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[Return to digest index] --------------------------------------------- This is a special digest of Co-Cure Research & Medical posts only Problems? Write to mailto:email@example.com --------------------------------------------- ---------------------------------------------------------------------- Date: Tue, 20 Mar 2007 08:06:37 +0100 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES: CFS/ME & FM papers, published since February 2007 Source: NCBI PubMed Date: March 20, 2007 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 scientific papers 1938-today, http://www.me-net.combidom.com/library/literature.htm#publications Search scientific papers, http://www.me-net.combidom.com/library/literature.htm#catalogue Figures computer analysis scientific papers, http://www.me-net.combidom.com/library/literature.htm#figure All popular papers 1900-today, http://www.me-net.combidom.com/library/literature.htm#popular CFS/ME & FM papers, published since February 2007 ------------------------------------------------- ___ Wallman KE, Sacco P. Sense of effort during a fatiguing exercise protocol in chronic fatigue syndrome. Res Sports Med. 2007 Jan-Mar;15(1):47-59. ___ Appel S, Chapman J, Shoenfeld Y. Infection and vaccination in chronic fatigue syndrome: Myth or reality? Autoimmunity. 2007 Feb;40(1):48-53. ___ Gulec H, Sayar K, Yazici Gulec M. The Relationship between Psychological Factors and Health Care- Seeking Behavior in Fibromyalgia Patients [Turkish]. Turk Psikiyatri Derg. 2007 Spring;18(1):22-30. ___ Sierpina V, Levine R, Astin J, Tan A. Use of mind-body therapies in psychiatry and family medicine faculty and residents: attitudes, barriers, and gender differences. Explore (NY). 2007 Mar-Apr;3(2):129-35. ___ Takken T, Henneken T, van de Putte E, Helders P, Engelbert R. Exercise Testing in Children and Adolescents with Chronic Fatigue Syndrome. Int J Sports Med. 2007 Mar 15. ___ Van Geelen SM, Sinnema G, Hermans HJ, Kuis W. Personality and chronic fatigue syndrome: Methodological and conceptual issues. Clin Psychol Rev. 2007 Jan 27. ___ Yunus MB. Fibromyalgia and Overlapping Disorders: The Unifying Concept of Central Sensitivity Syndromes. Semin Arthritis Rheum. 2007 Mar 10. ___ Nijs J, Demol S, Wallman K. Can submaximal exercise variables predict peak exercise performance in women with chronic fatigue syndrome? Arch Med Res. 2007 Apr;38(3):350-3. ___ Rowe PC, Lucas KE. Orthostatic intolerance in chronic fatigue syndrome. Am J Med. 2007 Mar;120(3):e13. ___ Bennett RM, Jones J, Turk DC, Russel IJ, Matallana L. An internet survey of 2,596 people with fibromyalgia. BMC Musculoskelet Disord. 2007 Mar 9;8(1):27. ___ Nordahl HM, Stiles TC. Personality styles in patients with fibromyalgia, major depression and healthy controls. Ann Gen Psychiatry. 2007 Mar 9;6(1):9. ___ Kumor K, Pierzchala K. The problem of fatigue in neurological disorders [Polish]. Wiad Lek. 2006;59(9-10):685-91. ___ Palomino RA, Nicassio PM, Greenberg MA, Medina EP Jr. Helplessness and loss as mediators between pain and depressive symptoms in fibromyalgia. Pain. 2007 Feb 28. ___ Baicus C, Baicus A. Spirulina did not ameliorate idiopathic chronic fatigue in four N-of-1 randomized controlled trials. Phytother Res. 2007 Mar 5. ___ Shorter E. Hysteria and catatonia as motor disorders in historical context. Hist Psychiatry. 2006 Dec;17(68 Pt 4):461-8. ___ Wigers SH, Finset A. Rehabilitation of chronic myofascial pain disorders [Norwegian]. Tidsskr Nor Laegeforen. 2007 Mar 1;127(5):604-8. ___ Rimes KA, Goodman R, Hotopf M, Wessely S, Meltzer H, Chalder T. Incidence, prognosis, and risk factors for fatigue and chronic fatigue syndrome in adolescents: a prospective community study. Pediatrics. 2007 Mar;119(3):e603-9. ___ Hjollund NH, Andersen JH, Bech P. Assessment of fatigue in chronic disease: a bibliographic study of fatigue measurement scales. Health Qual Life Outcomes. 2007 Feb 27;5:12. ___ Busch A. Hydrotherapy improves pain, knee strength, and quality of life in women with fibromyalgia. Aust J Physiother. 2007;53(1):64. ___ Van Houdenhove B, Luyten P. Stress, depression and fibromyalgia. Acta Neurol Belg. 2006 Dec;106(4):149-56. ___ Kobelt A, Grosch E, Wasmus A, Ehlebracht-Konig I, Schwarze M, Krahling M, Gutenbrunner C. Is It Possible to Predict Approval of Medical Rehabilitation by the Extent of Fatigue and Subjective Need for Rehabilitation? Development, Results and Acceptance of a Short Screening [German]. Rehabilitation (Stuttg). 2007 Feb;46(1):33-40. ___ Ang D, Kesavalu R, Lydon JR, Lane KA, Bigatti S. Exercise-based motivational interviewing for female patients with fibromyalgia: a case series. Clin Rheumatol. 2007 Feb 20. ___ Freedenfeld RN, Murray M, Fuchs PN, Kiser RS. Decreased pain and improved quality of life in fibromyalgia patients treated with olanzapine, an atypical neuroleptic. Pain Pract. 2006 Jun;6(2):112-8. ___ Harden RN, Revivo G, Song S, Nampiaparampil D, Golden G, Kirincic M, Houle TT. A critical analysis of the tender points in fibromyalgia. Pain Med. 2007 Mar-Apr;8(2):147-56. -------- (c) 2007 NCBI PubMed [Return to top] ------------------------------ Date: Tue, 20 Mar 2007 12:12:35 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Does Thalidomide Have an Analgesic Effect? Current Status and Future Directions Does Thalidomide Have an Analgesic Effect? Current Status and Future Directions Current Pain and Headache Reports 2007, 11:109-114 Veeraindar Goli, MD, Duke University Medical Center, 932 Morreene Road, Durham, NC 27705, USA. Email: goli0001 mc.duke.edu Dramatic relief of pain and life-altering changes in quality of life in some patients treated with immunomodulators such as thalidomide compel us to look more closely at unconventional mechanisms that may be involved in propagation of persistent pain. Tumor necrosis factor (TNF)-a, interleukin (IL)-1b, IL-6, and IL-10 are the cytokines with the most evidence in pain modulation. TNF-a and IL-1b seem to initiate neuropathic pain, IL-6 maintains such pain, and IL-10 inhibits this persistent pain. Thalidomide was found to be effective in animal models by inhibiting TNF-a production. Several case reports and case series in humans have demonstrated mixed results, with some patients having dramatic responses, especially in chronic intractable conditions such as complex regional pain syndrome. Thalidomide may be an alternative for some patients with intractable pain. However, use of thalidomide is limited by its neurotoxic and teratogenic effects. Newer analogues may significantly improve the risk/benefit of using such immunomodulators. Copyright © 2007 by Current Science, Inc. [Return to top] ------------------------------ Date: Tue, 20 Mar 2007 12:15:59 -0400 From: "Bernice A. Melsky" <bernicemelsky@VERIZON.NET> Subject: RES: Is There Genetic Polymorphism Evidence for Individual Human Sensitivity to Opiates? Is There Genetic Polymorphism Evidence for Individual Human Sensitivity to Opiates? Current Pain and Headache Reports 2007, 11:115-123 Makoto Nagashima, MD, PhD, Ryoji Katoh, MD, PhD, Yasuo Sato, MD, Megumi Tagami, MD, PhD, Shinya Kasai, PhD, and Kazutaka Ikeda, PhD Corresponding author: Kazutaka Ikeda, PhD, Department of Molecular Psychiatry, Tokyo Institute of Psychiatry, 2-1-8 Kamikitazawa, Setagaya-ku, Tokyo 156-8585, Japan. Email: ikedak prit.go.jp Opiate analgesics have been widely used for severe acute pain and chronic cancer-related pain. Individual differences in the effectiveness of opiates and their side effects limit the clinical benefits and increase risks of drug abuse. Genetic factors might affect variations of opiate sensitivity. The mu opioid peptide receptor (MOP) is the principal site of pharmacologic actions for most clinically important opiate drugs. Recent studies using various knockout mice and recombinant-inbred strain CXBK mice have indicated that the analgesic effect of morphine is dependent on the amount of the MOP. There are more than 100 polymorphisms identified in the human MOP (OPRM1) gene. These polymorphisms might be correlated with OPRM1 mRNA stability and opiate sensitivity, including opiate analgesia, tolerance, and dependence. More precise studies on the relationship between gene polymorphisms and opiate sensitivity will enable realization of personalized pain treatment by predicting opiate sensitivity and requirement for each patient. Copyright © 2007 by Current Science, Inc. [Return to top] ------------------------------ Date: Wed, 21 Mar 2007 08:57:50 -0400 From: Fred Springfield <fredspringfield VERIZON.NET> Subject: RES: The effect of cognitive behaviour therapy for chronic fatigue syndrome on self-reported cognitive impairments and neuropsychological test performance The effect of cognitive behaviour therapy for chronic fatigue syndrome on self-reported cognitive impairments and neuropsychological test performance. Journal: J Neurol Neurosurg Psychiatry. 2007 Apr;78(4):434-6. Authors: Knoop H, Prins JB, Stulemeijer M, van der Meer JW, Bleijenberg G. Affiliation: Expert Centre Chronic Fatigue, Radboud University Nijmegen Medical Centre, P O Box 9011, 6525 EC Nijmegen, The Netherlands. j.knoop nkcv.umcn.nl NLM Citation: PMID: 17369597 BACKGROUND: Patients with chronic fatigue syndrome (CFS) often have concentration and memory problems. Neuropsychological test performance is impaired in at least a subgroup of patients with CFS. Cognitive behavioural therapy (CBT) for CFS leads to a reduction in fatigue and disabilities. AIM: To test the hypothesis that CBT results in a reduction of self-reported cognitive impairment and in an improved neuropsychological test performance. METHODS: Data of two previous randomised controlled trials were used. One study compared CBT for adult patients with CFS, with two control conditions. The second study compared CBT for adolescent patients with a waiting list condition. Self-reported cognitive impairment was assessed with questionnaires. Information speed was measured with simple and choice reaction time tasks. Adults also completed the symbol digit-modalities task, a measure of complex attentional function. RESULTS: In both studies, the level of self-reported cognitive impairment decreased significantly more after CBT than in the control conditions. Neuropsychological test performance did not improve. CONCLUSIONS: CBT leads to a reduction in self-reported cognitive impairment, but not to improved neuropsychological test performance. The findings of this study support the idea that the distorted perception of cognitive processes is more central to CFS than actual cognitive performance. [Return to top] ------------------------------ Date: Wed, 21 Mar 2007 09:34:44 -0400 From: Co-Cure Moderator <ray CO-CURE.ORG> Subject: RES: Cold pressor pain sensitivity in monozygotic twins discordant for chronic fatigue syndrome Cold pressor pain sensitivity in monozygotic twins discordant for chronic fatigue syndrome. Journal: Pain Med. 2007 May-Jun;8(3):216-22. Authors: Ullrich PM, Afari N, Jacobsen C, Goldberg J, Buchwald D. Department of Rehabilitation Medicine, University of Washington, Seattle, WA, USA. NLM Citation: PMID: 17371408 Objective. Individuals with chronic fatigue syndrome (CFS) experience many pain symptoms. The present study examined whether pain and fatigue ratings and pain threshold and tolerance levels for cold pain differed between twins with CFS and their cotwins without CFS. Design. Cotwin control design to assess cold pain sensitivity, pain, and fatigue in monozygotic twins discordant for CFS. Patients and Setting. Fifteen monozygotic twin pairs discordant for CFS recruited from the volunteer Chronic Fatigue Twin Registry at the University of Washington. Results. Although cold pain threshold and tolerance levels were slightly lower in twins with CFS than their cotwins without CFS, these differences failed to reach statistical significance. Subjective ratings of pain and fatigue at multiple time points during the experimental protocol among twins with CFS were significantly higher than ratings of pain (P = 0.003) and fatigue (P < 0.001) by their cotwins without CFS. Conclusions. These results, while preliminary, highlight the perceptual and cognitive components to the pain experience in CFS. Future studies should focus on examining the heritability of pain sensitivity and the underlying mechanisms involved in the perception of pain sensitivity in CFS. [Return to top] ------------------------------ Date: Wed, 21 Mar 2007 15:11:33 +0100 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES,NOT: CFS and personality Source: Clinical Psychology Review Preprint Date: January 27, 2007 URL: http://www.sciencedirect.com/science/journal/02727358 Personality and chronic fatigue syndrome: Methodological and conceptual issues ------------------------------------------------------------------------------ Stefan M. van Geelen(a), Gerben Sinnema(a), Hubert J.M. Hermans(b), Wietse Kuis(c,*) a Department of Psychology, Wilhelmina Children's Hospital, University Medical Center Utrecht, The Netherlands b Faculty of Clinical Psychology and Personality, Radboud University Nijmegen, The Netherlands c Department of Immunology, Wilhelmina Children's Hospital, University Medical Center Utrecht, The Netherlands * Corresponding author. Division of Pediatrics, Wilhelmina Children's Hospital, University Medical Center Utrecht, P.O. Box 85090, KB.03.023.2, 3508 AB, Utrecht, The Netherlands. E-mail address: W.Kuis umcutrecht.nl (W. Kuis). Received 9 December 2005; received in revised form 29 November 2006; accepted 19 January 2007 Abstract Among clinical psychologists, consulting physicians, scientific researchers and society in general an image has emerged of patients with chronic fatigue syndrome (CFS) as perfectionist, conscientious, hardworking, somewhat neurotic and introverted individuals with high personal standards, a great desire to be socially accepted and with a history of continuously pushing themselves past their limits. The aim of this article is to (a) give a concise review of the main recent studies on personality and CFS, (b) address the major methodological problems in the study of personality in CFS and (c) discuss some of the conceptual assumptions that seem to limit the research on personality and CFS. The results of the reviewed studies range from no evidence of major differences between the personalities of patients with CFS and controls, to evidence of severe psychopathology and personality disorder in patients with CFS. Although personality seems to play a role in CFS, it is difficult to draw general conclusions on the relation between personality and CFS. It is argued that this is partially due to the diversity and heterogeneity in study methods, patient populations, control groups and CFS case definitions. Personality should be regarded as an important factor to be studied in CFS. However, additional studies are needed, not focusing exclusively on personality disorder, or personality considered on a general trait level. In recent developments in personality research, the continually evolving life narrative that makes sense of, and gives direction to, an individual's life is also regarded as an important aspect of personality. New insights into personality and CFS might be gained by systematically studying the self-narratives of patients with the syndrome. Keywords: Chronic fatigue syndrome; Personality; Clinical psychology; Narrative; Medicine 1. Introduction This article's main concern is the study of personality in the chronic fatigue syndrome (CFS). CFS is a syndrome of unknown origin. It is mainly characterized by a severely disabling fatigue and it is commonly associated with symptoms such as myalgias, headache, sleep disturbance, swollen lymph nodes and cognitive impairment. In recent years CFS has become a growing concern, not only for patients suffering from the illness and for their families, but also for medical science, clinical psychology and society in general. Some of these concerns already become apparent in defining what CFS is. In many cases, it is difficult to distinguish between idiopathic chronic fatigue, CFS and other unexplained medical conditions such as fibromyalgia, tension headache and irritable bowel syndrome, as these seem to be very similar and substantially overlapping (Aaron & Buchwald, 2001; Wessely, Nimnuan, & Sharpe, 1999). As no causes for CFS are found and definite markers for the illness are absent, the diagnostic process is usually extended and patients have to go through a whole battery of laboratory tests, physical examinations and psychological investigations before they are diagnosed with CFS. In 1988, the US Centers of Disease Control (CDC) proposed a set of diagnostic criteria to facilitate scientific research into CFS (Holmes et al., 1988). However, these criteria were criticized, not only because a large number of symptoms had to be present for a diagnosis of CFS, which might bias in favor of psychiatric morbidity (Katon & Russo, 1992), but also because it excluded such conditions as anxiety and depression, which some propose to be a result of the syndrome (Ray, 1991; Van Hoof, Cluydts, & De Meirleir, 2003). Therefore, less restrictive criteria were developed, amongst others in the UK by Sharpe et al. (1991). Consequently, the CDC criteria were also revised (Fukuda et al., 1994). At present these criteria are generally accepted and used for international research purposes. In Table 1 these criteria are presented. Estimations on the prevalence of CFS range from 37/100 000 (Lloyd, Hickie, Boughton, Spencer, & Wakefield, 1990), to 75-267/100 000 (Buchwald et al., 1995), and even 740/100 000 (Lawrie, Manders, Geddes, & Pelosi, 1997). However, these numbers are difficult to compare as different populations were studied and varying CFS case definitions were used. Estimations on the incidence of CFS are rare but, based on their assumptions with regard to the prevalence of CFS, Lawrie et al. (1997) estimated the annual incidence of CFS to be 370/100 000. Full recovery from CFS is unusual. In a recent review (Cairns & Hotopf, 2005) of studies on the prognosis of CFS, it was found that the median full recovery rate was only 5% and the median proportion of patients who had improved during follow-up was 39.5%. The prognosis for children and adolescents however, is generally somewhat better (Patel, Smith, Chalder, & Wessely, 2003). In a recent follow-up study of adolescent patients with CFS (Gill, Dosen, & Ziegler, 2004) it was found that, at a mean of 4.57 years after initial examination, 25% of the patients showed near to complete improvement and 31% showed partial improvement. Etiological studies into the possible causes of CFS have been abundant. Active viral infection has frequently been associated with the symptoms of CFS, but evidence for this hypothesis has not consistently been found. There appear to be no significant differences between patients with CFS and healthy controls in the prevalence of human herpes viruses, Epstein-Barr virus, cytomegalovirus, hepatitis C virus, adenovirus and parvovirus B19, amongst many others. (Buchwald, Ashley, Pearlman, Kith, & Komaroff, 1996; Koelle et al., 2003; Wallace, Natelson, Gause, & Hay, 1999). Immune dysfunction is another possible etiological factor that has been widely studied. Chronic lymphocyte overactivation with cytokine abnormalities in patients with CFS, associations between T cell markers and CFS, and associations between low natural killer cells and CFS have all been reported (Patarca-Montero, Antoni, Fletcher, & Klimas, 2001; Straus, Fritz, Dale, Gould, & Strober, 1993). However, in a recent systematic review of the immunology of CFS, the authors noted that studies supporting almost any conclusion regarding the presence, or absence of immunological abnormalities in CFS could now be found, and concluded that no consistent pattern could be identified (Lyall, Peakman, & Wessely, 2003). The same holds true of studies on the role of the neuroendocrine system in CFS. Disturbed neuroendocrineimmune system interactions, low circulating cortisol, high nocturnal melatonin, abnormalities in the relationship between cortisol and central neurotransmitter function, a disturbance of neurotransmitters in HPA axis function, and alterations in adrenal function in CFS have all been suggested and some evidence for these claims has been found (Cleare, Blair, Chambers, & Wessely, 2001; Demitrack et al., 1991; Kavelaars, Kuis, Knook, Sinnema, & Heijnen, 2000; Knook, Kavelaars, Sinnema, Kuis, & Heijnen, 2000; Segal, Hindmarsh, & Viner, 2005). Again however, in an extensive review on the neuroendocrinology of CFS, it was concluded that no consistent evidence of abnormalities could be found and that it was unclear whether neuroendocrine changes (if any) are primary or secondary to behavioral changes in sleep or exercise (Parker, Wessely, & Cleare, 2001). Along other lines of research, the psychiatric status of patients with CFS has received much attention. Several studies have reported a high prevalence of current psychiatric disorders in CFS, predominantly depression, somatization disorder and hypochondria (Ciccone, Busichio, Vickroy, & Natelson, 2003; Schweitzer, Robertson, Kelly, & Whiting, 1994). However, while some studies concluded that psychiatric illness in many cases predated the development of CFS (Katon, Buchwald, Simon, Russo, & Mease, 1991; Lane, Manu, & Matthews, 1991), other studies concluded that psychiatric disorder was concurrent with the onset of CFS and therefore more likely to be a consequence of, rather than a risk factor to CFS (Axe & Satz, 2000; Hickie, Lloyd, Wakefield, & Parker, 1990). In that case, CFS is not seen as a manifestation of an underlying psychiatric disorder and more somatic causes are presumed (Komaroff & Buchwald, 1998). Neuropsychological deficits and impaired cognitive functioning in patients with CFS have also received widespread attention, and have frequently been implied to be an important explanatory factor for some of the symptoms of CFS. People with CFS often complain of difficulties with memory and concentration. Several studies have described an impaired cognitive performance of patients with CFS on neuropsychological tests measuring speed of information processing, memory, motor speed and executive functioning (Busichio, Tiersky, Deluca, & Natelson, 2004; Cluydts & Michiels, 2001). Problems with neuropsychological functioning were found to be unrelated to depression, fatigue or anxiety (Short, McCabe, & Tooley, 2002) and have instead been related to low levels of physical activity (Vercoulen et al., 1998), a more extensive use of frontal and parietal brain regions (Lange et al., 2005) and even genetic traits (Mahurin et al., 2004). In contrast with this, many other studies have found no difference in cognitive performance between patients with CFS and controls, and no evidence of any neuropsychological deficits in CFS (Fry & Martin, 1996; Schmaling, DiClementi, Cullum, & Jones, 1994). However, although in many studies objectively no cognitive differences between patients with CFS and controls are found, patients with CFS consistently report cognitive complaints and underestimate their actual performance on neuropsychological tests. This difference between the subjective perception of cognitive impairment and the absence of any objective evidence has led some researchers to speculate that, in contrast to laboratory cognitive tests, in CFS everyday cognitive tasks may require excessive processing resources leaving patients with CFS diminished spare attentional capacity (Wearden & Appleby, 1996), and other researchers to suggest that patients with CFS set impossibly high standards of personal performance (Metzger & Denney, 2002). Other risk factors for the development of CFS that have been implied (and for which some evidence has been found) are birth order (Brimacombe, Helmer, & Natelson, 2002), family reinforcement of illness behavior (Brace, Scott-Smith, McCauley, & Sherry, 2000), maternal overprotection in relation to the formation of belief systems about activity avoidance (Fisher & Chalder, 2003) and a family history of physical and mental illness (Endicott, 1999). However, as with all of the etiological studies that have been discussed so far, the contrary conclusions can also be found. In a large birth cohort study into childhood predictors of CFS in adulthood, in which more than 11 000 people were followed up until the age of 30, no associations between maternal or child psychological distress, parental illness or birth order, and an increased risk of lifetime CFS were identified (Viner & Hotopf, 2004). There have also been many studies into possibly effective treatment strategies for CFS. However, presently there is no established, universally beneficial intervention for the management and treatment of CFS (Whiting et al., 2001). With regard to medical and pharmacological treatment, amongst others, intramuscular dialyzable leukocyte extract (Lloyd et al., 1993), intravenous immunoglobulin (Vollmer-Conna et al., 1997), hydrocortisone (McKenzie et al., 1998) and antidepressants (Vercoulen et al., 1996; Natelson et al., 1998) were investigated in placebo-controlled studies, without proving their effectiveness. Recently, the effects of galantamine hydrobromide (Blacker et al., 2004), polynutrient supplements (Brouwers, Van der Werf, Bleijenberg, Van der Zee, & Van der Meer, 2002), homeopathic treatment (Weatherley-Jones et al., 2004) and corticosteroids (Kakumanu, Mende, Lehman, Hughes, & Craig, 2003) have been studied in randomized controlled trials, but were also found to be ineffective. At the moment, only cognitive behavior therapy (Price & Couper, 2000; Prins et al., 2001; Sharpe, 1998) and graded exercise therapy (Wallman, Morton, Goodman, Grove, & Guilfoyle, 2004; Edmonds, McGuire, & Price, 2004) have shown some effectiveness, for a proportion of patients, in randomized controlled trials. So, CFS seems surrounded by controversy. Patients are confronted with a highly ambiguous illness that severely incapacitates them. In addition to this they suffer from the consequences of the unclear medical status of the disease. Due to the uncertainties surrounding the etiology of CFS, its symptomatology and the overall objective 'realness' of the syndrome, they are likely to encounter disbelief concerning their medical condition (Friedberg & Jason, 2001). At present it is being discussed whether the impact of labeling patients with a diagnosis of CFS is enabling, or rather disabling (Huibers & Wessely, 2006). In the absence of a clear biological marker for the illness, which would permit a definite diagnosis instead of a descriptive one, based almost solely on the exclusion of other disease entities, patients are often faced with skepticism by their families, employers, insurance companies, psychologists and physicians. In a recent study on illness experience in CFS it was found that lack of illness recognition ranked high as a source of dissatisfaction for patients and was thought to aggravate psychiatric morbidity (Lehman, Lehman, Hemphill, Mandel, & Cooper, 2002). In contrast with this, physicians participating in a study on their perspectives on patients with CFS (Asbring & Narvanen, 2003) expressed the view that patients seem to exaggerate the severity of their problems, and that there appears to be a discrepancy between their reported health and the way they look and behave. Although it has been widely recognized that a positive and co-operative caregiver-patient relationship is of the utmost importance in the successful treatment of CFS (Sharpe, Chalder, Palmer, & Wessely, 1997), uncertainty and conflicts about the causal attribution of the syndrome, in many cases, put this relationship under pressure. Steven et al. (2000) showed that one-third of a group of more than two-thousand general practitioners did not believe that CFS was a distinct syndrome and thought the most likely cause was depression. This finding was confirmed by another study in which it became clear that while most of the doctors participating in the study believed CFS to have a psychological cause, all of the patients attributed their illness to a physical cause (Deale & Wessely, 2001). This disagreement over the perceived origins of CFS was thought to largely account for the fact that two-thirds of the patients in this study were dissatisfied with the quality of the medical care they had received. This same dispute about the etiology of the syndrome, in combination with concerns about its nosological status, seems to have characterized and dichotomized medical and psychological thought on CFS. In spite of the great advances medical science has made in the explanation and treatment of diseases with an evident organic cause, the causes for CFS remain unclear and our understanding of the illness progresses only slowly. This "prototypical mind/ body problem" (Johnson, DeLuca, & Natelson, 1999, p. 258) seems to confront medicine with the limitations of the traditional paradigm, through which it has made such progress in the understanding and treatment of 'classical' diseases. As is now widely acknowledged the debates on chronic fatigue and immune dysfunction syndrome, neurasthenia, postviral fatigue syndrome, myalgic encephalomyelitis, chronic mononucleosis and chronic Epstein-Barr virus infection, as CFS was formerly known, were, and not uncommonly still are, characterized by a mind/body dualism that seems inherent to a biomedical model of thought, oriented towards monocausal explanation (Lewis, 1996; Taerk & Gnam, 1994; Ware, 1994). On the one hand, there are those who believe that CFS is initiated by a still unknown physical cause such as a chronic or relapsing viral infection, immunological deficiencies or abnormalities in the neuroendocrinological system. The absence of a clear and objective organic cause, on the other hand, leads others to relegate CFS to the realm of the mental and 'subjective' illnesses. In that case CFS is mostly thought of as a psychiatric disorder (e.g. a masked expression of depression, or a form of somatization), or a cognitive phenomenon. However, a more logical explanation of the variety of findings and opinions on CFS would be that the illness is multifactorial. Social, mental and somatic causes, and psychological and physical effects are not easily discernible, but instead appear to be interrelated. In recent years, a more biopsychosocial approach in the scientific research into CFS has become the standard (Main, Richards, & Fortune, 2000). In line with this approach (and in addition to the already mentioned studies) researchers have now also begun to study the iatrogenic factors in CFS (Deale & Wessely, 2001), associations in symptoms between patients with CFS and their parents (Van de Putte et al., 2006), the illness beliefs and attributions of patients with CFS (Deale, Chalder, & Wessely, 1998; Van Houdenhove, Neerinckx, Onghena, Lysens, & Vertommen, 2000), the psychological adjustment of patients with CFS (Van Middendorp, Geenen, Kuis, Heijnen, & Sinnema, 2001), the health-related quality of life of patients with CFS (Hardt et al., 2001), the locus of health control in patients with CFS (Van de Putte et al., 2005), the relationship between ethnicity and CFS (Luthra & Wessely, 2004), the coping strategies of patients with CFS (Ax, Gregg, & Jones, 2001), the influence of family members in CFS (Gray et al., 2001), the cultural and historical context of CFS (Abbey & Garfinkel, 1991; Ware, 1994; Ware & Kleinman, 1992; Wessely 1990; Wessely, 1996) and the personalities of individuals who have developed CFS (reviewed in this article). So, within the biopsychosocial model of CFS one of the aspects studied, that might have a perpetuating and even a predisposing role in the syndrome, is the personality of people suffering from CFS. Among clinical psychologists, consulting physicians, scientific researchers and in society in general, a typical image has emerged of patients with CFS as perfectionist, conscientious, hardworking, somewhat neurotic and introverted individuals with high personal standards, a great desire to be socially accepted and with a history of continuously pushing themselves past their limits. (Lewis, Cooper, & Bennett, 1994; Surawy, Hackmann, Hawton, & Sharpe, 1995). In addition to this, they are characterized as being particularly averse to any psychological or psychiatric explanation of the syndrome and extremely persistent in fixed beliefs concerning their illness, thereby reducing the chance of successful treatment (Sharpe, 1998). However, this image of people suffering from CFS was never really scrutinized, with most of the research activity concerning the individual with CFS focusing on psychopathology and possible psychiatric disorder. The aim of this article is to (a) give a concise review of the main recent studies on personality and CFS, (b) address the major methodological problems in the study of personality in CFS and (c) discuss some of the conceptual assumptions that seem to limit the research on personality and CFS. 2. Selection of studies The PubMed and PsychINFO databases from 1988 (when the original Centers for Disease Control criteria for CFS were first established) to November 2006 were searched using the keywords CFS and personality, CFS and psychology, CFS and individual, CFS and identity. On PubMed this generated 623 hits and on PsychINFO an additional 333 hits. All 956 abstracts were read. In addition the reference lists of the retrieved articles were examined. The intention in the selection of studies was to include all original articles describing primary research on personality and CFS. Review articles, articles describing studies without mentioning which CFS case definition criteria were used, or without an appropriate control group, and articles focusing exclusively on psychiatric morbidity, were all excluded. Using these criteria led to the inclusion of a final 16 studies.1 This review might not have captured all relevant studies. However, the discussed articles are the most important ones and can be seen as representative of the current state of affairs in the field. In Table 2 a concise overview of the main recent studies on the role of personality in CFS is given. 3. Results Studying these results, it soon becomes obvious that the findings regarding the association of personality and CFS are not definitive. Although some studies seem to confirm, for a proportion of patients, some of the aspects of the aforementioned stereotype of people suffering from CFS, other studies found no such evidence. Some findings however, seem to be more consistent than others. 3.1. Neuroticism All in all, there seems to be most empirical evidence for an increased level of neuroticism in patients with CFS. Taillefer, Kirmayer, Robbins and Lasry (2003) found significantly higher neuroticism scores in patients with CFS compared to the general population. Chubb et al. (1999) found increased scores in their CFS subjects with concurrent depression. Masuda, Munemoto, Yamanaka, Takei, and Tei (2002) found elevated neuroticism scores in their noninfectious CFS group, although not in their postinfectious CFS group. Fiedler et al. (2000), Blakely et al. (1991), Buckley et al. (1999) and Johnson, DeLuca and Natelson (1996) also found significant differences in neuroticism scores between patients with CFS and healthy controls and Rangel, Garralda, Levin, and Roberts (2000) found the related items of conscientiousness, worthlessness and emotional lability to be significantly more common in patients than in controls. However, most subjects in their study were recovered and their mothers, instead of the patients themselves, had been used as informants. Several other important limitations in the interpretation of these findings regarding neuroticism should also be mentioned. One study found elevated scores of neuroticism only in comparison to non-study recruited norm values for a general population (Taillefer et al., 2003). In addition, generally no differences in neuroticism between patients with CFS and other patients suffering from a chronic disease were found (Johnson et al., 1996; Taillefer et al., 2003; Wood & Wessely, 1999). Other studies used the MMPI to detect neuroticism (Blakely et al., 1991; Schmaling & Jones, 1996) which, due to its sensitivity to physical symptoms, has been found to perform poorly in CFS and to overestimate psychopathology in chronically ill populations (Johnson, De Luca, & Natelson, 1996) and finally, many of the findings of high neuroticism were later accounted for by co-morbid depression (Chubb et al., 1999; Fiedler et al., 2000; Johnson et al., 1996; Taillefer et al., 2003). 3.2. Personality disorder Furthermore, there also seems to be evidence for the prevalence of personality disorder in a proportion of patients with CFS. In the first study on personality and CFS, Millon et al. (1989) found elevated base rate means, above those of a non-clinical population, on the histrionic, schizoid and avoidant scales of the MCMI, measuring DSM axis II personality disorders. Henderson and Tannock (2004) also found quite a high level of personality disorder (39%), predominantly obsessive-compulsive personality disorders, in their sample of patients with CFS. Similar rates and findings were reported by Ciccone et al. (2003). In the study by Johnson et al. (1996), 37% of the subjects with CFS met the criteria for at least one personality disorder, predominantly histrionic and borderline personality disorders. So, there certainly seems to be a somewhat higher rate of personality disorder within the CFS population than in non-clinical populations, in which it is estimated to be between 10-19% (Moran, Coffey, Carlin, & Patton, 2006; Zimmerman & Corryell, 1990). However, personality disorder rates were similar in patients with CFS and those with other medical conditions (Johnson et al., 1996). Also, it should be noted that personality disorder was not found in the majority of patients. Furthermore, again there are some important confounding aspects and the generalizability of the findings in the abovementioned studies can be questioned. For example, some studies did not have a control group (Ciccone et al., 2003; Millon et al., 1989). Moreover, the MCMI that Millon et al. used includes many items that tap somatic concerns, thereby increasing the likelihood of a diagnosis of personality disorder in chronically ill patients. Co-morbid depression accounted for most personality pathology in one study (Johnson et al., 1996) and although this was not the case in the study by Henderson and Tannock, they only included patients attending a teaching hospital, who are likely to have a more severe form of CFS. 3.3. Perfectionism, social desirability and extroversion/introversion Although perfectionism, social desirability and introversion have commonly been referred to as some of the most characteristic features of the personalities of patients with CFS, the scientific evidence on this subject is far less clear-cut. White and Schweitzer (2000) found higher perfectionism scores in individuals with CFS than in their control group and Christodoulou et al. (1999) found the only difference between their CFS and MS groups to be an elevated persistence score, which they related to perfectionism. However, in contrast to these findings Wood and Wessely (1999), and Blenkiron, Edwards and Lynch (1999) did not find higher perfectionism scores in patients than in controls. There were three studies that specifically studied social desirability among patients with CFS (Buckley et al., 1999; Chubb et al., 1999; Wood & Wessely, 1999), but these studies revealed no differences between patients and control groups. With regard to extroversion and introversion, Masuda et al. (2002) found the members of their postinfectious CFS group to score higher on extroversion than controls, although the members of their noninfectious CFS group were found to be more introspective. And finally, while Buckley et al. found that patients with CFS scored significantly lower than their healthy controls on extroversion, Chubb et al. found the scores on extroversion of their CFS group not to be different from those of their healthy control group. 3.4. Personality: predisposing, initiating or perpetuating? So, the results vary from the uncovering of "evidence of severe personality pathology and affective distress" (Millon et al., 1989, p. 131), to the finding of "little evidence that any particular personality trait discriminates CFS patients [...] from other patients suffering a physically disabling condition" (Wood & Wessely, 1999, p. 395). However, even when evidence of abnormalities in the personality profiles of patients with CFS is found, there remains a considerable lack of clarity regarding the precise role of personality in the syndrome, and this is reflected in the conclusions these studies draw. For example, while Van Houdenhove, Neerinckx, Onghena, Lysens, and Vertommen (2001) conclude that "high 'action-proneness' and an associated 'overactive' lifestyle may be one of the factors playing a predisposing, initiating as well as a perpetuating role in CFS" (p. 575), Christodoulou et al. (1999) found no evidence to suggest that patients with CFS had any particular personality traits that would have predisposed them to develop their illness. Rangel et al. (2000) conclude that personality difficulty might either be a contributory factor to CFS, or result from the prolonged disease, and Buckley et al. (1999) and Blenkiron et al. (1999) conclude that the personality of subjects with CFS might have changed as a result of their disease. Although the impression of many psychologists, physicians and researchers, that the personality of patients is a factor in CFS, seems to be justified by clinical experience and is supported somewhat by the available research, decisive conclusions on this subject are difficult to draw on the basis of the relevant scientific studies. Even though these studies have scrutinized the aforementioned image of the 'typical' individual with CFS, no definitive conclusions for the patients as a group can be drawn, and a general and uniform answer to the question of the role of personality in CFS is hard to formulate. A provisional conclusion might be that it is "difficult to disentangle personality factors that may have contributed to the development of the condition from emotional reactions that are consequences of the debilitating symptoms and the mixed responses of others to the illness" (Lewis, 1996, p. 237). However, part of the reason for this opaqueness, seems to be due to a certain heterogeneity of the reviewed studies with regard to study methods, patient populations, control groups and CFS case definitions. Therefore, before discussing what seem to be some shared conceptual assumptions of these studies, in the next section some of the major methodological issues concerning the study of personality in CFS will be addressed. 4. Methodological issues regarding the study of personality in CFS 4.1. Study methods An obvious reason for the discrepancies in the conclusions of the studies discussed might be the use of different methods to measure personality. This diversity seems almost inevitable when we consider the variety and divergence in health care settings and traditions of personality research. However, even when using the same instruments there often was no uniformity in the findings. In three studies, all using the Multidimensional Perfectionism Scale (MPS) for example, a remarkable lack of consensus in the results emerges. While White and Schweitzer (2000) demonstrated higher perfectionism scores in individuals with CFS than in persons in their healthy control group, Wood and Wessely (1999) using the same MPS, found no differences in measures of perfectionism between the patients with CFS and the patients with rheumatoid arthritis in their control group. This difference might be explained by the fact that these studies used different control groups. However, Blenkiron et al. (1999) also used a healthy control group and in contrast with White and Schweitzer, they found the values for perfectionism on the MPS to be lower in their CFS sample than in their healthy control group. This example brings us to another issue in the possible explanation of the lack of uniformity in the major findings of the studies. 4.2. Control groups Another possible reason for a lack of consistency in the major findings could be that not all studies used comparable control groups. Whereas many studies used healthy individuals as (part of) their control group (Blakely et al., 1991; Blenkiron et al., 1999; Buckley et al., 1999; Christodoulou et al., 1999; Chubb et al., 1999; Fiedler et al., 2000; Johnson et al., 1996; Masuda et al., 2002; Rangel et al., 2000; Schmaling & Jones, 1996; White & Schweitzer, 2000), others used patients with fibromyalgia/chronic pain (Blakely et al., 1991; Van Houdenhove et al., 2001), depressed patients (Buckley et al., 1999; Chubb et al., 1999; Johnson et al., 1996), patients with multiple sclerosis (Christodoulou et al., 1999; Johnson et al., 1996; Taillefer et al., 2003), or patients with rheumatoid arthritis (Wood & Wessely, 1999). As a consequence, the results of the studies can only be interpreted relative to the specific control groups that were used. Certain differences between patients with CFS and controls that might be obvious with one control group, might become less significant, or even get completely lost with another. 4.3. Patient populations and CFS case definitions So, the results of a specific study can only be interpreted in the light of the control group that was used. However, this is of course rather common in medical and psychological research. Be that as it may, in the case of CFS the same applies to the patient groups that were included, which is far less usual. While most studies used adult patients with CFS, one study used adolescent patients with CFS of whom most were recovered (Rangel et al., 2000) and another study exclusively included combat exposed Gulf War veterans with CFS (Fiedler et al., 2000). Nevertheless, this would seem to leave all the studies using 'ordinary' adult individuals with CFS to be comparable. However, as different CFS case definitions were used, this is not the case. Some studies used the original CDC criteria of 1988 (Holmes et al., 1988), others the revised CDC criteria of 1992 (Schluenderberg et al., 1992), others the revised CDC criteria of 1994 (Fukuda et al., 1994), others the UK operational criteria of 1991 (Sharpe et al., 1991) and one New Zealand's McKenzie criteria of 1988 (McKenzie, 1988). To add to the confusion and making the different findings even more difficult to compare, some studies distinguished between noninfectious and postinfectious CFS patients (Masuda et al., 2002), some studies distinguished between patients with CFS and co-morbid psychiatric disorder/depression and patients with CFS without co-morbid psychiatric disorder/depression (Chubb et al., 1999; Fiedler et al., 2000), and one study only included non-depressed patients with CFS (Buckley et al., 1999). This brings us to the next important problem, the influence of depression on the study of CFS and personality. 4.4. CFS and depression Several studies on the psychiatric status of patients with CFS were discussed in the Introduction. However, as was mentioned there, depression is not an exclusionary criterion for the diagnosis of CFS and therefore inevitably plays an important role in the personality studies on CFS. As was noted by Buchwald (1996) and Wessely, Chalder, Hirsch, Wallace, and Wright (1996), amongst others, there is a considerable overlap between the criteria used for several psychiatric DSM-diagnoses (most notably depression) and CFS. As a consequence patients with symptoms required for a diagnosis of CFS, at the same time have symptoms fitting into a diagnosis of depression. When distinguishing between patients with or without depression, some found that depression had a great impact on the major findings of their study. In the study by Fiedler et al. (2000), the CFS with psychiatric co-morbidity group scored significantly higher than the CFS without psychiatric co-morbidity group on the neuroticism subscales of anxiety, hostility, self-consciousness, impulsivity and vulnerability. Chubb et al. (1999) found that the scores of patients with CFS were not different from those of healthy controls, except for those subjects with CFS who were concurrently depressed, where the scores resembled the scores of their depressed control group.Johnson et al. (1996) also found that most of the personality disorders in their CFS group were accounted for by the CFS group with concurrent depressive disorder. However, in contrast with these findings, Henderson and Tannock (2004) concluded that they were unable to account for the presence of personality disorder in their assessment of patients with CFS, by co-morbid depression. An additional problem is that the Beck Depression Inventory (BDI), which three of the studies used (Blakely et al., 1991; Johnson et al., 1996; Wood & Wessely, 1999), was found to perform poorly as a screener for depression in subjects with CFS (Farmer et al., 1996). All in all, the role of depression in CFS is extremely difficult to determine as there are at least three plausible relationships. It could be that depression is a predisposing, causative factor in CFS. On the other hand, it might be that "CFS is no more than depression masquerading as a physical illness" (Ray, 1991, p. 2), but it is also possible that depression is a reaction to the illness and to the lack of clarity that surrounds CFS. In this case it would be likely that depression is caused by the stress of being diagnosed with a disease of unknown origin, in combination with the absence of a standard treatment and the possible disbelief encountered in the health care setting. As it seems to be the case with many of the findings of abnormalities in CFS, the role of depression in the pathogenesis and perpetuation of CFS remains unclear. These questions of causality and nosology however, are somewhat beyond the reach of this article and will therefore not be discussed further.2 Nevertheless, by raising these questions we get to a more fundamental level of inquiry. In the next section some conceptual issues regarding the study of personality in CFS will be addressed. 5. Conceptual background of personality studies in CFS As mentioned, the methods used to study personality in CFS are quite diverse. Nonetheless, in the approach of the reviewed studies, a shared conceptual model regarding the possible association of personality and CFS, and the appropriate way to scientifically study it, seems to be reflected. Firstly, these studies have focused much of their attention on personality disorder. Psychological malfunctioning, rather than ordinary, non-pathological and everyday aspects of personality, which are commonly seen as a primary concern of personality psychology, has been a main interest of personality research in CFS so far. By such a focus on, and an overrepresentation of the psychopathological aspects of personality, it is easy to provide only a one-sided and too stringent image of the personality of individuals with CFS. Secondly, on the whole these studies have tended to conceptualize personality mainly in its most general and decontextualized structures. With the use of psychological tests like the Tridimensional Personality Questionnaire, the NEO Five-Factor Inventory and the Eysenk Personality Questionnaire, certain characteristics of personality, such as extroversion, neuroticism and social desirability can accurately be studied and compared. However, in this way personality is approached primarily in its most basic and undifferentiated structure, and only a limited understanding of personality is provided (Block, 1995). Although personality traits can provide a kind of dispositional signature of the person, few links have been made between traits and actual contextualized behavior (Funder, 2001) and it seems unlikely that the exclusive knowledge of such a basic structure of relatively non-conditional and noncontingent dispositional traits, or psychopathological personality profiles, is enough to wholly explain and account for the behavioral consequences of CFS, or the complex association between personality and the syndrome. Within the humanities and the social sciences, especially personality psychology, there has been an increasing awareness that persons do not merely act and experience on the basis of quantifiable, general traits. They primarily evaluate and motivate their behavior and beliefs in qualitative, contextualized terms (Richardson, Rogers, & McCaroll, 1998; Taylor, 1989). On the basis of these terms, persons assess their behavior, interpret themselves, articulate what they believe to be important, try to make sense of their past, give meaning to the present, direct their future projects and provide their life with purpose and unity (McAdams, 1995). Personality is not a static, independent, self-contained and decontextualized 'given', but is always dynamically constructed in dialogue with others, and against a 'meaningful' background provided by social practices and culturally shared moral values (Hermans, Kempen, & Van Loon, 1992; Taylor, 1995). In recent decades, the idea of the 'narrative' has emerged as a new metaphor not only within personality psychology (Hermans, 1996; Sarbin, 1986), but also within clinical psychology (Guignon, 1998; Hermans & Dimaggio, 2004; McLeod, 1997). >From this approach, persons are understood as the creators of meaning, and narrative thought is seen as the process by which these meanings are developed and changed (Bruner, 1991). The narrative is seen not only as a novel way of conceptualizing human experience and identity, but also as a useful clinical tool to help individuals understand why they act, and organize their lives, in certain ways, and to aid them in retelling and reorganizing their lifestory. In a broader concept of personality, than that which was used so far in the research on CFS, the lifestory could be seen as a special kind of psychosocial construction and individuals might be understood as trying to coauthor a thematically coherent and meaningful narrative with, and against the background of, their culture and social world. Dispositional traits and life narratives can be regarded as two different levels of personality (McAdams et al., 2004), each with their own methods of study, frameworks and taxonomies. In CFS, personality traits are usually studied through the use of standardized questionnaires and (semi) structured interviews in the search for abnormalities, or deviations from the average. The benefit and attraction of studying personality in this way is not only that it is rather time and cost effective, but also that it produces objective, quantifiable and comparable data and as such seems to be in accordance with the rigorous methods of the natural sciences. The downside to this approach is that, to a considerable extent, it decontextualizes human experience and behavior from its real life setting, and its social and cultural background. The usefulness and attraction of studying personality on the level of the life narrative, on the other hand, is that it can remain much closer to the continually evolving and subjectively experienced reality of the person. Starting from the assumption of normality, personality on this level is usually studied through an open dialogue in which the subject matters are decided, not primarily by the investigator, but in the first place by the person him - or herself. Just as with personality considered on a trait level however, the benefits to this approach also entail its main drawbacks. Besides being rather time-consuming, the obtained data might be difficult to compare and, because of their specific temporal and spatial context, be of a contingent and subjective nature. This can lead to the assumption that personality, considered as a developing lifestory changing through time, cannot be categorized, quantified or systematically researched (McAdams, 1995) and that it, because of this, cannot be studied in a proper methodical way. Within the scientific debates on CFS, some have tried to draw attention to the fact that the lifestories of the patients seem to have been neglected. Van Houdenhove (2002) for example, states that "much of the etiological and therapeutic controversies about the so called chronic fatigue syndrome (CFS)[...] may be due to the relative neglect of the patient's story - in clinical practice as well as in research. More specifically I believe that insufficient attention is being paid to the mostly significant context in which the illness began, and the possible connection between the illness and the patient's life history. [T]he patient's biography should be part of each diagnostic evaluation and considered an important focus of psychological/ psychiatric research in CFS." (p. 495) At present, there have been few who have addressed these concerns. Some qualitative studies have described, in narrative terms, the experience of patients of the impact of CFS as a disruption and disorganization of their pre-morbid lifestory and identity. The transformation and rewriting of those stories is depicted as an inescapable consequence of getting CFS and is usually followed by a subsequent quest for the restoration and reorganization of a meaningful autobiographical self-narrative (Bulow & Hyden, 2003; Clark & James, 2003; Whitehead, 2006). Currently however, the biggest challenge for those wishing to systematically study the association of personality, considered on the narrative level, and CFS, will be to do so with methods that are firmly based in psychological theories about personality and psychotherapy and that have been specifically designed to analyze and categorize a person's narrative into its most meaningful temporal constituents. Moreover, such methods should be psychometrically validated and not only allow a study of the idiosyncrasies of the single case, but these methods must also have been developed in such a way that they can be generalized to a population and that quantitative comparisons between different groups can be made (e.g. Baillio & Lyddon, 2000; Hermans & Hermans-Jansen, 1995; Van Geel & De Mey, 2003). 6. Conclusion Every science, whether it be psychology, medicine, physics or sociology, is based on a set of conceptual assumptions. Usually, when these disciplines are functioning satisfactory, these presuppositions remain implicit and there is no need to make them explicit. However, when problems arise that seem difficult to solve with the normal instruments of these sciences, we have to focus our attention explicitly on these conceptual assumptions and ask ourselves whether our understanding of the problem is not somehow obscured by the commonly accepted model of thought. For psychology and medicine, CFS poses exactly such a problem. In this article the first aim was to give a concise review of the current research on personality and CFS. There seems to be consistent evidence that patients with CFS often score higher on some personality traits, most notably neuroticism, than healthy controls. Furthermore, higher levels of DSM axis II diagnoses, most notably obsessive compulsive, histrionic and borderline personality disorders, within the CFS population, in comparison to healthy populations are found. However, there are some important confounding elements in these findings. When compared to patients with another chronic illness, the finding of specific personality differences is far less common and usually annulled. Additionally, the finding of divergence could often be explained by co-morbid depression/ psychiatric disorder. Another limitation is that, at times, instruments have been used to study certain aspects of personality (e.g. the MMPI, the BDI and the MCMI) that have later been found to perform inadequately for patients with CFS. And lastly, many studies eventually conclude that the found personality differences are consequences of the disease, rather than precipating factors and as such play no causal role in CFS. All in all, under careful scrutiny the previously mentioned stereotype of patients with CFS does not seem to be justified. Nonetheless, at present there do seem to be at least three overarching conclusions that can be drawn with regard to personality and CFS. Firstly, the heterogeneity of findings within the CFS groups implies that, on the trait or psychopathological level, there are no unique personality characteristics that are either a necessary condition for, or an unavoidable consequence of CFS. Secondly, although personality traits such as neuroticism and perfectionism are generally considered to be stable, non-conditional and not effected by life changes (Watson & Walker, 1996; Costa et al., 1986), most studies seem to agree on the possibility that the pre-morbid personalities of their subjects might have changed as a result of their condition. Diverse forms of chronic illness seem to be able to alter personality in similar ways and increased levels of neuroticism and introversion for example (not to mention depression), could well be a feature of many different diseases. In fact, the American Psychiatric Association acknowledges the possibility of personality change as a result of chronic illness (American Psychiatric Association, 1994). Thirdly, as a consequence of this, it can be concluded that cross-sectional designs in the long run will probably not be able to provide definitive answers to the question of the exact role of personality in CFS. In the section on the methodological problems of these personality studies it was suggested that some of the confusion that remains regarding the association between personality and CFS might be due to a variety in study methods, control groups and CFS case definitions. This diversity seems almost unavoidable. However, with regard to control groups, the substantial overlap between CFS and some psychiatric diagnoses (e.g. depression), and other unexplained medical conditions (e.g. fibromyalgia) is truly confusing in research, and makes patients from these populations difficult to compare. Age and sex matched healthy individuals, and patients with a somatic illness in which fatigue is also a main complaint (e.g. rheumatoid arthritis, multiple sclerosis) seem to be much better suited as control groups. With regard to study methods, the exclusion of general psychopathology or shared problems on a dispositional trait level in CFS has of course been essential and valuable in the personality research on CFS. However, the cross-sectional designs of the reviewed studies make inferences about causality very difficult. New insights might be gained by longitudinal designs, studying the predictive validity of certain personality traits as risk factors for the development of CFS. Prospective studies in clinical populations of mood disorders and emotional risk factors in relation to CFS for example, have already been able to provide some evidence regarding their precipating role (Moss-Morris & Spence, 2006; White et al., 2001). In addition, it will prove insightful to follow-up a cohort of patients with a relatively short illness duration (i.e. a recent diagnosis of CFS) in order to study whether certain personality characteristics, and levels of depression, changed as a consequence of prolonged illness duration. Finally, in the section on the conceptual background of the study on personality in CFS, it was argued that although the methods used so far were diverse, the studies seemed to share some basic conceptual assumptions regarding personality and the way to study it. Up to now, personality research in CFS has either been in search for personality disorder and psychological malfunctioning, or has been conducted on a general, non-relational trait level. Nevertheless, the fact that to a large extent personality is something that can only exist in, and develop through the inherent relations and dialogues with family, peers, colleagues, media, society and culture in general, must be taken in account. In previous issues of this journal a similar perspective has been brought forward by Dwairy (2002, 1997) with regard to the understanding of the personality and (mental) health within collective cultures, but it also seems particularly true in the study of CFS. Future personality research in CFS should not only take the abovementioned methodological issues into account and be of a more longitudinal nature, but should also be directed towards, and become aware of the dialogically constructed, historically contextualized and indissoluble relational terms by which persons understand, evaluate and articulate themselves. Modern individualized society, to a considerable degree, is focused on achievement, consumption and success, and is characterized by a plurality of rapid economical, political, religious, technological and cultural changes. Against this background, modernity confronts people in a whole new fashion with a multiplicity of problems and possible ways of life and the need, and imperative, to find and develop a meaningful identity. New insights into the possible difficulties and stumbling-blocks in the personality of individuals with CFS might be gained, if research attention would also concentrate on systematically and comparatively studying individuals with CFS, as socioculturally embedded agents who are trying to construct a coherent and intelligible self-narrative. Notes 1 Millon et al. (1989), being the first to study the role of personality in CFS, was included although the study lacked an appropriate control group. 2 See, for example, Abbey and Garfinkel (1990), Moss-Morris and Petrie (2001), and Swartz (1988) for some of the articles concerned with the relation between CFS and depression, Wessely et al. (1999) and Aaron and Buchwald (2001) for a more general discussion concerning the nosological status of CFS, and Bolton (2001) and Borch-Jacobsen (2001) for a more philosophical and a historical discussion of nosological problems in the definition of psychiatric disorders. The authors are grateful to Elise van de Putte, Coralie Fuchs, Gaston Franssen, Marc Slors and anonymous reviewers of this journal for their constructive remarks and suggestions on an earlier draft of this article. Preparation of this manuscript was supported by a Netherlands Organization for Scientific Research Grant (400-03-469). Tables Table 1. US Centers for Disease Control case definition of CFS, 1994 -------------------------------------------------------------------------------- Diagnostic criteria: At least 6 months of persistent or recurring fatigue for which no physical explanation has been found and which * is of new onset, that is to say it has not been lifelong * is not the result of ongoing exertion * is not substantially alleviated by rest * severely limits functioning In combination with four or more of the following symptoms, persistent or regularly recurring over a period of six months and which must not have predated the fatigue: * self-reported impairment in memory or concentration * sore throat * tender cervical lymph nodes * muscle pain * multi-joint pains * headache * unrefreshing sleep * post-exertional malaise lasting 24 h or longer Exclusionary criteria: * any medical condition that may explain the presence of chronic fatigue * a psychotic, major or bipolar depressive disorder (but not an uncomplicated depression) * dementia * anorexia or bulimia nervosa * alcohol abuse or the use of drugs * severe obesity -------------------------------------------------------------------------------- Table 2 Primary research on personality in CFS ---------------------------------------------------------------------------------------------------------------------------------------------------- Study Number of participants Study methods Major findings ---------------------------------------------------------------------------------------------------------------------------------------------------- Henderson and 61 patients with CFS (CDC, 1994 Structured Clinical Interview for 39% of the CFS group, 73% of the Tannock (2004) (Fukuda et al., 1994)) DSM-III-R Diagnoses (SCID-II) depressed group and 4% of the 40 psychiatric inpatients healthy group were diagnosed with with depressive disorder personality disorders. Cluster C 45 healthy controls disorders (avoidant, dependent, obsessive-compulsive, self-defeating and passive-aggressive) were the most common in both the CFS and depressed group. Personality disorder in patient with CFS could not be accounted for by co-morbid depression. Taillefer et al., 45 patients with CFS (CDC, 1988 Illness Worry Scale, Neo Five-Factor There was no difference between the (2003) (Holmes et al., 1988)) Inventory (NEO-FFI), SCL-90R groups on neuroticism, depressive 40 patients with multiple sclerosis Depression Scale, Symptom symptoms, or on the SIQ. The CFS Interpretation Questionnaire (SIQ) group did have significantly higher scores than the MS group on the Illness Worry Scale. When the CFS group was divided into more and less depressed patients, the neuroticism scores were found to be significantly higher than the general population in the more depressed CFS group. Masuda et al., 16 patients with postinfectious Holmes Social Readjustment Rating The stress, maladjustment, marked (2002) CFS (CDC, 1992 Scale, Cornell Medical Index (CMI), anxiety, depressive tendency and (Schluenderberg et al., 1992)) Maudsley Personality Inventory (MPI), hypertense state scores of both CFS 20 patients with noninfectious Yatabe-Guilford test, Self-rating groups were significantly higher than in CFS (CDC, 1992 Depression Scale (SDS) the control group. (Sharpe et al., 1992)) No significant differences between 20 healthy controls both CFS groups on these scores were observed. However members of the postinfectious CFS group were diagnosed as social extroverts, while those in the noninfectious CFS group were neurotic and introspective. Van Houdenhove A randomized sample of a 100 Questionnaire for Habitual The patients and their significant others et al., (2001) patients out of 124 patients with Action-proneness (HAB) scored the questionnaire similar. These CFS (CDC, 1994 scores were higher than the norm values, (Fukuda et al., 1994)) suggesting that high "action-proneness" 68 patients with fibromyalgia and an associated "overactive" lifestyle (FM) may be one of the factors playing a predisposing, initiating as well as a perpetuating role in CFS and FM. White and Schweitzer 44 patients with CFS (CDC, 1994 Multidimensional Perfectionism Scale The study demonstrated higher (2000) (Fukuda et al., 1994)) (MPS), Rosenberg Self-Esteem Scale perfectionism scores and lower self- 44 healthy controls (RSE), Courtauld Emotional Scale esteem in individuals with CFS, than in (CECS), Marlowe-Crowne Social individuals in the healthy control group. Desirability Scale (MCS) The results suggest that individuals with CFS have a maladaptive perfectionist personality style. Rangel et al., 25 adolescent patients with CFS Personality Assessment Schedule (PAS), Subjects with CFS demonstrated (2000) (Oxford Criteria, 1991 (Sharpe et Kiddie-SADS Psychiatric Interview increased scores for introspection, al., 1991)) At the time of the study (K-SADS), Children's Global Assessment sensitivity, conscientiousness, two-thirds (n = 17) had recovered Scale (CGAS), Child Behaviour vulnerability, lability and worthlessness. and the subject's mothers were used Checklist (CBCL) Personality difficulty may either be a as informants contributory factor to CFS in children, or 15 healthy controls result from the prolonged disease. Fiedler et al. 35 veterans with CFS (CDC, 1994 Combat Exposure Scale (CES), Operation Measures of personality and negative (2000) (Fukuda et al., 1994)) and co- Desert Storm Survey (ODS Survey), coping strategies (as well as self-reported morbid psychiatric disorder Childhood Traumatic Events Scale, combat and chemical exposures) 23 veterans with CFS and no co- Psychiatric Epidemiology Research significantly differentiated healthy morbid psychiatric disorder Interview-Life Events Scale (PERI), veterans from those with CFS. On the 45 healthy veterans Neuroticism, Extroversion, Openness neuroticism subscales of anxiety, hostility, Personality Inventory (NEO-PI), Toronto depression, self-consciousness, Alexithymia Scale (TAS), Marlowe- impulsivity and vulnerability the CFS/ Crowne Social Desirability Scale psychiatric group scored significantly higher than the two other groups. Veterans with CFS reported a poorer ability to identify and communicate feelings than did healthy controls. Chubb et al. 62 patients with CFS (CDC, 1994 Eysenck Personality Questionnaire Patients with CFS and concurrent (1999) (Fukuda et al., 1994)) and 48 (EPQ), Attributional Style depression scored significantly higher healthy controls completed the Questionnaire (ASQ) than individuals with CFS without EPQ. concurrent depression or healthy 50 patients with CFS (CDC, 1994 controls on the neuroticism subscale. (Fukuda et al., 1994)), 100 healthy On the social desirability subscale subjects controls and 37 depressed patients with CFS did not differ from the controls. completed the ASQ. Scores on both questionnaires show no difference between patients with CFS and healthy controls except for those subjects with CFS who are also concurrently depressed. In these cases the scores resemble patients with depression. Buckley et al. 30 non-depressed patients with Revised NEO Five-Factor Higher scores on neuroticism and (1999) CFS (CDC, 1994 (Fukuda et al., Inventory, Eysenk introversion in patients with CFS than 1994)) Personality Questionnaire in healthy controls. Lower neuroticism in 20 patients with major depressive CFS than MDD patients. Patients with disorder (MDD) CFS reported increased postmorbid 15 healthy controls neuroticism and introversion, suggesting that personality may have changed as a result of the illness. Christodoulou et al. 38 patients with CFS (CDC,1994 Diagnostic Interview Schedule Personality profiles of CFS and MS (1999) (Fukuda et al., 1994)) (Q-DIS), Tridimensional subjects were generally similar. Both 40 patients with multiple sclerosis Personality Questionnaire (TPQ) the MS and the CFS groups showed 40 healthy controls elevated levels of Harm Avoidance and lower levels of Reward Dependence in comparison to healthy subjects. The only difference was on the dimension of persistence, where the CFS group displayed preserved persistence and the MS group showed a reduction. There was no evidence to suggest that patients with CFS possessed an unusual level of negativity that would have predisposed them to develop their illness. Wood and Wessely 101 patients with CFS (Oxford MacLean's questionnaire on attitudes Alexithymia scores were greater in the (1999) Criteria, 1991 (Sharpe et al., 1991) towards mental illness, Social Desirability RA patient group and social adjustment and CDC, 1994 (Fukuda et al., Questionnaire, Defensiveness Scale of was poorer in the CFS group. No 1994)) Adjective Check List, Twenty-Item differences were found between CFS 45 patients with rheumatoid Toronto Alexithymia Scale, and RA patients in measures of arthritis (RA) Tridimensional Personality Questionnaire, perfectionism, attitudes towards mental Multidimensional Perfectionism Scale, illness, defensiveness, social desirability, Beck Depression Inventory (BDI) Social or sensitivity to punishment. There was Adjustment Scale (SAS) no evidence from this study of major differences between the personalities of patients with CFS and patients with RA. Blenkiron et al., 40 patients with CFS (CDC, 1994 Multidimensional Perfectionism Scale, Women more than men with CFS tend (1999) (Fukuda et al., 1994)) Chalder Fatigue Questionnaire, Hospital to set lower expectations and standards 31 healthy controls Anxiety and Depression Scale (HAD) for others. The values for perfectionism found on the MPS were lower in the CFS sample (reflecting fewer perfectionist traits) than in the control group. This may indicate that the CFS respondents in this survey had already moderated their perfectionist tendencies and reset their standards to cope with the unpredictabilities of the disorder. Schmaling and Jones 53 patients with CFS Minnesota Multiphasic Personality The aggregate MMPI profile of (1996) (Approximately CDC, Inventory (MMPI) patients with CFS suggests that they 1988/ 1994 (Holmes et al., 1988; have significant physical complaints Fukuda et al., 1994)) and difficulties with cognitive 43 healthy controls functioning, are concerned about their symptoms, and are emotionally distressed. Their profile is similar to that of patients with chronic pain. Johnson et al., 35 patients with CFS (CDC, 1988/ The NEO Neuroticism Scale, Personality The study found progressively higher (1996) 1992 (Holmes et al., 1988; Sharpe Diagnostic Questionnaire-Revised (PDQ- rates of personality disorders (PD) and et al., 1992)) R), Beck Depression Inventory neuroticism from healthy controls 20 patients with multiple sclerosis through CFS and MS (who did not 24 depressed patients differ) to the depressed group. The 40 healthy controls most common PD's among subjects with CFS were histrionic (23%) and borderline (17%). The CFS group with concurrent depressive disorder (34% of the CFS group) was found to account for most of the personality disorder. Blakely et al. 58 patients with CFS (McKenzie Minnesota Multiphasic Personality Progressively more elevated scores on (1991) (New Zealand) criteria, 1988) Inventory, Beck Depression Inventory, most scales from healthy controls 81 patients with chronic pain (CP) General Health Questionnaire (GHQ) through chronic pain to patients with 104 healthy controls Lazarus ways of Coping (WoC) CFS were found. The individuals with CFS showed more deviant personality traits reflecting emotionality or neuroticism, inward hostility, self- criticism and guilt, although personality profiles fell into different groups. The hypothesis is brought forward that in CFS we are dealing with a particular subpopulation of patients with CP, who are particularly extreme and relatively homogenous in their endorsement of CFS symptoms. Millon et al. 24 patients with CFS (CDC, 1988 Millon Clinical Multiaxial Inventory Evidence of severe personality (1989) (Holmes et al., 1988)) (MCMI-II), Profile of Mood States pathology and affective distress was No appropriate control group Hamilton Rating Scale of Depression found. Anxiety, somatic disorder and (HAM-D), Folstein Mini-Mental depression were particularly prominent. Examination The Wechsler Memory Scale Histrionic (33%), schizoid (29%) and (WMS) avoidant, narcissistic and aggressive/ sadistic (each 25%) personality scales were pathologically elevated. ---------------------------------------------------------------------------------------------------------------------------------------------------- References Aaron, L.A., & Buchwald, D. (2001). A review of the evidence for overlap among unexplained clinical conditions. Annals of Internal Medicine, 134, 868-881. Abbey, S.E., & Garfinkel, P.E. (1990). Chronic fatigue syndrome and the psychiatrist. Canadian Journal of Psychiatry, 35, 625-633. Abbey, S.E., & Garfinkel, P.E. (1991). Neurasthenia and chronic fatigue syndrome: The role of culture in the making of a diagnosis. American Journal of Psychiatry, 148, 1638-1646. American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: American Psychiatric Association. Ax, S., Gregg, V.H., & Jones, D. (2001). Coping and illness cognitions: Chronic fatigue syndrome. Clinical Psychology Review, 21, 161-182. Axe, E., & Satz, P. (2000). Psychiatric correlates in chronic fatigue syndrome. Annals of Epidemiology, 10, 458. Asbring, P., & Narvanen, A. (2003). Ideal versus reality: Physicians perspectives on patients with chronic fatigue syndrome (CFS) and fibromyalgia. Social Science & Medicine, 57, 711-720. Baillio, J.N., & Lyddon, W.J. (2000). The self-confrontation method and the assessment of depression: A between groups comparison study. Constructivism in the Human Sciences, 5, 89-96. Blacker, C.V., Greenwood, D.T., Wesnes, K.A., Wilson, R., Woodward, C., Howe, I., et al. (2004). Effect of galantamine hydrobromide in chronic fatigue syndrome: A randomized controlled trial. Journal of the American Medical Association, 292, 1195-1204. Blakely, A.A., Howard, R.C., Sosich, R.M., Campbell Murdoch, J., Menkes, D.B., & Spears, G.F.S. (1991). Psychiatric symptoms, personality and ways of coping in chronic fatigue syndrome. Psychological Medicine, 21, 347-362. Blenkiron, P., Edwards, R., & Lynch, S. (1999). Associations between perfectionism, mood, and fatigue in chronic fatigue syndrome. The Journal of Mental and Nervous Disease, 187, 566-570. Block, J. (1995). A contrarian view of the five-factor approach to personality description. Psychological Bulletin, 117, 187-215. Bolton, D. (2001). Problems in the definition of 'mental disorder'. The Philosophical Quarterly, 51, 182-199. Borch-Jacobsen, M. (2001). Making psychiatric history: Madness as folie à plusieurs. History of the Human Sciences, 14, 19-38. Brace, M.J., Scott Smith, M., McCauley, E., & Sherry, D.D. (2000). Family reinforcement of illness behavior: A comparison of adolescents with chronic fatigue syndrome, juvenile arthritis, and healthy controls. Journal of Developmental and Behavioral Pediatrics, 21, 332-339. Brimacombe, M., Helmer, D.A., & Natelson, B.H. (2002). Birth order and its association with the onset of chronic fatigue syndrome. Human Biology, 74, 615-620. Brouwers, F.M., Van der Werf, S., Bleijenberg, G., Van der Zee, L., & Van der Meer, J.W.M. (2002). The effect of a polynutrient supplement on fatigue and physical activity of patients with chronic fatigue syndrome: A double-blind randomized controlled trial. Quarterly Journal of Medicine, 95, 677-683. Bruner, J. (1991). The narrative construction of reality. Critical Inquiry, 18, 1-21. Buchwald, D. (1996). Defining chronic fatigue syndrome. In S.E. Straus (Ed.), Chronic fatigue syndrome (pp. 45-60). New York: Marcel Dekker. Buchwald, D., Ashley, R.L., Pearlman, T., Kith, P., & Komaroff, A.L. (1996). Viral serologies in patients with chronic fatigue and chronic fatigue syndrome. Journal of Medical Virology, 50, 25-30. Buchwald, D., Umali, P., Umali, J., Kith, P., Pearlman, T., & Komaroff, A.L. (1995). Chronic fatigue and the chronic fatigue syndrome: Prevalence in a Pacific Northwest health care system. Annals of Internal Medicine, 123, 81-88. Buckley, L., MacHale, S.M., Cavanagh, J.T.O., Sharpe, M., Deary, I.J., & Lawrie, S.M. (1999). Personality dimensions in chronic fatigue syndrome and depression. Journal of Psychosomatic Research, 46, 395-400. Bulow, P.H., & Hyden, L. (2003). In dialogue with time: Identity and illness in narratives about chronic fatigue. Narrative Inquiry, 13, 71-97. Busichio, K., Tiersky, L.A., Deluca, J., & Natelson, B.H. (2004). Neuropsychological deficits in patients with chronic fatigue syndrome. Journal of the International Neuropsychological Society, 10, 278-285. Cairns, R., & Hotopf, M. (2005). A systematic review describing the prognosis of chronic fatigue syndrome. Occupational Medicine, 55, 20-31. Christodoulou, C., Deluca, J., Johnson, S.K., Lange, G., Gaudino, E.A., & Natelson, B.H. (1999). Examination of Cloninger's basic dimensions of personality in fatiguing illness: Chronic fatigue syndrome and multiple sclerosis. Journal of Psychosomatic Research, 47, 597-607. Chubb, H.L., Jones, I., Hillier, J., Moyle, C., Sadler, S., Cole, T., et al. (1999). Chronic fatigue syndrome - Personality and attributional style of patients in comparison to healthy controls and depressed individuals. Journal of Mental Health, 8, 351-359. Ciccone, D.S., Busichio, K., Vickroy, M., & Natelson, B.H. (2003). Psychiatric morbidity in the chronic fatigue syndrome: Are patients with personality disorder more physically impaired? Journal of Psychosomatic Research, 54, 445-452. Clark, J.N., & James, S. (2003). The radicalized self: The impact on the self of the contested nature of the diagnosis of chronic fatigue syndrome. Social Science & Medicine, 57, 1387-1395. Cleare, A.J., Blair, D., Chambers, S., & Wessely, S. (2001). Urinary free cortisol in chronic fatigue syndrome. American Journal of Psychiatry, 158, 641-643. Cluydts, R., & Michiels, V. (2001). Neuropsychological functioning in chronic fatigue syndrome: A review. Acta Psychiatrica Scandinavica, 103, 84-93. Costa, P.T., McCrae, R.R., Zonderman, A.B., Barbano, H.E., Lebowitz, B., & Larson, D.M. (1986). Cross-sectional studies of personality in a national sample: 2. Stability in neuroticism, extraversion and openness. Psychology and Aging, 1, 144-149. Deale, A., Chalder, T., & Wessely, S. (1998). Illness beliefs and treatment outcome in chronic fatigue syndrome. Journal of Psychosomatic Research, 45, 77-83. Deale, A., & Wessely, S. (2001). Patients' perceptions of medical care in chronic fatigue syndrome. Social Science & Medicine, 52, 1859-1864. Demitrack, M., Dale, J., Straus, S., Lawe, L., Listwak, S.J., Kruesi, M.J., et al. (1991). Evidence for impaired activation of the hypothalamic pituitary-adrenal axis in patients with chronic fatigue syndrome. Journal of Clinical Endocrinology and Metabolism, 73, 1224-1234. Dwairy, M. (1997). A biopsychosocial model of metaphor therapy with holistic cultures. Clinical Psychology Review, 17, 719-732. Dwairy, M. (2002). Foundations of psychosocial dynamic personality theory of collective people. Clinical Psychology Review, 22, 343-360. Edmonds, M., McGuire, H., & Price, J. (2004). Exercise therapy for chronic fatigue syndrome. Cohrane Database of Systematic Reviews, 3 CD003200. Endicott, N.A. (1999). Chronic fatigue syndrome in private practice psychiatry: Family history of physical and mental health. Journal of Psychosomatic Research, 47, 343-354. Farmer, A., Chubb, H., Jones, I., Hillier, J., Smith, A., & Borysiewicz, L. (1996). Screening for psychiatric morbidity in subjects presenting with chronic fatigue syndrome. British Journal of Psychiatry, 168, 354-358. Fiedler, N., Lange, G., Tiersky, L., DeLuca, J., Policastro, T., Kelly-McNeil, K., et al. (2000). Stressors, personality traits, and coping of Gulf War veterans with chronic fatigue. Journal of Psychosomatic Research, 48, 525-535. Fisher, L., & Chalder, T. (2003). Childhood experiences of illness and parenting in adults with chronic fatigue syndrome. Journal of Psychosomatic Research, 54, 439-443. Friedberg, F., & Jason, L.A. (2001). Chronic fatigue syndrome and fybromyalgia: Clinical assessment and treatment. Journal of Clinical Psychology, 57, 433-455. Fry, A.M., & Martin, M. (1996). Fatigue in the chronic fatigue syndrome: A cognitive phenomenon? Journal of Psychosomatic Research, 41, 415-426. Fukuda, K., Straus, S.E., Hickie, I., Sharpe, M., Dobbins, J.G., Komaroff, A., et al. (1994). The chronic fatigue syndrome: A comprehensive approach to its definition and study. Annals of Internal Medicine, 121, 953-959. Funder, D.C. (2001). Personality. Annual Review of Psychology, 52, 197-221. Gill, A.C., Dosen, A., & Ziegler, J.B. (2004). Chronic fatigue syndrome in adolescents. Archives of Pediatrics and Adolescent Medicine, 158, 225-229. Gray, D., Parker-Cohen, N.Y., White, T., Clark, S.T., Seiner, S.H., Achilles, J., et al. (2001). A comparison of individual and family psychology of adolescents with chronic fatigue syndrome, rheumatoid arthritis, and mood disorders. Journal of Developmental and Behavioral Pediatrics, 22, 234-242. Guignon, C. (1998). Narrative explanation in psychotherapy. American Behavioral Scientist, 41, 558-577. Hardt, J., Buchwald, D., Wilks, D., Sharpe, M., Nix, W.A., & Egle, U.T. (2001). Health-related quality of life in patients with chronic fatigue syndrome: An international study. Journal of Psychosomatic Research, 51, 431-434. Henderson, M., & Tannock, C. (2004). Objective assessment of personality disorder in chronic fatigue syndrome. Journal of Psychosomatic Research, 56, 251-254. Hermans, H.J.M. (1996). Voicing the self: From information processing to dialogical interchange. Psychological Bulletin, 119, 31-50. Hermans, H.J.M., & Hermans-Jansen, E. (1995). Self-narratives. The construction of meaning in psychotherapy. New York, NY: The Guilford Press. Hermans, H.J.M., & Dimaggio, G. (Eds.). (2004). The dialogical self in psychotherapy Brunner-Routledge: Hove and New York. Hermans, H.J.M., Kempen, H.J.G., & Van Loon, R.J.P. (1992). The dialogical self: Beyond individualism and rationalism. American Psychologist, 47, 23-33. Hickie, I., Lloyd, A., Wakefield, D., & Parker, G. (1990). The psychiatric status of patients with the chronic fatigue syndrome. British Journal of Psychiatry, 156, 534-540. Holmes, G.P., Kaplan, J.E., Gantz, N.M., Komaroff, A., Schonberger, L.B., Strauss, S.S., et al. (1988). Chronic fatigue syndrome: A working case definition. Annals of Internal Medicine, 108, 387-389. Huibers, M.J., & Wessely, S. (2006). The act of diagnosis: Pros and cons of labelling chronic fatigue syndrome. Psychological Medicine, 36, 895-900. Johnson, S.K., DeLuca, J., & Natelson, B.H. (1996). Personality dimensions in the chronic fatigue syndrome: A comparison with multiple sclerosis and depression. Journal of Psychiatric Research, 30, 9-20. Johnson, S.K., DeLuca, J., & Natelson, B.H. (1999). Chronic fatigue syndrome: Reviewing the research findings. Annals of Behavioral Medicine, 21, 258-271. Kakumanu, S.S., Mende, C.N., Lehman, E.B., Hughes, K., & Craig, T.J. (2003). Effect of topical nasal corticosteroids on patients with chronic fatigue syndrome and rhinitis. Journal of the American Osteopathic Association, 103, 423-427. 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, 378-379. Katon, W.J., & Russo, J.E. (1992). Chronic fatigue syndrome criteria. A critique of the requirement for multiple physical complaints. Archives of Internal Medicine, 152, 1604-1609. Kavelaars, A.M.A.A., Kuis, W., Knook, L.M.E., Sinnema, G., & Heijnen, C.J. (2000). Disturbed neuroendocrineimmune interactions in chronic fatigue syndrome. Journal of Clinical Endocrinology and Metabolism, 85, 692-696. Knook, L.M.E., Kavelaars, A.M.A.A., Sinnema, G., Kuis, W., & Heijnen, C.J. (2000). High nocturnal melatonin in adolescents with chronic fatigue syndrome. Journal of Clinical Endocrinology and Metabolism, 85, 3690-3692. Koelle, D.M., Barcy, S., Huang, M.L., Ashley, R.L., Corey, L., Zeh, J., et al. (2003). Markers of viral infection in monozygotic twins discordant for chronic fatigue syndrome. Clinical Infectious Diseases, 35, 518-525. Komaroff, A.L., & Buchwald, D.S. (1998). Chronic fatigue syndrome: An update. Annual Review of Medicine, 49, 1-13. Lane, T.J., Manu, P., & Matthews, D.A. (1991). Depression and somatization in the chronic fatigue syndrome. American Journal of Medicine, 91, 335-344. Lange, G., Steffener, J., Cook, D.B., Bly, B.M., Christodoulou, C., Liu, W.C., et al. (2005). Objective evidence of cognitive complaints in chronic fatigue syndrome. Neuroimage, 26, 513-524. Lawrie, S.M., Manders, D.N., Geddes, J.R., & Pelosi, A.J. (1997). A population- based incidence study of chronic fatigue. Psychological Medicine, 27, 343-353. Lehman, A.M., Lehman, D.R., Hemphill, K.J., Mandel, D.R., & Cooper, L.M. (2002). Illness experience, depression, and anxiety in chronic fatigue syndrome. Journal of Psychosomatic Research, 52, 461-465. Lewis, S. (1996). Personality, stress, and chronic fatigue syndrome. In C.L. Cooper (Ed.), Handbook of stress, medicine, and health (pp. 233-249). Boca Raton, FL: CRC Press. Lewis, S., Cooper, C.L., & Bennett, D. (1994). Psychosocial factors and chronic fatigue syndrome. Psychological Medicine, 24, 661-671. Lloyd, A.R., Hickie, I., Boughton, C.R., Spencer, O., & Wakefield, D. (1990). The prevalence of chronic fatigue syndrome in an Australian population. Medical Journal of Australia, 153, 522-528. Lloyd, A.R., Hickie, I., Brockman, A., Hickie, C., Wilson, A., Dwyer, J., et al. (1993). Immunological and psychological therapy for patients with chronic fatigue syndrome: A double-blind, placebo-controlled trial. American Journal of Medicine, 94, 197-203. Luthra, A., & Wessely, S. (2004). Unloading the trunk: Neurastenia, CFS and race. Social Science & Medicine, 58, 2363-2369. Lyall, M., Peakman, M., & Wessely, S. (2003). A systematic review and critical evaluation of the immunology of chronic fatigue syndrome. Journal of Psychosomatic Research, 55, 79-90. Main, C.J., Richards, H.L., & Fortune, D.G. (2000). Why put new wine in old bottles: The need for a biopsychological approach to the assessment, treatment, and understanding of unexplained and explained symptoms in medicine. Journal of Psychosomatic Research, 48, 511-514. Mahurin, R.K., Claypoole, K.H., Goldberg, J.H., Arguelles, L., Ashton, S., & Buchwald, D. (2004). Cognitive processing in monozygotic twins discordant for chronic fatigue syndrome. Neuropsychology, 18, 232-239. Masuda, A., Munemoto, T., Yamanaka, T., Takei, M., & Tei, C. (2002). Psychosocial characteristics and immunological functions in patients with postinfectious chronic fatigue syndrome and noninfectious chronic fatigue syndrome. Journal of Behavioral Medicine, 25, 477-485. McAdams, D.P. (1995). What do we know when we know a person? Journal of Personality, 63, 365-369. McAdams, D.P., Anyidoho, N.A., Brown, C., Huang, Y.T., Kaplan, B., & Machado, M.A. (2004). Traits and stories. Links between dispositional traits and narrative features of personality. Journal of Personality, 72, 761-784. McKenzie, R. (1988). Myalgic Encephalomyelitis Syndrome. Therapeutic Notes, vol. 205. New Zealand Department of Health Circulation. McKenzie, R., O'Fallon, A., Dale, J., Demitrack, M., Sharma, G., Deloria, M., et al. (1998). Low-dose hydrocortisone for treatment of chronic fatigue syndrome: A randomized controlled trial. Journal of the American Medical Association, 280, 1061-1066. McLeod, J. (1997). Narrative and psychotherapy. London: Sage. Metzger, F.A., & Denney, D.R. (2002). Perception of cognitive performance in patients with chronic fatigue syndrome. Annals of Behavioral Medicine, 24, 106-112. Millon, C., Salvato, F., Blaney, N., Morgan, R., Mantero-Atienza, E., Klimas, N., et al. (1989). A psychological assessment of chronic fatigue syndrome/ chronic Epstein-Barr virus patients. Psychology and Health, 3, 131-141. Moran, P., Coffey, C., Carlin, J.B., & Patton, G.C. (2006). Dimensional characteristics of DSM-IV personality disorders in a large epidemiological sample. Acta Psychiatrica Scandinavica, 113, 233-236. Moss-Morris, R., & Petrie, K.J. (2001). Discriminating between chronic fatigue syndrome and depression: A cognitive analysis. Psychological Medicine, 31, 469-479. Moss-Morris, R., & Spence, M. (2006). To "lump" or to "split" the functional somatic syndromes: Can infectious and emotional risk factors differentiate between the onset of chronic fatigue syndrome and irritable bowel syndrome? Psychosomatic Medicine, 68, 463-469. Natelson, B.H., Cheu, J., Hill, N., Bergen, M., Korn, L., Denny, T., et al. (1998). Single-blind, placebo phase-in trial of two escalating doses of selegiline in the chronic fatigue syndrome. Neuropsychobiology, 37, 150-154. Parker, A.J.R., Wessely, S., & Cleare, A.J. (2001). The neuroendocrinology of chronic fatigue syndrome. Psychological Medicine, 31, 1331-1345. Patarca-Montero, R., Antoni, M., Fletcher, M.A., & Klimas, N.G. (2001). Cytokine and other immunological markers in chronic fatigue syndrome and their relation to neuropsychological factors. Applied Neuropsychology, 8, 51-64. Patel, M.X., Smith, D.G., Chalder, T., & Wessely, S. (2003). Chronic fatigue syndrome in children: A cross sectional survey. Archives of Disease in Childhood, 88, 894-898. Price, J.R., & Couper, J. (2000). Cognitive behaviour therapy for adults with chronic fatigue syndrome. Cochrane Database of Systematic Reviews, 2, CD001027. Prins, J.B., Bleijenberg, G., Bazelmans, E., Elving, L.D., De Boo, T.M., Severens, J.L., et al. (2001). Cognitive behaviour therapy for chronic fatigue syndrome: A multicentre randomised controlled trial. Lancet, 357, 841-847. Rangel, L., Garralda, E., Levin, M., & Roberts, H. (2000). Personality in adolescents with chronic fatigue syndrome. European Child and Adolescent Psychiatry, 9, 39-45. Ray, C. (1991). Chronic fatigue syndrome and depression: Conceptual and methodological ambiguities. Psychological Medicine, 21, 1-9. Richardson, F.C., Rogers, A., & McCaroll, J. (1998). Toward a dialogical self. American Behavioral Scientist, 41, 496-515. Sarbin, T. (Ed.). (1986). Narrative psychology: The storied nature of human conduct. New York: Praeger. Schluenderberg, A., Straus, S.E., Peterson, P., Blumenthal, S., Komaroff, A., Spring, S.B., et al. (1992). Chronic fatigue syndrome research - Definition and medical outcome assessment. Annals of Internal Medicine, 117, 325-331. Schmaling, K.B., DiClementi, J.D., Cullum, C.M., & Jones, J.F. (1994). Cognitive functioning in chronic fatigue syndrome and depression: A preliminary comparison. Psychosomatic Medicine, 56, 383-388. Schmaling, K.B., & Jones, J.F. (1996). MMPI profiles of patients with chronic fatigue syndrome. Journal of Psychosomatic Research, 40, 67-74. Schweitzer, R., Robertson, D.L., Kelly, B., & Whiting, J. (1994). Illness behaviour of patients with chronic fatigue syndrome. Journal of Psychosomatic Research, 38, 41-49. Segal, T.Y., Hindmarsh, P.C., & Viner, R.M. (2005). Disturbed adrenal function in adolescents with chronic fatigue syndrome. Journal of Pediatric Endocrinology & Metabolism, 18, 295-301. Sharpe, M. (1998). Cognitive behaviour therapy for chronic fatigue syndrome: Efficacy and implications. American Journal of Medicine, 105, 104s-109s. Sharpe, M., Archard, L., Banatvala, J., Borysiewicz, L., Clare, A., David, A., et al. (1991). A report. Chronic fatigue syndrome: Guidelines for research. Journal of the Royal Society of Medicine, 84, 118-121. Sharpe, M., Chalder, T., Palmer, I., & Wessely, S. (1997). Chronic fatigue syndrome. A practical guide to assessment and management. General Hospital Psychiatry, 19, 185-199. Short, K., McCabe, M., & Tooley, G. (2002). Cognitive functioning in chronic fatigue syndrome and the role of depression, anxiety, and fatigue. Journal of Psychosomatic Research, 52, 475-483. Steven, I.D., McGrath, B., Qureshi, F., Wong, C., Chern, I., & Pearn-Rowe, B. (2000). General practitioners' beliefs, attitudes and reported actions towards chronic fatigue syndrome. Australian Family Physician, 29, 80-85. Straus, S.E., Fritz, S., Dale, J.K., Gould, B., & Strober, W. (1993). Lymphocyte phenotype and function in the chronic fatigue syndrome. Journal of Clinical Immunology, 13, 30-40. Surawy, C., Hackmann, A., Hawton, K., & Sharpe, M. (1995). Chronic fatigue syndrome: A cognitive approach. Behavioural Research and Therapy, 33, 535-544. Swartz, M.N. (1988). The chronic fatigue syndrome - One entity or many? The New England Journal of Medicine, 319, 1726-1728. Taerk, G., & Gnam, W. (1994). A psychodynamic view of the chronic fatigue syndrome. The role of object relations in etiology and treatment. General Hospital Psychiatry, 16, 319-325. Taillefer, S.S., Kirmayer, L.J., Robbins, J.M., & Lasry, J. (2003). Correlates of illness worry in chronic fatigue syndrome. Journal of Psychosomatic Research, 54, 331-337. Taylor, C. (1989). Sources of the self. Cambridge, MA: Harvard University Press. Taylor, C. (1995). The dialogical self. In R.F. Goodman & W.R. Fisher (Eds.), Rethinking knowledge: Reflections across the disciplines (pp. 57-66). Albany, NY: State University of New York Press. Van de Putte, E.M., Engelbert, R.H.H., Kuis, W., Sinnema, G., Kimpen, J.L.L., & Uiterwaal, C.S.P.M. (2005). Chronic fatigue syndrome and health control in adolescents and parents. Archives of Disease in Childhood, 90, 1020-1024. Van de Putte, E.M., Van Doornen, L.J., Engelbert, R.H.H., Kuis, W., Kimpen, J.L.L., & Uiterwaal, C.S.P.M. (2006). Mirrored symptoms in mother and child with chronic fatigue syndrome. Pediatrics, 117, 2074-2079. Van Geel, R., & De Mey, H. (2003). Self, other, positive, and negative affect scales of the selfconfrontation method: Factorial structure and unidimensionality. Personality and Individual Differences, 35, 1833-1847. Van Hoof, E., Cluydts, R., & De Meirleir, K. (2003). Atypical depression as a secondary symptom in chronic fatigue syndrome. Medical Hypotheses, 61, 52-55. Van Houdenhove, B. (2002). Listening to CFS: Why we should pay more attention to the story of the patient. Journal of Psychosomatic Research, 52, 495-499. Van Houdenhove, B., Neerinckx, E., Onghena, P., Lysens, R., & Vertommen, H. (2000). Attributions in chronic fatigue syndrome and fibromyalgia syndrome in tertiary care. The Journal of Rheumatology, 27, 1051-1055. Van Houdenhove, B., Neerinckx, E., Onghena, P., Lysens, R., & Vertommen, H. (2001). Premorbid "overactive" lifestyle in chronic fatigue syndrome and fibromyalgia. An etiological factor or proof of good citizenship? Journal of Psychosomatic Research, 51, 571-576. Van Middendorp, H., Geenen, R., Kuis, W., Heijnen, C., & Sinnema, G. (2001). Psychological adjustment of adolescent girls with chronic fatigue syndrome. Pediatrics, 107, e35. Vercoulen, J.H., Bazelmans, E., Swanink, C.M., Galama, J.M., Fennis, J.F., Van der Meer, J.W., et al. (1998). Evaluating neuropsychological impairment in chronic fatigue syndrome. Journal of Clinical and Experimental Neuropsychology, 20, 144-156. Vercoulen, J.H., Swanink, C.M., Zitman, F.G., Vreden, S.G., Hoofs, M.P., Fennis, J.F., et al. (1996). Randomised, double-blind, placebo-controlled study of fluoxetine in chronic fatigue syndrome. Lancet, 347, 858-861. Viner, R., & Hotopf, M. (2004). Childhood predictors of self reported chronic fatigue syndrome/myalgic encephalomyelitis in adults: National birth cohort study. British Medical Journal, 329, 941-945. Vollmer-Conna, U., Hickie, I., Hadzi-Pavlovic, D., Tymms, K., Wakefield, D., Dwyer, J., et al. (1997). Intravenous immunoglobulin is ineffective in the treatment of patients with chronic fatigue syndrome. American Journal of Medicine, 103, 38-43. Wallace, H.L., Natelson, B., Gause, W., & Hay, J. (1999). Human herpesviruses in chronic fatigue syndrome. Clinical and Diagnostic Laboratory Immunology, 6, 216-223. Wallman, K.E., Morton, A.R., Goodman, C., Grove, R., & Guilfoyle, A.M. (2004). Randomised controlled trial of graded exercise in chronic fatigue syndrome. Medical Journal of Australia, 180, 444-448. Ware, N. (1994). An anthropological approach to the chronic fatigue syndrome. In S.E. Straus (Ed.), Chronic fatigue syndrome (pp. 85-97). New York: Marcel Dekker. Ware, N., & Kleinman, A. (1992). Culture and somatic experience: The social course of illness in neurasthenia and chronic fatigue syndrome. Psychosomatic Medicine, 54, 546-560. Watson, D., & Walker, L.M. (1996). The long-term stability and predictive validity of trait measures of affect. Journal of Personality and Social Psychology, 70, 567-577. Wearden, A.J., & Appleby, L. (1996). Research on cognitive complaints and cognitive functioning in patients with chronic fatigue syndrome (CFS): What conclusions can we draw? Journal of Psychosomatic Research, 41, 197-211. Weatherley-Jones, E., Nicholl, J.P., Thomas, K.J., Parry, G.J., McKendrick, M.W., Green, S.T., et al. (2004). A randomised, controlled triple-blind trial of the efficacy of homeopathic treatment for chronic fatigue syndrome. Journal of Psychosomatic Research, 56, 189-197. Wessely, S. (1990). Old wine in new bottles: Neurasthenia and 'ME'. Psychological Medicine, 20, 35-53. Wessely, S. (1996). The history of chronic fatigue syndrome. In S.E. Straus (Ed.), Chronic fatigue syndrome (pp. 13-44). New York: Marcel Dekker. Wessely, S., Chalder, T., Hirsch, S., Wallace, P., & Wright, D. (1996). Psychological symptoms, somatic symptoms, and psychiatric disorder in chronic fatigue and chronic fatigue syndrome: A prospective study in the primary care setting. American Journal of Psychiatry, 153, 1050-1059. Wessely, S., Nimnuan, C., & Sharpe, M. (1999). Functional somatic symptoms: One or many? Lancet, 354, 936-939. White, C., & Schweitzer, R. (2000). The role of personality in the development and perpetuation of chronic fatigue syndrome. Journal of Psychosomatic Research, 48, 515-524. White, P.D., Thomas, J.M., Kangro, H.O., Bruce-Jones, W.D.A., Amess, J., Crawford, D.H., Grover, S.A., et al. (2001). Predictions and associations of fatigue syndromes and mood disorders that occur after infectious mononucleosis. Lancet, 358, 1946-1954. Whitehead, L. (2006). Toward a trajectory of identity reconstruction in chronic fatigue syndrome/myalgic encephalomyelitis: A longitudinal qualitative study. International Journal of Nursing Studies, 43, 1023-1031. Whiting, P., Bagnall, A., Sowden, A.J., Cornell, J.E., Mulrow, C.D., & Ramirez, G. (2001). Interventions for the treatment and management of chronic fatigue syndrome: A systematic review. Journal of the American Medical Association, 286, 1360-1368. Wood, B., & Wessely, S. (1999). Personality and social attitudes in chronic fatigue syndrome. Journal of Psychosomatic Research, 47, 385-397. Zimmerman, M., & Coryell, W.H. (1990). Diagnosing personality disorders in the community. A comparison of self-report and inteview measures. Archives of General Psychiatry, 47, 527-531. -------- (c) 2007 Elsevier/ScienceDirect B.V. [Return to top] ------------------------------ Date: Wed, 21 Mar 2007 15:33:19 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Normal cerebrospinal fluid levels of hypocretin-1 (orexin A) in patients with fibromyalgia syndrome Normal cerebrospinal fluid levels of hypocretin-1 (orexin A) in patients with fibromyalgia syndrome. Sleep Med. 2007 Mar 16; [Epub ahead of print] Taiwo OB, Russell IJ, Mignot E, Lin L, Michalek JE, Haynes W, Xiao Y, Zeitzer JM, Larson AA. University of Minnesota, Department of Veterinary and Biomedical Sciences, Rm 295, Animal Science/Veterinary Medicine Building, 1988 Fitch Avenue, St. Paul, MN 55113, USA. PMID: 17369087 BACKGROUND: The hypothalamic neuropeptide hypocretin (orexin) modulates sleep-wake, feeding and endocrine functions. Cerebrospinal fluid (CSF) hypocretin-1 (Hcrt-1) concentrations are low in patients with narcolepsy-cataplexy, a sleep disorder characterized by hypersomnolence and rapid eye movement (REM) sleep abnormalities. METHODS: We determined CSF Hcrt-1 concentrations of patients with the fibromyalgia syndrome (FMS), a condition characterized by fatigue, insomnia and in some cases daytime hypersomnolence. RESULTS: Basal CSF levels of Hcrt-1 in FMS did not differ from those in healthy normal controls. CONCLUSIONS: These findings suggest that abnormally low Hcrt-1 is not a likely cause of fatigue in FMS. [Return to top] ------------------------------ Date: Wed, 21 Mar 2007 15:37:31 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: Long-term opioid contract use for chronic pain management in primary care practice. A five year experience. Long-term opioid contract use for chronic pain management in primary care practice. A five year experience. J Gen Intern Med. 2007 Apr;22(4):485-90. Hariharan J, Lamb GC, Neuner JM. Division of General Internal Medicine, Medical College of Wisconsin, Froedtert East Clinic Bldg., Suite E4200, 9200 West Wisconsin Avenue, Milwaukee, WI, 53226, USA, firstname.lastname@example.org. PMID: 17372797 BACKGROUND: The use of opioid medications to manage chronic pain is complex and challenging, especially in primary care settings. Medication contracts are increasingly being used to monitor patient adherence, but little is known about the long-term outcomes of such contracts. OBJECTIVE: To describe the long-term outcomes of a medication contract agreement for patients receiving opioid medications in a primary care setting. DESIGN: Retrospective cohort study. SUBJECTS: All patients placed on a contract for opioid medication between 1998 and 2003 in an academic General Internal Medicine teaching clinic. MEASUREMENTS: Demographics, diagnoses, opiates prescribed, urine drug screens, and reasons for contract cancellation were recorded. The association of physician contract cancellation with patient factors and medication types were examined using the Chi-square test and multivariate logistic regression. RESULTS: A total of 330 patients constituting 4% of the clinic population were placed on contracts during the study period. Seventy percent were on indigent care programs. The majority had low back pain (38%) or fibromyalgia (23%). Contracts were discontinued in 37%. Only 17% were cancelled for substance abuse and noncompliance. Twenty percent discontinued contract voluntarily. Urine toxicology screens were obtained in 42% of patients of whom 38% were positive for illicit substances. CONCLUSIONS: Over 60% of patients adhered to the contract agreement for opioids with a median follow-up of 22.5 months. Our experience provides insight into establishing a systematic approach to opioid administration and monitoring in primary care practices. A more structured drug testing strategy is needed to identify nonadherent patients. [Return to top] ------------------------------ Date: Fri, 23 Mar 2007 15:36:45 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: res: FMS -pivotal trial for chronic pain ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 23 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ http://www.pipelinereview.com/joomla/content/view/10541/106/ Pipeline Review Fralex Therapeutics Inc. initiates pivotal trial for chronic pain associated with fibromyalgia ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ 22 Mar 2007 Announced the initiation of RELIEF, its pivotal study for the treatment of chronic pain associated with fibromyalgia. The trial will evaluate the safety and effectiveness of the Company's non-drug, in-home therapy, Complex Neural Pulse(TM) (CNP(TM)). The first clinical trial site in Ottawa, Ontario, has been initiated and patient screening and recruitment will begin shortly. TORONTO, Canada | Mar 22, 2007 | Fralex Therapeutics Inc. (TSX: FXI) ("Fralex" or the "Company"), a medical technology company developing neuromodulation therapy, today announced the initiation of RELIEF, its pivotal study for the treatment of chronic pain associated with fibromyalgia. The trial will evaluate the safety and effectiveness of the Company's non-drug, in-home therapy, Complex Neural Pulse(TM) (CNP(TM)). The first clinical trial site in Ottawa, Ontario, has been initiated and patient screening and recruitment will begin shortly. "We are pleased that we have achieved our milestone of initiating the RELIEF trial within the first quarter of 2007 and look forward to initiating further clinical sites in Canada and the U.S. in the coming weeks," said Avi Grewal, President and CEO of Fralex. "We believe that CNP will significantly advance the practice of medicine in the treatment of various chronic, debilitating conditions by offering a non-invasive, relatively low-cost treatment option. Patients can regain control of their lives without having to deal with possible addiction issues, or other side effects that themselves seriously affect quality of life." The RELIEF trial will enrol between 200 and 300 subjects across 13 centres in the U.S. and Canada, and is being conducted under an Investigational Device Exemption (IDE) from the U.S. Food and Drug Administration (FDA) and an Investigational Testing Authorization (ITA) from Health Canada. Subjects will be randomized on a one-to-one basis to receive CNP or placebo for 12 weeks. The primary efficacy endpoint will be a statistically and clinically significant difference between the active and placebo groups in the proportion of the subjects who achieve a 30% or greater reduction in their NRS pain scores. About Fibromyalgia Fibromyalgia is a chronic, debilitating condition characterized by widespread musculoskeletal (MSK) pain, disturbed sleep, and fatigue along with multiple painful tender points, which are widely and symmetrically distributed. According to the American Pain Society, fibromyalgia is estimated to affect eight to twelve million people in the United States. Fibromyalgia is one of the most commonly diagnosed conditions in pain clinics in the United States. No treatments have been specifically approved for fibromyalgia in the United States or Canada. About FRALEX: FRALEX is a medical technology company focused on developing and commercializing Complex Neural Pulse(TM) or CNP(TM), a novel neuromodulation therapeutic technology for chronic pain, which utilizes specifically designed, low-frequency electromagnetic pulses. FRALEX is proceeding with its FDA-approved pivotal clinical trial (the "RELIEF" trial) to evaluate the safety and effectiveness of this technology in the treatment of chronic pain associated with fibromyalgia. The trial is to be conducted in 2007 and 2008 at leading medical centres within the US and Canada. For more information on FRALEX, please visit www.fralex.com; further details on the RELIEF trial will be posted on www.clinicaltrials.gov. Certain statements contained in this release containing words like "believe", "intend", "may", "expect", and other similar expressions, are forward-looking statements that involve a number of risks and uncertainties. Factors that could cause actual results to differ materially from those projected in the Company's forward-looking statements include the following: market acceptance of Company's technologies and products; the ability to obtain financing; Company's financial and technical resources relative to those of its competitors; Company's ability to keep up with rapid technological change; government regulation of therapeutic technologies; the Company's ability to enforce its intellectual property rights and protect its proprietary technologies; the ability to obtain and develop partnership opportunities; the timing of commercial product launches; the ability to achieve key technical milestones in key products and other risk factors identified from time to time in the Company's filings. SOURCE: Fralex Therapeutics Inc [Return to top] ------------------------------ Date: Fri, 23 Mar 2007 16:23:50 +0100 From: Jan van Roijen <j.van.roijen CHELLO.NL> Subject: not,med: clinical guidelines often influenced by industry ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 23 March 2007 <<<< Editorship : j.van.roijen chello.nl Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ http://www.bmj.com/cgi/content/extract/334/7586/171 BMJ 2007;334:171 (27 January), doi:10.1136/bmj.39104.406065.DB News US clinical guidelines often influenced by industry, NEJM says ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Janice Hopkins Tanne 1 New York Many clinical guidelines for doctors in the United States are influenced by the pharmaceutical industry and special interest groups, said an article in the New England Journal of Medicine last week (2007;356:331-3). "The quality of guidelines varies considerably," and some are controversial, says a commentary by the journal's national correspondent, Robert Steinbrook. Meanwhile, the National Institutes of Health (NIH) cancelled a conference that it had planned on guidelines for screening pregnant women for herpes, after it received a protest letter from the Center for Science in the Public Interest. The organisation's letter said that four out of five of the speakers had undisclosed ties to drug firms that made antiviral drugs (BMJ 2007;334:115). The letter was signed by Richard Horton, editor of the Lancet; two former editors of the New England Journal of Medicine, Marcia Angell and Jerome Kassirer; 41 other physicians and scientists, including the head . . . [Full text of this article] http://www.bmj.com/cgi/content/full/334/7586/171 `````` Related Article Who should call the tune? James R Philp BMJ 2007 334: 491. [Extract] http://www.bmj.com/cgi/content/extract/334/7592/491-c This article has been cited by other articles: (Search Google Scholar for Other Citing Articles) Philp, J. R (2007). Who should call the tune?. BMJ 334: 491-491 [Full text] http://www.bmj.com/cgi/content/full/334/7592/491-c Rapid Responses: Read all Rapid Responses http://www.bmj.com/cgi/eletters/334/7586/171 An additional hazard of clinical guidelines. Joseph A Sonnabend bmj.com, 27 Jan 2007 [Full text] http://www.bmj.com/cgi/eletters/334/7586/171#155455 US clinical guidelines often influenced by industry-referral to NICE in UK Judy Gordon bmj.com, 28 Jan 2007 [Full text] http://www.bmj.com/cgi/eletters/334/7586/171#155522 [Return to top] ------------------------------ Date: Fri, 23 Mar 2007 12:36:26 -0400 From: "Bernice A. Melsky" <bernicemelsky VERIZON.NET> Subject: RES: The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation. Med Hypotheses. 2007 Mar 19; [Epub ahead of print] Katz DL, Greene L, Ali A, Faridi Z. Yale Prevention Research Center, Yale University School of Medicine, 130 Division Street, Derby, CT 06418, USA; Yale University School of Public Health, Yale University School of Medicine, 60 College Street, New Haven, CT 06520, USA. PMID: 17376601 Fibromyalgia syndrome (FMS) is a condition of chronic muscle pain and fatigue of unknown etiology and pathogenesis. There is limited support for the various hypotheses espoused to account for the manifestations of FMS, including immunogenic, endocrine, and neurological mechanisms. Treatment, partially effective at best, is directed toward symptomatic relief without the benefit of targeting known, underlying pathology. A noteworthy commonality among partially effective therapies is a vasodilatory effect. This is true both of conventional treatments, unconventional treatments such as intravenous micronutrient therapy, and lifestyle treatments, specifically graduated exercise. The pain of fibromyalgia is described in terms suggestive of the pain in muscles following extreme exertion and anaerobic metabolism. Taken together, these characteristics suggest that the pain could be induced by vasomotor dysregulation, and vasoconstriction in muscle, leading to low-level ischemia and its metabolic sequelae. Vasodilatory influences, including physical activity, relieve the pain of FMS by increasing muscle perfusion. There are some preliminary data consistent with this hypothesis, and nothing known about FMS that refutes it. The hypothesis that the downstream cause of FMS symptoms is muscle hypoperfusion due to regional vasomotor dysregulation has clear implications for treatment; is testable with current technology; and should be investigated. [Return to top] ------------------------------ Date: Sun, 25 Mar 2007 16:08:09 +0200 From: "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM> Subject: RES,NOT: CFS and CBT Source: Journal of Neurology, Neurosurgery, and Psychiatry Vol. 78, #4, pp 434-436 Date: March 21, 2007 URL: http://jnnp.bmj.com/cgi/content/full/78/4/434 http://www.jnnp.com [Short report] The effect of cognitive behaviour therapy for chronic fatigue syndrome on self-reported cognitive impairments and neuropsychological test performance --------------------------------------------------------------------------- Hans Knoop, Judith B Prins, Maja Stulemeijer, Jos W M van der Meer, Gijs Bleijenberg Hans Knoop, Gijs Bleijenberg, Expert Centre Chronic Fatigue, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands Judith B Prins, Maja Stulemeijer, Department of Medical Psychology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands Jos W M van der Meer, Department of Internal Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands Correspondence to: H Knoop, Expert Centre Chronic Fatigue, Radboud University Nijmegen Medical Centre, P O Box 9011, 6525 EC Nijmegen, The Netherlands; j.knoop nkcv.umcn.nl Received 26 June 2006 Revised 14 November 2006 Accepted 15 November 2006 Abstract Background Patients with chronic fatigue syndrome (CFS) often have concentration and memory problems. Neuropsychological test performance is impaired in at least a subgroup of patients with CFS. Cognitive behavioural therapy (CBT) for CFS leads to a reduction in fatigue and disabilities. Aim To test the hypothesis that CBT results in a reduction of self-reported cognitive impairment and in an improved neuropsychological test performance. Methods Data of two previous randomised controlled trials were used. One study compared CBT for adult patients with CFS, with two control conditions. The second study compared CBT for adolescent patients with a waiting list condition. Self-reported cognitive impairment was assessed with questionnaires. Information speed was measured with simple and choice reaction time tasks. Adults also completed the symbol digit-modalities task, a measure of complex attentional function. Results In both studies, the level of self-reported cognitive impairment decreased significantly more after CBT than in the control conditions. Neuropsychological test performance did not improve. Conclusions CBT leads to a reduction in self-reported cognitive impairment, but not to improved neuropsychological test performance. The findings of this study support the idea that the distorted perception of cognitive processes is more central to CFS than actual cognitive performance. Abbreviations: CBT, cognitive behavioural therapy; CFS, chronic fatigue syndrome; CIS, checklist individual strength; CIS-conc, checklist individual strength-concentration; SDMT, symbol digit modalities task; SIP-ab, sickness impact profile-alertness behaviour; SOCI, self-observation of cognitive impairment -------------------------------------------------------------------------------- Chronic fatigue syndrome (CFS) is characterised by severe fatigue, lasting longer than 6 months and leading to functional impairment. The fatigue is not the result of a known organic disease or ongoing exertion, and not alleviated by rest. According to the Centre for Disease Control definition of CFS, impaired concentration and/or memory is an additional symptom criterion.1 The level of self-reported cognitive impairments in CFS is high2 and contributes to the social and occupational dysfunctions of patients with CFS.3 Studies evaluating neuropsychological functioning in patients with CFS with neuropsychological tests yielded conflicting results.4 Reduced speed of (complex) information processing is the most consistently found impairment.3 5 6 However, several studies found no cognitive impairments7 and other studies identified a subset of patients with defective performance.8 9 Fatigue-related cognitions and behaviour can perpetuate CFS.10 Several controlled trials have shown that cognitive behavioural therapy (CBT) aimed at these perpetuating factors leads to a reduction in fatigue and disabilities.11 The first hypothesis tested was that CBT for CFS also results in a reduction of self-reported cognitive impairments. The second hypothesis was that the neuropsychological test performance of patients with CFS improves after CBT. Data of two previous CBT trials12 13 were used to test the hypotheses. MATERIALS AND METHODS Patients The first study from which data were used compared the effects of CBT for adults with CFS with natural course and support groups12 in a multicentre randomised controlled trial. Assessments were done at baseline, and at 8 and 14 months. An intention-to-treat analysis showed a reduction in fatigue and functional impairment after CBT. In two of the three participating treatment centres, neuropsychological tests were part of the assessments. Consequently, data from neuropsychological test performance were available for a subset of 233 (78 CBT; 76 natural course; 79 support group) of the total group of 278 patients. The mean (SD) age of this group was 36.8 (10.2) years, 182 (78%) were female and median illness duration was 41 months. The second study was a randomised controlled trial comparing CBT for adolescents with CFS13 with a waiting list condition. A total of 69 patients were randomly assigned to the conditions. Assessments were done at baseline and at 5 months. The results showed a greater decrease in fatigue and functional impairment in the CBT group. Neuropsychological data of 67 patients were available (33 CBT; 34 waiting list). The mean (SD) age of the group was 15.6 (1.3) years, 59 (88%) were female and median illness duration was 18 months. Questionnaires assessing self-reported cognitive impairments Checklist individual strength-concentration In both studies, the severity of concentration problems over the past 2 weeks was assessed with the subscale concentration of the checklist individual strength (CIS) that consists of five items on a seven-point scale. The score can range between 5 and 35.3 12 13 Sickness impact profile-alertness behaviour In adults, the self-observed effect of cognitive impairments on daily functioning was assessed with the subscale sickness impact profile-alertness behaviour (SIP-ab) of the sickness impact profile.14 The subscale has 10 items, each item is weighed and the score can range between 0 and 777. No such instrument was available for adolescents. Self-observation of cognitive impairment In adolescents, the frequency of cognitive impairments was determined with a structured diary. Patients rated both concentration and memory impairment separately on a daily self-observation list four times a day for 12 days (0=no impairment; 1=impaired). The percentage of concentration problems and memory problems (both number of assessments with a problem divided by 48 times 100) were added and then divided by two to calculate the mean percentage of incidents of cognitive impairment. Neuropsychological tests Reaction time task The reaction time task consisted of two subtests, simple and choice reaction time tasks. Both are described in detail elsewhere.8 15 In a previous study, the reaction times of patients with CFS were slower than that of healthy controls on both tasks.8 Symbol digit modalities task The symbol digit modalities task (SDMT)16 was used in the adult study as a measure of complex attention. In previous studies, patients with CFS scored lower than a matched healthy control group.8 9 Statistical analysis Statistical analysis was performed using SPSS V.12.01. Significance was assumed at p,0.05. A multivariate analysis of variance was performed with self-reported cognitive impairment and reaction time as dependent variables and treatment as fixed factor. Univariate tests and post hoc analysis are reported if the multivariate test was significant. For the SDMT, a univariate analysis was performed, as data were available for a subset of 174 patients as the SDMT was added later to the test battery. In the adult study, the dependent variables were the change scores at 14 months from baseline and in the adolescent study, it was at 5 months from baseline. Reaction times were transformed by a logarithm transformation. For adults, if data at 14 months were missing and data 8-months post-treatment were available, the second were used. In all other cases, missing data were replaced with estimates derived by single imputation (missing variable analysis regression in SPSS with baseline value as predictor). For significant treatment effects, effect sizes were calculated. RESULTS Nineteen adult patients (8%) had missing checklist individual strength-concentration (CIS-conc) and SIP-ab post-treatment data. One patient had missing data on both reaction time tasks at baseline, for 44 (19%) patients only baseline data and for 30 (17%) patients only a baseline SDMT score was available. Two adolescent patients had no SOCI scores at baseline. For 4 (6%) patients the CIS-conc and SOCI at second assessment were missing. Two patients had no baseline reaction time and for 13 (20%) adolescents the reaction times at the second assessment were missing. In both studies, there were more data missing from neuropsychological tests than from questionnaires as some patients were willing to mail the questionnaires, but refused to undergo a second neuropsychological assessment. Self-reported cognitive impairments Adults The multivariate test (Pillai's trace) showed a significant change in self-reported cognitive impairments (F(4,460)=4.76; p=0.001). The univariate tests showed a significant effect of treatment on the change in CIS-conc and SIP-ab (F(2,230)=8.94; p<0.001 and F(2,230)=4.42; p=0.013). Following CBT, the decrease in CIS was significantly greater than in both the natural course (p,0.001) and the support group (p=0.001; table 1). There was a significantly greater decrease in SIP-ab score after CBT compared with natural course (p=0.004). The difference between CBT and support group failed to reach significance (p=0.055). Adolescents The multivariate test showed a significant treatment effect on self-reported cognitive impairments (F2,62=5.03; p=0.009). Univariate tests showed that the decrease in the CIS-conc and SOCI score was significantly larger in the CBT group (F(1,63)=6.4; p=0.014 and F(1,63)=6.28; p=0.015). Neuropsychological test performance Adults There was no significant effect of treatment on either reaction time task (F(4,458)=0.44; p=0.783). There was no significant treatment effect on the SDMT (F(2,171)=0.73; p=0.484). Adolescents Multivariate tests showed no significant treatment effect on either reaction time task (F(2,62)=0.34; p=0.714). DISCUSSION The hypothesis that self-reported cognitive impairments decrease after CBT in patients with CFS was confirmed. Only one comparison in the adult study, measuring cognitive impairments more indirectly, showed an effect in the expected direction without reaching significance. The results of the original adolescent study13 already indicated that concentration problems decrease after CBT. In that study, the concentration problems were assessed with a single item evaluating these problems retrospectively over a period of 6 months. This assessment can be easily influenced by situational circumstances and memory biases, which can be prevented by the use of a diary as in the present study. No support could be found for the hypothesis that neuropsychological test performance improves after CBT. A methodological problem is that in a substantial part of the patients the neuropsychological data of the second assessment were missing. Furthermore, in our analysis we assumed that dropout occurred at random, whereas patients may drop out for non-random reasons. We repeated the analyses, but only on patients who completed both assessments. Again, there was no significant treatment effect. Our interpretation is that this indicates that improvement in self-reported cognitive impairments after CBT is independent of the change in neuropsychological test performance. A discrepancy between subjectively reported disabilities versus objectively measured performance is not limited to the current study. Mahurin et al17 found that the objective cognitive functioning of monozygotic twins discordant for CFS did not differ, whereas the twin with CFS reported more cognitive impairments. Metzger and Denney18 showed that patients with CFS underestimated their cognitive performance. In the study by Vercoulen et al,8 most patients with CFS reported concentration and memory problems, whereas only a small percentage showed an impaired performance. Given the fact that patients with CFS perceive their cognitive processes as impaired but underestimate their actual performance, one would expect that an effective treatment of CFS would lead to a more accurate perception of one's performance. The results of the present study are consistent with this prediction. CBT resulted in decreased complaints about cognitive functioning, but not in a change in performance. This is also in line with the hypothesis that a distorted perception of symptoms and performance is a crucial element of CFS.10 ACKNOWLEDGEMENTS The authors thank Theo Fiselier for contributing to the selection of adolescent patients with CFS, Lammy Elving for contributing to the selection of adult patients and Ria te Winkel and Lida Nabuurs for assisting in data collection. Funding: The Health Insurance Council (College van Zorgverzekeraars) funded the adult CBT study. The Children's Welfare Stamps Netherlands (Stichting Kinderpostzegels Nederland) and the ME Foundation (ME Stichting) funded the adolescent CBT study. Competing interests: none. TABLE Table 1 Estimated treatment effect in change score (95% CI) on the dependent variables ------------------------------------------------------------------------------------------------------ Self-reported cognitive impairments Adults CBT Natural course Support group CIS-conc -7.4 (-9.1 to -5.7)+ -2.7 (-4.4 to -1.0)** -3.4 (-5.1 to -1.8)** SIP-ab -116 (-156 to -76)++ -31 (-72 to -10)** -61 (-100 to -21) Adolescents CBT Waiting list CIS-conc -6.8 (-10.5 to -3.5)+++ -0.9 (-4.2 to +2.5)* SOCI -7.9 (-12.8 to -2.9)1 0.9 (-4.1 to +6.0)* ------------------------------------------------------------------------------------------------------ Neuropsychological test performance Adults CBT Natural course Support group Simple reaction time (ms) 9 (-9 to 27) -5 (-23 to 14) 6 (-12 to 24) Choice reaction time (ms) -24 (-51 to 3) -27 (-54 to 1) -26 (-53 to 1) SDMT 2.8 (0.8 to 4.8) 2.3 (0.2 to 4.4) 4 (2 to 6) Adolescents CBT Waiting list Simple reaction time (ms) -30 (-53 to -8) -18 (-41 to 4) Choice reaction time (ms) -12 (-29 to 6) -10 (-28 to 8) ------------------------------------------------------------------------------------------------------ CBT, cognitive behavioural therapy; CIS-conc, checklist individual strength-concentration; SDMT, symbol digit modalities task; SIP-ab, sickness impact profile-alertness behaviour; SOCI, self- observation of cognitive impairment. * Significantly different from the CBT condition, p,0.05. ** Significantly different from the CBT condition, p,0.01. + Cohen's d based on change within treatment condition=1.3. ++ Cohen's d=0.6. +++ Cohen's d=0.4. REFERENCES 1 Fukuda K, Straus SE, Hickie I, et al. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med 1994;121:953-9. 2 Vercoulen JHMM, Swanink CMA, Fennis JFM, et al. Dimensional assessment of chronic fatigue syndrome. J Psychosom Res 1994;38:383-92. 3 Michiel V, Cluydts R. Neuropsychological functioning in chronic fatigue syndrome: a review. Acta Psychiatr Scand 2001;103:84-93. 4 Cho, HJ, Skowera, A, Cleare A, et al. Chronic fatigue syndrome: an update focusing in phenomenology and pathophysiology. Curr Opin Psychiatry 2006;19:67-73. 5 Moss-Morris R, Petrie KJ, Large RG, et al. Neuropsychological deficits in chronic fatigue syndrome: artefact or reality? J Neurol Neurosurg Psychiatry 1996;60:474-7. 6 Tiersky LA, Johnson SK, Lange G, et al. The neuropsychology of chronic fatigue syndrome: a critical review. J Clin Exp Neuropsychol 1997;19:560-86. 7 Dipino RK, Kane RL. Neurocognitive functioning in chronic fatigue syndrome. Neuropsychol Rev 1996;6:47-60. 8 Vercoulen JH, Bazelmans E, Swanink CM, et al. Evaluating neuropsychological impairment in chronic fatigue syndrome. J Clin Exp Neuropsychol 1998;20:144- 56. 9 Van der Werf S, Prins JB, Jongen P, et al. Abnormal neuropsychological findings are not necessarily a sign of cerebral impairment: a matched comparison between chronic fatigue syndrome an multiple sclerosis. Neurol Neuropsychol Behav Neurol 2000;13:199-203. 10 Prins JB, Van der Meer JWM, Bleijenberg G. Chronic fatigue syndrome. Lancet 2006;376:346-55. 11 Whiting P, Bagnall AM, Sowden AJ, et al. Interventions for the treatment and management of chronic fatigue syndrome; a systematic review. J Am Med Assoc 2001;286:1360-8. 12 Prins JB, Bleijenberg G, Bazelmans E, et al. Cognitive behaviour therapy for chronic fatigue syndrome: a multicentre randomised controlled trial. Lancet 2001;357:841-7. 13 Stulemeijer M, de Jong LWAM, Fiselier TJW, et al. Cognitive behaviour therapy for adolescents with chronic fatigue syndrome: randomised controlled trial. BMJ 2005;330:7481-6. 14 Berger M, Bobbit RA, Carter WB, et al. The sickness impact profile: development and final revision of a health status measure. Med Care 1981;19:787-805. 15 Jolles J. Maastricht aging study: determinants of cognitive aging. Maastricht: Neuropsychological Publishers, 1995. 16 Stinnissen J, Willems PJ, Coetsier L, et al. Handleiding bij de Nederlandse bewerking van de WAIS [Manual of the Dutch edition of the WAIS]. Amsterdam: Swets and Zeitlinger, 1970. 17 Mahurin RK, Claypoole KH, Goldberg JH, et al. Cognitive processing in monozygotic twins discordant for chronic fatigue syndrome. Neuropsychology 2004;18:232-9. 18 Metzger FA, Denney, DR. Perception of cognitive performance in patients with chronic fatigue syndrome. Ann Behav Med 2002;24:106-12. -------- (c) 2007 BMJ Publishing Group Ltd. [Return to top] ------------------------------
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