Abstract
The research for this thesis has been conducted in three consecutive studies: Fatigue in Teenagers-I (FIT-I) in 2002, FIT-II in 2004 and FIT-III in 2006. In each FIT-study different research questions were formulated on the basis of the biopsychosocial model. The three FIT-studies resulted in the chapters of this thesis.
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These chapters appear in the chronological order of the FIT-studies. FIT-I and FIT-II both have a cross-sectional study design in which adolescents with CFS are compared with healthy adolescents. FIT-III is a follow-up of the patients who participated in FIT-I and FIT-II. Chapter 2 focuses on a constitutional biological factor, which may partly explain the symptoms of fatigue and pain in the CFS. The main question is whether constitu-tional laxity of the connective tissues is more frequently present in adolescents with CFS than in healthy controls.
Chapter 3 investigates health beliefs, one of the psychological factors that determine health behaviour both in the adolescents and in their parents. Although health behaviour is often the focus of treatment, very little is known about the beliefs in families with an adolescent with CFS, neither as a predisposing nor as a maintaining factor.
Chapter 4 reports the findings of research in the relation between fatigue and other somatic symptoms, both in adolescents with CFS and healthy adolescents. Chapter 5 is the first article of the FIT-II study. In this chapter the association of symp-toms in children and in their parents is explored within the biopsychosocial model, with possible genetic contributions on the one hand, and possible psychosocial contributions on the other hand. The second goal of the study was to establish the relation between fatigue and psychological distress in the adolescents with CFS. Chapter 6 explores a set of symptoms in the CFS adolescents, namely neurocognitive symptoms, which are frequently present without a clear substrate. We applied a neuro-cognitive measurement tool for interference control. The tool measures the ability to protect a response from interruption by competing responses or events. The goal of the study was to investigate whether adolescents with CFS show a lesser degree of interference control than healthy adolescents. The second goal was to explore the importance of familial factors by examining the interference control in the parents of both groups.
Chapter 7 is another reflection on a possible neurobiological basis for CFS. Sensory gating is the ability to be protected from the load of sensory information by filtering sensory stimuli, and is a critical function of all sensory systems. We hypothesized that adolescents with CFS and possibly one of their parents would show deficient sensory gating. A deficient sensory gating might be one of the biological factors predisposing or maintaining CFS-like symptoms.
Chapter 8 is based on the hypothesis that children's early object relations may possibly have an etiologic relationship to CFS. It may be one of the psychological factors involved. Alexithymia, defined as an inability to recognize and describe emotions, has its origin in an insecure and disorganized development of attachment in childhood. It is hypothesized that adolescents with CFS exhibit more alexithymia than healthy adolescents. The second hypothesis is that alexithymia unfavourably affects the outcome of CFS. To answer this last question we used the data of the FIT-III study.
Chapter 9, finally, is the general discussion in which the findings from the three FIT-studies are discussed within the biopsychosocial model.
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