Gene Expression in Chronic Fatigue Syndrome

Chronic Fatigue Syndrome (CFS) is a disorder of unknown origin likely affecting multiple physiological processes. CFS is often a diagnosis of exclusion following a history of 6 months or more where patients may experience partial to full recovery, relapse or a worsening in symptoms and hence deterioration in health (Brkic et al., 2011). The clinical manifestations include moderate to severe fatigue, muscle pain, swollen lymph nodes, headaches, impaired sleep and cognition (Fukuda et al., 1994). A diagnosis of CFS is made using questionnaires which include Centre for Disease Prevention and control criteria for CFS, the Australian, British and Canadian CFS classifications and the recently developed World Health Organisation’s International Classification of Diseases for CFS (Carruthers et al., 2011, Carruthers et al., 2003; Fukuda et al., 1994; Lloyd et al., 1990; Sharpe et al., 1991). CFS is a heterogeneous and multifactorial disorder. Mechanisms to explain the underlying factors and processes that are responsible for disease progression and symptom profile of this disorder remains to be established. However, research has demonstrated that CFS impacts the endocrine, neurological, immune and metabolic processes resulting in impaired physiological homeostasis (Brenu et al., 2010; Demitrack, 1997; Schwartz et al., 1994). While these processes are likely compromised and collectively contribute to ill health in CFS patients, CFS remains a disorder lacking a clear molecular or biochemical cause.