John Richardson

John Richardson, MB, BS, (1915-2002) was a British family practice physician who spent many years caring for and researching ME patients. He was a founding Member of the Newcastle Research Group, a member of the Melvin Ramsay Society, and the Environmental Medicine Association. He served as the Chairman of the 1989 Cambridge Symposium on the Clinical and Scientific Basis of Myalgic Encephalomyelitis. and the book that followed, The Clinical and Scientific Basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, edited by Byron Hyde, was dedicated to Dr. Richardson.

In 2001, Dr Richardson wrote a book describing the relationship between exposure to enteroviruses or toxins such as organophosphates and onset of myalgic encephalomyelitis and other organ pathologies.

Richardson's research was involved in demonstrating an association between ME, enterovirus infection, and hypothalamic dysfunction, brainstem hypoperfusion , and brain pathology at autopsy.

Just prior to his death in 2002, he produced a document containing guidelines for physicians on diagnosing and treating ME patients.

Notable studies

 * 2002, Toxins and Immunity in Chronic Fatigue Syndrome"'Abstract - In this paper, Dr. Richardson illustrates links between exposure, absorption and effects of viruses, bacteria, and inorganic toxins, and their toll on the immune system, as potential causes of chronic symptomatology as seen in chronic fatigue syndrome.'"
 * 2002, Myalgic Enchephalomyelitis: Guidelines for Doctors
 * 2001, Viral Isolation from Brain in Myalgic Encephalomyelitis - Case Report
 * 2000, Four Cases of Pesticide Poisoning, Presenting as “ME,” Treated with a Choline and Ascorbic Acid Mixture"'Abstract - Objectives: 1. To demonstrate in four patients, in whom the correct diagnosis of pesticide poisoning had been missed, the injustices inflicted on them when they are told ME does not exist. 2. To show how closely the features of such poisoning, especially by organochlo-rines, resemble those of the much more classic ME which is usually due, at least in the author's practice in the northern region of the UK, to persistent enteroviral infection. 3. To draw attention to a new and apparently successful form of treatment with an oral mixture of choline and ascorbic acid. 4. To suggest reasons why this treatment merits further scientific investigation. Setting: A charity based private practice involved in the investigation of viral mediated disease. Subjects: Four patients, two male and two female, each referred with a diagnosis of ME. Intervention: a. Samples of blood were sent to Biolab Medical Unit where a variety of pesticide residues, including the very persistent organochlorines, were identified and progress in detoxification was monitored, b. All four cases were treated orally with a choline and ascorbic acid mixture. Results: After a variable number of months, during the early phase of which the blood levels of some of the toxins rose, possibly due to mobilization from fatty stores, all symptoms cleared as blood levels fell. Key Messages: The term ME comprises a number of clinical features, characterizing a patient who is ill. To refuse to recognize their existence does the patient much injustice. Some cases of ME may be found to have pesticide poisoning. The possibility of it should always be borne in mind. The source may be either in the UK or abroad. A positive enquiry and a single blood test will provide a diagnosis. Organochlorines may persist in the body for many years, as may the symptoms derived from them. A detoxification program based on oral administration of a choline and ascorbic acid mixture has shown much promise and deserves verification of its value. Conclusions: Amongst the group of clinical features known as ME, the possibility of pesticide poisoning should always be borne in mind. Treatment with choline and ascorbic acid mixture is worth trying, pending its more formal investigation.'"
 * 1998, Relationship Between SPECT Scans and Buspirone Tests in Patients with ME/CFS'' Abstract - "The purpose of this exercise was to study the relationship between the detail shown on the SPECT brain scans with those seen in the buspirone tests. Thirty-nine patients are included in this study. These patients were selected from a large number who had been referred to Dr. Richardson from various parts of the country by their doctors because of a tentative diagnosis of ME/CFS. All the selected patients were confirmed by Dr. Richardson as suffering from ME/CFS taking into account the subjective scoring methods, clinical examination, virology and buspirone tests. This study is an attempt to link together the results of the previously described techniques to investigate possible areas of impaired cellular function in brain which may have purely neuroneura! effects or possibly neurohormonal effects. 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/CFS patients. The completion of this buspirone test and SPECT scan can be deemed to be basic complementary evidence for the positive diagnosis of ME/CFS."


 * 1995, Disturbance of Hypothalamic Function and Evidence for Persistent Enteroviral Infection in Patients with Chronic Fatigue Syndrome"'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 (Bakheir, 1992). 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 CFS/ME and evidence of persistent enteroviral infection, as shown by the repealed detection of the group specific protein of enteroviruses, VPI, 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 CFS/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 signiftcantly 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 CFS/ME. It represents a quantifiable biochemical alteration to be found in this group of patients.'"

Book

 * Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies

Obituary

 * 2003, In Memoriam - John Richardson, Physician, 6th February 1915–18th July 2002
 * 2002, Obituary in the BMJ

Learn more

 * 2014, "ME/CFS - Dr. John Richardson and the Enterovirus Connection" by [[Erica Verrillo] at Onward Through the Fog]