intervention on physician-patient interaction and health outcome. METHODS: Sixty-seven FMS patients of an outpatient university setting that had been included in a randomized controlled trial were followed up. They were either treated in an SDM group or in an information group. Both groups saw a computer based information tool on FMS, but only the SDM group was treated by doctors which underwent a special SDM communication training. A comparison group of 44 FMS patients receiving treatment as usual was recruited in rheumatological practices. We assessed patients and their doctors using a combined qualitative and quantitative approach. Patients and doctors were followed-up after 3 months (T2) and after 1 year (T3). RESULTS: The significantly best quality of physician-patient interaction was reported by patients and doctors of the SDM group, followed by the information group. Coping had more often improved in the SDM group than in the information group. However directly health related outcome variables had not improved in any of the groups at T3. CONCLUSION: An SDM intervention can lead to an improved physician-patient relationship from the patients' and from the doctors' perspective. PRACTICE IMPLICATIONS: It should be considered to include SDM in standard care for FMS patients. [Return to top] ------------------------------ Date: Thu, 19 Oct 2006 13:17:34 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx> Subject: RES: Improving management of musculoskeletal disorders in primary care: the Joint Adventures Program Improving management of musculoskeletal disorders in primary care: the Joint Adventures Program. Clin Rheumatol. 2006 Oct 18; [Epub ahead of print] Petrella RJ, Davis P. Department of Family Medicine, University of Western Ontario, London, Ontario, Canada. PMID: 17047890 Musculoskeletal disorders represent a large and growing clinical challenge to primary care clinicians. Unfortunately, there appears to be a gap in current training and continuing education to meet this challenge. We used script concordance within a continuing medical education program entitled "Joint Adventures" to assist family physicians to acquire the knowledge, skills, and tools they need to improve their management of musculoskeletal disorders. Program workshops were coordinated through a national continuing education program of the College of Family Physicians of Canada. A group of 54 experts in musculoskeletal disorders including family physicians, rheumatologists, and orthopedists developed cases for six areas of management that were identified by family physicians during a needs survey delivered at a national scientific congress in primary care. Script concordance methodology was used in the Joint Adventures workshop to address knowledge gaps or lack of group consensus in the six areas including (1) diagnosis of osteoarthritis, (2) treatment and management of osteoarthritis, (3) treatment and management of rheumatoid arthritis, (4) diagnosis and treatment of back pain, (5) diagnosis and treatment of fibromyalgia and diagnosis, and (6) treatment of shoulder pain. Each workshop session included 5-30 family physicians, a specialist expert, and a family physician facilitator. Before each session, a group needs assessment was conducted to identify which one or two of the six cases would be used. Perceived knowledge and skill acquisition, self-assessed change in practice, and satisfaction with the program were measured at the conclusion of each session and again at 3 months post program. All programs were delivered from March 2003 to September 2005. Six hundred and fifty family physicians from across Canada completed the program. In general, participants reached concordance with each case. Measures of knowledge and skill acquisition and self-assessed change in practice were significantly improved with high rates of program satisfaction. The Joint Adventures program provided family physicians with knowledge and skills that changed their care of musculoskeletal disorders. This was achieved using consensus that was sensitive to local needs. Further use should be evaluated in other areas of medical practice as well. [Return to top] ------------------------------ Date: Thu, 19 Oct 2006 22:53:54 +0200 From: Jan van Roijen <j.van.roijen@xxxxx.xx> Subject: not,med: A Hummingbirds Guide to ME Newsletter -October 2006 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 19 oktober 2006 <<<< Editorship : j.van.roijen@chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: "Jodi Bassett" <jodibassett@bigpond.com> A Hummingbirds Guide to ME Newsletter ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ October 2006 Hello and welcome to the 'A Hummingbirds Guide to Myalgic Encephalomyelitis' e-newsletter for October 2006. As always I hope it finds you and yours all doing as well as possible. This month I have just one small new project to announce, as well as a few new great articles by other authors. I've been resting up after finally finishing the huge CBT and GET database last month, including the essay 'Smoke and Mirrors' which, if anyone missed it, is available at: http://www.ahummingbirdsguide.com/cbtandget.htm ```````` A new Translations page: Calling all translators! Since my website began I've been interested in having translations available, as much as is possible. Myalgic Encephalomyelitis (M.E.) is an illness that has occurred in epidemic and sporadic forms all over the world. Unfortunately the bulk of information on M.E., particularly the good quality and unbiased information, is mostly only available in English. For the benefit of the many thousands of people with M.E around the world this has to change. In time, I hope to be able to present here links to at least the basic texts on this site (which quote and reference some of the best information on M.E. available by many of the world's leading M.E. experts), in at least most of the most commonly used languages. For this to happen however, translators are urgently needed! If you would be willing to translate even just 2 pages of text into another common language please contact me. For more information, and to see some of the texts currently available in other languages see: http://www.ahummingbirdsguide.com/translations.htm `````````` Outstanding new articles by other authors The following new(ish) articles by some of the world's leading M.E experts and advocates are highly recommended. 1. A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome (an extract, PDF format) by Dr Byron Hyde M.D. This is simply one of the best (if not THE BEST) articles on the illness. It contain valuable information both politically and medically and should be essential reading for anyone with an interest in M.E. or CFS. (See the quote at the end of the newsletter for a brief sample.) Also, for anyone who hasn't read Hyde's 2003 The Complexities of Diagnosis this is also very highly recommended. Links to both texts are available at: http://www.ahummingbirdsguide.com/whyde.htm Also, a review of Dr Hyde's essential M.E. textbook, including a selection of quotes from the book, is now available at: http://www.ahummingbirdsguide.com/hydetextbookreview.htm 2. Myalgic Encephalomyelitis (ME): a review with emphasis on key findings in biomedical research by Professor Hooper 2006, printed in the BMJ A quote: 'Undoubtedly the perverse use of chronic fatigue syndrome, to impose a psychiatric definition for ME/CFS by allying it to fatigue syndromes, has delayed research, the discovery of effective treatment(s), and care and support for those suffering from this illness I would propose that the use of CFS should now be abandoned and that, following the Minister of Health's assurances, the WHO definition is now accepted and used in all official documentations. The excellent work on the biological aspects of ME, already carried out by several leading research groups, now requires significant funding.' A link to this paper is available at: http://www.ahummingbirdsguide.com/whooper.htm 3. Submission to the Parliamentary Inquiry into progress in the scientific research of M.E. by the 25% Severe ME Group/Greg Crowhurst This paper includes comments from 25% members on CBT, GET and the effect of the 'psychiatric' approach to M.E. and makes very clear the high level of suffering caused by these inappropriate interventions and theories. This is utterly compelling reading and great work by Greg Crowhurst/25% Group. A link to this paper is available at: http://www.ahummingbirdsguide.com/w25group.htm 4. Illustrations of Clinical Observations and International Research Findings from 1955 to 2005 that demonstrate the organic aetiology of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome by Malcolm Hooper, Eileen Marshall and Margaret Williams, 12th December 2005 This 175 page paper has been around for a while, but is still well worth drawing attention to for those who are not aware of it. It was prepared for the recent Gibson inquiry. The paper is also available as a PDF download from MEAction UK. Links to the webpage and the PDF download are available at: http://www.ahummingbirdsguide.com/wmarwillhoopgibsonenqui.htm (There are likely many more papers that could be included in this list, but I wanted to keep it (relatively) brief.) `````````` That's it for this month! Best wishes as always to everyone and all the best in your ongoing battle with M.E. (or your loved one's battle with M.E.) - until next month! If you're still waiting for a reply to an email you wrote me, hopefully it will be coming soon, I'm up to April 2006 now! Jodi Bassett -- A Hummingbirds Guide to Myalgic Encephalomyelitis: www.ahummingbirdsguide.com Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. The CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process. It is (a) a partial mix of infectious mononucleosis /glandular fever, (b) a mix of some of the least important aspects of M.E. and (c) what amounts to a possibly unintended psychiatric slant to an epidemic and endemic disease process of major importance. Any disease process that has major criteria, of excluding all other disease processes, is simply not a disease at all; it doesn't exist. M.E. and CFS should be separated as definitions. They are not the same. Dr Byron Hyde MD ```````````````` A HUMMINGBIRDS GUIDE E-NEWSLETTER NOTES: 1. if you'd like to unsubscribe from this list, just reply to this newsletter (or email me and quote the number 4). 2. Permission is given for you to forward this email provided it is unedited. If you do so however, can you please make sure to delete my email address from the top of the email so I don't end up added to even more spam lists! Thank you. 3. If you have received this newsletter as a forwarded e-mail and would now like to subscribe to the newsletter yourself, see: www.ahummingbirdsguide.com/websiteenewsletter.htm for details. 4. To read past newsletters/site updates see the 'What's New' section on the website at: http://www.ahummingbirdsguide.com/whatsnew.htm [Return to top] ------------------------------ Date: Fri, 20 Oct 2006 01:09:30 +0200 From: Jan van Roijen <j.van.roijen@xxxxx.xx> Subject: res: ME/CFS -thalamus malfunction? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 20 oktober 2006 <<<< Editorship : j.van.roijen@chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ http://www.cfs-healing.info/ Clinical CFS-study in Switzerland ~~~~~~~~~~~~~~~~~~~~~~~~~~ (Warning: I suffer from ME-CFIDS-CFS myself and due to brain-fog I can not guarantee that the information in this report is 100% accurate!) 18. October 2006 "Cerebral Volumetry and Diffusion Tensor Imaging of the Thalamus with Chronic Fatigue Syndrome" This clinical CFS-study in Switzerland is currently in progress. It takes place in the capital of Switzerland, Berne. (At the Insel Spital; departement of psychosomatic medicine / general internal medicine.) Physician in charge is Dr. med. Stefan Begré Dr. Begré's team recently checked my brain with a magnetic resonance tomography device. (Translation!? Magnetic Resonance Imaging (MRI)? German: "Magnet Resonanz Tomographie MRT") 60 patients with ME-CFIDS-CFS and a control group with 60 healthy patients will undergo measurements/brain scans with magnetic resonance tomography. (The 60 ill subjects are being tested rigorously via many questionnaires and personal interrogation to make sure that they suffer from the 'real deal', and to assess the various CFS-subgroups.) Dr. Begré and his fellow researchers suspect a serious malfunction of the thalamus; they also don't want to exclude the possibility of the additional influence of some (yet not discovered?) virus. As soon as the results of my brain scan arrive, I will publish them here. I posted info about this study here for German speakers: Informationen über diese studie für Deutsch sprechende: Cfs-board.de/forum http://www.cfs-board.de/cfsforum/thread.php?threadid=272 Brain Scan / Neuroimaging (Wikipedia) http://en.wikipedia.org/wiki/Brain_scan ```````````````````` 19. October 2006 Some questions I got via email and forum posts: What is the actual thalamus malfunction? If we only knew! I guess they are not sure - they suspect a 'general imbalance' of the thalamus, if I understood Dr. Begré correctly. What exactly is the function of the thalamus? Wikipedia says: - There is not a single thalamic function... - The thalamus also plays an important role in regulating states of sleep and wakefulness... - Thalamic nuclei have strong reciprocal connections with the cerebral cortex... ...are believed to be involved with consciousness. - The thalamus plays a major role in regulating arousal, the level of awareness and activity. - An animal with a severely damaged or severed thalamus suffers permanent coma. - Many different functions are linked to the system to which thalamic parts belong... : ... sensory systems ... auditory, somatic, visceral, gustatory and visual systems. - A major role of the thalamus is devoted to "motor" systems. Newer research suggests that thalamic function is even more complicated. Livescience.com (~jvr: see below) http://www.livescience.com/humanbiology/060817_brain_boot.html Thalamus (Wikipedia) http://en.wikipedia.org/wiki/Thalamus If the thalamus indeed controls and regulates all those functions a lot of our CFS-symptoms would really be the logical consequence of a thalamus imbalance! Where are links to more information on the study? Dr. Begré said a scientific paper is going to be published soon. I keep you updated. fox Switzerland www.cfs-healing.info `````````````````````` http://www.livescience.com/humanbiology/060817_brain_boot.html Your Brain Boots Up Like a Computer By Abigail W. Leonard Special to LiveScience posted: 17 August 2006 As we yawn and open our eyes in the morning, the brain stem sends little puffs of nitric oxide to another part of the brain, the thalamus, which then directs it elsewhere. Like a computer booting up its operating system before running more complicated programs, the nitric oxide triggers certain functions that set the stage for more complex brain operations, according to a new study. In these first moments of the day, sensory information floods the system-the bright sunlight coming through the curtains, the time on the screeching alarm clock-and all of it needs to be processed and organized, so the brain can understand its surroundings and begin to perform more complex tasks. "The thinking part of the brain is applying a sort of stencil to the information coming in and what the nitric oxide is doing is allowing more refinement of that stencil," says Dwayne Godwin, an associate professor at Wake Forest University and lead author of the study, which was funded by the National Eye Institute. The little two-atom molecule, it seems, is partly responsible for our ability to perceive whatever it is we're sensing. The finding, published last week in the journal Neuroscience, changes the way scientists understand nitric oxide's role in the brain, and it also has them rethinking the function of the thalamus, where it is released. The thalamus was thought to be a fairly primitive structure, sort of a gate that could either open and allow sensory information to stream into the cortex, the higher functioning part of the brain, or cut off the flow entirely. Godwin says the new research shows it's more accurate to think of the thalamus not as a gate but as a club bouncer, who doesn't simply allow a huge rush of people to go in or no one at all, but picks and chooses whom to let in and out. "Instead of vision being a process going straight from eye to cortex, it's more of a loop," Godwin explained. "This constitutes a new role for the thalamus in directing, not just modulating." While this study is the first to identify nitric oxide's role in the thalamus, elsewhere in the body it was already known to have an important, if somewhat different function. The molecule is actually integral to controlling blood flow and is, in fact, the molecule Viagra targets in order to increase blood flow to the penis. The teeny molecule might have other medical uses. "This study shows a unique role for nitric oxide. It may help us to someday understand what goes wrong in diseases that affect cognitive processing, such as attention deficit disorder or schizophrenia, and it adds to our fundamental understanding of how we perceive the world around us," Godwin said. [Return to top] ------------------------------ Date: Fri, 20 Oct 2006 11:58:46 -0400 From: Fred Springfield <fredspringfield@xxxxx.xxx> Subject: RES: Translation and validation of the Dutch language version of the CDC Symptom Inventory for Assessment of Chronic Fatigue Syndrome (CFS) Translation and validation of the Dutch language version of the CDC Symptom Inventory for Assessment of Chronic Fatigue Syndrome (CFS). Journal: Popul Health Metr. 2006 Oct 18;4(1):12 [Epub ahead of print] Author: Vermeulen RC. NLM Citation: PMID: 17049095 ABSTRACT: BACKGROUND: In a study by Wagner et al. the CDC Symptom Inventory was validated in a population that was selected from the inhabitants of a city in the USA, and proved reliable for the assessment of the symptoms accompanying the Chronic Fatigue Syndrome (CFS). The Dutch translation of the CDC Symptom Inventory is compared to the original, and the psychometric properties are presented for patients in a tertiary care setting. METHODS: A total of 139 consecutive patients who visited the CFS Center Amsterdam for the first time were asked to complete the CDC Symptom Inventory in the Dutch Language Version (DLV) together with the usual set of questionnaires. Sixty-one patients had Chronic Fatigue (CF) and 78 patients fulfilled the criteria for CFS. Forty-three healthy accompanying persons completed the CDC Symptom Inventory DLV, the Physical Functioning scale of the Medical Outcome Survey Short Form-36 DLV, and the Fatigue and Concentration scales of the Checklist Individual Strength (CIS-20). RESULTS: The healthy control group contained fewer women and was overall older than the patient groups. The influence of gender on the CDC Symptom Inventory DLV was significant but the effect of age was not. The Dutch version had a good internal consistency and convergent validity. The results were comparable to the original English version, but the sex-related difference needs further study. CONCLUSION: The Dutch version of the CDC Symptom Inventory is a reliable tool for the assessment of the secondary criteria for CFS. The results show that it is comparable to the outcome of studies in English-speaking countries. [Note: This is an Open Access article. It is available for free in PDF at http://www.pophealthmetrics.com/content/pdf/1478-7954-4-12.pdf .] [Return to top] ------------------------------ Date: Fri, 20 Oct 2006 23:18:06 +0200 From: Jan van Roijen <j.van.roijen@xxxxx.xx> Subject: not,med: Dr Derek Enlander -London & New York ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 20 October 2006 <<<< Editorship : j.van.roijen@chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: Clopez794@aol.com Dr Derek Enlander -London & New York ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ * Dr Derek Enlander a prominent CFS / ME physician will visit London on Monday Oct 30th. He will see a limited number of patients during his stay. You may contact his secretary Joy if you would like further information * New CFS FATIGUE Clinic opening ON FIFTH AVENUE in New York CONTACT: MISH3961@AOL.COM Chris, NY CFS Association [Return to top] ------------------------------ Date: Sat, 21 Oct 2006 14:01:07 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xx> Subject: RES: Alpha1-Antitrypsin Polymorphism in Fibromyalgia Syndrome Patients from the Asturias Province in Northern Spain: A Significantly Higher Prevalence of the PI*Z Deficiency Allele in Patients Than in the General Population Alpha1-Antitrypsin Polymorphism in Fibromyalgia Syndrome Patients from the Asturias Province in Northern Spain: A Significantly Higher Prevalence of the PI*Z Deficiency Allele in Patients Than in the General Population Journal of Musculoskeletal Pain (ISSN: 1058-2452,)Volume: 14 Issue: 3, (2006), Page Range: 5 - 12 DOI: 10.1300/J094v14n03_02 Ignacio Blanco MD, Daniel Arbesú PhD, Daniel Al Kassam MD, Frederick J. de Serres PhD, Enrique Fernandez-Bustillo PhD, Carmen Rodriguez MD Background: Recent evidence suggests that the alpha1-antitrypsin [AT] gene may play a role in the pathogenesis of the fibromyalgia syndrome [FMS]. The objective of the present study is to compare the AT gene frequency between FMS patients and the general population [GP] from the central region of the Asturias Province in Northern Spain. Method: The AT proteinase inhibitor phenotypes were characterized by isoelectric focusing on serum from a cohort of 250 individual FMS subjects, who fulfilled the American College of Rheumatology criteria for FMS, and on serum from a control cohort of 1,111 GP subjects. The FMS subjects [238 females and 12 males] were enlisted from an outpatient hospital clinic setting. The mean age of the FMS cohort was of 49.02 years. The GP control cohort [45 percent males and 55 percent females] was enrolled using an epidemiological technique of simple random sampling in the general population from the same region of Asturias. The GP sample size was 1,111, the mean age was of 46.2 years. Mean outcome measures were AT-PI phenotyping characterization [performed by isoelectric focusing] and AT serum concentration [measured by nephelometry]. Results: Calculated mean allele frequencies for PI*S and PI*Z [the two most frequent AT deficiency alleles] were 64 [95 percent confidence interval [CI]: 45-90] and 40 [CI: 25-62] per 1,000, respectively, for the FMS cohort, as compared with 100 [CI: 88-113] and 19.7 [CI: 14.5-26.6] per 1,000 for the GP cohort. Calculated prevalences [Hardy-Weinberg statistics formula] were 1/14 in FMS versus 1/29 in GP for MZ; 1/195 in FMS versus 1/254 in GP for SZ; and 1/625 in FMS versus 1/2,573 in GP for ZZ. For PI*Z, the calculated odd ratio among FMS versus GP was 2.06 [CI: 1.16-3.63]. A binomial proof [contrast hypothesis] stated that FMS AT-Z gene frequency differed significantly from the GP Z gene frequency [P = 0.007]. Conclusion: The most common AT severe-deficient allele [i.e., PI*Z] has been found with a two-fold higher frequency in the FMS cohort than in the GP cohort. The high odds ratio found for PI*Z indicates a significant difference for PI*Z frequency in the FMS cohort as compared with the GP cohort. Our findings suggest that AT deficiency might play an important role in FMS development and clinical expression in, at least, a subset of FMS subjects. Keywords: Alpha1-antitrypsin, alpha1-antitrypsin allelic polymorphism, SERPINA1, fibromyalgia syndrome [Return to top] ------------------------------ Date: Sat, 21 Oct 2006 15:47:52 -0400 From: Fred Springfield <fredspringfield@xxxxx.xxx> Subject: RES: Special problems of children with ME/CFS and the enteroviral link Special problems of children with ME/CFS and the enteroviral link. Journal: J Clin Pathol. 2006 Sep 11; [Epub ahead of print] Author: Colby J. Affiliation: Tymes Trust, United Kingdom. NLM Citation: PMID: 16935964 Since 1997, it has been known that ME/CFS constitutes the biggest cause of long term sickness absence from school, in both staff and pupils. The scale of the problem in children is substantial, and the pattern of illness in schools suggests a prominent role for virus infection, for example, the clustering of cases. The Dowsett/Colby study of 1997, researching long term sickness, reported on a school roll of 333,024 pupils and 27,327 staff, and found a prevalence of 70/100,000 in pupils and 500/100,000 in staff; 39% of cases were in clusters of 3 or more. The peak age was 14-16 years. The illness is known to be potentially very severe and chronic. In addition, the Tymes Trust has reported that many affected children struggle for recognition of their needs and feel bullied by medical and educational professionals. Children should have time to recover sufficiently before returning to school; sustainable, energy-efficient and often home-based education is important here, to fulfil legal obligations. Research is needed into viruses that trigger childhood ME, for example, enteroviruses, and into the neurocognitive defects caused by ME. We should recognise the value of previous biological research and records of outbreaks and I recommend that ME be made notifiable due to the encephalitic nature of the effects commonly reported in this illness. Key Words: Chronic Fatigue Syndrome, Myalgic encephalomyelitis, children, enterovirus, schools [Return to top] ------------------------------ Date: Sun, 22 Oct 2006 14:21:39 -0400 From: "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx> Subject: RES: Abnormally Low Antibody Markers of Elastin Synthesis in Patients with Fibromyalgia Syndrome Abnormally Low Antibody Markers of Elastin Synthesis in Patients with Fibromyalgia Syndrome Journal of Musculoskeletal Pain (ISSN: 1058-2452,)Volume: 14 Issue: 3, (2006), Page Range: 13 - 19 DOI: 10.1300/J094v14n03_03 Keith K. Colburn MD, John A. Rambharose MD, Marilyn C. Malto BS, Stephan Baydanoff PhD, Lawrence B. Sandberg MD, PhD, Lora M. Green PhD. Keith K. Colburn MD, Chief of Rheumatology, Medical-111R & Research Service-151, Jerry L. Pettis Memorial Veteran Medical Center, Loma Linda, CA, 92350, Keith.Colburn@med.va.gov John A. Rambharose MD, Department of Rheumatology, Loma Linda University School of Medicine, Loma Linda, CA, 92354 Marilyn C. Malto BS, Department of Rheumatology, Loma Linda University School of Medicine, Loma Linda, CA, 92354 Stephan Baydanoff PhD, Professor and Chairman, Department of Biology, Pleven, Pleven, Bulgaria Lawrence B. Sandberg MD, PhD, Professor, Microbiology & Biochemistry, Loma Linda University Graduate School, Loma Linda, CA, 92354 Lora M. Green PhD., Molecular Immunologist, Department of Rheumatology, Loma Linda University School of Medicine, Loma Linda, CA, 92354, lgreen@dominion.llumc.edu Background: Antibodies [Abs] to tropoelastin [elastin precursor] and alpha-elastin [elastin breakdown product] are found in serum of all human subjects and correlate with their respective serum peptide levels; however, peptide levels vary with age and some disease states. This study was undertaken to determine if serum elastin Abs reflective of elastin metabolism were altered in patients with fibromyalgia syndrome [FMS] by determining the ratio of serum antitropoelastin to anti-alpha-elastin Ab levels. Method: Serum samples from 20 female patients with FMS were compared with samples from 19 age-matched healthy normal control subjects for the levels of anti-elastin Abs directed against tropoelastin and alpha elastin using enzyme-linked immunosorbent assays. Results: Anti-tropoelastin Abs in the sera of patients with FMS were decreased relative to the levels measured in healthy subjects [P < 0.0002]. The ratios of anti-tropoelastin to anti-alphaelastin Abs were 1.98 versus 1.01 for control and FMS subjects, respectively. This suggested a decrease in elastin production in patients with FMS. There were no differences in the average values of anti-alpha-elastin Abs in the FMS patients sera compared to the average value of the control samples, suggesting there was no differences in elastin destruction. Conclusions: Variations in elastin metabolism were detected in sera of patients with FMS. This suggests an altered elastin metabolism in terms of reduced elastin production in patients with FMS. The relationship between elastinmetabolism and disease pathology is currently being explored. Keywords: Anti-elastin antibodies, fibromyalgia syndrome, elastin metabolism [Return to top] ------------------------------ Date: Sun, 22 Oct 2006 21:43:15 +0200 From: "Dr. Marc-Alexander Fluks" <fluks@xxx.xx> Subject: RES,NOT: Mortality in CFS and CF Source: Psychological Medicine Vol 36, #9, pp 1301-1306 Date: September 2006 URL: http://journals.cambridge.org/action/displayJournal?jid=PSM Mortality in a cohort of chronically fatigued patients ------------------------------------------------------ Wayner Smith(*), Carolyn Noodan, and Dedra Buchwald Departments of Psychiatry and Behavioral Sciences and Medicine, University of Washington, Seattle, WA, USA * Address for correspondence: W.R. Smith, Ph.D., Harborview Medical Center, 325 9th Avenue, Box 359797, Seattle, WA 98104, USA. (Email: wrsmith@u.washington.edu) ABSTRACT Background. Comprehensive studies of mortality among patients with chronic fatigue (CF) and chronic fatigue syndrome (CFS) have not been published, but several sources suggest that CFS is associated with an elevated risk for suicide. Method. Data on 1201 chronically fatigued patients followed in a university- affiliated tertiary-care clinic for up to 14 years were submitted to the Center for Disease Control and Prevention (CDC) National Death Index (NDI) to evaluate all-cause and suicide-caused death rates against standardized mortality rates (SMRs). We used Life Table Analysis to examine the influence of sex and diagnoses of CFS and depression. Results. All-cause mortality in chronically fatigued patients was no higher than expected, but suicide-caused death rates were more than eight times higher than in the US general population. The significant elevation in the SMR of suicide was restricted to those who did not meet criteria for CFS [SMR_CF=14.2, 95% confidence interval (CI) 5.7-29.3 versus SMR_CFS=3.6, 95% CI 0.4-12.9]. Among chronically fatigued patients who did not meet CFS criteria, those with a lifetime history of major depression (MD) had higher suicide-caused death rates than among their non-depressed counterparts (SMR_MD=19.1, 95% CI 7.0-41.5 versus SMR_NMD=5.6, 95% CI 0.1-31.4), although the difference was not significant. Conclusions. CFS does not appear to be associated with increased all-cause mortality or suicide rates. Clinicians, however, should carefully evaluate patients with CF for depression and suicidality. BACKGROUND Chronic fatigue (CF) is a common complaint in clinical settings that may result from diverse medical and psychological conditions. Chronic fatigue syndrome (CFS) is an illness characterized by at least 6 months of persistent and severe fatigue that is associated with unrefreshing sleep, myalgia, headache and neuropsychological disturbances. The case definition for CFS, developed by the Center for Disease Control and Prevention (CDC), allows a diagnosis of CFS to be considered only after other causes of fatiguing illness have been excluded, such as hepatitis, cancer, neurological diseases and diabetes (Fukuda et al. 1994). By definition, persons with CFS are free of most major medical conditions and therefore might be expected to have mortality rates similar to, or lower than, those for the general population. However, most psychiatric conditions are not exclusionary and rates of depressive, anxiety and other psychiatric disorders are high among patients with CF (Wessely et al. 1996) and CFS (Krusei et al. 1989; Katon et al. 1991; Lane et al. 1991). It is not known whether major depression (MD), along with the profound life changes engendered by these conditions, results in elevated rates of suicide among individuals with CF and CFS. Comprehensive studies on mortality among persons with chronically fatiguing illnesses have not been published, although one review found no increased mortality or suicide (Joyce et al. 1997). Nonetheless, reports of death and suicide attributed to CFS have been disseminated by the lay press and the internet (Australian Broadcast Corporation, 2001; Guardian Unlimited, 2001), highlighted in testimony from medical experts (Cable News Network, 2001), and reported in consumer-group publications (Chronic Fatigue and Immune Deficiency Syndrome Association of America, 1998; Allison Hunt Memorial Foundation, 1999). However defined, CFS is linked by these sources to an increased risk of suicide. We analyzed data obtained on 1201 patients evaluated at a tertiary referral clinic over a period of 12-14 years to determine if CF or CFS carried an increased risk for mortality. We used the CDC's National Death Index (NDI) to confirm death. The main objectives were to evaluate whether all-cause mortality and suicide death rates differed significantly among patients with CF or CFS from those for the general US population. METHOD Setting and sample Patients were adults seen at an academic referral center devoted to the evaluation and treatment of CF. All clinic patients were evaluated with a standardized, comprehensive review of their medical and psychiatric history, physical examination, and routine laboratory studies as recommended by the CDC (Fukuda et al. 1994). Other laboratory studies were obtained as clinically indicated. Patients were not required to meet the CDC's criteria for CFS to be seen at the clinic, but information was collected on each criterion in the case definition. Patients provided written, informed consent to use the data elements gathered during their clinic visits, a procedure that was approved by the institutional human subjects office. Identification of deaths Personal identifiers (name, social security number, date of birth, and sex) and date of the initial clinic visit were submitted to the NDI for patients who were first evaluated prior to 2002. Matches were determined based on the probabilistic match score provided by the NDI. Also provided for each potential match were the date of death and an ICD-9 or ICD-10 code indicating all causes of death for patients who died prior to 31 December 2001, which, at the time of the analysis in 2003, were the most recent data available. ICD-10 codes were translated into corresponding ICD-9 codes for analytic purposes because the software had not yet been upgraded to recognize ICD-10 codes. Although only the primary cause of death was considered in the analysis, we carefully inspected both the primary and the ancillary death codes to ensure that all suicide-caused mortality was captured. Diagnoses CFS status was assessed at the initial clinic visit according to the 1994 CDC criteria (Fukuda et al. 1994) using self-report items on the pattern, intensity and timing of fatigue and the ancillary symptoms. Retained in the current study were patients who endorsed problematic fatigue with an onset date at least 6 months prior to the examination. The presence of exclusionary diagnoses was determined by a physical examination and the attending physician's interview and review of the medical history, and by follow-up medical evaluations such as polysomnography. A trained research assistant administered the National Institute of Mental Health Diagnostic Interview Schedule Version III-A, a structured interview that assigns current and lifetime psychiatric diagnoses based on DSM-III-R criteria (Robins & Helzer, 1985). Lifetime and current MD were determined using the structured psychiatric interview. Patients who were chronically fatigued but did not meet the CDC case definition of CFS were excluded for the following reasons: (1) fatigue that was lifelong, remitted with rest, did not result in a substantial decrease in function, or was associated with an insufficient number of ancillary symptoms, (2) the presence of an exclusionary medical condition (i.e. one that could cause fatigue), including polysomnographically verified sleep disorders, or (3) the presence of an exclusionary psychiatric condition, consisting of a history of psychosis, eating disorder or alcohol or substance abuse within 2 years prior to the fatigue onset. Data analysis Patients who reported at least 6 months of fatigue and were not missing data for key variables (date of birth, social security number, sex, race, date fatigue began, initial examination date, and CFS and lifetime MD diagnoses) were considered in the analyses. Of the 1395 patients undergoing their index clinic visit between December 1988 and December 2001, 1201 (86%) met these criteria and were included in the final sample. We computed standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) for all-cause mortality and suicide by comparing observed death rates in the referral clinic cohort to general population rates in the USA from 1960 to 1999. SMRs were adjusted for sex, race, age and calendar time. We computed SMRs for the entire cohort and stratified by sex, fatigue duration prior to clinic entry, and CFS and depression diagnoses. Follow-up time began at the date of the first clinic visit and ceased on the date of death or 31 December 2001, whichever was earlier. We set the start of follow-up time at the date of clinic entry because it was the time when patients first came under observation. If we had started the follow-up period at the reported onset of fatigue, we would have introduced a bias due to incomplete observation of risk. Instead we chose to assess differences in the duration of fatigue prior to clinic entry by performing a stratified SMR analysis. Patients were stratified according to quartile of fatigue duration: <2, 2-3.9, 4-7.9 and >=8 years prior to clinic entry. All analyses were conducted using the Life Table Analysis System version 1.0d (Waxweiler et al. 1983) developed by the National Institute for Occupational Safety and Health. Stratified SMRs were tested for heterogeneity or trend using methods developed by Breslow & Day (1987). RESULTS As of 31 December 2001 the mean amount of time our sample patients were followed was 9 years (S.D.=4 years). Nearly 80% of the patients had been followed for at least 5 years. The mean age of the clinic patients at their initial evaluation was 48 p/m 13 years, and the majority were female (77%). The sample was 94% Caucasian, which is typical of the clinic, even though the greater metropolitan area is approximately 75% Caucasian. Over half the sample met all the 1994 diagnostic criteria for CFS (53%); 55% met criteria for lifetime MD. At the time of assessment the group with CF not meeting CFS criteria more frequently met criteria for current MD than did the CFS group (24% v. 14%). Among the 560 patients in the group with CF not meeting criteria, 135 (25%) were excluded from the CFS group by not meeting the symptom criterion, 36 (7%) were excluded for medical conditions, 30 (6%) were excluded for psychiatric or substance abuse conditions, and 329 (62%) had more than one exclusion. Among the 1201 clinic patients, 38 (3%) were deceased. The most common causes of death as listed by the NDI were cancers (n=9, 24%), suicide (n=9, 24%) and heart disease (n=3, 8%). Two deaths each (5%) occurred from renal failure, human immunodeficiency virus (HIV) complications, chronic obstructive pulmonary disease, and chronic liver disease, and one each (3%) from cerebrovascular disease, pneumonia, effects of alcohol dependence, asthma, motor vehicle accident, phlebitis, atherosclerosis, diaphragmatic hernia, and stroke. Table 1 shows the SMRs for our sample according to cause of death and sex. Overall, chronically fatigued patients did not experience all-cause mortality at higher rates than the general US population (SMR=0.9, 95% CI 0.6-1.2) and the SMRs for males and females were similar (p=0.51). The overall SMR for suicide was 8.6 (95% CI 3.9-16.3). The SMRs for suicide were elevated in both men (8.9, 95% CI 2.9-20.8) and women (8.2, 95% CI 2.2-21.0), but did not differ according to sex (p=0.91). Table 1 also shows the SMRs for the clinic sample according to cause of death and diagnosis of CFS. The SMRs for all-cause mortality in patients with CF not meeting criteria and those with CFS were 1.0 and 0.7, respectively. Neither SMR differed significantly from 1, nor were the ratios different from each other (p=0.22). The SMRs for death due to suicide were elevated for both patients with CF and CFS when compared to expected rates (SMR_CF=14.2, SMR_CFS=3.6). However, the SMR was significant only for chronically fatigued patients who did not meet the CDC criteria for CFS (p<0.01) (i.e. did not meet fatigue or symptom severity criteria or had an exclusionary condition). Among these chronically fatigued patients, further stratification by lifetime MD revealed a larger SMR for depressed than non-depressed patients (19.1, 95% CI 7.0-41.5 v. 5.6, 95% CI 0.1-31.4), but the difference was not significant (p=0.23). We also examined whether the SMRs for all-cause mortality or suicide increased with fatigue duration prior to clinic entry (results not shown). We found no evidence that the SMR for all-cause mortality increased with fatigue duration (p_trend=0.51). Although the rate of death due to suicide was significantly elevated in most strata when compared to expected rates (SMR range 7.7-9.2), the rate of suicide did not increase with fatigue duration (p_trend=0.91). DISCUSSION This study is the first to examine SMRs among a well-defined population of fatigued patients. We found that overall mortality was not higher than expected in our sample of 1201, mostly female, chronically fatigued Caucasian clinic patients. Suicide, however, occurred at a higher rate than in the general population, but this increase was significant only among those who did not meet diagnostic criteria for CFS. The SMR for suicide was higher among non-CFS patients with lifetime MD episodes than among their non-depressed counterparts, although this finding did not reach statistical significance. Because neither death nor suicide has ever been rigorously examined among individuals with CF and CFS, we cannot directly compare our findings to other data. However, in a study comparing depressed CFS patients with depressed patients without CFS, the CFS group experienced less worthlessness and higher selfesteem than the purely depressed group (Powell et al. 1990). Similarly, others have found that chronically fatigued adolescents without MD endorsed many secondary symptoms of depression but were less likely than depressed psychiatric clinic patients to report primary depressive symptoms such as depressed mood, guilt and suicidality (Smith et al. 1991). In our study, the co-occurrence of a CFS-exclusionary condition or MD disorder appeared to increase the risk of suicide among chronically fatigued patients. MD is a well-recognized risk factor for suicide (APA, 1994) and is itself not exclusionary for CFS. Yet it often co-exists with other psychiatric diagnoses (APA, 1994) that preclude a diagnosis of CFS, such as mania, melancholia, psychosis, eating disorders and substance abuse (Fukuda et al. 1994). These exclusionary diagnoses increase the risk of suicide (Bongar, 1991) and may explain the greater SMR for suicide in the CF patients not meeting CFS criteria. In addition to psychiatric illnesses, other risk factors for suicide include chronic, debilitating medical illness and dissatisfaction with medical care (Bongar, 1991). By definition, the chronically fatigued group not meeting the CFS case definition had a higher proportion of patients with debilitating medical illness, and may have contained a higher proportion who were disappointed and dissatisfied with their health care because of failure to be diagnosed with CFS after an extensive medical work-up. This study has several additional limitations. First, for a study of this type, our sample size was relatively small and the follow-up period short. A related issue is that SMRs may be inflated if patients recovered and were no longer fatigued during the follow-up period. However, in our previous work using self-reported disability measures with follow-ups averaging 1.7 years, we showed that the rate of recovery was low in our clinic population (Bombardier & Buchwald, 1995). Second, the reliance of the NDI on state death certificates has led some early researchers to question the accuracy and completeness of suicide as a cause of death (Nelson et al. 1978; Taylor, 1982). However, the NDI has very high sensitivity in detecting true deaths (Fisher et al. 1995), and more recent work suggests adequate reliability for suicide (Rockett & Thomas, 1999). Third, our results may not be generalizable to primary-care or community- based samples of fatigued patients because of our tertiary-care setting and the under-representation of non-Caucasians in the sample. Finally, we used the index examination date as the date when the follow-up period began rather than the date of reported fatigue onset. To do otherwise would have systematically biased the true mortality rate due to incomplete observation of risk. Nonetheless, we examined the duration of prior fatigue in a stratified analysis and saw no effect of longer fatigue duration on all-cause or suicide mortality. In summary, the all-cause mortality rate among this sample of 1201 chronically fatigue clinic patients followed for up to 12-14 years was similar to that of the general population. The subgroup that failed to meet the CFS case definition experienced greater than expected rates of death by suicide. Larger non-clinical samples and longer periods of follow-up might provide a different view, but these data underscore the need for clinicians to not dismiss the potentially serious consequences of a chronically fatiguing condition, especially when accompanied by major depression. ACKNOWLEDGMENTS We thank Dr Jack Goldberg of University of Washington Department of Epidemiology for his valuable guidance in conceptualizing this study. We are grateful to the clinic patients who made us aware of the risk of tragic events among those with chronically fatiguing conditions. This work was supported in part by grant U19 AI38429 from the National Institute of Allergy and Infectious Diseases (to Dr Buchwald). DECLARATION OF INTEREST None. TABLE Table 1. Standardized mortality ratios (SMRs) for all chronically fatigued patients according to sex or diagnosis --------------------------------------------------------------------------- All-cause mortality Suicide ------------------------ ------------------------- Observed SMR 95% CI Observed SMR 95% CI deaths deaths --------------------------------------------------------------------------- Sex Male 15 1.0 0.6-1.8 5 8.9 2.9-20.8 Female 23 0.8 0.5-1.3 4 8.2 2.2-21.0 All patients 38 0.9 0.7-1.3 9 8.6 3.9-16.3 Diagnosis of CF^a With MD 14 1.1 0.6-1.8 6 19.1 7.0-41.5 Without MD 10 1.0 0.5-1.8 1 5.6 0.1-31.4 All CF patients 24 1.0 0.7-1.5 7 14.2 5.7-29.3 Diagnosis of CFS With lifetime MD 10 0.9 0.4-1.6 1 3.2 0.1-18.0 Without lifetime MD 4 0.5 0.1-1.2 1 4.0 0.1-22.2 All CFS patients 14 0.7 0.4-1.2 2 3.6 0.4-12.9 --------------------------------------------------------------------------- CI, confidence interval; MD, major depression. ^a Chronic fatigue (CF) not meeting criteria for chronic fatigue syndrome (CFS). REFERENCES Allison Hunt Memorial Foundation (1999). Medical diagnosis, suicide and chronic fatigue syndrome (http://www.ahmf.org/99King.html). Accessed 26 June 2005. APA (1994). Diagnostic and Statistical Manual of Mental Disorders (4th edn). American Psychiatric Press: Washington, DC. Australian Broadcast Corporation (2001). Radio National. Life Matters, 23 January 2001 (http://www.abc.net.au/rn/talks/lm/stories/s125970.htm). Accessed 26 June 2005. Bombardier, C. H. & Buchwald, D. (1995). Outcome and prognosis of patients with chronic fatigue vs. chronic fatigue syndrome. Archives of Internal Medicine 155, 2105-2110. Bongar, B. (1991). The Suicidal Patient: Clinical and Legal Standards of Care. The American Psychological Association: Washington, DC. Breslow, N. E. & Day, N. E. (1987). Statistical Methods in Cancer Research: Volume II - The Design and Analysis of Cohort Studies. International Agency for Research on Cancer: Lyon. Cable News Network (2001). Chronic fatigue syndrome: more than being tired (http://archives.cnn.com/2001/HEALTH/conditions/12/24/chronic.fatigue/index.html). Accessed 24 June 2005. Chronic Fatigue and Immune Deficiency Syndrome Association of America (1998). What is CFS/ME ? (http://www.cfids-me.org/whatis.html). Accessed 25 June 2005. Fisher, S. G., Weber, L., Goldberg, G. & Davis, F. (1995). Mortality ascertainment in the veteran population: alternatives to the National Death Index. American Journal of Epidemiology 141, 242-250. Fukuda, K., Straus, S. E., Hickie, I., Sharpe, M. C., Dobbins, J. G. & Komaroff, A. (1994). The chronic fatigue syndrome; a compre- hensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Annals of Internal Medicine 121, 953-959. Guardian Unlimited (2001). Eton boy in suicide pact with depressed mother. London, UK, 6 April 2001. Joyce, J., Hotopf, M. & Wessely, S. (1997). The prognosis of chronic fatigue and chronic fatigue syndrome: a systematic review. Quarterly Journal Medicine 90, 223-233. Katon, W. J., Buchwald, D. S., Simon, G. E., Russo, J. E. & Mease, P. J. (1991). Psychiatric illness in patients with chronic fatigue and those with rheumatoid arthritis. Journal of General Internal Medicine 6, 277-285. Kruesi, M. J., Dale, J. & Straus, S. E. (1989). Psychiatric diagnoses in patients who have chronic fatigue syndrome. Journal of Clinical Psychology 50, 53-56. Lane, T. J., Manu, P. & Matthews, D. A. (1991). Depression and somatization in the chronic fatigue syndrome. American Journal of Medicine 91, 335-344. Nelson, F. L., Farberow, N. L. & MacKinnon, D. R. (1978). The cer- tification of suicide in eleven western states: an inquiry into the validity of reported suicide rates. Suicide and Life-Threatening Behavior 8, 75-88. Powell, R., Dolan, R. & Wessely, S. (1990). Attributions and self- esteem in depression and chronic fatigue syndromes. Journal of Psychosomatic Research 34, 665-673. Robins, L. N. & Helzer, J. E. (1985). Diagnostic Interview Schedule (DIS): Version III-R. Washington University: St Louis. Rockett, I. R. H. & Thomas, B. M. (1999). Reliability and sensitivity of suicide certification in higher-income countries. Suicide and Life-Threatening Behavior 29, 141-149. Smith, M. S., Mitchell, J., Corey, L., Gold, D., McCauley, E. A., Glover, D. & Tenover, F. C. (1991). Chronic fatigue in adolescents. Pediatrics 88, 195-202. Taylor, S. (1982). Death certificates underestimate suicide rates. In Durkheim and the Study of Suicide (ed. S. Taylor). St Martin's Press: New York. Waxweiler, R., Beaumont, J., Henry, J., Brown, D., Robinson, C., Ness, G., Wagoner, J. & Lemen, R. (1983). A modified life-table analysis system for cohort studies. Journal of Occupational Medicine 25, 115-124. Wessely, S., Chalder, T., Hirsch, S., Wallace, P. & Wright, D. (1996). Psychological symptoms, somatic symptoms, and psychiatric dis- order in chronic fatigue and chronic fatigue syndrome: a pro- spective study in the primary care setting. American Journal of Psychiatry 153, 1050-1059. -------- (c) 2006 Cambridge University Press [Return to top] ------------------------------ Date: Mon, 23 Oct 2006 04:31:41 +0200 From: Jan van Roijen <j.van.roijen@xxxxx.xx> Subject: med: Link Vaccine & ME ? ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 23 October 2006 <<<< Editorship : j.van.roijen@chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ http://www.nzherald.co.nz/section/story.cfm?c_id=1&objectid=10407140 The New Zealand Herald National News Monday October 23, 2006 Ministry downplays link between vaccine and ME ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ The Ministry of Health says vaccines are not linked to the rare condition chronic fatigue syndrome, but it is monitoring developments in Norway, where recipients of a meningococcal B vaccine are being studied for a possible link. The vaccine was given to more than 130,000 teenagers in the late 1980s in Norwegian trials and was the parent of the vaccine against the epidemic strain of meningococcal disease in New Zealand. It was used in trials in New Zealand, but not in the mass vaccination programme in which more than 1 million young people have been vaccinated, the ministry says. After a payout by Norway's patient injury compensation authority to a person with chronic fatigue syndrome (also called myalgic encephalomyelitis or ME) in 2003 following the trials, reportedly 70 more people who took part have been diagnosed with the condition. Around 180,000 people took part in the vaccine trials, of whom around 136,000 received the vaccine, the rest having placebo injections, the ministry says. NZ vaccination programme director Dr Jane O'Hallahan said yesterday the ministry was in contact with Norway's public health institute. She understood from an official at the institute that the cohort which took part in the Norwegian trials, now aged 29-33, had a rate of chronic fatigue syndrome "no higher than before or after that birth cohort. We need to get that confirmed ... which is what we are seeking to do at the moment." Dr O'Hallahan said no cases of chronic fatigue syndrome had been recorded in the database of adverse events following vaccination in the New Zealand programme. ```````````````` http://www.stuff.co.nz/stuff/0,2106,3836567a10,00.html Sunday Star Times Did vaccine put our kids at risk? ~~~~~~~~~~~~~~~~~~~~~~~~~~ 22 October 2006 By GREG MEYLAN The jab used to vaccinate more than a million Kiwi children against meningococcal disease is being investigated for a possible link to chronic fatigue syndrome. The Health Ministry says it will closely monitor the work of a panel of international medical experts set up to oversee a study into the safety of the vaccine, which was developed in Norway. Earn Money Working for AVON! The move follows a documentary screened in Norway last week in which doctors, including Professor Ola Didrik Saugstad, expressed concerns about the vaccine's safety. New Zealand and Norway are the only countries to have used the vaccine. The vaccine, developed in the late 1980s, was tested on 180,000 Norwegian teenagers who each received two doses. The study will determine whether or not those people are more likely to have chronic fatigue syndrome - myalgic encephalopathy (ME). The vaccine was never used outside the trial in Norway and the epidemic waned naturally. New Zealand bought the vaccine in 2001 and in 2004 and it was declared safe after small trials here and data from Norway. Since then, 1.1 million Kiwi children under 20 have received three shots of the vaccine, about 200,000 of whom were aged 13 to 17. Saugstad claimed a correlation between 19 people who had been part of the vaccine trial and their later diagnosis with ME. A Norwegian website says Saugstad is related to someone with ME and is involved in the Norwegian ME Association. The same site dates the Norwegian National Institute of Public Health's decision to investigate a link between vaccinations against meningitis and ME to March. Following the first documentary, 250 people in Norway came forward with ME symptoms, 160 of whom Saugstad said warranted further investigation. New Zealand immunisation programme director Dr Jane O'Hallahan said they were concerned about events in Norway and were monitoring events closely. However, she stressed that nothing had caused them to question the vaccine's safety. She said vaccines had been implicated in ME before but had never been proven. ME mostly strikes adults aged 25 to 40, but can also afflict children and teenagers. The latest Norwegian documentary said that at the time New Zealand bought the vaccine, the Norwegian government had made one compensation payment to a teenager who had been paralysed from the waist down as a result of the vaccine and another who had contracted ME. Speaking to the Sunday Star-Times, Saugstad said he wrote to a New Zealand colleague about his concerns before the vaccination programme began here and was told the New Zealand authorities would passively monitor for ME. "I wrote back and said in order to find out you need to go out and ask: do you have this and this symptom?" Saugstad said. In March, Saugstad asked if New Zealand had had any cases of ME related to the vaccine and was told by a member of New Zealand's safety evaluation team, Dr Stewart Reid, that there had been none. Reid said the ministry would wait and see if any cases appeared that could be linked to a vaccination and then consult on whether a wider investigation was required. A diagnosis for ME cannot be made unless a patient has been suffering fatigue for at least six months and only then if other causes have been ruled out. Saugstad said some of the Norwegian teens fell ill with flu-like symptoms quickly, and others became ill slowly after months or years. A meeting between Saugstad and Norwegian health officials on Wednesday agreed an international panel should oversee the study into the possibility of a link. The New Zealand ME Society's medical adviser Dr Ros Vallings said she had seen no increase in cases of ME in her GP practice and knew of no increases reported to the society. ```````````````````````` http://www.radionz.co.nz/news/latest/200610221904/meningococcal_b_vaccine_linked_with_me2 Radio New Zealand Meningococcal B vaccine linked with ME ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Posted at 7:07pm on 22 Oct 2006 The meningococcal B vaccination is being investigated for a possible link to chronic fatigue syndrome. The move follows the screening of a documentary in Norway in which doctors questioned the vaccine's safety. The head of New Zealand's immunisation programme, Jane O'Hallahan, says a panel of medical experts are now investigating the claims. She says talk of a link between the vaccine and chronic fatigue syndrome is not new, but she will be monitoring the medical panel's findings closely. ```````````````` http://www.stuff.co.nz/stuff/0,2106,3836816a11,00.html STUFF NATIONAL NEWS Meningococcal B vaccine claims rejected ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ 23 October 2006 By PAUL MULROONEY Health Ministry officials have defended the quality of New Zealand's meningococcal B vaccine amid international concerns its parent vaccine may contribute to chronic fatigue syndrome. Norwegian professor Ola Didrik Saugstad has questioned the safety of the vaccine, which has been used only in Norway and New Zealand. He claimed a link between 19 people who had been part of the Norwegian vaccine trial and their later diagnosis with the syndrome myalgic encephalopathy (ME). Sponsored Links Findout how to get quake safeNew Zealand meningococcal immunisation programme director Jane O'Hallahan said while the vaccines were similar they were not identical. Norway's use of the parent vaccine, tested in two doses on up to 180,000 teenagers, is now the subject of a study into its safety by a panel of international experts. Following limited trials in New Zealand, and approval in 2004, a similar vaccine was used on 1.1 million New Zealanders aged under 20. Dr O'Hallahan said New Zealand officials were monitoring the situation in Norway, with regular briefings given to Health Minister Pete Hodgson, but there was no scientific evidence linking chronic fatigue to the New Zealand vaccine. "The key difference is the (meningococcal) strain circulating in Norway has been replaced with the strain of the disease circulating here. It is a strain-specific vaccine." AdvertisementAdvertisementWhile the health ministry was aware of one case in Norway in which a vaccine recipient had later developed ME, she rejected claims by vaccine sceptics, the Immunisation Awareness Society, that the ministry had overlooked any earlier concerns. But immunisation society spokeswoman Sue Claridge said the developments highlighted its concerns with the long term effects of such vaccines. "We expressed concern at the time of the immunisation campaign that it had not been adequately tested." Medsafe technical specialist Stewart Jessamine said the quality of the manufacturing site for the New Zealand vaccine continued to meet international standards. The Immunisation Advisory Centre, an independent agency connected to Auckland University, found there were no unexpected side effects from the New Zealand vaccine. [Return to top] ------------------------------ Date: Mon, 23 Oct 2006 14:14:28 +0200 From: "Dr. Marc-Alexander Fluks" <fluks@xxx.xx> Subject: RES: CFS/ME & FM papers, published since September 2006 Source: NCBI PubMed Date: October 20, 2006 URL: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi Topic=((chronic fatigue) OR (myalgic encephalomyelitis)) OR fibromyalgia Ref: In the update, you will only find journals that are indexed by Medline (PubMed). All papers 1938-today, http://www.me-net.dds.nl/library/literature.html#publications Search papers, http://www.me-net.dds.nl/library/literature.html#catalogue Figures computer analysis: http://www.me-net.dds.nl/library/literature.html#figure CFS/ME & FM papers, published since September 2006 -------------------------------------------------- ___ Van Houdenhove B. What is the aim of cognitive behaviour therapy in patients with chronic fatigue syndrome? Psychother Psychosom. 2006;75(6):396-7. ___ Gielissen MF, Verhagen S, Witjes F, Bleijenberg G. Effects of cognitive behavior therapy in severely fatigued disease- free cancer patients compared with patients waiting for cognitive behavior therapy: a randomized controlled trial. J Clin Oncol. 2006 Oct 20;24(30):4882-7. ___ Vermeulen RC. Translation and validation of the Dutch language version of the CDC Symptom Inventory for Assessment of Chronic Fatigue Syndrome (CFS). Popul Health Metr. 2006 Oct 18;4(1):12. ___ Petrella RJ, Davis P. Improving management of musculoskeletal disorders in primary care: the Joint Adventures Program. Clin Rheumatol. 2006 Oct 18. ___ Calandre EP, Hidalgo J, Rico-Villademoros F. Use of ziprasidone in patients with fibromyalgia: a case series. Rheumatol Int. 2006 Oct 13. ___ Torenbeek M, Mes CA, van Liere MJ, Schreurs KM, ter Meer R, Kortleven GC, Warmerdam CG. Favourable results of a rehabilitation programme with cognitive behavioural therapy and graded physical activity in patients with the chronic-fatigue syndrome [Dutch]. Ned Tijdschr Geneeskd. 2006 Sep 23;150(38):2088-94. ___ Jonker K, van Hemert AM. Treatment of patients with the chronic-fatigue syndrome [Dutch]. Ned Tijdschr Geneeskd. 2006 Sep 23;150(38):2067-8. ___ Ardic F, Ozgen M, Aybek H, Rota S, Cubukcu D, Gokgoz A. Effects of balneotherapy on serum IL-1, PGE(2 )and LTB (4) levels in fibromyalgia patients. Rheumatol Int. 2006 Oct 11. ___ Tastekin N, Birtane M, Uzunca K. Which of the three different tender points assessment methods is more useful for predicting the severity of fibromyalgia syndrome? Rheumatol Int. 2006 Oct 7. ___ Wood PB, Patterson Ii JC, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL. Reduced Presynaptic Dopamine Activity in Fibromyalgia Syndrome Demonstrated With Positron Emission Tomography: A Pilot Study. J Pain. 2006 Oct 3. ___ Chambers D, Bagnall AM, Hempel S, Forbes C. Interventions for the treatment, management and rehabilitation of patients with chronic fatigue syndrome/myalgic encephalomyelitis: an updated systematic review. J R Soc Med. 2006 Oct;99(10):506-20. ___ Crawley E. Chronic fatigue syndrome in young people: the spectrum and the myths. Br J Hosp Med (Lond). 2006 Sep;67(9):452-3. ___ Schikler KN. Potential polygenic influences on chronic fatigue syndrome. Pediatrics. 2006 Oct;118(4):1799-800; author reply 1800. ___ O'dowd H, Gladwell P, Rogers CA, Hollinghurst S, Gregory A. Cognitive behavioural therapy in chronic fatigue syndrome: a randomised controlled trial of an outpatient group programme. Health Technol Assess. 2006 Oct;10(37):1-140. ___ Zucker DR, Ruthazer R, Schmid CH, Feuer JM, Fischer PA, Kieval RI, Mogavero N, Rapoport RJ, Selker HP, Stotsky SA, Winston E, Goldenberg DL. Lessons Learned Combining N-of-1 Trials to Assess Fibromyalgia Therapies. J Rheumatol. 2006 Oct;33(10):2069-77. ___ Cacace E, Ruggiero V, Anedda C, Denotti A, Minerba L, Perpignano G. Quality of life and associated clinical distress in fibromyalgia [Italian]. Reumatismo. 2006 Jul-Sep;58(3):226-9. ___ Van Staden WC. Conceptual issues in undifferentiated somatoform disorder and chronic fatigue syndrome. Curr Opin Psychiatry. 2006 Nov;19(6):613-8. ___ Amital D, Vishne T, Rubinow A, Levine J. Observed effects of creatine monohydrate in a patient with depression and fibromyalgia. Am J Psychiatry. 2006 Oct;163(10):1840-1. ___ Vervoort T, Crombez G, Buysse A, Goubert L, De Backer T, Ickes W. Brief Report: The Accuracy of Parents for the Thoughts and Feelings of Their Adolescent Suffering from Chronic Fatigue: A Preliminary Study of Empathy. J Pediatr Psychol. 2006 Sep 29. ___ Cook DB, Nagelkirk PR, Poluri A, Mores J, Natelson BH. The influence of aerobic fitness and fibromyalgia on cardiorespiratory and perceptual responses to exercise in patients with chronic fatigue syndrome. Arthritis Rheum. 2006 Sep 28;54(10):3351-3362. ___ Hammond A, Freeman K. Community patient education and exercise for people with fibromyalgia: a parallel group randomized controlled trial. Clin Rehabil. 2006 Oct;20(10):835-46. ___ Maes M, Mihaylova I, Leunis JC. Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): Indication for the involvement of gram- negative enterobacteria in the etiology of CFS and for the presence of an increased gut-intestinal permeability. J Affect Disord. 2006 Sep 26. ___ Cole JA, Rothman KJ, Cabral HJ, Zhang Y, Farraye FA. Migraine, fibromyalgia, and depression among people with IBS: a prevalence study. BMC Gastroenterol. 2006 Sep 28;6:26. ___ Liedberg GM, Burckhardt CS, Henriksson CM. Young women with fibromyalgia in the United States and Sweden: Perceived difficulties during the first year after diagnosis. Disabil Rehabil. 2006 Oct 15;28(19):1177-84. ___ Jones KD, Adams D, Winters-Stone K, Burckhardt CS. A comprehensive review of 46 exercise treatment studies in fibromyalgia (1988-2005). Health Qual Life Outcomes. 2006 Sep 25;4:67. -------- (c) 2006 NCBI PubMed [Return to top] ------------------------------ Date: Mon, 23 Oct 2006 14:12:14 -0400 From: Fred Springfield <fredspringfield@xxxxx.xxx> Subject: RES: What is the aim of cognitive behaviour therapy in patients with chronic fatigue syndrome? Letter to the Editor: What is the aim of cognitive behaviour therapy in patients with chronic fatigue syndrome? Journal: Psychother Psychosom. 2006;75(6):396-7. Author: Van Houdenhove B. Affiliation: Department of Liaison Psychiatry, University Hospital Gasthuisberg BE3000Leuven, Belgium. E-Mail: <boudewijn.vanhoudenhove@uz.xxxxxxxx.xx.xx> NLM Citation: PMID: 17053343 We read with great interest the article by Bazelmans et al. [1], [see http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0506B&L=CO-CURE&P=R3050 ] in which the authors reported their unexpected ‘negative’ results of group cognitive behaviour therapy (CBT) in patients with chronic fatigue syndrome (CFS). In short, although patients mentioned less fatigue after the therapeutic programme, this symptomatic improvement was not refl ected by a higher level of functioning. The authors speculated about four possible reasons for their fi ndings: the therapists might have laid too much emphasis on rest and waited too long before encouraging patients to resume activity; the therapists might have been too inexperienced in treating CFS patients; the group therapy format might have been less effective compared to individual CBT, or the patient group might have been too unselected. In our opinion, however, another possibility could be considered. The patients’ symptomatic amelioration might have been due to the fact that they had learned to better manage their energy, not exceed their limits and avoid peaks of activity which might eventually have resulted in a decrease of their global activity level. Thus, according to this interpretation, the reported results of the group CBT programme were not that negative! The above shows that the aim of CBT (and graded exercise therapy, which is often associated with CBT) in CFS patients is far from clear-cut. Indeed, in CBT-oriented literature concerned with CFS, different treatment goals can be discerned. Some authors suggest that the therapist should mainly incite patients to diminish their somatic focus and correct inappropriate physical attributions [2, 3] . However, the usefulness of this goal is doubtful since the majority of patients with CFS and the largely overlapping fi bromyalgia syndrome (FM) seems to accept a combined psychological/somatic causation of their illness [4] . According to other authors, the therapist should in the fi rst place tackle the patients’ activity avoidance or irregular activity patterns (outburst of activity followed by prolonged periods of rest), and stimulate them to engage in a graded exercise program in order to fi ght physical deconditioning [5] . However, most CFS patients do not show kinesiophobia [6, 7] and loss of exercise capacity does not seem to play a major role in the pathophysiology of CFS [8, 9] . Moreover, recent physical therapists do not recommend ‘pure’ graded exercise therapy in CFS patients (i.e. progressively increasing physical effort irrespective of possible symptom worsening), but modulate exercises by an individualized pacing scheme [10] . Finally, some CBT therapists are convinced that patients should, at the end of the therapy, stop considering themselves as CFS sufferers, even claim their therapy being curative [11] , while others point to the patients’ lasting vulnerability necessitating long-term adaptation to prevent relapse [9, 12] . In our own daily practice with patients suffering from CFS/FM, we base our group CBT programme on the following pathophysiological working hypothesis: both CFS and FM result from a ‘loss of resilience’ of the stress system, after a prolonged period of physical or mental overburdening in which the system functions ‘in overdrive’ [12, 13] . Given the fact that direct treatment of this neurobiological dysregulation is at present not available, we explain to the patients that the recovery of their stress system might be indirectly facilitated under the following conditions: First, they should accept their ailment and functional limitations and work through the painful grieving process resulting from the fact that CFS means giving up many important things in life. Second, they should realistically adapt to their effort intolerance by learning to carefully pace activities in order to avoid post-exertional malaise refl ecting abnormal immune activation [12] . In many patients, this implies abandoning their previous ‘overactive’ lifestyles, which may be rooted in narcissistic, perfectionistic or counter-dependent tendencies [14] . Third, they should try to gradually increase their physical and mental activity level, again without provoking post-exertional malaise. And fourth, they should realize that long-term readjustment of lifestyle, life-goals and priorities is a conditio sine qua non to maintain symptomatic amelioration and regain stress system resilience. In sum, if our hypothesis is correct (namely that the aetiopathogenesis of CFS/FM is based on long-lasting physical and/or mental overburdening, leading to severe and persistent disturbances of the stress system in vulnerable individuals), the aim of CBT should be to help patients find a ‘new equilibrium’, taking fully account of their personal illness and life history [13, 15] . In terms of McEwen’s [16] neurobiological stress paradigm, this aim could also be formulated as ‘restoring allostasis’. References 1 Bazelmans E, Prins JB, Lulofs R, van der Meer JW, Bleijenberg G: Cognitive behaviour group therapy for chronic fatigue syndrome: a non-randomized waiting list controlled study. Psychother Psychosom 2005; 74: 218 224. 2 Chalder T, Power MJ, Wessely S: Chronic fatigue in the community: ‘a question of attribution’. Psychol Med 1996; 26: 791800. 3 Moss-Morris R, Charon C, Tobin R, Baldi JC: A randomized controlled graded exercise trial for chronic fatigue syndrome: outcomes and mechanisms of change. J Health Psychol 2005; 10: 245259. 4 Neerinckx E, Van Houdenhove B, Lysens R, Vertommen H, Onghena P: Attributions in chronic fatigue syndrome and fi bromyalgia syndrome in tertiary care. J Rheumatol 2000; 27: 10511055. 5 Fulcher KY, White PD: Strength and physiological response to exercise in patients with chronic fatigue syndrome. J Neurol Neurosurg Psychiatry 2000; 69: 302307. 6 Nijs J, Vanherberghen K, Duquet W, De Meirleir K: Chronic fatigue syndrome: lack of association between pain-related fear of movement and exercise capacity and disability. Phys Ther 2004; 84: 696705. 7 Gallagher AM, Coldrick AR, Hedge B, Weir WR, White PD: Is the chronic fatigue syndrome an exercise phobia? A case control study. J Psychosom Res 2005; 58: 367373. 8 Bazelmans E, Bleijenberg G, van de Meer JW, Folgering H: Is physical deconditioning a perpetuating factor in chronic fatigue syndrome? A controlled study on maximal exercise performance and relations with fatigue, impairment and physical activity. Psychol Med 2001; 31: 107114. 9 Pardaens K, Haagdorens L, Van Wambeke P, Van den Broeck A, Van Houdenhove B: How relevant are exercise capacity measures for evaluating treatment effects in chronic fatigue syndrome? Results of a prospective, multidisciplinary outcome study. Clin Rehabil, 2006;20:5666. 10 Wallman KE, Morton AR, Goodman C, Grove R: Exercise prescription for individuals with chronic fatigue syndrome. Med J Aust 2005; 183: 142 143. 11 Prins J, Bleijenberg G, van der Meer JM: Chronic fatigue syndrome and myalgic encephalomyelitis. Lancet 2002; 359: 1699. 12 Van Houdenhove B, Egle UT: Fibromyalgia: a stress disorder? Piecing the biopsychosocial puzzle together. Psychother Psychosom 2004; 73: 267 275. 13 Van Houdenhove B, Neerinckx E, Onghena P, Vingerhoets A, Lysens R, Vertommen H: Daily hassles reported by chronic fatigue syndrome and fi bromyalgia patients in tertiary care: a controlled quantitative and qualitative study. Psychother Psychosom 2002; 71: 207213. 14 Van Houdenhove B, Neerinckx E, Onghena P, Lysens R, Vertommen H: Premorbid ‘overactive’ lifestyle in chronic fatigue syndrome and fi bromyalgia. An etiological factor or proof of good citizenship? J Psychosom Res 2001; 51: 571576. 15 Van Houdenhove B: Listening to CFS. Why we should pay more attention to the story of the patient. J Psychosom Res 2002; 52: 495499. 16 McEwen BS: Stressed or stressed out: what is the difference? J Psychiatry Neurosci 2005; 30: 315318. [Return to top] ------------------------------

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