What is ME?  What is CFS?

 

 

             INFORMATION FOR  CLINICIANS AND LAWYERS

                             

                                                            December 2001

 

 

 

 

 

                                            

   

                                                                            E.P. Marshall (1)

                                                                            M. Williams (1)

M. Hooper (2)    

 

(1)  ME Research (UK)

      (British Library Registered)

      c/o The British Library

      Science Reference & Information Services

      Boston Spa, Wetherby,

      West Yorkshire LS 23  7BQ, UK

 

(2)   Emeritus Professor of Medicinal Chemistry  

      Department of Life Sciences

      University of Sunderland

      SR2  7EE, UK

 

 

                                                                                        

 

 

                                           CONTENTS

 

 

 

 

 

 

History and Classification of Myalgic Encephalomyelitis (ME)………………..3

 

Description of ME………………………………………………………………….4

 

Symptoms Documented in ME……………………………………………………6

 

Evidence of Abnormalities in ME…………………………………………………10

 

Precipitating Factors in ME……………………………………………………….13

 

Physical Signs Found in ME……………………………………………………….15

 

Changing Definitions: History of Chronic Fatigue Syndrome (CFS)………….. 17

 

How “CFS” Displaced ME in the UK……………………………………………..18

 

The UK  Chief Medical Officer’s Report on “CFS/ME”…………………………27

 

Caution needed by Lawyers……………………………………………………….. 29

 

Conclusion……………………………………………………………………………30

 

 

 

 

 

 

 

 

 

 

 

 

 

                               What is ME?   What is CFS?

 

                    INFORMATION FOR CLINICIANS AND LAWYERS

                                                   December 2001

  

 

 

History and Classification of Myalgic Encephalomyelitis

 

Myalgic Encephalomyelitis (ME) has been documented in the medical literature from 1934. [1] The Wallis description of ME (not Chronic Fatigue Syndrome, known as CFS – see below) was in 1957. [2]  Sir Donald Acheson’s  (a former UK Chief Medical Officer) major review of ME was in 1959. [3]  In 1962, the distinguished neurologist Lord Brain included it in the standard textbook of neurology. [4]  ME has been formally classified by the World Health Organisation as a neurological disorder in the International Classification of Diseases (ICD) since 1969 (ICD-8: Vol I: code 323, page 158; Vol II (Code Index)

page 173).  On 7th April 1978 the Royal Society of Medicine held a symposium on ME at which ME was accepted as a distinct entity.  The symposium proceedings were published in The Postgraduate Medical Journal in November that same year. [5]  The Ramsay case description was published in 1981. [6]   Since 1989, the Medical Information Service of the British Library has produced quarterly updates on the disorder: these updates (known as CATS, or Current Awareness Topics) compile published international research and clinical evidence about the condition and contain abstracts of published articles.  The Centres for Disease Control (the US federal agency charged with the containment of diseases and known internationally as the CDC) designates it for funding status as  “A serious legitimate diagnosis CDC PRIORITY 1 disease of public health importance”.

 

ME remains classified in the current ICD as a neurological disorder (ICD 10. G.93.3) and the World Health Organisation has confirmed that there are no plans to reclassify it as a psychiatric disorder in the next revision of the ICD (due in 2003).

 

Chronic Fatigue Syndrome (CFS) is listed in ICD-10 as a term by which ME is also known, as is the term Postviral Fatigue Syndrome (PVFS). The term “CFIDS”, or Chronic Fatigue and Immune Dysfunction Syndrome, is used by some groups in the US.

 

 

Description of Myalgic Encephalomyelitis

 

ME / ICD-CFS is a serious, disabling and chronic organic (ie. physical not mental) disorder: 80% of patients do not get better.[7]  According to US statistics provided by the Centres for Disease Control (CDC), only 4% of patients had full remission (not recovery) at 24 months.[8]  International expert Daniel Peterson is on record as stating about ME / ICD-CFS:

 

        “In my experience, (it) is one of the most disabling diseases that I care for, far

          exceeding HIV disease except for the terminal stages”. [9]

 

American researchers found that the quality of life is particularly and uniquely disrupted in ME / ICD-CFS and that all participants related profound and multiple losses, including loss of jobs, relationships, financial security, future plans, daily routines, hobbies, stamina and spontaneity.  Activity was reduced to basic survival needs for some subjects.  The researchers found that the extent of the losses experienced by sufferers was devastating, both in number and intensity. [10]

 

Australian researchers found that patients with this disorder had more dysfunction than those with multiple sclerosis, and that in ME / ICD-CFS the degree of impairment is more extreme than in end-stage renal disease and heart disease, and that only in terminally ill cancer and stroke patients was the sickness impact profile (SIP) greater than in ME /ICD-CFS. [11]

 

The incidence of ME / ICD-CFS is known to be rising: in April 1994, the insurance company UNUM (one of the largest disability insurers) reported that in the five years from 1989 - 1993, mens’ disability claims for CFS increased 360%, whilst womens’ claims for CFS increased 557%.  No other disease category surpassed these rates of increase.

In order of insurance costs, ME/ICD-CFS came second in the list of the five most expensive chronic conditions, being three places above AIDS.  At the Fifth American Association of Chronic Fatigue Syndrome International Research and Clinical Conference held in January 2001 in Seattle, the Associate Director of the University of Washington’s CFS Research Centre (Dr N Afari) confirmed that the incidence is indeed rising.

 

Of potential significance is the fact that American researchers have demonstrated that in ME / ICD-CFS, a particular pathway in the body which is affected by viruses can also be affected by chemicals. [12]  

 

The strike rate is higher than multiple sclerosis.  Comparisons have been made between the prevalence of ME /ICD-CFS and MS in the UK, in the USA [13] and in Australia [14] and have been estimated to be three times, twice and equivalent respectively.  Prevalence estimates in Britain vary by a factor of 8, which is a reflection of the problem of definition.

In the UK it is generally believed that at least 300,000 suffer from the disorder; some psychiatrists, however (see below), having themselves broadened the case definition to include psychiatric disorders, claim that there are over one million “CFS” sufferers in the UK, of which they assert 75% have a psychiatric disorder. [15]

 

Estimated direct NHS costs are said to be from £180 million to just over £1 billion per annum, depending on the choice of prevalence estimates, with total costs ranging from

£879 million to nearly £16 billion. [16]

 

ME/ ICD-CFS is a multi-system disorder, one form of which can be associated with enteroviruses related to the poliomyelitis virus [17].  Virally-induced ME used to be known as “atypical poliomyelitis”.  There are acknowledged similarities and overlaps between ME  and the post-polio syndrome (PPS), particularly concerning the nature and source of the pathophysiology, including virological evidence that enteroviruses persist in the human central nervous system.  Specifically, the mechanism of the incapacitating exhaustion is identical in the two conditions (ie. in ME and PPS). [18]  In ME there are chronic sequelae and the effects may be neurological, hormonal, autoimmune and myalgic, which may include the myocardium. [19]

 

 

Symptoms documented in Myalgic Encephalomyelitis

 

In ME, symptoms are seemingly without end.  There is a remarkable variability of signs and symptoms from day to day and even from hour to hour: Hyde and Jain [20] (quoting Pellew) describe this variability:

 

            “A patient examined in the morning might have nystagmus, which would

              disappear at midday, recur later, disappear later and recur the next day”.  

 

This waxing and waning in the same patient in the same day is typical of almost all findings in ME / ICD-CFS and may lead to medical scepticism.

 

The most apparent features are extreme post-exertional muscle fatiguability, which is quite distinct from chronic “fatigue” or tiredness, together with recurrent nausea and profound, incapacitating malaise. It is striking how consistent are the symptoms that characterize this condition. [21]  The exhaustion experienced by patients is extreme:

 

          “the disabling weakness and exhaustion a patient with ME / ICD-CFS

            experiences is so profound that “fatigue” is probably an insult”. [22]

 

ME commonly starts with abdominal pain and diarrhoea, together with a persistent headache and / or vertigo, with a stiff neck and back, together with generalised myalgia, described as intense and burning. Muscles are tender to palpation and muscle spasm is not uncommon.  There may be severe, intractable pain in particular groups of muscles, most notably in the neck and in the shoulder and pelvic girdles: the more severely affected are unable to stand unsupported for more than a few minutes. There is sometimes segmental pain in the chest wall.

 

In the more severely affected, dizziness is a particularly striking and chronic feature, as is persisting dysequilibrium and ataxia, with patients frequently bumping into things and becoming bruised. There is impaired neuromuscular coordination, particularly with fine finger movements. In the severely affected, there may be difficulty with swallowing; choking fits are not infrequent. There may be difficulty with voice production, particularly if speaking is sustained.

 

There may be seizures, although these are found only in the most severe cases.

 

In the most severe cases, photophobia and hyperacusis are common, as is tinnitus; often there is parasthesia.

 

Hypersomnia is prevalent, especially in the early stages of the disorder; this may be replaced by reversed sleeping patterns, with vivid and disturbing dreams; unrefreshing sleep is common.

 

Abdominal pains often recur; especially in the severely affected, there are usually chronic problems with diarrhoea and frequency of micturition, including nocturia. Bladder and bowel control may be insecure.

 

Cardiac arrythmias are very common, with pronounced tachycardia and an uncomfortably pounding heart; there may be paroxysmal attacks of angina-like chest pain. Cardiac pain is a recognised feature: patients may be convinced they are suffering a heart attack. Myocarditis was a common symptom in an analysis of 1,000 ME/ ICD-CFS patients seen in Glasgow, where clinicians were struck by the often-occurring association of patients

with ME/ICD-CFS with acute chest pain resembling coronary thrombosis.[23]  A significant number of cases of Syndrome X strongly resemble ME / ICD-CFS clinically, and nuclear magnetic resonance spectroscopy studies of skeletal muscle in patients with Syndrome X show abnormalities that are identical to those found in patients with ME / ICD-CFS.[24]    Syndrome X is characterised by typical anginal pain with a normal coronary angiogram:[25] in both Syndrome X and ME / ICD-CFS, blood supply to the heart muscle seems to be going haywire, but in Syndrome X there is desensitivity of the cell endothelium, whilst in ME / ICD-CFS there is heightened sensitivity of the cell endothelium.  Syndrome X has been defined as a cluster of symptoms secondary to resistance of insulin-mediated glucose uptake; [26]  it has been seen in association with increased risk for coronary heart disease due to enhanced growth and proliferation of arterial smooth muscle cells and highly elevated levels of cholesterol.

 

In the more severely affected, palindromic arthropathies regularly recur; spontaneous periarticular bleeds are frequent, especially in the fingers, which become swollen and painful, making the patient appear even more clumsy.

 

Pancreatitis is not uncommon and may cause acute, severe pain: pancreatic exocrine insufficiency leads to malabsorption, which is a well-recognised feature found in the more severely affected; some patients have almost non-existent pancreatic exocrine function. Some patients have been shown to have achlorhydria.

 

Food intolerance is a prominent feature across all degrees of severity: multiple sensitivities to normal foods and household chemicals (including perfumes, chemical treatments of furniture and carpets such as flame-retardants and glues in chipboard), petrol and agricultural chemicals are frequent. Intolerance to alcohol and to medicinal drugs, particularly to antidepressants, is virtually pathognomonic.[27]  Patients have to be cautious about all drugs but especially those acting on the central nervous system (ie. anaesthetics), as there is an increased occurrence of adverse reaction. [28]

 

ME affects not only the central nervous system but the autonomic and peripheral nervous systems as well. Sympathetic nervous system dysfunction is integral to ME  /  ICD-CFS pathology [29] and includes blurred and double vision, with difficulty in focusing and visual accomodation; eyes may be dry and eyelids are often swollen and painful. Typical autonomic symptoms include alternate sweating and shivering, with marked thermodysregulation. Patients experience orthostatic hypotension and symptoms of hypovolaemia, with blood pooling in the legs and insufficient blood flow to the brain: patients may feel faint, shaky and nauseous; they can be tearful and observably pale and they may experience severe distress.

 

Heightened sensory input awareness might be called an “acid test” for ME / ICD-CFS:

one world expert claims that it is possible to make a diagnosis by taking a patient into a shopping mall (he calls it the Mall Test) because with all the lights, noise, echoes, smells, movement and confusion, a sufferer would be ready to explode. [30]

 

In the more severely affected, commonly there is difficulty with breathing, with sudden attacks of breathlessness and dyspnoea on minimal effort; the administration of oxygen may be necessary.

 

Rashes may occur; mouth ulcers may be recurrent and may be painful and severe to the extent that speaking and eating may be affected.

 

Hands and feet are frequently cold, blanched and / or purple, with painful vascular spasms seen in the fingers.

 

 

Vascular headaches are common and recurring. [31]

 

In females, ovarian-uterine dysfunction is not uncommon; in males, prostatitis and impotence may occur.

 

Many patients can walk only very short distances and require a wheelchair. There is difficulty with simple tasks such as climbing stairs and dressing.

 

Problems with short-term memory are common:[32]  cognitive impairment is significant and includes difficulty with memory sequencing, processing speed, word searching; dyslogia, spatial organisation, calculation (dyscalculia), and particularly with decision-making.  In relation to the degree of cognitive impairment, American researchers found that

 

      “the performance of the CFIDS patients was sevenfold worse than either the

        control or the depressed group.  These results indicated that the memory deficit in

        CFIDS was more severe than assumed by the CDC criteria.  A pattern emerged of        

        brain behaviour relationships supporting neurological compromise in CFIDS”. [33]

    

Uncharacteristic emotional lability is very common; there may be an increased irritability.

Patients are often understandably anxious and afraid.

 

There may be significant and permanent damage to skeletal or cardiac muscle as well as to

other end-organs including the liver, pancreas, endocrine glands and lymphoid tissues, [34] 

with evidence of dysfunction in the brain stem. Injury to the brain stem results in disturbance of the production of cortisol (required for stress control) via damage to the hypothalamus and to the pituitary and adrenal glands, and patients react extremely adversely to stress.

 

Cycles of severe relapse are characteristic and common, together with the evolution of further symptoms over time. ME is rarely listed as the cause of death, although after decades of illness, death from end-organ damage (mainly cardiac or pancreatic failure)

is known to occur.

 

 

 

Suicide rates are high [35] and are said to be the most common cause of death in ME and to be related to the current climate of disbelief and rejection of welfare support. [36] 

 

 

Evidence of abnormalities in ME

 

Despite beliefs and assertions to the contrary, in ME there is evidence of inflammation of the central nervous system (CNS); that is what helps to differentiate ME from other forms of CFS. There are many references in the medical literature to inflammation of the CNS in ME and in ICD- CFS  [37] [38] [39] [40] [41] [42]  but such CNS inflammation is not found in all variants of CFS. It is incorrect to deny the existence of CNS inflammation in ME / ICD-CFS. In some cases of ME, as in multiple sclerosis, there is evidence of oligoclonal bands

in the cerebrospinal fluid. [43] [44] 

 

It is accepted by the most experienced ME clinicians that some degree of encephalitis has occurred both in patients with ME and in those with post-polio syndrome: the areas chiefly affected include the upper spinal motor and sensory nerve roots and the spinal

nerve networks traversing the adjacent brain stem (which is always damaged). [45]  In nearly every patient there are signs of disease of the central nervous system. [46]  Recent research continues to support neurological involvement. [47] [48] [49] [50] [51] [52]  [53] 

There is a substantial literature on the neuroendocrine dysfunction which has been demonstrated in ME / ICD-CFS, particularly the known dysfunction of the hypothalamic-pituitary-adrenal axis (HPA axis), leading to a disordered stress response.

 

There is mounting international evidence that ME / ICD-CFS is an autoimmune disorder, with similarities to systemic lupus erythematosus.[54] [55]  Evidence of antilamin antibodies has been found in the blood of ME / ICD-CFS patients: antibodies against this protein are proof of autoimmunity and of damage to brain cells.  The occurrence of autoantibodies to an intra-cellular protein like lamin B1 provides laboratory evidence for an autoimmune component in ME / ICD-CFS. [56] [57]

 

In the UK, patients with autoimmune features and neurological signs and symptoms are usually the most sick and as such they are excluded from studies of “CFS” or chronic fatigue undertaken by psychiatrists, so the results of UK studies from which such patients are excluded are not representative of the true situation.

 

A particularly important piece of research in these patients has demonstrated sensitivity of the vascular endothelium to acetylcholine (a major neurotransmitter and vascular dilator) and this finding may have implications for many other cholinergic pathways (which are extensive throughout the body). [58]

 

In ME / ICD-CFS there is evidence of disruption in ion channels in the cell membranes; changes in ion channel function from time to time offer a rational basis to explain the fluctuating symptoms, and such ion channel changes are known to be induced by physical activities, stress and fasting. If sodium channels are blocked in the open mode, this causes entry of sodium into neural tissues and muscles. This ingress of sodium is followed by water, which in turn leads to swelling of the neural tissues, a phenonmenon observed both electron microscopically and by laser scanning microscopy. Acquired ion channel abnormalities in the myocardium could explain the pathogenesis of Syndrome X and may form the basis of cardiac dysfunction in both Syndrome X and in ME / ICD-CFS. [59] 

 

Australian researchers have found that total body potassium (TBK) is significantly lower in patients with ME / ICD-CFS; they suggest that abnormal potassium handling by muscles in the context of low overall body potassium may contribute to muscle fatigue in this disorder. [60]  Burnett reports that there is a reduced flux of potassium across the cell membrane (which fits in with a channelopathy) and that patients will feel more ill the lower the potassium levels.  TBK results for ME / ICD-CFS patients have also been shown by others to be significantly lower than those for controls; this fits with other metabolic abnormalities in these patients, such as impaired water metabolism. [61]

 

There is convincing evidence that patients with ME / ICD-CFS reach exhaustion more rapidly that normal subjects: the use of 31 P-nuclear magnetic resonance (31 P-NMR)

has now provided positive evidence of defective oxidative capacity in such patients. [62]

These findings show that there is a continued loss of post-exertional muscle power

(giving an additional loss of power), with delayed recovery for at least 24 hours, whereas sedentary controls recovered full muscle power after 200 minutes.

 

A genetic component to ME / ICD-CFS is strongly suggested by HLA phenotyping analysis in the laboratory of Paul Terasaki at UCLA School of Medicine.  Terasaki is one of the world’s leading experts in HLA typing and he found 46% of ME / ICD-CFS patients were HLA-DR4 positive. [63]  However, in a small study of only 58 patients, Wessely (a UK psychiatrist – see below) found no association between HLA genotype and CFS and claims there is no significant difference in HLA frequencies between patients and controls. [64]

 

In the February 2000 issue of The American Journal of Medicine, Anthony Komaroff 

(Assistant Professor of Medicine at Harvard and a world expert on this disorder) summarised key points in an Editorial:

 

 

       “Many controlled studies have compared patients with age-matched and gender-

         matched healthy control subjects.  Objective biological abnormalities have been

         found significantly more often in patients with the syndrome than in the

         comparison groups.  The evidence indicates pathology of the central nervous

         system and immune system.  What is the evidence of central nervous system

         pathology?    Magnetic resonance imaging has revealed areas of high signal

         in the white matter. Single photon emission computed tomography (SPECT)

         signal abnormalities also are found more often in patients, abnormalities like those

         seen in patients with encephalopathy due to the acquired immunodeficiency

         syndrome (AIDS) and unlike the findings in patients with depression. Autonomic

         nervous system testing has revealed abnormalities of the sympathetic and

         parasympathetic systems that are not explained by depression or physical

         deconditioning.  Studies of hypothalamic and pituitary function have revealed

         neuroendocrine abnormalities not seen in healthy control subjects and opposite

         to those found in depression.  There is considerable evidence from different

         investigators, using different technologies and studying different groups of

         patients, of a state of chronic immune activation.  In summary, there is now  

         considerable evidence of an underlying biological process in most patients (which)

         is inconsistent with the hypothesis that (the syndrome) involves symptoms

         that are only imagined or amplified because of underlying psychiatric distress.

         It is time to put that hypothesis to rest”. [65]

        

                    

 

Precipitating Factors

 

Precipitating factors are acknowledged to include stress, [66] [67] [68]   exposure to toxic chemicals, [69] [70]  and physical trauma - particularly a motor vehicle accident. [71] [72]  

There is convincing evidence that when combined with physical trauma, chemical or biological insult, stress potentiates the condition and that the disorder may be due in part to multiple chemical and / or biological exposures which have been shown to increase the permeability of the blood brain barrier (BBB), leading to a significant brain injury. [73] [74] [75]   Evidence of BBB breakdown in ME / ICD-CFS was presented at the international conference held in London in April 1999:  scientists in Israel have shown that severe stress (physical or mental) can produce breakdown of the BBB; if that barrier is broken, small amounts of substances which are normally outside the brain could produce brain injury.  It is postulated that in the case of ME / ICD-CFS, a person already under physical or mental stress is exposed to an agent (viral or chemical) which crosses the BBB, enters the brain, and produces long-term dysfunction.[76]

 

John Dwyer, Professor of Medicine at the University of New South Wales, Australia, states that his team has seen ME / ICD-CFS stimulated by vaccination and that they have seen it both with vaccinations such as those for influenza and also with the use of material which is not live, such as that in a tetanus toxoid injection.  [77] [78]  

 

The disorder is known sometimes to occur or worsen after anaesthetics, [79] [80] [81]  and to be related to some infections (both viral and bacterial).  There is a considerable literature on the viral aspects of the disorder, the most implicated viruses being Coxsackie B [82]  [83] and Human Herpes Virus 6 (HHV6). [84] [85]    HHV-6 has been found in patients suffering from ME / ICD-CFS and also in MS; it has also been linked to other autoimmune conditions such as systemic lupus erythematosus (SLE or lupus).

 

 

Physical signs found in ME

 

In cases of severe ME there are definite physical signs indicative of physical illness and not of abnormal illness behaviour. Some of these signs are often present in less severely affected cases but in the UK are dismissed or trivialised in order to comply with the currently-favoured psychiatric definition of CFS. Not all patients have all signs, but throughout the ME literature, the following are common in the sickest patients.

 

Observable signs include a typically swinging low-grade temperature, nystagmus; sluggish visual accommodation; abnormality of vestibular function with a positive Romberg test; abnormal tandem or augmented tandem stance; abnormal gait; hand tremor; incoordination; cogwheel movement of the leg on testing; muscular twitching or fasciculation; hyper-reflexia without clonus; facial vasculoid rash; vascular demarcation which can cross dermatomes with evidence of Raynaud’s syndrome and / or vasculitis; [86]  mouth ulcers; [87] [88]   hair loss; [89]  [90]  [91]  [92]  [93]  a labile blood pressure (sometimes as low as

84/48 in an adult at rest); flattened or even inverted T-waves on 24 hour Holter monitoring [94]  (a standard 12 lead ECG is usually normal); orthostatic tachycardia; shortness of breath (patients show significant reduction in all lung function parameters tested); [95]   abnormal glucose tolerance curves;  liver involvement [96] [97] [98] [99]  [100]

(an enlarged liver or spleen may not be looked for in ME, so missed) and destruction of fingerprints: (atrophy of fingerprints is due to perilymphocytic vasculitis and vacuolisation of fibroblasts [101]). 

 

In his Testimony before the FDA Scientific Advisory Committee on 18th February 1993, Dr Paul Cheney (Professor of Medicine at Capital University; Medical Director of the Cheney Clinic, North Carolina and one of the world’s leading exponents on ME /ICD-CFS) testified as follows:

 

       “ I have evaluated over 2,500 cases.  At best, it is a prolonged post-viral syndrome

          with slow recovery.  At worst, it is a nightmare of increasing disability with both

          physical and neurocognitive components.  The worst cases have both an MS-like

          and an AIDS-like clinical appearance.  We have lost five cases in the last six

          months. The most difficult thing to treat is the severe pain.  Half have abnormal

          MRI scans.  80% have abnormal SPECT scans.  95% have abnormal cognitive-

          evoked EEG brain maps.  Most have abnormal neurological examination.  40%

          have impaired cutaneous skin test responses to multiple antigens.  Most have

          evidence of T-cell activation.  80% have evidence of an up-regulated 2-5A antiviral

          pathway.  80% of cases are unable to work or attend school.  We admit regularly to

          hospital with an inability to care for self”.

 

People with ME are permanently excluded from being blood donors.[102]

 

Twenty-five per cent of sufferers are severely affected and are either house or bed bound; they are invisible and for the most part, they are ignored and abandoned to their own fate. 

A major Report by the charity Action for ME [103] found that 77 % of sufferers experienced severe pain; over 80% had felt suicidal as a result of the illness; 70% are either never able, or are sometimes too unwell to attend a doctor’s clinic; 65% (nearly two out of three) have received no advice from their GP on managing this illness; 80% of those who are currently bedridden by ME report that a request for a home visit by a doctor has been refused; many people do not receive state benefits to which they are clearly entitled.

 

Despite all this verifiable and authenticated international research, much of the current perception of ME, both medical and lay, is beset by confusion and misinformation.

 

There are still doctors who dismiss the condition as non-existent and too many sick children are still being forcibly removed from their parents and placed in institutional care where they are forced to undergo inappropriate exercise regimes under the care of psychiatrists.

Very recently, there have been two tragic ME cases involving children: in one case social workers, accompanied by uniformed police officers, appeared unannounced on the doorstep to take away a child under a Child Protection Order; the other child had been made a Ward of Court.

 

In July 2001, the appalling treatment of children with ME / ICD-CFS was the subject of a major feature written by the Countess of Mar in The Daily Telegraph. [104]  Cases such as these have been only too common since the late 1980s: support for families in such situations is available from the mother of a child who was compelled to go to the High Court to stop the local Council and NHS Healthcare Trust from using child protection procedures to force her sick son into psychiatric treatment without his parents’ consent and in disregard of competent but differing medical opinion  (telephone: Val Broke Smith: 01564 - 778649).

 

Refusal by some doctors to accept what is known about ME /ICD-CFS may raise the question of whether or not such doctors are in breach of their contract of employment

if that contract requires them to keep abreast of advancing medical knowledge. Guidance issued by the General Medical Council (GMC) requires that doctors  “must observe and keep up to date with the laws and statutory codes of practice which affect your work.” [105] The law cannot be used to enforce alternative treatment on a patient already receiving competent medical treatment just because doctors disagree.

 

The fact that so many doctors do not keep reasonably up-to-date about ME / ICD-CFS has enormous implications for patients. [106]

 

 

Changing Definitions: History of Chronic Fatigue Syndrome (CFS)

 

In the US in the late 1970s and 1980s there seemed to be a remarkable rise in incidence of a condition indistinguishable from ME, with manifestations of serious neuro-immune disease and profound incapacity, to the extent that the powerful insurance industry became alarmed. The insurance industry was concerned that, because there is no National Health Service in the US: 

 

             “the field could change from an epidemiological investigation into                

               a health insurance nightmare”. [107]

 

The result was a determination to suppress the true symptomatology and to construct a new case “definition” for which insurers could not reasonably be liable: the condition was henceforth to be called ‘chronic fatigue syndrome’ or CFS and emphasis was to be on chronic “fatigue” as the primary symptom.  The case definition required every sign of organic illness to be excluded before the diagnosis of “CFS” could be made. As a result, the view that patients were clearly afflicted by serious neuro-immune illness was to be strenuously down-played for many years. [108]

 

“CFS” did not come into existence until 1988.  As a basis for sound scientific research, it has been a disaster. “CFS” is not a single diagnostic entity and “fatigue” is not a disorder, it is a symptom. The term “CFS” is now applied to a heterogeneous group as a non-specific label which embraces many different medical and psychiatric conditions in which tiredness and fatigue are prominent.

 

The first definition of CFS  (1988 Holmes et al) concentrated on “fatigue” persisting for at least six months; it expressly excluded the cardinal features of ME which had been documented for decades despite the fact that ten years earlier, the UK Royal Society of Medicine had accepted ME as a distinct nosological entity. In 1988 in the US, the eighteen strong panel of medical scientists and clinicians charged with formulating a new case definition and new name could not agree:  two of the most experienced members refused to sign the final document and withdrew from the panel because the proposed definition and new name were too different from the ME with which they were so familiar.[109]  Those two members were Dr Alexis Shelokov from the US and Dr Gordon Parish from the UK. Dr Parish now lives in Scotland and is curator of the Ramsay Archive, which is possibly the world’s largest collection of medical papers on ME which pre-date 1988.

 

 

How “CFS” displaced ME in the UK

 

At about the same time (1988) in the UK, psychiatrist Simon Wessely rose to prominence.

Wessely leads a group of UK doctors, mostly but not exclusively psychiatrists, who have colloquially become known as the “ Wessely School”.[110]  Wessely is now Professor of Epidemiological and Liaison Psychiatry at Guy’s, King’s and St Thomas’ School of Medicine, London and at The Institute of Psychiatry, where he is Director of both the CFS Research Unit and the Gulf War Illness Research Unit. He is well-known for his strongly-held beliefs that neither ME nor Gulf War Syndrome exists, [111] and that such patients are mentally, not physically, ill.

 

Since the late 1980s he and his close colleagues have assiduously attempted to obliterate recorded medical history by insisting that there is no such disorder as “ME”, claiming that previous studies of ME “reflect those who seek treatment rather that those who suffer the symptoms”, [112]  even though those studies were published in peer-reviewed prestigious medical journals and span over sixty years.

 

Despite the fact that the International Classification of Diseases is approved by all the countries who are part of the World Health Assembly, Wessely believes the WHO got it wrong about ME, writing in the Lancet:

 

         “The inclusion in the tenth revision of the International Classification of Diseases

           (ICD-10) of benign myalgic encephalomyelitis as a synonym for postviral

           fatigue syndrome under Diseases of the Nervous System seems to represent

           an important moral victory for self-help groups in the UK.  Neurasthenia remains

           in the Mental and Behavioural Disorders chapter under Other Neurotic Disorders.

           Neurasthenia would readily suffice for ME.  Applying more stringent criteria for

           CFS in the hope of revealing a more neurological sub-group succeeds only in

           strengthening the association with psychiatric disorders.  We believe this latest

           attempt to classify fatigue syndromes will prevent many people from seeing the  

           world as it actually is”. [113]

 

In the ICD classification the section entitled “Mental and Behavioural Disorders” (section F-48.0 subtitled “Other Neurotic Disorders”) includes  “neurasthenia” and “fatigue syndrome”. ME, CFS and PVFS are specifically excluded from the psychiatric section F-48.

 

Wessely’s views of those afflicted by ME / ICD-CFS are well-known, and may be summarised in just two illustrations:

 

        “The description given by a leading (doctor) at The Mayo Clinic remains accurate:

          ‘the doctor will see that they are neurotic and he will often be disgusted with

          them’ ” [114]

 

         “There lies at the heart of CFS not a virus (or) immune disorder, but a distortion

           of the doctor-patient relationship”  [115]

 

 

Wessely’s determination to eradicate ME as a legitimate medical entity seems never to cease. Perhaps his most blatant attempt to change the WHO classification from neurological to psychiatric can be found in his contribution to the WHO Guide to Mental Health in Primary Care (November 2000) in which ME is notoriously re-classified as a mental disorder. Psychiatrists at King’s College Hospital and The Institute of Psychiatry are designated as one of the WHO Collaborating Centres and as such are entitled to use the WHO logo. Use of the WHO logo implies that contributions carry WHO sanction, but in this particular instance, such is not the case and Wessely’s actions brought forth international condemnation.  The WHO has confirmed that what Wessely published about the classification of ME in the Guide to Mental Health in Primary Care did not carry WHO approval, stating

 

         “It is possible that one of the several WHO Collaborating Centres in the United

           Kingdom presented a view that is at variance with WHO’s position”. [116]       

 

The present confusion has been compounded by the fact that the term “CFS” has been included by the WHO in the latest revision of the International Classification of Diseases as one of the terms by which ME has become known. In practice, this has come to mean that when referring to “CFS”, some doctors (mostly some UK psychiatrists led by Simon Wessely) are talking about psychiatric illness involving “chronic fatigue”, whilst international experts are talking about ICD- CFS, which is synonymous with ME. 

 

It is important to be aware that published international research on CFS  (as distinct from UK psychiatric research on CFS) reflects patients who are likely to have ME rather than psychiatric disorder.

 

The essence of the confusion concerns the use in the UK of the combined term “CFS/ME”,  given that “CFS” means different things to different people. 

 

On the one hand there is an extensive published record by the UK “psychiatric CFS” school promoting their view that ME no longer exists and that CFS  (a term they use interchangeably with chronic or long-term “fatigue” [117] [118]) is a psychiatric (behavioural) disorder with no physical signs which is perpetuated by aberrant “illness beliefs” and “personality” [119]  which is best managed by a form of psychotherapy known as cognitive behavioural therapy (CBT) and delivered according to a “management plan” administered by psychotherapists. Wessely himself has published over 200 papers mostly on his own view of CFS but his beliefs are not supported by international experts and there is stringent criticism of his papers in the peer-reviewed medical literature (see below).

 

On the other hand, ME /ICD-CFS is formally classified as a neurological disorder in the WHO International Classification of Diseases. The whole area of terminology has become a minefield for the unwary, to the serious detriment of patients.

 

This dichotomy has been summarised by Fred Friedberg, Clinical Professor in the Department of Psychiatry at the State University of New York:

 

         “descriptive studies of CFS patients in England, the US and Australia suggest

           that the CFS population studied in England shows substantial similarities to

           depression, somatization and phobic patients, while the US and Australian

           research samples have been clearly distinguished from depression patients and

           more closely resemble fatiguing neurological illnesses”. [120]

 

It is important to be familiar with the fact that “chronic fatigue” and chronic “fatigue syndromes” do not equate with chronic fatigue syndrome (CFS) or with ME. 

 

Following an erroneous News Release in 1990 about this point, the American Medical Association was forced to issue a correction which said:  “A news release in the July 4 packet confused chronic fatigue with chronic fatigue syndrome; the two are not the same. We regret the error and any confusion it may have caused.  AMA Science News Editor: John Hammarley” [121] 

        

Wessely’s beliefs, however, have flooded the UK literature; he is adviser to the UK Government and to the Ministry of Defence and his wife (psychiatrist and GP Dr Clare Garada) is Senior Policy Adviser to the Department of Health.

 

Specifically, Wessely and those who agree with him officially advise that no investigations should be performed to confirm the diagnosis; [122]  particularly, they emphasise that immunological abnormalities (documented by worldwide researchers as underlying the disorder) should not “deflect the clinician from the (psychiatric) approach….and should not focus attention towards a search for an ‘organic’ cause”.  In this respect it is notable that it has been convincingly demonstrated that changes in different immunological parameters correlate with particular aspects of ME / ICD-CFS symptomatology and with measures of disease severity, lending further support to the concept of immunoactivation of  T- lymphocytes. [123]   Such findings seem to be intentionally diverted by Wessely and his colleagues, who officially advise Government that the performing of medical investigations on patients with ME or CFS is neither necessary nor appropriate and that doing so merely reinforces sufferers’ “dysfunctional belief” that they are physically ill,

from which they seek to obtain secondary gain in the form of sickness benefits and from the relinquishing of personal responsibility for their imagined ill-health.

 

Wessely and his associates ignore the fact that ME is often confused with multiple sclerosis. [124]  They also ignore the evidence that ME /ICD-CFS has features of autoimmune disorder and features of allergy and multiple chemical sensitivity (MCS), [125] [126] [127] [128] [129] [130]  which is now officially recognised in the International Classification of Diseases, (ref: ICD 10: SGBV:3.1:code T78.4: Chemical Sensitivity Syndrome, Multiple). Data presented at the American Association for Chronic Fatigue Syndrome (AACFS) Fifth International Research and Clinical Conference in Seattle in January 2001 showed that MCS was present in 42.6% of patients compared with 3.8% of controls. [131]  Wessely, however, asserts that MCS does not exist and that along with fibromyalgia (in apparent contempt of the fact that FM is formally classified as a legitimate physical disorder in the International Classification of Diseases under Soft Tissue Disorders ref ICD-10 M.79.0 ), conditions such as irritable bowel syndrome, pre-menstrual tension, globus hystericus, tension headache and chronic fatigue syndrome should all be classed as one entity because, he claims, all occur more frequently in women and all are associated with unnecessary expenditure of medical resources and are afforded unjustified credibility largely because of “an artefact of medical specialisation”: Wessely believes this one entity to be a psychiatric disorder which he terms a “functional somatic syndrome”. [132] 

 

Psychiatrists who do not subscribe to the “Wessely School” doctrine point out that “somatic syndromes” are simply assumed to be without a physical cause, but this assumption is never tested or validated; they advise that it is a mistake to diagnose mental illness in people with ME / ICD-CFS because of the unproven and incorrect assumption that their physical complaints are of psychological origin. [133]

 

Wessely and colleagues also dismiss the evidence that immune abnormalities documented in ME/ ICD-CFS follow a recognisable, consistent and reproducible pattern, with clear evidence of an immune activation state.

 

It is true that the immune system dysfunction is not reflected in any of the currently used case definitions, hence the international support for a name change.  Currently, the favoured choice supported by the internationally renowned immunologist and ME /ICD-CFS expert Professor Nancy Klimas (of the University of Miami) is for NEIDS or

Neuro-Endocrine-Immune Dysfunction Syndrome or for CNDS (Chronic Neuroendocrineimmune Dysfunction Syndrome), both of which accurately reflect the nature of the underlying organic pathoaetiology.

 

It may well be the case that ME is one of the recognised conditions which are characterised by chronic post-exertional fatiguability, but ME is different in clinical presentation from other chronic fatigue syndromes.  The evidence speaks for itself.

Other postviral fatigue states are clinically in contrast to the three cardinal features of ME.[134]  Other fatigue states which may follow flu, measles, chickenpox, herpes or mononucleosis lack not only the clinical but also the laboratory features of ME. [135]

 

There are no less than nine case definitions of CFS. [136]  The two most commonly used (the UK 1991 Oxford case definition which was drawn up by Wessely and his associates and the US 1994 CDC case definition, in the formulation of which Wessely participated) both unequivocally state that patients with CFS have no physical signs. In the US, in Australia and on the Continent, such a stipulation is now accepted as being unsatisfactory and apart from the UK (where the forthcoming Chief Medical Officer’s Report on CFS/ME  (see below) is likely to state that “on present evidence, (subgrouping CFS) may be considered a matter of semantics and personal philosophy”), there is an increasing clamour within the medical fraternity for the urgent need to study sub-groups of “CFS”  [137] [138] [139] [140] [141] [142]  because those with ME / ICD-CFS always do have observable physical signs and abnormal immunological laboratory results.

 

The overriding difficulty is that some clinicians in some medical disciplines apparently fail to see them, have no desire to look for them or even deny their significance and existence.

It is the case that some of those doctors have been funded for many years by sources with links to the same industry which manufactures the chemicals which may be contributing to the rise in incidence of chemically-induced ME / ICD-CFS.  They have also been funded by the insurance industry and by private interests such as The Linbury Trust which belongs to the Sainsbury (supermarket) family.

 

Since 1991, the Linbury Trust has funded over £4 million for research into CFS (which they call “chronic fatigue”), almost all of it by Wessely and his psychiatrist colleagues.

 

Since 1996, David Sainsbury (now Lord Sainsbury of Turville) has donated £7 million to the UK Labour Party. He is currently Minister for Science; as such, he has responsibility for the Office of Science and Technology and the Chemical and Biotechnology industries, as well as all the Research Councils, including the Medical Research Council. 

 

The MRC, itself often now funded by partnership schemes with industry, is on record as regularly funding research into “chronic fatigue” by psychiatrists and others who subscribe to Wessely’s views (who then claim that their results relate to “CFS”), whilst regularly declining to fund applications for research submitted by suitably qualified non-psychiatrists into the physical basis of ME, claiming of those applications: “none have been of sufficiently high scientific quality to merit funding”. [143]

 

This is notable, given that the psychiatric research done by Wessely’s close colleagues and co-authors which the MRC has funded has been rigorously criticised on the grounds that it is methodologically flawed and biased and that it relies on a highly selective and misrepresentative choice of references, including citing too many of their own studies as references.   [144] [145] [146] [147] 

 

In a letter to Wessely (made widely available), the Countess of Mar brought to his personal attention the fact that questions have been asked about his methodology, the selection of evidence he utilises, the obvious bias, and the lack of balance and objectivity.[148]   That same letter continued

 

             “You must recognise that you and your colleagues have an enormous

               influence on the treatment meted out to a very large group of sick people.

               How you managed to achieve this influence is a matter for conjecture”.

              

   

The Office of Science and Technology monitors all government funding of research grants and controls official science policy and it is “policy” which determines the research which

is funded: “The Department funds research to support policy”. [149]

 

It is the case that in 1998, Wessely joined a Board of the Medical Research Council but it is unthinkable that he would be asked to read, report on or referee anything to do with his own work. It is also the case, however, that from 1989 to 1992  the MRC granted the Institute of Psychiatry £92,000 for research on “chronic fatigue”.

 

Since 1988, psychiatrists of the “Wessely School” have been funded not only by the MRC but by Wellcome Training Fellowships in Clinical Epidemiology; by a Wellcome Research Fellowship in Epidemiology; by the Wellcome Trust; by ICI Pharmaceuticals; by Pfizer UK; by Duphar Pharmaceuticals; by The Linbury Trust; by the Medical Policy Group of the Department of Social Security; by the Department of Health;  by Private Patients Plan by BUPA and by the US Department of Defense.

 

If influential doctors can succeed in portraying ME as non-existent and CFS as psychiatric in origin, then the chemical companies and the governments who granted them product licences would not be at risk of being accountable should there turn out to be a provable link with the synergistic effects of so many chemicals, daily exposure to which is now impossible to avoid due to the huge increase in chemical usage. It is this prevailing use of so many chemicals which is thought to be chronically stimulating the immune system. [150]

In the shadows is also the massive insurance industry, which cannot ever face liability for chemical injury or environmental illness without considerable strain and even collapse.

 

Accountability becomes more remote if all research which demonstrates the link between chemicals and the present upsurge in chemically-induced ME / ICD-CFS is blocked, dismissed, trivialised, ignored or discredited.

 

As well as being advisors to the UK Government, some of this same group of doctors are also known to have indisputable long-term commitment to the insurance industry and have acted as advisors to it, notably Professor Wessely and his close colleague and co-author Michael Sharpe, also a psychiatrist who claims to be a specialist in “CFS”.  Many illustrations could be provided; only one is mentioned here. On 17 May 1995 both Wessely and Sharpe were the main speakers at a symposium held at the London Business School entitled “Occupational Health Issues for Employers” at which they advised employers how best to deal with employees who are on long-term sickness absence with “ME”.  Information presented included informing attendees that ME/CFS has also been called “the malingerer’s excuse”. Another speaker at this conference was Dr John le Cascio, Vice President of UNUM.

 

 

Just three extracts from a copy of UNUM’s  “Chronic Fatigue Syndrome Management Plan” seem significant:

 

(i)      Diagnosis:  Neurosis with a new banner

(ii)    UNUM stands to lose millions if we do not move quickly to address this increasing  

  problem

(iii)  attending physicians (must) work with UNUM rehabilitation services in an effort to  

       return the patient / claimant back to maximum functionality with or without

       symptoms.

 

 

Apart from those mentioned, there are other areas related to ME / ICD-CFS in which Wessely is known to have special interests, none of which he usually declares.

 

One of these is PRISMA, which stands for Providing Innovative Service Models and Assessments.  It is based in Germany and is a multi-national healthcare company working with insurance companies; it arranges rehabilitation programmes for those with “CFS” and its recommended management is cognitive behavioural therapy, placing heavy emphasis on training sufferers to “regain a normal life again”. PRISMA claims to be especially concerned with long-term disability from the perspective of government, service providers and insurance companies.  It claims to have developed a “unique treatment programme”  for “hopeless” cases (it specifically includes those with ME /CFS), claiming that such patients “avoid physical exercise and social activities, as they fear these may trigger new bouts of complaints”.  In the PRISMA Company Information, Professor Simon Wessely is listed as a Corporate Officer. He is a member of the Supervisory Board; in order of seniority, he is higher than the Board of Management.  He is listed as a “world expert” in the field of  “medically unexplained illnesses, including Chronic Fatigue Syndrome”. [151]   Is it possible that Wessely is recommending to the Chief Medical Officer a management programme for “CFS” which is known to be harmful for those with ME / ICD-CFS [152] and which is provided by a company of whose Supervisory Board he is a member?

 

Another area with which Wessely is known to be involved is the organisation now called HealthWatch, but which used to be called The Campaign Against Health Fraud. This UK organisation, now a charity, is known for its zealous views which are antagonistic towards alternative and complementary medicine, and towards those who believe in environmental and chemically-induced illness, including multiple chemical sensitivity.  It is a campaigning organisation which in the past has accepted funding from both pharmaceutical companies and the health insurance industry. [153]  [154]  In the Campaign’s own literature, it states that it plans a programme of public information and that its aims are “to oppose…unnecessary treatment for non-existent diseases”.  The same document lists Simon Wessely as a “leading member of the campaign”, together with other doctors including other psychiatrists and Dr David Pearson of Manchester. [155]  It is the case that Wessely asserts that ME is a “non-existent” disease. [156]  [157] 

 

Pearson became notorious [158] for his evidence for the Defence in the High Court in London in 1991 [159] in which he relied upon an unauthorised draft report from the Royal College of Physicians entitled Allergy: Conventional and Alternative Concepts despite a letter from solicitors for the Royal College of Physicians (Field Fisher Waterhouse) forbidding him to use it; the letter, dated 18th October 1991, stated  “The College is not in a position to endorse the contents or conclusions of the draft you have seen…we must ask that this letter be brought to the attention of the Judge”. The draft report upon which Pearson relied in evidence was subsequently subjected to stringent critical review and was withdrawn; it was substantially amended on the grounds that Fellows of the College found it to be wildly inaccurate and misleading, but the Judge (Mr Justice McPherson) did not know this and found against the Plaintiff (who could not obtain Legal Aid to mount an appeal).  It is difficult to know how significantly the Judge was influenced by the inaccurate draft report, but it is likely that he would have been influenced by an apparently prestigious report supposedly backed by the Royal College of Physicians.

 

The HealthWatch website has links to other Internet sites, including amongst others the Advertising Standards Authority, a body which regulates advertising and which HealthWatch members have used to discipline alternative therapy practitioners; the American Council on Science and Health, a powerful group which is sponsored by multinational industry including pharmaceutical companies; the Association of Broadcasting Doctors; the Food and Agriculture Organisation; Net Doctor; NHS Direct Online; the UK Department of Health and the Cochrane Collaboration (a sibling of the Centre for Reviews and Dissemination based at the University of York, which carried out the review of the literature for the Chief Medical Officer’s forthcoming report and which recommended cognitive behavioural therapy as “best practice” management of CFS/ME.

The Chief Medical Officer has himself confirmed in writing [160] that it was Wessely’s own database which formed the basis of that literature review; it is a matter of record that Wessely himself was adviser to the team which carried out the review).

 

 

The Chief Medical Officer’s Working Group on CFS/ME

 

In 1998 the UK Chief Medical Officer (CMO) set up a Working Group to produce an official Report on ME and CFS: many people hoped and believed that the aim was to produce accurate information about the condition so that UK clinicians would be brought up to date with current scientific knowledge.  In reality, the remit of the CMO’s advisory group was narrow: it was restricted to just one single aspect, namely to advising UK clinicians as to the best way of managing the disorder, it being acknowledged that currently, there is no effective treatment.

 

Of special concern is the fact that the remit specifically dictated that ME and CFS should be considered as one entity: this has been particularly problematic, because the most influential members of the Working Group are Simon Wessely and his psychiatrist colleagues.  Psychiatrists and those who agree with Wessely’s beliefs are heavily represented on the Working Group and it is known that their beliefs about the nature and management of the disorder have dominated the proceedings.

 

To the concern of many researchers and clinicians, advice that only the most basic screening should be carried out on patients with CFS/ME is likely to be enshrined in the CMO’s forthcoming Report, the final draft of which specifically advises that no immunological tests and no nuclear medicine scans should be carried out on patients suspected of suffering from “CFS/ME” (even though it is these two areas which are delivering the strongest evidence of organic pathoaetiology). 

 

Also of concern is the fact that whilst Deputy Chair of the CMO’s Working Group on CFS/ME, Professor Anthony Pinching of St Bartholomew’s Hospital, London published an article in Prescribers’Journal in which he asserted that “over-investigation can (cause patients) to seek abnormal test results to validate their illness”. [161]   Such views are in stark contrast to those expressed by international researchers, whose clear message is that basic laboratory testing is not sufficient for patients with ME / ICD-CFS, and that more advanced immunological and neurological tests are necessary. [162] 

 

As long ago as 1994, world-renowned ME/ ICD-CFS clinician and researcher

Daniel Peterson stated in his Introduction to an International Research and Scientific Conference: [163]

 

        “I take great issue with the current recommendations that no additional testing

         should ever be done.  I believe there are indications for more advanced testing”.

 

As recently as July 2001, the American Medical Association issued a statement, explaining that 90% of ME / ICD-CFS patients show normal test results on basic investigations, and that studies designed for specific subgroups are needed.  Anthony Komaroff, Associate Professor of Medicine at Harvard and an undisputed world expert on the disorder, said:

 

        “Researchers are already using imaging technology to measure brain hormones

          and are examining the function of the immune system.  There is considerable

          evidence already that the immune system is in a state of chronic activation in

          many patients with CFS”. [164]

 

In the UK, it seems that clinicians are to be advised that it is inappropriate and unnecessary even to look for such pathology in those who are thought to have this disorder.

 

The final draft of  the CMO’s forthcoming report states that management is to be psychiatric (cognitive behavioural therapy and graded exercise), and that future NHS services for “CFS/ME” patients “ideally would adopt a biopsychosocial model of care---

The components of such a service are facilities for activity management”.

 

In the final draft of November 2001, there is no recommendation (nor even any acknowledgment of the need) for the urgent establishment of centres of excellence which would provide facilities to look at the underlying immunology, neurology, endocrinology or the molecular biology of ME / ICD-CFS, but only for more psychiatric services; the need for provision of in-patient care or suitable respite care for such very sick people is notable by its absence.

 

 

Caution Needed by Clinicians and Lawyers

 

It is essential to be ever mindful of the fact that it is unsafe to assume that the most prolific published author on a subject is necessarily the unquestioned expert on that subject.  This is especially true in relation to ME / ICD-CFS, where Wessely is keen to promote himself as a medico-legal expert.[165]

 

In any medical discipline, the selective or multiple reporting of studies as if they were different trials, sometimes by  “shifting first authorship”, makes it difficult to detect duplicate publications in different journals: examples of this practice in psychiatry include one trial which had been published (in one form or another) in 83 separate publications. [166]

 

Once again, however, medical science is seeking to expose such deliberate manipulation of the facts. Undeclared competing interests which in reality underlie numerous published biomedical studies are again in the spotlight, with editors of JAMA  (Journal of the American Medical Association) and the BMJ Publishing Group now looking for ways to ensure that the studies which they publish are free from hidden bias. [167]  This supports the acknowledgment by medical science that the problem not only exists but is considerable, and that it is essentially a form of scientific misconduct. [168]  In an Editorial in 2000 in the journal Psychological Medicine entitled “Publication Bias”  [169] Gilbody and Song state

 

     “Despite psychological researchers being the first to recognize the importance of

       publication bias (Sterling, 1959), this issue has been all but ignored in the sphere of 

       mental health. Publication bias needs to be dealt with if psychiatry is going to become

       more ‘evidence-based’.  The continued existence of publication bias represents an

       abuse of the trust that patients give and is essentially a form of scientific misconduct.

       The recognition of the potential consequences of publication bias has led to important        

       advances in its minimization and detection.  However, these methods are rarely

       employed when they should be in psychiatry.  This is unfortunate when, compared to

       other specialities, psychiatry is likely to be especially prone to publication bias.

 

     “The cornerstone of evidence-based medicine is the belief that good quality research

       should form the basis of clinical practice and decision-making. It is largely published

       research that forms the ‘knowledge base’ of the evidence movement. A fundamental

       difficulty arises when published research results are a biased sample of all research

       results. 

 

       “A consequence is the danger that readers of journals are more likely to see studies

         showing results in a certain direction”.

 

In the UK, nowhere is this more pertinent than in the field of ME / ICD-CFS.

 

 

Conclusion

 

Clinicians and lawyers need to be fully aware of the political undercurrents surrounding the reality of ME, ICD-CFS and CFS.

 

They need to come to their own conclusions about what might motivate a group of doctors to disassemble a formally classified neurological disorder and endeavour to replace it by a much larger category of psychiatric “behavioural” illness.

 

They need to consider how, despite there being such an extensive worldwide literature on the organic nature of ME / ICD-CFS, a group of UK doctors has come to exert such influence over the rest of the UK medical community to the extent that discussion of the biomarkers of serious organic pathology is rarely published in the UK medical journals, with the result that UK clinicians are effectively being deprived of the opportunity to obtain an informed and balanced over-view of the reality of their patients’ suffering, as the literature they are most likely to see reflects only the views of Wessely and his associates.

 

Lawyers may wish to reflect on some of the practical consequences of the denial of ME / ICD-CFS; these include:

 

--- refusal and denial of state benefits: those with a psychiatric diagnostic label are denied

     the higher rates of some state benefits and do not usually qualify for the Disability  

     Living Allowance (DLA), which requires that the recipient has a physical disability

 

--- difficulties in obtaining insurance benefit if unable to work through ill-health (some

     health insurance companies expressly exclude psychiatric illness)

 

--- difficulties in obtaining private health care insurance (again, some companies do not

     provide cover for psychiatric disorders)

 

--- difficulties in obtaining early retirement on health grounds

 

--- unfit patients are forced to return to work

 

--- inappropriate treatment (some ME sufferers have been threatened with being sectioned

     under the Mental Health Act unless they comply with psychiatric treatment)

 

--- withdrawal of Out of Area Treatment / Transfers for those with ME / ICD-CFS 

     (necessary if no suitable clinician is available within the patient’s own Health Authority

     area; there is a marked lack of appropriate referrals, eg to neurologists, immunologists

     endocrinologists etc )

 

--- lack of appropriate service provision within the NHS

 

--- special problems for children and young people with ME.

 

Lawyers may wish to consider that on 23rd November1999 the House of Commons Select Health Committee produced its report looking at adverse clinical incidents, unexpectedly poor outcomes to treatment, failures in medical care, poorly-performing doctors and the NHS complaints procedures; the Select Committee took evidence and representations from at least eight people about ME. [170]

 

It may also be of interest to lawyers to know that the opinion of an eminent Leading Counsel (a member of the House of Lords) has been obtained and that this Opinion is unequivocal.  It states:

 

             “ On the document you have sent me there is an overwhelming case for

               the setting up of an immediate independent investigation as to whether

               the nature, cause and treatment of ME as considered by the Wessely

               School is acceptable or consistent with good and safe medical practice.

 

             “ There is substantial doubt as to whether such could be the case in view

                of the clear division of medical opinion.

 

              “A formal request should be made to set up such an enquiry, at which interested

                parties could be represented by Counsel.  It is all but essential that a reputable

                firm of solicitors should be instructed: an approach to Lord Mishcon would be

                well advised”. [171]

 

 

Lawyers may wish to consider if a small group of exceptionally influential doctors should be allowed to determine public policy without there being some external moderation.

 

They may wish to consider why disease definition has become socially constructed, resulting in political tensions between sufferers, medical science and the modern State,

a consequence of which is the intentional construction of “mental illness” by some groups of medical professionals resulting in stigma caused by the on-going denial. [172]

 

If clinicians and lawyers are unaware of this background and accept the readily proffered psychiatric explanations as if objective and based on sound scientific research, they will be unable to support their patients / clients with ME / ICD-CFS and will risk failing in their professional duty in this difficult area.

 

 


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    Paul LA et al  European Journal of Neurology 1999:6:63-69

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[64]  Lack of association between HLA genotype and chronic fatigue syndrome. Underhill JA,

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[65]  The Biology of the Chronic Fatigue Syndrome. Anthony L Komaroff  Am J Med 2000:108:

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    1996:31:1:7-18

[67]  Neuroendocrinology of Chronic Fatigue Syndrome. TG Dinan. Presented at the First World 

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[68]  Critical life events, infection and symptoms during the year preceding CFS. Theorell T et al

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[74]  Stress and Combined Exposure to Low Daily Doses of Pyridostigmine Bromide, DEET and 

    Permethrin in Adult Rats Causes Blood Brain Barrier Disruption and Neurochemical and

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[75] Objective Evidence of Brain Impairment in the Chemical Syndrome.  KH Kilburn.  ibid 

[76] Blood Brain Barrier Breakdown in Myalgic Encephalomyelitis. Behan W, Gow JW, Curtis F

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[77] personal communication (10 February 1992) from John Dwyer, Professor of Medicine,

   University of New South Wales, Australia 

[78] Is CFS linked to Vaccinations? Charles Shepherd.  The CFS Research Review 2001:2:1:6-8

[79] New light on the causes and management of postviral fatigue syndrome. Charles Shepherd.

   Modern Medicine 1988:287

[80] Environmental Medicine in Clinical Practice. H Anthony, S Birtwhistle, K Eaton, J Maberly.

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[82] Persistence of enteroviral RNA in Chronic Fatigue Syndrome is associated with the abnormal 

   production of equal amounts of positive and negative strands of enteroviral RNA.

   L Cunningham, NE Bowles et al  J Gen Virol 1990:71:6:1399-1402

[83] Evidence for Enteroviral Persistence in Humans. DN Galbraith et al  J Gen Virol 1997: 

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[84] Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS).

   DV Ablashi et al  J Clin Virol 2000: (3):16:179-191

[85] Evidence of Active HHV6 Infection and its Correlation with RNase L Low Molecular Weight

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[86] The Clinical and Scientific Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome

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[87] Outbreak at The Royal Free. ED Acheson. Lancet 20 August 1955:304-305

[88] M.E. Post-Viral Fatigue Syndrome. Dr Anne Macintyre. Unwin Hyman 1989

[89] Chronic Fatigue and Immune Dysfunction Syndrome: a Patient Guide. CFIDS Assn. 1989

[90] The Disease of a Thousand Names. DS Bell. Pollard Publications, New York 1991

[91] How do I diagnose a patient with CFS?  J.Goldstein. In: The Clinical and Scientific Basis of

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[92] Chronic Fatigue Sydrome: evaluation of a 30-criteria score and correlation with immune

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[93] Viral Isolation from Brain in Myalgic Encephalomyelitis (A Case Report).  John Richardson

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[94] Cardiac involvement in patients with CFS as documented with Holter monitor and biopsy data

   AM Lerner et al  Infectious Diseases in Clinical Practice 1997:6:327-333

[95] Lung function test findings in patients with chronic fatigue syndrome, De Lorenzo et al.

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[96] Icelandic Disease (Benign Myalgic Encephalomyelitis or Royal Free Disease). AM Ramsay

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[97] The ‘chronic mononucleosis’ syndromes. Komaroff AL   Hosp Pract 1987 (May):71-75

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[99] Chronic Fatigue Syndrome and Depression: Biological Differentiation and Treatment

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[100] Symptom patterns in long-duration chronic fatigue syndrome. F.Friedberg et al

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[101] Presentation by Dr Paul Cheney. CFS National Consensus Conference, Sydney,

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[102] Guidelines for the Blood Transfusion Service in the UK 1989:5.42 / 5.44 / 5.410; Department

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[103] Severely Neglected: ME in the UK.  Report from Action for ME.  March 2001

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[105] Good Medical Practice.  pub The General Medical Council, UK

[106] The position of Australian psychiatry in the CFS debate. N Phillips. Presented at The Alison

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[107] Osler’s Web: Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic.  Hillary

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[108]  ibid  (page 268)

[109]  ibid  (page 218)

[110]  Hansard (Lords) 19th December 1998:1013

[111]  Ill-defined notions. Ziauddin Sardar. New Statesman, 5th February 1999

[112]  Chronic Fatigue Syndrome.  Joint Royal Colleges’ Report CR54. RCP Publications Unit, 1996

[113]  Chronic Fatigue, ME, and ICD-10  David A, Wessely S. Lancet 1993:342:1247-1248

[114]  Chronic fatigue and myalgia syndromes.  Wessely S.  In: Psychological Disorders in General

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[115]  Chronic fatigue syndrome: an update. Anthony J Cleare, Simon C Wessely. Update (Recent

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[116] Letter from Dr B Saraceno, Director, Department of Mental Health 16 October 2001

[117] A Research Portfolio on Chronic Fatigue. ed. Robin Fox for The Linbury Trust. pub. The

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[118] New research ideas in Chronic Fatigue. ed. Richard Frackowiak and Simon Wessely for

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[119] Final draft of CMO’s Report on CFS/ME, November 2001

[120] A Subgroup Analysis of Cognitive Behavioural Treatment Studies.  Fred Friedberg.

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[121]JAMA issues correction. Journal of the American Medical Association 1990 (referring to the

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[122] Chronic Fatigue Syndrome. Report of a Joint Working Group of the Royal Colleges of

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[124]  The Differential Diagnosis between Multiple Sclerosis and Chronic Fatigue Postviral

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[127]  Allergy and the chronic fatigue syndrome. Stephen E Straus, Janet Dale et al  J All Clin

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[128]  History of the chronic fatigue syndrome. Stephen E Straus. Rev Inf Dis 1991:13:1:S2-S7

[129]  Epidemiology of Chronic Fatigue Syndrome. Paul Levine. Clin Inf Dis 1994:18:1:S57-S60

[130]  Comparison of patients with chronic fatigue syndrome,fibromyalgia and multiple chemical

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[131]  Multiple Chemical Sensitivity in CFS.  JN Baraniuk et al.  AACFS Seattle, Jan 2001 # 124

[132]  Functional somatic syndromes: one or many: S Wessely, C Nimnuan, M Sharpe 

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[133]  How to differentiate CFS from psychiatric disorder. E.Stein.  Presented at The Alison Hunter 

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[134]  Myalgic encephalomyelitis or what?  AM Ramsay. Lancet 1988:100

[135]  ibid: 101

[136]  Report from The National Task Force on Chronic Fatigue Syndrome, Post Viral Fatigue

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[137]  Editorial: Roberto Patarca- Montero Journal of Chronic Fatigue Syndrome 2000:7:4:1

[138]  Politics, Science, and the Emergence of a New Disease: the case of Chronic Fatigue

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[139]  Conference calls for serious research. T Lupton  CFIDS Chronicle 2001:14:1:12-13

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[141]  A Definition-based Analysis of Symptoms in a Large Cohort of Patients with CFS.

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[143]  Written reply from the Parliamentary Under-Secretary of State for Health, 18 January 1996  

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[144]  The Royal Colleges’ Report on CFS: Insidiously Biased and Potentially Harmful. T Hedrick

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[145]  Editorial: Frustrating Survey of Chronic Fatigue. Lancet 1996:348:971

[146]  Why doctors are failing ME sufferers. Richard Horton (Editor of The Lancet):

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[147]  Chronic Fatigue Syndrome.  TE Hedrick Quarterly Journal of Medicine 1997:90:723-727

[148]  Letter to Professor Wessely from the Countess of Mar  18th February 2000

[149]  Hansard 11th May 2000: 461W - 462W

[150]  Human endogenous retrovirus: nature, occurrence and clinical implications in human

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[152]  Medical and Welfare Bulletin. 2001:2:8  pub by The ME Association, Essex, UK

[153]  Hansard (Lords), 28th April 1993:364-382

[154]  Hansard (Lords), 10th May 1995:66-68

[155]  Subscription Form for CAHF (now HealthWatch), 1990

[156]  Microbes, Mental Illness, the Media and ME: The Construction of Disease. Simon Wessely.

     The 9th Eliot Slater Memorial Lecture, The Institute of Psychiatry, London, 12th May 1994

[157]  Eradicating ME: Report of a meeting held on 15th April 1992 at Belfast Castle. Pfizer / Invicta

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[158]  Dirty Medicine. Martin J Walker pub:  Slingshot Publications, BM Box 8314, London 1993

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[160]  Letter from Professor Liam Donaldson, CMO, September 1999, ref PO319/99

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[162]   Immunological studies on the blood of patients with Gulf War Syndrome. A.Vojdani.

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[163]   Introduction to Research and Clinical Conference.  Daniel L Peterson.  Journal of CFS 1995:

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      held at Fort Lauderdale, Florida, 7th - 10th October 1994, co-sponsored by the National

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[164]  American Medical Association Statement, Co-Cure: 17th July 2001

[165]  Letters. Simon Wessely. The CFIDS Chronicle, Summer 1994:77

[166]  Publication bias and the integrity of psychiatric research. Editorial: SM Gilbody, F Song

     Psychological Medicine 2000:30:253-258

[167]  Biomedical Journals Ponder the Failures and Remedies of Peer Review.  Joan Stephenson

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[170] Sixth Report: Procedures Related to Adverse Clinical Incidents and Outcomes in Medical

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[171] Written Opinion from Leading Counsel (2, Kings Bench Walk) Temple, London) 6th April 2000

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