Journal of Psychosomatic Research 60 (2006) 549 – 550
Editorial
Chronic fatigue and chronic fatigue syndrome: pathogenesis and measurement scales There are many terms that are used to describe what is now most generally referred to as chronic fatigue syndrome (CFS). Similarly, there are many approaches taken to evaluate its causative factors, from psychological to behavioral dimensions and neuroscientific investigations. The criticism could be made that most of these studies consider a single dimension (e.g., how mood or sleep impact or relate to CFS). Two papers in this issue explore issues as diverse as natural killer cell activity (NKCA) [1] and a concept referred to as baction pronenessQ [2], and how these biological and psychological functions alter or are altered by CFS. Part of the problem stems from studies in single centers, with each group focusing on a useful but inevitably narrowly defined perspective. It would seem that it would take considerable political will to conduct large multicenter studies simultaneously investigating several possible biological, psychological, and social elements of CFS to be able to arrive at a heuristic model of bio-psycho-social relevance. I have previously emphasized the issue of measurement in chronic fatigue and CFS [3,4]. In this issue, we have more finely delineated scales to measure fatigue in specific circumstances (e.g., postsurgery and in contrast with sleepiness) [5,6]. The correlation between fatigue and sleepiness exists, but is low [7,8], and hitherto has been fraught with the accusation that one was comparing apples and oranges when using a standard fatigue scale and was comparing it to a standard sleep scale that had no direct relation to the other scale. Bailes et al. [6] go some way to address this issue. The mistake of increasingly viewing sleepiness and fatigue as interchangeable has been recognized [7–9]. However, it would still be the case that most patients would not tease apart the distinction between fatigue and sleepiness without being asked directly to do so. Furthermore, many patients referred, for example, to a sleep clinic for bsleepinessQ identify bfatigueQ as their primary concern [9]. An Australian study [10] evaluated the relationship between emotional intelligence and subjective fatigue, showing an inverse relationship with many mediating variables including social support and sleep quality. Van Houdenhove et al. [2] showed that action proneness, which is high in patients prior to the onset of CFS, can be modified 0022-3999/06/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jpsychores.2006.04.008
by cognitive–behavioral therapy and physical (graded exercise) interventions and can be potentially adjusted to a midpoint of what may be seen as an overdrive prior to the onset of CFS and an underdrive with the onset of the disorder. The paper gives support to the validity of the two interventions and raises key issues of bburnout Q in fatigue and, while not explicitly stated, there is the possibility that, for some individuals, there is the vacillation between low action and high action (a lack of gain control), which acts as a perpetuating factor for the fatigue. In a very different attempt to consider pathoplastic factors in CFS, Siegel et al. [1] evaluated NKCA in CFS patients and concluded that those with lower levels of NKCA had worse cognition and more daytime dysfunction. This study highlights a key approach in this field of research in that, in addition to comparing measures with normal controls (where NKCA is repeatedly found to be lower) [11–15], one needs to subdivide the pool of CFS patients as one can anticipate differences in subgroups. This may, in turn, lead to a recognition of certain clusters of factors (for example and completely hypothetically, a traumatic experience plus sleep changes may lead to a slightly different phenotype of CFS compared with high action proneness and unusually low NKCA, which lead to a different constellation or pattern of what we currently see as phenotypic CFS). The implication is that different treatment modalities may be applicable to different groups of fatigued patients and subgroups of CFS patients. While I applaud Bailes et al. [6] for grappling with the issue of fatigue versus sleepiness, I disagree with their final comments implying that patients with sleep disorders have sleepiness but not fatigue. Their contribution is creating the possibility of measuring relationships. Patient populations suffering from conditions that traditionally have been considered to have fatigue as a dominant symptom (e.g., hepatitis C) often have an underlying sleep problem. Such patient groups may derive specific benefit from sleep-related interventions. A New Zealand group provides a description of perioperative fatigue and fulfills its own conclusion of offering a bmore comprehensive assessment of fatigue than provided by the measures most widely used in postsurgical
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Editorial /Journal of Psychosomatic Research 60 (2006) 549 – 550
fatigue literature to dateQ [5]. The final scale they produced has five subscales: bfeelings of fatigue,Q bfeelings of vigor,Q bimpact on concentration,Q bimpact on energyQ and bimpact on daily activitiesQ. These provide an interesting counterpoint to the description of an adjectival checklist (FACES), which set out to distinguish between fatigue and sleepiness and came to a set of five subscales: fatigue, anergy, consciousness, energized and sleepiness [16]. In this issue, our group provides the first two complete scales that are used specifically to measure alertness [17]. We anticipate a rapid increase in the understanding of the relationship between fatigue and alertness, and between sleepiness and alertness, by using some of these scales in specific populations and with specific treatment interventions. The combination of improved measurement skills and scales, together with a heuristic approach to the pathogenesis of fatigue, in general, and of chronic fatigue, in particular, is likely to advance our understanding of this field and to lead to effective treatment interventions. Colin M. Shapiro Department of Psychiatry and Opthalmology University of Toronto and Toronto Western Hospital UHN, Toronto, ON, Canada Tel.: +1 416 603 5699 Fax: +1 416 603 5036 E-mail address:
[email protected]
References [1] Siegel SD, Antoni MH, Fletcher MA, Maher K, Segota MC, Klimas N. Impaired natural immunity, cognitive dysfunction, and physical symptoms in patients with chronic fatigue syndrome: preliminary evidence for a subgroup? J Psychosom Res 2006;60:559 – 66. [2] Van Houdenhove B, Bruyninckx K, Luyten P. In search of a new balance. Can high daction-pronenessT in patients with chronic fatigue syndrome be changed by a multidisciplinary group treatment? J Psychosom Res 2006;60:623 – 5.
[3] Shapiro CM. Chronic fatigue—chronically confusing but growing information. J Psychosom Res 2004;56:153 – 5. [4] Shapiro CM, Moller HJ. Chronic fatigue: listen and measure. J Psychosom Res 2002;52:427 – 36. [5] Paddison JS, Booth RJ, Hill AG, Cameron LD. Comprehensive assessment of peri-operative fatigue: development of the identity– consequence fatigue scale. J Psychosom Res 2006;60:615 – 22. [6] Bailes S, Libman E, Baltzan M, Amsel R, Schondorf R, Fichten, CS. Brief and distinct empirical sleepiness and fatigue scales. J Psychosom Res 2006;60:605 – 13. [7] Shen J, Barbera J, Shapiro CM. Distinguishing sleepiness and fatigue: focus on definition and measurement. Sleep Med Rev 2006; 10:63 – 76. [8] Shen J, Botly LC, Chung SA, Gibbs AL, Sabanadzovic S, Shapiro CM. Fatigue and shift work. J Sleep Res 2006;15:1 – 5. [9] Hossain JL, Ahmad P, Reinish LW, Kayumov L, Hossain NK, Shapiro CM. Subjective fatigue and subjective sleepiness: two independent consequences of sleep disorders? J Sleep Res 2005;14:245 – 53. [10] Brown RF, Schutte NS. Direct and indirect relationships between emotional intelligence and subjective fatigue in university students. J Psychosom Res 2006;60:585 – 93. [11] Natelson BH, Haghigi MH, Ponzio NM. Evidence for the presence of immune dysfunction in chronic fatigue syndrome. Clin Diagn Lab Immunol 2002;9:747 – 52. [12] Maher K, Klimas NG, Fletcher MA. Immunology of chronic fatigue syndrome. In: Jason LA, Fennell PA, Taylor RR, editors. Handbook of chronic fatigue syndrome. Australia7 John Wiley and Sons, 2003. p. 1 – 38. [13] Fletcher MA, Maher K, Klimas NG. Natural killer cell function in chronic fatigue syndrome. Clin Appl Immunol Rev 2002;2:129 – 39. [14] Whiteside TL, Friberg D. Natural killer cells and natural killer cell activity in chronic fatigue syndrome. Am J Med 1998;105(3A); 27S – 34S. [15] Levine PH, Whiteside TL, Friberg D, Bryant J, Colclough G, Herberman RB. Dysfunction of natural killer activity in a family with chronic fatigue syndrome. Clin Immunol Immunopathol 1998;88:96 – 104. [16] Shapiro CM, Flanigan M, Fleming JA, Morehouse R, Moscovitch A, Plamondon J, Reinish L, Devins GM. Development of an adjective checklist to measure five FACES of fatigue and sleepiness. Data from a national survey of insomniacs. J Psychosom Res 2002;52:467 – 73. [17] Shapiro CM, Auch C, Reimer M, Kayumov L, Heslegrave R, Huterer N, Driver H, Devins GM. A new approach to the construct of alertness. J Psychosom Res 2006;60:595 – 603.