The Hummingbirds' Foundation for M.E.

The Hummingbirds' Foundation for M.E. (HFME) is fighting for the recognition of M.E.,
and for patients to be accorded the same basic human rights as those with similar
disabling and potentially fatal neurological diseases such as M.S.

Articles sorted by author: Dr Richardson

Highly recommended authors: Dr Byron Hyde and Dr. Elizabeth Dowsett. Click here to read the full list of recommended authors.

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Read Putting research and articles into context and A warning on CFS and ME/CFS research and advocacy

The late Dr Richardson had over 50 years experience in treating M.E. and studying M.E. and was still seeing patients with ME two weeks before his death in July at the age of 87.

As The Committee for Justice and Recognition of M.E.  explain: 'No physician has had more experience with ME patients than Dr John Richardson, developing invaluable expertise and insight from his five decades of examining and treating patients and conducting research.'

Dr Richardson also served as a mentor to the preeminent M.E. expert Dr Byron Hyde

Articles by Dr John Richardson

Myalgic Encephalomyelitis: Guidelines for Doctors (PDF) Journal: J of Chronic Fatigue Syndrome, Vol. 10(1) 2002, John Richardson, MB BS

Click here for a version in Microsoft Word

'As with poliomyelitis, the symptoms in M.E. are somewhat diffused but do involve the nervous system. We should consider the terms applied to the effects of infection in the nervous system due to the poliovirus, which is the enterovirus. The term ANTERIOR POLIOMYELITIS referred to cases where the ANTERIOR horns of the spinal cord were chiefly affected. These neurons subserve EFFERENT outgoing neurological impulses. Hence the effects were on the "motor" system with some paralysis. The term POSTERIOR POLIOMYELITIS was also used to define lesions in the POSTERIOR horns of the spinal cord.

These neurons subserve AFFERENT neurological impulses. The enteroviral groups to which we refer in these guidelines have been shown to have a propensity for, and cause the pathology in these AFFERENT impulse conducting neurons. Hence, the results are more noticeable to the patient than the doctor, which is not so with poliomyelitis. These pathological results may not be confined to the nervous system but may result in neurohormonal or other differing end organ effects.

In CNS cases seen over 4-5 decades by one of us (Dr. John Richardson, MB BS) the computerized records, when analyzed, reveal that the male cases with M.E. numbered 224 and females 469. From these figures it can be shown, that besides the female preponderance, the total number of varying CNS syndromes are greater for females as can be seen in the table.'

Richardson, J. n.d., ‘M.E., The Epidemiological and Clinical Observations of a Rural Practitioner,The Clinical and Scientific Basis of Myalgic Encephalomyelitis / CFS, Hyde, Byron M.D. (ed) The Nightingale Foundation, Ottawa, pp. 85-94.

For information on this book, and for purchasing details, see the Review of this textbook. See the following book also:

Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies by John Richardson

From Neurology to Mitochondia Richardson J, Costa DC. J CFS 1998, 4(3)

Initial considerations suggested that in the SPECT scans, the fields of hypoperfusion which were shown to be significant demonstrated localised areas with diminished metabolic requirements. This could be related to diminished cell function which occurred as a result of mitochondrial dysfunction, possibly due to viral infection. This has been well demonstrated by Behan and coworkers.

It should be noted that mitochondria, as the name implies, are the "nuclear power house" of the cell, from "mitosis" to "apoptosis." During cell life, this mitochondrial "power" results in the generation of energy in the form of ion gradients and ATP synthesis. Mitochondria mediate energy generation through the oxidation of food material which has passed through the blood-brain-barrier (BBB). To this end, mitochondria also contain the enzymes for the Krebs and other fatty acid cycles, and thus govern the respiratory cell pathway of oxygen. Therefore, mitochondrial dysfunction results in a decrease in cell respiration. For instance, abnormal carnitine metabolism in ME/CFS patients is one of the energy metabolic dysfunctions in mitochondria. Carnitine itself is an amino acid used for the transport of fatty acids across the cell membrane to the matrix, a process which is catalysed by the co-enzyme carnitine palmitoxyl transferase. The resulting decrease in oxidation is no doubt the reason for the lack of perfusion requirements demonstrated in the SPECT scans.

Mitochondria contain DNA and RNA by means of which they replicate. This relates to the development of cells with the formation of deutoplasm and a large increase in protoplasm and mitochondria, which leads to the formation and future function of specialised cells. Other physiological aspects that may underlie the SPECT abnormalities seen in ME/CFS should be considered, such as the anatomical divisions of the brain with enormous variations in function. The latter variations are seen in both the neuroneural and neurohormonal control of the whole body. Consideration should be given to the BBB, as this possibly has some effect on the means of access to the higher centres of viruses or toxins as well as normal nourishment, with the areas above the BBB being possibly more protected than those beneath. However, viruses and other material, e.g., toxins and certain drugs which are fat soluble, may pass this BBB.

(This article is taken/available from the TCJRME website)

Relationship Between SPECT Scans and Buspirone Tests in Patients with ME John Richardson, MB, BS,  Durval Campos Costa, MD, MSc, PhD Journal of Chronic Fatigue Syndrome, Vol. 4(3) 1998 

'All patients within this study displayed hypoperfusion in some brain area as shown by their SPECT scans (see Appendix, Table 1.1). *Thirty-five (90%) showed hypoperfusion in the regions comprising: *Twenty-four (62%) in the Brain Stem *Twenty (51%) in the Caudate Nuclei *Nine (23%) showed hypoperfusion in both Brain Stem and Caudate Nuclei regions *Thirty (77%) cases demonstrated hypoperfusion in the regions comprising:  *Twenty-four (62%) in the Temporal Lobes *Twelve (31%) in the Parietal Lobes *Nine (23%) in the Frontal Lobes

The significance of these results is to confirm that there is actual evidence of neurological dysfunction which results in the continuing morbidity in these ME patients.'

Full article with Tables and Figures available by ordering from Haworth Press 

Disturbance of hypothalamic function and evidence for persistent enteroviral infection in patients with chronic fatigue syndrome. Richardson J. Journal of Chronic Fatigue Syndrome 1995; 1(2): 59-66.

Abstract: It has been suggested that one of the major effects of persistent virus infections in the production of disorders such as the chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is on the hypothalamus (1). Buspirone, which is one of the anxiolytic drugs of the azapyrone group, causes a release of prolactin by stimulation of serotonin 5-hydroxytryptamine (5-HT) receptors. The buspirone-prolactin response was studied in a subgroup of patients with ME and evidence of persistent enteroviral infection, as shown by the repeated detection of the group-specific protein of enteroviruses, VP1, in the blood. Family controls who were asymptomatic were studied at the same time. In addition to the response to buspirone, diurnal variations in cortisol and prolactin levels were studied. It was found that the patients with ME had much greater rises in prolactin levels one hour after buspirone compared to controls. Cortisol levels were elevated in the patients, but the rise was not significantly different between the two groups. There was a significant association between the pattern of sleep disturbance, which we speak of as the OWL syndrome, and the ratio of pre- and post-buspirone prolactin levels. This study shows that there is a hypothalamic disturbance in the patients who also had evidence of enteroviral infection as part of the disorder of ME. It represents a quantifiable biochemical alteration to be found in this group of patients.

Full article with Tables and Figures available by ordering from Haworth Press 

Viral Isolation from Brain in Myalgic Encephalomyelitis  (A Case Report) J. Richardson

J. Richardson is affiliated with Newcastle Research Group, Belle Vue, Grange Road, Ryton, Tyne & Wear, NE40 3LU, England. Journal of Chronic Fatigue Syndrome, Vol. 9(3/4) 2001, pp. 15-19 

Full article with Tables and Figures available by ordering from Haworth Press 

BMJ 2002;325:716 ( 28 September ) Obituaries: John Richardson, General practitioner whose records on coxsackie infection won him worldwide fame

'The international reputation that John Richardson acquired in the field of myalgic encephalitis (ME) research sprang from the records that he kept for 40 years of enteroviral infections, mostly coxsackie virus. He realised that enteroviral infections were endemic among his practice population on the south bank of the Tyne, spreading from one family to another and from one generation to the next.'

In Memoriam: John Richardson, Physician, 6th February 1915-18th July 2002 Contributors: Byron M. Hyde, Nightingale Research Foundation, Ottawa, Canada