The Sydney CFS Conference '98
On Saturday 14th February 1998, the day after the Clinical and Scientific Conference ended, the Alison Hunter Memorial Foundation held an Information Day for people with CFS and their families.
My Mum and I arrived around 10:30am, and already the auditorium was three quarters full. The turn-out was so big the organisers had to turn people away! I was surprised and delighted that so many people came. The League's club did a wonderful job of hosting us - every table had a jug of iced water and some glasses, which they kept refreshed all day. Sponsors of the event, who helped to make it all possible - so I'm giving them a plug :) - were Brita water filters, Discount Vitamins Direct, Planet Ark, Yakult and (I think?) Effalax. Tim Roberts, a doctor from Newcastle University, and Christine Hunter organised the conference and welcomed us to the patient's day.
The first speaker was Dr Peter Rowe, a pediatrician from Johns Hopkins medical school in Baltimore, USA. He began with the example of a 16 year old female patient who had gradual-onset fatigue. He noticed that when she stood up, blood pooled in her calves and ankles, to the extent that her legs appeared blotchy and purplish. He conducted a 'standing test' on her, and found that when she stood, her heart rate rose sharply. They then did a Tilt Table Test, which exacerbated all of her CFS symptoms, and in particular her low blood pressure. This indicated that she had Neurally Mediated Hypotension (NMH), and they treated her with an increased salt intake, and the drug 'Florinef'. Within 2 weeks, his patient's symptoms improved - she was able to return to work, and her heart rate and blood pressure responses improved. 2 years later she is still better.
The second important finding Dr Rowe and his researchers have observed is that an allergy to cow's milk protein can make the symptoms of NMH worse. In many cases a strict no cow's milk diet helps the symptoms of low blood pressure. Dr Rowe also mentioned that children who experience bad allergies during early childhood, but then recover from them as they grow older, may find them re-activated by a virus (or other cause of CFS) during their teen years.
A third observation is that patients with hypermobility of their joints (known as Ehlers-Danloss Syndrome, or double-jointedness) are more pre-disposed to hypotension. These people are able to bend fingers backwards, hold a leg behind their neck and stand, bent over, with their legs straight and their hands flat on the floor. The theory is that the extraordinary 'stretchiness' of these people's ligaments and skin might mean they have more elastic blood vessels, and that the vessels in their legs might stretch and accomodate more blood. So when they stand up, more blood pools in their legs than usual. This condition is independent of CFS, and seems to be hereditary.
Randomised trials are currently being conducted to find the best treatment-medicine for NMH.
The second speaker was Dr David Bell, who spoke about general principles of treating children with CFS. Dr Bell feels that becoming ill during childood, and the treatment of that illness, can affect the identity of the child and the development of their personality and ability to cope into adulthood. He gave as his example the case of a woman and her son he treated during the Lindenville outbreak of CFS in America. This woman brought her sick son to Dr Bell, and her ability to describe and understand her son's symptoms led Dr Bell to ask if she had experienced them herself. She revealed that she had had similar symptoms in her youth, but had been told quite forcefully that they were all in her head and that she was just imagining them. This treatment was reinforced by a teacher who, when the woman's leg leapt due to (uncontrollable) myclonic jerks, would hit her for distracting the class. Dr Bell's patient used to put the leg of her desk on her foot to prevent her leg moving. She believed that her symptoms were imaginary to such an extent that when she experienced Grand Mal seizures later in life, seizures severe enough to cause her to bite herself and lose consciousness, she refused treatment on the grounds that "she was just imagining it". Her son's illness was very unsettling for this woman because it forced her to confront the idea that her illness was real.
Dr Bell said that the 'imaginary' line can ruin a person's self-respect, self-image and even interrupt the development of their personality during their formative years. He feels not diagnosing CFS causes a great deal of harm, and he is dismayed by a recent editorial in the Journal of the American Medical Association which discouraged the diagnosis of CFS in children. The label for this illness, inadequate as it is, is important because it allows a child to put the illness into context, and allows them to accept their limitations. He said he thinks YPWCs are courageous, and at that point I fervently wished all of my YPWC friends could be beamed into the auditorium to hear such supportive and encouraging words. If only all doctors were so understanding.
The third speaker was Professor Martin Lerner, from Michigan. His experience is with adults with CFS. He believes a critical part of the illness is the involvement of the heart. He and his researchers are working with this paradigm: "The CFS is a persisting viral infection of the heart producing primary myocardial disease." A 24-hour Electro-cardiogram (ECG) on a patient with CFS showed heart waves increased later in the day. It also showed that the 'T-waves' on the graph became flattened or inverted. These abnoraml heart waves increased with an increase in acitvity, which parallels people with CFS (PWCs) feeling worse during exercise. The T-wave abnormalities become more common as CFS progresses, and people with more severe cases of CFS have worse abnormalities.
The professor and his team studied the strength of heart muscles in his patients with CFS. They found hypokinesis, tardokinesis and biventricular dilation. 24% of their patients have these abnormalities. Also, myofibres in the heart of a healthy patient are parallel, but a biopsy of the heart muscle in CFS patients showed myofibre disarray, which is called cardiomyopathy. The researchers' suspicion is that a virus is causing this.
Professor Lerner's advice on treatment is that patients shouldn't over-exercise; they should try to do some exercise but not so much that they experience these abnormal heart waves. He believes moderate exercise and no alcohol is important. The T-wave abnormality reverses immediately after exercise is halted.
Professor Gary Scoop from Adelaide was the fourth speaker. He is a medical doctor, and a researcher in the field of exercise physiology. He has experience in monitoring exercise performance, such as the tests elite atheletes go through to measure their fitness. His findings on PWCs are that they do not become de-conditioned because of their illness, and that their 'exercise engine' is not effected. The nature of CFS means exercise makes pain and fatigue worse, and therefore compliance with training programs is poor. There is a belief among physicians that exercise for PWCS is harmful, and he believes this is true. His advice is to "maintain a low intensity, but not completely sedentary, life-style."
There are two main tests of fitness: the 'maximal oxygen uptake', which indicates how much exercise a patient can cope with, and the 'lactate/anaerobic threshhold test' which indicates how much exercise a patient can take before building up lactic acid (which causes muscle pain). Because PWCs are wary of participating in strenuous tests because of the exacerbation of symptoms they will cause, Professor Scoop conducted sub-maximal oxygen uptake tests on CFS patients. These showed that aerobic capacities were only marginally lower than for the ordinary population, which indicates that the PWCs have not become de-conditioned and possess the normal ability to exercise. The difference is that compared to normal people, PWCs fatigue earlier. In terms of cardio-respitory function, PWCs are normal, so early exhaustion is due to the illness, not a lack of fitness. Professor Scoop explained that in this case, exercise training programs won't help because PWCs are no less fit than normal people. He recommends only mild exercise, as excessive exercise might do damage, and we only need to be as fit as our lifestyle requires.
Dr Judith Ford, also from Adelaide, spoke fifth. She is a geneticist interested in the toxic effects of chemical exposure on genes. It is her theory that chemical exposure cases are a sub-group of CFS patients. She is not sure whether chemical exposure either (a) damages cells which puts them at increased risk of infection, or (b) directly injures chromosomes in cells.
Dr Ford explained, with the aid of slides, the ways in which chromosomes can be damaged. Chromosomes 'break' when damaged by chemical or radiation exposure, and form 'ring chromosomes' or 'dicentric chromosomes'. These can be found in samples from patients immediately after their exposure, but they disappear from the body fairly quickly. After that, only difficult-to-find chromosome damage remains. The remaining forms of chromosome damage are 'inversion's and 'reciprocal translocation's. One may only find 3 damaged chromosomes in 100 cells a period of time after the exposure has occurred, and consequently few labs are willing to do this tedious work. Dr Ford can arrange these tests at her labs however. The results they find can be used in legal cases.
Dr Ford also mentioned that chemical exposure can re-activate viruses, such as Epstein-Barr virus, and cited research which showed that workers in chemical industries had a higher rate of viral infection than normal.
Dr Jeorg Haier from the Instute of Molecular Medicine, California, was the sixth speaker. He discussed the similarities between Gulf War Syndrome (GWS) and CFS. His research team began by examining GWS sufferers, and noticed that the main three symptoms of GWS - fatigue, cognitive problems, and pain - were the same as for CFS. In 1993 and 1994, the US Government studied families of GWS sufferers, and found that 70% of their spouses were also sick, along with the majority of their children born after the Gulf War. The researchers surmised then that the disease must have been transmissable, ruling out the possibility that it was caused by chemical exposure or was psychological in origin. They suspected mycoplasmas, a primitive variety of bacteria which live naturally on the roof of the mouth, were the cause. Mycoplasmas normally live attached to, or inside, cells, and are very slow-growing. Consequently they are hard for both the immune system, and researchers, to find. These microorganisms have been known for some time to cause CFS - and GWS-like symptoms . The researchers developed a special DNA test - previous test were tedious and less effective - to find mycoplasmas in white blood cells. They found that 72.4% of PWCs have mycoplasmas in their blood stream, and of these, 43.0% had a strain of mycoplasma called 'mycoplasma fermentens', which is particularly aggressive.
The treatment, recommended for mycoplasma-positive patients only, is a cycle of different antibiotics. Each antibiotic (listed below) is taken for 6 weeks, followed by a 2 week break, and then another 6 week course of the next antibiotic, and so on. (Because the mycoplasmas are so slow-growing, the 2 week break does not allow them to build up to previous levels during the treatment.)
