Chronic Fatigue Syndrome (CFS) is a complex, debilitating disorder, characterised by prolonged, persistent, medically unexplained fatigue lasting for at least six months and accompanied by several other unexplained physical, constitutional and neuropsychological symptoms.
At present, the underlying aetiology (cause or manner of causation) and pathophysiology of CFS is unknown, however growing evidence is suggesting that CFS is heterogeneous, meaning it will likely prove to have no single or simple aetiology.
With CFS aetiology and pathophysiology unclear or unknown, diagnostic testing is not available. As such, clinical diagnosis of CFS is made based on the following criteria.
The presentation of persistent, debilitating fatigue lasting more than six months, with other known medical or psychological conditions excluded by clinical diagnosis, as well as four or more of the following symptoms:
- substantial impairment in short-term memory and/or concentration (severe enough to reduce levels of occupational, social or personal activities)
- sore throat
- tender cervical or axillary lymph nodes
- muscle pain
- multi-joint pain without swelling or redness
- headaches of a new type, pattern or severity
- unrefreshing sleep (fatigue does not improve with rest/sleep)
- post-exertional weakness or discomfort, lasting more than 24 hours.
While many ideas have been put forward regarding the aetiology and pathophysiology of CFS, it is generally believed that CFS is a multifactorial disorder – one in which numerous factors integrate to create the symptoms or presentation. A number of these factors are explored below.
Clinically, CFS often follows an infectious episode, and thus infectious agents are a strong argument for the aetioogy of CFS. Many people report never feeling well since an infection such as influenza, mononucleosis, Lyme disease and Epstein-Barr virus.
CFS may be the result of a complex interplay between an infectious agent and/or a dysfunctional immune response in susceptible individuals.
Exposure to infectious agents along with increased susceptibility to infection, results in immune dysfunction, including elevated levels of pro-inflammatory cytokines, especially interleukins, which may explain some CFS symptoms such as fatigue and flu-like symptoms. High levels of interleukin 6 may be responsible for symptoms such as apathy, sleepiness, loss of appetite, poor focus/concentration and heightened pain sensitivity.
Many studies show that people with CFS have increased levels of immune cells and components including interleukins and cytokines. Dysfunction (number and responsiveness) of natural killer cells has been seen in people with CFS.
Research has shown evidence of a neuroendocrine pathway explaining the connection between stress hormones and CFS.
Several studies have demonstrated abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis. Many patients with CFS have been shown to exhibit hypocortisolism: reduced basal cortisol output has been found in serial samples of blood, saliva or 24-hour urinary output.
There is evidence for heightened negative feedback and glucocorticoid receptor function and for impaired adrenocorticotropic hormone (stimulates the adrenal cortex) and cortisol responses, however no evidence indicates a specific or uniform dysfunction of the HPA axis.
Disturbance of central nervous system function
Some MRI (brain structure) and SPECT (brain function) studies have shown consistent abnormalities, including abnormalities in white matter and reduced blood flow to many areas of the brain, most notably the brain stem.
Life-altering events (i.e. serious injury, stress, trauma, surgery, grief, loss and bereavement, pregnancy and labour etc.) may precede CFS. In this way, CFS mimics post-traumatic stress disorder.
Coexisting psychological distress or psychiatric disorder may also contribute to neurocognitive deficits.
Family and twin data suggests that prolonged fatigue/CFS may be familial, with possible genetic predisposition.
Differential gene expression has been documented in patients suffering from CFS, compared with healthy controls.
Being female increases risk of CFS.
A person’s vulnerability to CFS may relate to their personality. Having introverted or neurotic tendencies, characterised by avoidant behaviour and anxiety, increases the likelihood of developing CFS.
As CFS is a multifactorial disorder, the above factors must be taken into consideration when planning treatment, and treatment must also be tailored to each individual’s history and presentation of the disorder.
If you suffer from a fatigue syndrome such as CFS, have the above factors been taken into consideration within your treatment plan? If not, book an appointment with one of our naturopaths to find out how we can help enhance your treatment plan and outcomes.
Written by Perri Baldwin BHSc