Affiliations: Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan
Note: [] Correspondence to: Dr. Takakazu Oka, Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Tel.: +81 092 642 5317; Fax: +81 092 642 5336; E-mail: [email protected]
Abstract: This article reviews the influence of psychological stress on chronic fatigue syndrome (CFS). Studies have demonstrated that psychological stress is involved in the CFS onset, exacerbation, and/or relapse, while early life stress acts as a risk factor toward the development of CFS in later life. CFS patients may have disrupted stress systems, including HPA axis hypofunction and ANS alterations characterized by sympathetic overactivity and low vagal tone. Individuals with CFS respond to psychological stress differently from healthy subjects in that CFS patients show a blunted (or similar) activation of the HPA axis and SNS and attenuation of proinflammatory cytokine induction, whereas psychological stress increases cytokine levels in healthy subjects. It is not fully understood how such disrupted stress systems and differential stress responsiveness contribute to the pathophysiology of CFS. Further studies are necessary to determine whether laboratory stress can fully replicate typical daily stress and how stress responsiveness is related to psychological stress-induced exacerbation of CFS symptoms. This article also reviews the role of psychological stress in low-grade fever in CFS and the role of adaptive or maladaptive coping in the severity of CFS symptoms.
