The conference was in two parts - Research (2 days) and Clinical (2 days). There were about 400 delegates including many CFS patients; the daily program ran from 8 a.m. to 8 p.m. with no designated breaks - so it was difficult to meet people, and impossible to attend every talk or workshop! The following is a brief summary of interesting research.

Research Conference

The research program was summarised by Dr. Tony Komaroff:

1) Epidemiology

A telephone survey of a cross section of the San Francisco population found an incidence of 2 per 1000 who seemed to meet the 1994 criteria for CFS. With further checks to exclude other conditions (history and lab tests), the real incidence would probably be lower. It is significant that CFS in San Francisco was more common among blacks and native Americans, and in lower income groups; this refutes the typical stereotype of 'white, affluent, middle class females'! A study of the prevalence of CFS in adolescents found that it exists but is less common than in adults, and below ten years is unusual. Further studies of the true incidence in young people should be done.

Dr. Keiji Fukuda, chairman of the 1994 group that developed the latest criteria for diagnosing CFS, presented a four year study on Gulf War veterans with a CFSlike illness. This study has proven that Gulf War Syndrome exists as a real clinical disorder. They found that GWS could be defined as a multisystem illness, that overlaps with depression, post-traumatic stress disorder and CFS, and has categories of mild, moderate and severe illness.


2) Immunology

Dr. Tan presented a study looking at tests that are associated with connective tissue disorders such as rheumatoid arthritis, lupus, and Sjogren's syndrome. He found a high rate of lupus autoantibodies, about 70%. More importantly, they found particular antibodies to cell proteins (anti-nuclear envelope antibodies), not found before, that appeared to be unique to CFS, and might help to distinguish CFS from other autoimmune disorders. With further research this might be a diagnostic test - here Dr. Komaroff described what a perfect diagnostic test should show: it would have to be nearly 100% positive in CFS people, and nearly 100% negative in healthy controls! So far, no diagnostic markers fulfil this statistic.

Dr. Suhadolnik presented his discovery of a new low molecular weight '2-5A binding protein' - evidence of an enzyme system that is turned on by viral infection. This test was positive in all 10 CFS patients, and negative in all 10 controls. If this held out in hundreds of individuals, we would have a diagnostic test, which would also point to the biology of the illness (ie ongoing infection). However, other researchers have had breakthrough tests, which were not confirmed in later tests.

Dr. Nancy Klimas and colleagues in Miami have found a pattern of cytokines produced by T-cells, which potentially could be a diagnostic fingerprint - but again this requires very sophisticated technology, not always available to general physicians.

Dr. Barker and Dr. Levy continued their studies on T-cells. Some believe that although there are many immunological studies in CFS, no abnormality holds up throughout. But there are two robust findings found in nearly all studies - one is the low Natural Killer cell function and another is activation of a subset of T-cells, CD8 cells, first reported by Dr. Levy. They reported here a new marker of activation of T-cells, but of more interest is the finding of abnormal function of this subset of T-cells in CFS compared to these T-cells in healthy people.


3) Microbiology

Dr. John Gow and Dr. Len Archard (UK) presented conflicting evidence of their findings of enteroviruses in muscle biopsies of people with CFS. Dr. Archard, using a molecular biological technique, found pieces of enterovirus in 30% of CFS subjects, more often when those patients had objective evidence of abnormal muscle fatigability (an abnormal lactate response to exercise). But Dr. Gow's group found no evidence of 'full length enterovirus' in muscle specimens from CFS patients. According to Dr. Komaroff "the two results aren't necessarily incompatible, but this is an area that needs further work".


4) Neuropsychiatry

Dr. Tavio from Italy presented the results of a study using Positron Emission Tomography (PET), which assesses brain metabolism. They found 'significant hypometabolism in right frontal cortex and in the brainstem, in 18 CFS patients, compared with healthy people'. By comparison, a control group with depression had greater reduction in metabolism in the frontal cortex, but no hypometabolism in the brainstem. (This correlates with the reduced brainstem perfusion in M.E. found by Dr. Costa's team at the Middlesex hospital.)

Dr. John Gow, Glasgow, presented (on behalf of Prof P. Behan) results of neuro-endocrine studies on people exposed to organophosphates - most were sheep farmers. These patients were clinically identical to CFS/ME. They performed various tests of neuroendocrine function, and found the same abnormalities in these tests that were found previously in CFS. These findings also suggest involvement of the hypothalamus in OP poisoned workers, as in CFS.

Dr. Natelson's group tested the observation from many patients that following physical exertion they feel much worse - not only weak and painful muscles, but their thinking becomes impaired. They performed tests of cognitive function in CFS and healthy sedentary subjects before, immediately after and 24 hours after a formal, exhaustive treadmill test. The CFS patients before the exercise test did not score differently in cognitive function, but immediately after, and 24 hours after exercise even more so, the CFS group performed significantly worse than the healthy controls. This is the first test that systematically and objectively confirms what the patients say about the effects of exercise on the brain.

Dr. LA Jason presented a study that assessed the usefulness of psychiatric interviews, in which 18 people with CFS were each tested for psychiatric diagnoses (DSM IIIR, Axis l) twice, once using Diagnostic Interview Schedule (DIS) and once using Structured Clinical Interview (SCID). The incidence of current psychiatric diagnosis using DIS interview was 50%, and using SCID was only 22%. That of life psychiatric diagnosis using DIS was 61%, compared to 44% using SCID. Thus 'Psychiatric co-morbidity rates are influenced by the type of interview instrument used and the examiner's bias towards scoring of CFS symptoms. These findings help explain the large discrepancies in findings of psychiatric illness in people with CFS'.


Other studies

Dr. Evingarde from Stockholm looked at levels of folate and vitamin B12 both in blood and in spinal fluid, and found low to normal levels in the blood. But in the spinal fluid they found absent vitamin B12 in CFS. However, they did not compare with healthy controls, in whom it is presumed they will have detectable B12.

Dr. Kuratsune from Japan updated us on a series of studies on a particular energy system involving acylcarnitine. He previously reported low levels of this in the blood in CFS, and has now expanded this to nearly 150 patients, in whom there is still significantly low acylcarnitine.

Dr. Sharpe from Oxford reported on his study of Cognitive Behaviour Therapy (CBT), which led to clinical improvement in a significant number of CFS patients. He said clearly that this does not mean that the illness is fundamentally psychological and CBT is also used in patients with well recognised organic illnesses.

Dr. Komaroff's team in Boston found that various abnormalities of the reproductive system in women may be more common in CFS. The endocrine abnormalities suggested could possibly encourage a state of chronic immune activation.

Dr. Strauss reported on the results of a cortisone replacement therapy clinical trial. Previous work has suggested two abnormalities in CFS - low levels of cortisol, and possibly low levels of a brain hormone secreted by the hypothalamus called CRH, both of which could explain fatigue. Low dose hydrocortisone in a pill was tested in a placebo-controlled trial. There was no significant improvement in the patients who had the cortisone compared to those who had placebo. However, even in these low doses, the hydrocortisone suppressed the HPA axis, which can be hazardous for patients. So on the basis of no improvement and one significant adverse side effect, Dr. Strauss recommended against this type of therapy.


Clinical Conference

1) Dr. Richard Bruno, Director of the Kessler Post-Polio Institute, gave a presentation about the similarities in clinical symptoms, and neurological investigations (neuropsychology, brain scans, neuroendocrinology, and electroencephalogram) between post-polio fatigue and CFS. He postulated a 'brain fatigue generator' in the brain, which would have evolved as a protective mechanism for mammals, to make them rest when exhausted. Dr. Bruno then described how polio virus damage to the BFG could be a model for the severe fatigue in post-polio syndrome and in CFS, with damage to neurones (nerve cells) that make dopamine. A clinical trial of a dopamine stimulating drug is currently under way, but its usefulness in CFS is not yet known.

2) Drs. David Bell and Jim Jones presented results of a study looking at 170 adolescents with CFS, between 1985 and 1996, by extensive questionnaires that asked about coping styles, psychosocial function, levels of fatigue, functional activity and social support. The results showed that there is no correlation between coping style and fatigue severity, nor between social support and fatigue severity. Maladaptive coping was associated with worse self esteem and perceived self competence The results suggested that CFS as defined in this study is not a psychiatric illness.

3) Dr. Peter Rowe described the physiology of neurally mediated hypotension (NMH), and studies showing a strong association between NMH, CFS and fibromyalgia syndrome. He also presented an ongoing, randomised, clinical trial of fludrocortisone for CFS patients with NMH. He advised that proven NMH in CFS (he uses the tilt-table test) does not respond to taking extra salt alone. In his fludrocortisone trial, all patients received a potassium supplement as well as fludrocortisone or placebo. He mentioned other therapy useful for treating NMH: licorice (not to be taken with fludrocortisone), clonidine, beta-blockers, vasoconstrictors, and SSRI antidepressants. (Note, results of this trial will be published in due course. Until then, CFS/ME people are advised that they should not ask their GPs to prescribe fludrocortisone!)

4) Treatment and Rehabilitation. A number of physicians gave brief accounts of their treatment strategies, and a panel of therapists spoke of their views on rehabilitation. These will be published in the Spring Perspectives, together with a talk by Dr. Alexis Shelokov about the history of M.E. and CFS since 1953.

Acknowledgment: Reprinted from Perspectives, January 1997, magazine of the M.E. Association (UK).

Reprinted from Emerge, Autumn 1997.