Diary

Sarah Rigby

Last week I walked home from Shepherd’s Bush Green. It isn’t far – people who come to visit say it takes them about ten minutes – but it felt like a considerable achievement. I haven’t been able to walk that far since I’ve lived in this part of London. It wasn’t just that I could cover the distance – at a push I could have done that six months ago – but I didn’t have any pain in the days which followed, which was an indication of how much I’ve improved. Two years ago, when I first moved here, I couldn’t comfortably walk from one room of my flat to another, and when I tried to ignore the pain and go further, it always got worse.

At that time I didn’t make a link between using muscles in the normal way and the pain in them increasing. In fact, I had very little idea what was happening to me. For three months, taking increasing amounts of medication, I’d been struggling to live normally, but just after I moved my GP suggested that I stop taking painkillers, which he felt were dangerous if used for an extended period. Without them, I had to stop working. Every step I took sent waves of pain up the right-hand side of my body (for some reason the pain was always worse on the right side) and I had severe and constant headaches in my temples and at the base of my skull. The other symptoms I’d had since having flu in March continued: swollen glands, a constant sore throat, night sweats, dizziness, bowel disturbances and temperature fluctuations – I was also unusually thirsty, hungry and tired. I was sleeping for about 14 hours a day but was exhausted while I was awake; I was eating more than usual but within three weeks had lost a stone and a half in weight, and couldn’t put it back on for more than a year. Later I developed blurred vision in my right eye, tinnitus in my right ear and recurrent insomnia. More frightening than any of this was the fact that I found it very difficult to concentrate: when I tried to read, or to listen to the radio, I often couldn’t keep the meanings of the words in my mind for long enough to make sense of a sentence.

Unless they’ve known someone with the condition, most people wouldn’t recognise these as symptoms of what one consultant I saw described as a ‘textbook case’ of ME, or Chronic Fatigue Syndrome. In the last few years the illness has attracted a great deal of publicity – partly because it’s still very controversial, partly because it affects so many people (approximately 150,000 in the UK). There’s disagreement about what the condition should be called, about how many people have it, about whether there are subgroups within the Syndrome, but most of all about what it is and whether or not it exists. Many people I meet have a view on whether it’s a genuine illness or not, but strikingly, hardly any of them even have a clear idea of its symptoms. The three most common opinions about ME are that it doesn’t exist at all, except in name; that it just involves feeling slightly more tired than usual; and that it’s a psychological illness.

The Chief Medical Officer, Kenneth Calman, announced on 16 July that a new working group is to be set up to help GPs deal with ME, which he recognised as ‘debilitating’ and ‘a real entity’. This should go some way towards dislodging two of the more common assumptions from the minds of doctors, though public opinion will be slower to change. The third – that ME is a psychological illness – continues to be contested. Matthew Hotopf, of the Institute of Psychiatry, recently described ME as ‘a grey area’. Appearing on ITV’s Link, Hotopf said: ‘The main thing about ME is that it cannot be understood by any single biological or psychological mechanism. You have to have an integrated approach which takes both into account.’ On the same progamme, Ellen Gouldsmit, a psychologist with a special interest in ME, argued that ‘we must start distinguishing between the various fatigue syndromes. The literature doesn’t make sense if you treat CFS as one disease ... The evidence is overwhelming that it isn’t. There are some groups where physical factors like the immune system are involved, and they’re not being looked at.’

When my GP eventually said that he thought I had postviral syndrome, and then casually went on to call it ME, I was astonished. I didn’t know much about ME, and thought that its symptoms were very different from mine. My immediate suspicion was that he simply didn’t know what was wrong with me and was reaching for a convenient term to explain it away. But as I found out more about ME, I realised he was probably right. My friends and family were relieved by the new diagnosis; not surprisingly, they didn’t know what it meant. ‘You’re so lucky,’ one of my friends said, thinking that in return for feeling tired I’d have a few months off work to read, sunbathe and sleep. ‘I could really do with some of that.’ Several others said that they were tired, too – perhaps they had ME as well. Many congratulated me on being so thin. Later, when I’d got a bit better and was just about managing to work three days a week so long as I didn’t try to do anything else, the usual line was how nice it’d be to work only on alternate days.

Describing the symptoms again and again gets very boring. But no matter how hard I tried to explain that I couldn’t read, or that I was in far too much pain to get outside at all or, later, that most of the time I wasn’t at work I spent asleep, it rarely made an impact. Once the term ‘ME’ has been mentioned it’s difficult for people not to click into their own preconceptions about the illness. Even when I could hardly walk, and when the headaches were so bad that I found it hard to talk coherently on the phone, I got calls from friends wondering if I wanted to go out for a drink that evening. Why wasn’t I better yet? Did I know that long-distance running was supposed to cure ME?

One of the hardest things for other people to understand about ME is that it imposes definite physical limitations, and unless it’s properly handled the severity of the illness can fluctuate wildly. During the first few months I was ill, I was convinced that I’d recover quickly and that I had a very mild case which wouldn’t interfere with my life. I carried on working; the pain steadily increased. Inexplicably, it was worse in the afternoons than in the mornings; days when I could do nothing were followed by reasonably good days. A few hours after using a computer or writing, the pain in my right arm became worse, until turning a key in a lock or dialling numbers on a telephone was unbearable.

Eventually I realised there was a pattern. The consultants I’ve seen since have confirmed it. In his paper ‘The Clinical Identity of the Myalgic Encephalomyelitis Syndrome’, A. Melvin Ramsay noted the presence of ‘a unique form of muscle fatiguability whereby, even after a minor degree of physical effort, three, four, five days or longer elapse before full muscle power is restored’, and stated that this phenomenon ‘is virtually a sheet-anchor in the diagnosis of ME and without it a diagnosis should not be made’. Many consultants who see ME patients advise them to use the pain as a guide to gauge exactly what they can and can’t do. The idea is to rest when the muscles are overtired and start to hurt. At this stage the pain tends to be a mild ache – like having flu – and it’s possible to rest until it disappears. Ignoring it and pressing on usually makes it worse. It is estimated that only about 30 or 40 per cent of those with ME ever make a total recovery. About 30 per cent experience some improvement but 20-25 per cent are bed or wheelchair-bound indefinitely. What seems to make the difference is how much rest is taken in the early, acute stage of the illness but even after that, careful management is crucial.

It’s also very frustrating. When I wasn’t actually in pain, my instinct was to assume I was better and go out – and that would bring the symptoms on again. Friends couldn’t understand why I could go to see them one day, looking and seeming fine, and then be worse again the next. I tried to remember that my situation was much better than average: I had the most common and most easily recognised kind of ME, that is preceded by an obvious virus. I had GPs who knew a fair amount about it and a very supportive boyfriend. As time went on most of my friends tried to find out more about what was wrong with me. Many people with ME have a very different experience and become isolated. The yachtswoman Clare Francis, who developed ME about twenty years ago, describes having ‘pretended’ her illness ‘wasn’t happening’ in her Foreword to Anne Maclntyre’s Post-Viral Syndrome: How to Live with It: ‘I covered up the gaping holes in my life with lies and evasions: while I slept all day, my answering machine said I was out; when I stumbled over words and walked into things I joked about having had a late night; and my social life was reduced to almost nothing by constantly pleading a previous engagement.’

Until ten years ago it was fashionable to question the authenticity of ME. People with the symptoms tended to be told that there was nothing wrong with them or that they had emotional problems. But antidepressants didn’t cure them and exercise made them substantially worse. The absence of a diagnosis made it difficult to understand the illness, or to explain it to other people – relationships often broke down as a result. Without the support of a doctor it was impossible to arrange sick leave or to apply for invalidity benefits, which meant that sufferers had to try to carry on working until they’d made the illness so much worse that they were completely unable to continue.

These problems still occur to some extent, but if doctors don’t all agree about what ME is, many more now accept that it does exist. The ME Association estimates that between 10 and 20 per cent of GPs are still sceptical; it emphasises that getting an informed doctor very much depends on where you happen to live. Bristol is a good place; Lincoln is not. Older doctors, it is thought, are much more likely to see it as a nonsense illness. Three months before the 1996 report of the Royal Colleges of Physicians, Psychiatrists and General Practitioners concluded that ME was a ‘genuine and serious debilitating condition which is poorly understood and poorly managed by many GPs’, I was seeing a neurologist who didn’t believe in it. He accepted that the symptoms I had were those generally diagnosed as ME, but insisted that the term itself was meaningless. Instead, he used a different formula: ‘migraine-limb-pain-syndrome’, which he said explained all my symptoms. More than a year after I first got ill, a different consultant confirmed that I had ‘Post-Viral Chronic Fatigue Syndrome’. Five years ago, it’s said, it often took patients about two years to get a consultant’s diagnosis; a year is about average now.

The World Health Organisation lists ME as a disease of the nervous system in its ‘International Classification of Diseases’. The Departments of Health and Social Security describe it as ‘a debilitating and distressing condition with a physical basis’. In the UK doctors are almost evenly split on whether it is predominantly a psychological or a physical illness. Sceptics, such as Elaine Showalter, an American professor of English whose 1997 book about hysteria included a controversial chapter on CFS, point out that, despite extensive research, nobody yet knows what causes ME. It often occurs after a virus, but there is no evidence of prolonged viral infection. There is still no diagnostic test: most routine investigations show up no abnormalities and diagnosis is made on case-history and by exclusion. Women seem more prone to it than men (roughly 65 per cent of sufferers are female). Some cases are mild; others are severe. Patients experience remissions and severity can seem to fluctuate. Not everyone has the same set of symptoms. Patients and some doctors claim that over-exertion makes the illness worse. Moreover, it is said, ME is a predominantly Western disease: rural workers in India don’t get it – the implication is that only those who can afford ME actually develop it.

Multiple Sclerosis shares some symptoms with ME. As recently as the Sixties, before widespread MRI scanning made diagnosis easier, there were those in the early stages of MS who had similar trouble being taken seriously: their symptoms couldn’t be confidently assigned, and some people are said to have been told they had ‘hysterical paralysis’. (Another parallel is syphilis, which was originally said to be a sign of neurosis; TB was for some time thought to affect only those with a ‘tubercular personality’.) Until it was demonstrated that brain abnormalities associated with MS showed up on MRI scans and on EEG tests, there was no accepted test for the disease. It is still not known what causes MS, although the most recent research suggests that a combination of factors, including genetic predisposition, is involved, and that onset may be triggered by a virus. Like lupus and myasthenia gravis, two potentially fatal conditions, MS affects more women than men – the MS Society puts the ratio at 3-2. Susceptibility is thought to be partly related to climate: its incidence is much higher in temperate than in tropical regions. Like ME, MS is unpredictable. Some people have only one attack in a lifetime; others experience MS as a chronic illness with very gradual deterioration and periods of remission, but about 15 per cent become quickly and severely disabled. It is said that no one case of MS is the same as another; symptoms vary. None of this is to say that MS is the same as ME, of course; but it shows that other neurological illnesses do have similar characteristics.

Simon Wessely, the psychiatrist on whose research Showalter leant heavily, has since written a short, unrelated article in the Guardian, silently contradicting her assumption that CFS is mainly a middle-class problem: ‘My clinics do contain more teachers, doctors and nurses than one would expect,’ he said, ‘but when we extended our studies to general practice and the community we found that CFS was common in all social classes.’ In the same article he also accepted that the condition could be triggered by a virus – an idea which Showalter had scornfully rejected in her book – but added that he didn’t think it was simply a case of prolonged viral activity. He also pointed out that ‘many ME patients are not depressed. Several research teams have shown that the stress hormone cortisol, which is exceptionally high in classic major depression, is inexplicably low in CFS.’ Charles Shepherd, the medical adviser to the ME Association, believes that Showalter ‘had not read around enough from the research point of view’: ‘She just wasn’t aware of most of the research that’s going on or most of what’s been shown about neuro-imaging, muscular abnormalities and so on.’ Nonetheless, her chapter on CFS got a great deal of publicity.

In October 1996, the Royal Colleges concluded, after a two-year investigation, that ME existed but that this name was misleading and the condition ought to be described as Chronic Fatigue Syndrome; that a quarter of a million people in the UK might have it and that it was a physical as well as a psychological illness. They estimated that 75 per cent of cases had a co-existent psychiatric disorder, such as anxiety or depression. No progress on the cause of the illness had been made, however.

The ME charities quickly pointed out that the research committee had been dominated by psychiatrists. Only one GP had been included although GPs inevitably see more CFS than other doctors. The charities agreed that the social consequences of having ME could result in depression but estimated that this was present in only a quarter of cases (roughly the same as for other chronic illnesses) and stressed that it was not an initial characteristic of the illness. They agreed that the term ‘myalgic encephalomyelitis’ was misleading (there is no evidence of inflammation in the brain) but warned that the term CFS would blur the distinctions between ME (which they felt should be diagnosed according to strict criteria) and other long-term illnesses in which fatigue was significant, some of which might be psychiatric conditions. The reactions from medical journals were mixed: the BMJ welcomed the report, but the Lancet described it as ‘biased and inconclusive and of little help to patients or their physicians’. In the Observer, the Lancet’s editor, Richard Horton, described the conclusions as ‘a cardboard case’, adding that it ‘interpreted every piece of evidence pointing to a biological cause ... in a negative light ... the sensible conclusion should surely be that there is reasonable doubt that chronic fatigue has a psychological basis.’

Though no one yet knows what causes ME, there is no shortage of hypotheses. Around three-quarters of cases are preceded by a noticeable virus – chickenpox, glandular fever or gastric flu, or occasionally something as seemingly harmless as a sore throat – which then seems to disappear. Early theories that the initial infection is a retrovirus have been disproved. There are thought to be other possible initial precipitants in addition to viral infections: vaccines and pesticides which stimulate the immune system are candidates. The most convincing explanations centre on the idea that ME may have several contributory causes, and emerges when one or more long-term but dormant problems coincide with a period of ill-health or stress which suppresses the immune system. It is thought increasingly likely that there are subgroups within ME, and that each may have different causes and symptoms.

There is also conflicting evidence about what keeps the illness going. According to Shepherd, many researchers now agree that there are neurological problems associated with ME. Bloodflow to the brain stem may be affected and there is some evidence of irregularities in the chemical transmitters in the brain, especially serotonin and acetylcholine – problems which may be the result of an overactive or disturbed immune system’s response to the initial virus or toxin. The hypothalamus, which controls hormonal production, sleep and appetite may be affected. SPECT tests – a form of scanning not in general use – are said to show a deprivation of oxygen to the brain. Several current research studies are concentrating on brain hormones and chemical transmitters, and on a possible weakness in (or build up of toxins around) the blood-brain barrier. A nationwide trial is currently underway on one drug, Galanthamine, which slows the destruction of acetylcholine in the brain. Several smaller studies are currently testing the use of cortisol replacement.

What puzzles many observers is why establishing a cause matters so much to patients. After all, they say, no illness is ever completely psychological or completely physical. Of course there is some truth in this: stress can be a contributory factor in heart disease and some cancers, and it has been shown that women are more likely to develop breast cancer following a major bereavement. Very recent research has pointed to the damaging effect of long-term stress on the immune system (short-term stress, apparently, can be good for it). While stress and emotional pressure may contribute as much to the onset of ME as to any other illness, they are unlikely to be the only causes – and the debate about the other causes affects diagnosis and treatment. No one is going to stop looking for a cure for cancer because we know that stress can be a contributory factor, but there is pressure to do exactly that with ME.

ME patients aren’t simply worried that the illness will be proved to be a form of depression. On the whole they will do anything to get better, and most have tried anti-depressants at some point. Many GPs prescribe them for a time because they’re unsure about the extent to which psychological and social factors are involved in the Syndrome – and while some types do help to correct sleeping patterns, they don’t cure ME. According to Charles Shepherd, the only double-blind study involving a placebo and an anti-depressant used fluoxetine (Prozac) and concluded that it ‘does not have a beneficial effect on any characteristic of CFS’.

Shepherd emphasises that the patients he sees tend not to mind who they’re referred to as long as the specialist has some understanding of ME. Patients who have some psychological symptoms tend to be conscious of them, and usually have no problem with seeing a psychiatrist – ‘it’s the ones who have a clear cut case of ME, which started with a virus, and developed into muscle pain and fatigue and who have no psychological symptoms who get annoyed with GPs who tell them that it’s all in the mind and they should see a psychiatrist. There’s no point seeing a psychiatrist who knows nothing about ME just as there’s no point seeing a neurologist who doesn’t understand it. The consultants who get five-star ratings are the ones who ... can give good advice about lifestyle management.’ The problem is that those who see ME as a purely psychological illness often don’t give good advice. When patients are told that it’s important to drive themselves on physically, ignoring pain, they tend to have spectacular relapses. Of course it’s more important to find a cure for ME than to worry about its causes. But the nature of ME is central to the way patients are encouraged to manage it. And for the time being, at least, good management is essential to most recoveries.