What is M.E. or Myalgic Encephalomyelitis

The Nightingale Research Foundation
Byron M. Hyde, M.D.

M.E. can be either epidemic or sporadic, but always is characterized by its acute
onset. M.E. was first called Benign Epidemic Myalgic Encephalomyelitis, benign simply
because the epidemics were only infrequently associated with patient death. However,
deaths did occur.

Deaths were documented in the 1934 Las Angeles, the 1947 Iceland epidemics and the 1955 Cumberland epidemics. Over 60 M.E. epidemics have been described. Benign was soon dropped due to the severe and chronic disability associated with this illness.
One important clue as to the CNS injury occurred in the Iceland epidemics circa 1947
when three children fell ill and died of Parkinson-like illness. The three children were all
younger than 10 years of age, strongly suggesting that M.E. in the Iceland Akureyri
epidemic was associated with an injury of the CNS in the basal ganglia area of the brain.

<...>


It has been shown that the normal accelerated antibody response to viral or
immunological invasion is blocked in M.E. with the significantly decrease in number and
activity of NKC (Natural Killer Cells), the primary response to infection. This failure of
the NKC system allows the viral or immunological pathogen to persist for a sufficiently
long time that this infectious pathogen is recognized as self, not susceptible to the normal
human antibody response.

This blocking of the normal immune or inflammatory
response, allows the pathogen to cause long standing disease of multiple organs,
particularly the CNS (Central Nervous System = brain+ spinal cord), muscle, vascular
systems of the body and to a lesser extent various other organs and systems.
Not until the 1984 North American epidemics, that continued on up until 1989 in large
numbers, usually peaking during the August to Christmas periods was there physiological
brain imaging in place to ascertain brain injury.

It was shown that a significant majority of these epidemic, cluster and sporadic patients had persistent pathophysiological hypoperfusion brain changes that could be measured by brain SPECT and brain PET. D

The Injury to the CNS is not a theory: In M.E. the irregular diffuse attack upon the
CNS (central nervous system) can be measured by various techniques first noted by Drs.
Jay Goldstein and Ismael Mena in California in 1998. They pathological findings include abnormal persisting changes in:

(a) Brain SPECT (Single Photon Emission Computed Tomography)
(b) Quantitative EEG (QEEG Scan or BEAM Scan in the USA) or
(c) Brain PET (Positron emission tomograph) and even the inexpensive
(d) Transcranial Doppler as developed at Harbor View Hospital in Seattle.
(e) Neuropsychological Testing