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Chronic Fatigue syndrome / Myalgic Encephalomyelitis

Background

Chronic Fatigue syndrome / Myalgic Encephalomyelitis: CFS/ME; Myalgic Encephalomyelitis or Encephalopathy; ME; Epidemic Neuromyasthenia; Post Viral Fatigue syndrome; PVFS; Chronic Fatigue and Immune Dysfunction syndrome - CFIDS (in USA and Canada)

Myalgic Encephalomyelitis appears on the World Health Organisation's International Classification of diseases list (G93.3, ICD-10) as a neurological disease.

Myalgic Encephalomyelitis is a distinctive clinical syndrome first reported in patients after outbreaks of viral infections in 1950s and was characterised by persistent fatigue, muscle pain (myalgia), symptoms suggestive of brain and spinal cord dysfunction (encephalomyelitis) and conspicuous deterioration of symptoms after physical exertion. Only limited neuropathological studies have been possible in ME. There is no significant abnormality in muscles and peripheral nerves, but there are abnormal inclusion bodies in brain (corpora amylacea) and inflammatory changes in the dorsal root ganglion of spinal nerve root. Post-viral fatigue syndrome was used to describe a similar syndrome where patients could clearly trace the onset of their illness back to a viral infection. However, ME-type symptoms are also known to follow other infections (for example, Lyme disease and Q fever), post-infective neurologic diseases (such as Guillain-Barré syndrome) immunisation or exposure to neurotoxins (for example, ciguatera fish poisoning). The quality of fatigue in ME is disabling and comparable to fatigue in Multiple Sclerosis. The term chronic fatigue syndrome was introduced in 1988 by the Centers for disease Control (Atlanta, USA) to describe medically unexplained, persistent or relapsing fatigue of new onset. ME/PVFS was subsumed within this new designation. CFS is a broad diagnostic category and patients with psychiatric causes of chronic fatigue may be offered a diagnosis of CFS. The term chronic fatigue and immune dysfunction syndrome is still preferred in the USA and Canada because research studies in the 1980s showed subtle immunological changes in elevation of cytotoxic T cells, pro-inflammatory cytokines and low natural killer cell activity. In the absence of better pathologic data, CFS/ME is likely to be used as the most preferred clinical descriptor. Recent research on DNA microarray and gene profiling of patients with CFS/ME suggest changes due to increased oxidative stress, accelerated apoptosis (programmed cell death) and altered immune regulation.

The prevalence of CFS/ME is estimated to be at least 2 in 1,000 adult population (that is around one hundred and fifty thousand people in UK). All age groups are affected although onset is rare below the age of seven and above the age of sixty years. The most common age of onset is between mid-teens and mid-forties, in previously fit and often, physically active individuals. ME is more prevalent in females than males (similar to multiple sclerosis) and may be one of the common medical reasons of long time school absenteeism in children.

What are the symptoms? View What are the symptoms?

Medical text written October 2001 by Dr A Chaudhuri. Last reviewed December 2007 by Dr A Chaudhuri, Consultant Neurologist, Essex Centre for Neurosciences, Queen’s Hospital, Romford, UK. 

 

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