A study of the earliest recorded outbreak of epidemic M.E. in the UK appeared in the Thesis of Dr. Andrew Wallis, a Scottish physician, in 1957. It discusses an epidemic in Cumberland in Northern England in 1955. His definition of the chronic disease included the following features:
Acheson's 1959 paper was based on research at the Royal Free Hospital into the 1955 outbreak there. An excerpt is reproduced below. It was a medical paper, and hence contains much technical terminology that I have tried to translate in parentheses [...].
After an acute or subacute onset with headache, symptoms of gastro-intestinal or upper respiratory upset, muscular pains and low or absent fever, an unusual type of paresis [slight or partial paralysis] develops which is rarely associated with the classic signs of lower motor neurone or pyramidal tract involvement [the pyramidal tracts are four columns of motor fibers of which two run on each side of the spinal cord].
This is often accompanied by paraesthesiae [a sensation of pricking, tingling, or creeping on the skin], sometimes by sensory loss, and occasionally by painful muscular spasms, myoclonus [irregular involuntary contraction of a muscle] or other types of involuntary movement. As the paresis recovers a curious jerky muscular contraction on volition has been noted in some instances. Involvement of the cranial nerves and the bladder may occur [the cranial nerves are the 12 paired nerves that arise from the lower surface of the brain with one of each pair on each side and pass through openings in the skull to the periphery of the body].
Recovery has usually been completed within three months. In a proportion of cases, a well defined state of chronic ill health has developed, characterised by fluctuating myalgia and paresis, partial remission and exacerbation, and depression with emotional lability [instability] and lack of concentration.
some who have continued to research ME have preferred the name Myalgic
Encephalopathy, since the -myelitis ending of the original name implies
inflammation of myelin tissue by an infective agent, and it is not clear
that this accurately represents the disease process in chronic or endemic
cases. On the other hand, Encephalopathy can be demonstrated
by autopsy, SPECT, QEEG, and PET scans and sometimes MRI.
Onset may be sudden and without apparent cause, for example a sudden attack of acute vertigo. There is usually a history of infection of the upper respiratory tract or, occasionally, the gastrointestinal tract. All cases have low grade pyrexia (up to 38 deg C) usually subsiding within a week.
Subsequently there is persistent and profound fatigue, accompanied by a medley of symptoms such as headache, giddiness and a number of muscle symptoms such as pain, cramp, twitching, tenderness and weakness (especially after excercise). Other symptoms include paraesthesia, frequency of micturition [urination], blurred vision and/or diplopia, hyperacusis (sometimes alternating with deafness or normal hearing), tinnitus, fainting attacks which may be the result of hypoglycaemia and a general sense of "feeling awful".
Once the syndrome is fully established there are three groups of symptoms:
Other Common Features