Despite the many unknowns in relation to CFS, there is significant room for improvement in provision of the diagnosis and supportive care. There is clear evidence for a genetic contribution to CFS from family and twin studies, suggesting that a large scale genome-wide association study is warranted. Further functional neuroimaging studies are needed. A growing body of evidence suggests CFS arises from functional (non-structural) changes in the brain, but of uncertain character and location. These studies have largely resolved what the condition is not: ongoing infection, immunological disorder, endocrine disorder, primary sleep disorder, or simply attributable to a psychiatric condition. To receive a chronic fatigue syndrome diagnosis, you must be experiencing chronic fatigue lasting at least six months that is not improved by rest or sleep. There have been numerous small case-control studies seeking to identify the biological basis of the condition. Studies of the underlying pathophysiology clearly implicate a range of different acute infections as a trigger for onset in a significant minority of cases, but no other medical or psychological factor has been reproducibly implicated. Although several different diagnostic criteria are proposed, for clinical purposes only three elements are required: recognition of the typical fatigue history and physical examination to exclude other medical or psychiatric conditions which may explain the symptoms and a restricted set of laboratory investigations. The core symptom of fatigue affects both physical and cognitive activities, and features a prolonged post-activity exacerbation triggered by tasks previously achieved without difficulty.
There is no diagnostic test, validated biomarker, clear pathophysiology or curative treatment. Chronic fatigue syndrome (CFS) is a prevalent condition affecting about one in 100 patients attending primary care.