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Ataxia is movement without coordination or the loss of full control of bodily movements. In most conditions, it is because parts of the nervous system that control movement and balance are affected. Few theories exist on the cause of ataxia in ME/CFS. A 2000 study by Chaudhuri, et al, suggested that either cellular ion channel subunits that produce electrical signals across cell membranes or the proteins that regulate them are abnormal, possibly due to toxin exposure.[1]

Notable studies[edit | edit source]

  • 2000, The symptoms of chronic fatigue syndrome are related to abnormal ion channel function

    "Abstract: The pathogenesis of chronic fatigue syndrome (CFS) is unknown but one of the most characteristic features of the illness is fluctuation in symptoms which can be induced by physical and/or mental stress. Other conditions in which fluctuating fatigue occurs are caused by abnormal ion channels in the cell membrane. These include genetically determined channelopathies, e.g. hypokalemic periodic paralysis, episodic ataxia type 2 and acquired conditions such as neuromyotonia, myasthenic syndromes, multiple sclerosis and inflammatory demyelinating polyneuropathies.Our hypothesis is that abnormal ion channel function underlies the symptoms of CFS and this is supported also by the finding of abnormal cardiac-thallium201 SPECT scans in CFS, similar to that found in syndrome X, another disorder of ion channels. CFS and syndrome X can have identical clinical symptoms. CFS may begin after exposure to specific toxins which are known to produce abnormal sodium ion channels. Finally, in CFS, increased resting energy expenditure (REE) occurs, a state influenced by transmembrane ion transport. The hypothesis that ion channels are abnormal in CFS may help to explain the fluctuating fatigue and other symptoms."[1]

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References[edit | edit source]

  1. 1.0 1.1 Chaudhuri, A; Watson, WS; Pearn, J; Behan, PO (2000), "The symptoms of chronic fatigue syndrome are related to abnormal ion channel function", Medical Hypotheses, 54 (1): 59-63, doi:10.1054/mehy.1998.0822, PMID 10790725