Understanding Chronic Fatigue Syndromeby Shefali Sabharanjak, PhD | October 26, 2012
Chronic fatigue syndrome (CFS) has baffled scientists and doctors alike, for quite some time now. The syndrome had to be diagnosed by elimination of other neurological and psychological maladies rather than be recognized by its own unique symptoms. Typically, patients report feelings of listlessness (anergy), depression, joint and muscle pain and headaches. Another remarkable symptom of this syndrome is the development of severe exhaustion, post-exercise. It is easy enough to see that these symptoms overlap with several other known malaises. CFS affects 0.2-1% of the population in the US. Women are more susceptible to CFS but patients from all age groups have been reported as well.
Viral infections were thought to be the root cause of CFS, typically infection with the XMRV (Xenotropic Murine Related Retrovirus). However, this theory has been discarded owing to conclusive evidence that patient samples in this study were found to be contaminated. Also, absence of the virus in body fluids of patients with confirmed CFS has been reported.
Recent research actually indicates that CFS is a complex syndrome of the nervous as well as immune systems. Blood supply to the brain was found to be reduced in CFS patients when compared to that seen in normal people. Exposure to cadmium is a possible factor that may cause reduced blood flow to the brain seen in CFS patients. There are structural changes in the brain as well. CFS patients show reduced grey matter as well as white matter in occipital lobes. These structural deficits may result in abnormal visual processing as well as reduced eye-limb coordination.
Researchers from the Queen Elizabeth Hospital, Adelaide, have reported changes in the structure of the brain stem in CFS patients. Grey matter (cell bodies of neurons) is reduced in the brainstem of CFS patients and altered regulation of blood supply to various parts of the brain is also observed. Alterations in the functions of astrocytes are thought to cause these changes. Astrocytes are star-shaped cells in the brain which provide nutrients to neurons and also have a role to play in tissue repair following brain trauma. The study indicates defects in astrocytes as well as trauma to the brain stem can contribute to structural abnormalities in the brain that lead to the development of CFS.
Another model for understanding this complex disease suggests that a combination of immune factors such as increased levels of pro-inflammatory cytokines and changes in brain pathology may by jointly responsible for the development of CFS. This model can therefore accommodate the fact that CFS has been known to set in after patients have experienced a bout of infection from various known pathogens (apart from XMRV). This model suggests that infections could trigger a pro-inflammatory response as well as deplete antioxidants from the body. These changes may contribute to development of CFS.
Therapeutic approaches to CFS are limited. Supplementation with magnesium and zinc has been suggested if cadmium is detected in patients with CFS. Current therapies focus on providing relief from specific symptoms. Scientific evidence, however, indicates that an efficient therapeutic strategy can emerge only after the neuronal correlates of this disease are understood.
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Morris G, & Maes M (2012). A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Metabolic brain disease PMID: 22718491
Pacini S, Fiore MG, Magherini S, Morucci G, Branca JJ, Gulisano M, & Ruggiero M (2012). Could cadmium be responsible for some of the neurological signs and symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Medical hypotheses, 79 (3), 403-7 PMID: 22795611
Puri BK, Jakeman PM, Agour M, Gunatilake KD, Fernando KA, Gurusinghe AI, Treasaden IH, Waldman AD, & Gishen P (2012). Regional grey and white matter volumetric changes in myalgic encephalomyelitis (chronic fatigue syndrome): a voxel-based morphometry 3 T MRI study. The British journal of radiology, 85 (1015) PMID: 22128128
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