The pathophysiology of cancer-related fatigue: current controversies

• Published in: Supportive care in cancer Vol. 26; no. 10; pp. 3353 - 3364
• Main Authors: O’Higgins, C. M., Brady, B., O’Connor, B., Walsh, Declan, Reilly, R. B.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-10-2018; Springer; Springer Nature B.V
• Subjects: Adrenal glands; ATP (Adenosine triphosphate); Cancer; Circadian rhythm; Cytokines; Fatigue; Health aspects; Hypotheses; Medicine; Medicine & Public Health; Muscle proteins; Nursing; Nursing Research; Oncology; Pain Medicine; Rehabilitation Medicine; Review Article; Hypothalamic-pituitary-adrenal axis; Cancer-related fatigue; Proinflammatory cytokines; Pathophysiology; Serotonin; Neuromuscular abnormalities
• ISSN: 0941-4355; 1433-7339
• DOI: 10.1007/s00520-018-4318-7

Fatigue is one of the most common and debilitating cancer symptoms, and is associated with impaired quality of life. The exact pathophysiology of cancer-related fatigue (CRF) is poorly understood, but in any individual, it is likely multifactorial and involves inter-related cytokine, muscular, neurotransmitter, and neuroendocrine changes. Underlying CRF mechanisms proposed include central and peripheral hypotheses. Central mechanisms include hypotheses about cytokine dysregulation, hypothalamic-pituitary-adrenal-axis disruption, circadian rhythm disruption, serotonin, and vagal afferent nerve function while peripheral mechanisms include hypotheses about adenosine triphosphate and muscle contractile properties. Currently, these hypotheses are largely based on evidence from other conditions in which fatigue is characteristic. The purpose of this article is to provide a narrative review of the literature and present the current controversies in the pathophysiology of CRF, particularly in relation to central and peripheral hypotheses for CRF. An understanding of pathophysiology may facilitate direct and simple therapeutic interventions for those with cancer.