It is with great sadness that we learned of the death of Dr J. Gordon Parish, aged 92, on September 13th at his home in the village of Stanley in rural Perthshire. Dr Parish was one of the group of trustees who founded ME Research UK (originally called MERGE) in 2000, becoming a valued patron thereafter. Without his intellectual and financial support, particularly in the very early days, the charity would not have survived and prospered. He was a great advocate of the need to recognize ME as a distinct clinical entity, and through the years he kept a close interest in the scientific projects funded by ME Research UK, particularly those on muscle and brain which he saw as key to understanding the biology of the disease. He also wrote the occasional article for our magazine, Breakthrough, including “Myalgic encephalomyelitis – a muscle/brain disorder”, the magazine summary of which is given below.
After his war-time medical training, Dr Parish took up posts in the North of England, and it was while working in Durham in the mid 1950s that he contracted ME, recovering thereafter but suffering recurrences of the original illness at various times over the next 60 years. Afterwards, the family moved to Canada but returned to England where Dr Parish ended his working life as a Consultant in Rehabilitation Medicine at Mary’s Hospital in Colchester. It was there that he saw many patients with an ME-like illness similar to his own, and Dr Parish became dedicated to their care and convinced of the need for scientific investigation of the disease. It was his firm belief that ME had an infectious cause, probably viral, and he devoted much of his spare time to writing scientific letters and articles, and to identifying outbreaks of the illness as they appeared in the scientific literature. By the end of the 1970s, he had identified 47 possible epidemics of ME across the world, from Los Angeles (1934) to Southampton, England (1979). Over time, he not only tabulated these epidemics (table available on the ME Research UK website) but brought together an extensive archive of the literature on each, which he made available to researchers. A summary of the information he collected appears as Chapters 1 and 16 of “The Clinical and Scientific Basis of ME/CFS” published by the Nightingale Research Foundation in 1992 (free download available).
Dr Parish was the last survivor of a handful of British medical doctors who diagnosed and treated people with ME, and who became leading advocates of the need to recognise, diagnose, investigate and treat the disease (notable others include Dr A. Melvin Ramsay, Dr John Richardson and Dr Betty Dowsett). Through their valiant efforts, extending from the 1950s to the present day, the existence of ME and its effects on the lives of patients and their families was not lost to history. As Dr Vance Spence, Chairman of ME Research UK, says: “The ME world owes an enormous debt to their quiet persistence, their professional approach and their dedication to keeping the flame alive.”
Myalgic encephalomyelitis – a muscle/brain disorderBy Dr J. Gordon Parish, Patron of ME Research UK
Epidemics of myalgic encephalomyelitis were reviewed in a classic scientific paper by Acheson in 1959, and subsequent investigations have established that between 1934–79 there were at least forty-seven outbreaks of epidemic proportions of a similar illness, all well-documented, distributed geographically, for example in North America and the UK.
Many of the findings described by Acheson are very much relevant to our understanding of ME today. The disease was initially thought to resemble poliomyelitis until distinguishing features occurred; however, no patient developed the paralysis and muscle wasting seen in poliomyelitis which is a disease of the spinal cord. In essence, he described as a systemic infectious illness, characterised by marked muscle fatigability (not just weakness); muscle pain, tenderness and swelling; and variable involvement of the central nervous system. Similarly, Henderson and Shelokov in their review in 1959, found that the affected muscles were tender either diffusely or in focal discrete areas, which felt “oedematous, doughy or rubbery in consistence.” They also mentioned the association of behavioural disturbances with brain cell disorders such as cranial nerve palsies and hemiparesis with extensor plantar response an occasional finding in some epidemics, an association clearly illustrated by Melvin Ramsay in a report of serious of sporadic cases in North West London in 1955/6.
ME Research UK has funded research which has revealed abnormalities in the function of blood vessels and blood cells. However, abnormalities of blood vessels have also been described in the papers describing the epidemics. Infectious material was transferred from patients to monkeys during an epidemic in Adelaide, Australia in 1949-1950. The only abnormalities discovered at autopsy were minute red spots along the course of the sciatic nerves, found to be localised collections of inflammatory cells which had also infiltrated the area where the nerve roots come out of the spinal cord. Again, during the North of England epidemic in 1955 Andrew Wallis described findings in a patient in her fifties, who developed the characteristic febrile illness leaving her debilitated and emotional. During the next fifteen months she continued to run a low grade fever with continued mental deterioration before she died. The post-mortem revealed numerous small haemorrhages around blood vessels in the cerebral cortex extending into the mid-brain, which were considered to be the cause of her death.
Myalgic encephalomyelitis is a muscle/brain disorder, which occurs as clusters of cases in families, in institutions such as hospitals or schools, and in specific areas, but also sporadically. It is an infectious disease with an incubation period of 5 to 8 days. Acheson in 1959 used the expression “in a greater or lesser degree” to describe “the symptoms and signs of damage to the brain and spinal cord” in this disease. This expression can also be applied to the febrile illness and muscle involvement. Many patients recover, while others have relapses with reactivation of features of the initial illness and further damage to new areas of the brain or muscles, and in extreme cases deterioration may lead to death. After activity the recovery of muscle power is prolonged to an extent not recorded in any other disease. The association between these findings in muscle and vascular abnormalities in blood vessels and blood components needs to be explored, and for research purposes patients with these physical signs should not be coupled with patients, whose main illness is chronic fatigue on exertion and who do not have these signs.