When I saw Dr Dowsett In September 1994 she gave me a
document call
"ME In a Nutshell" which is on the official part of my site. This
page is just here for those in the know. I had reason to consult Dr Dowsett
by phone and she was kind enough to send me these new notes. I think they are
fairly self-explanatory so I have OCR’ed them. I there were a few pictures
but I have not included them since I am not sure Dr Dowsett would want it on
the Internet. I forgot to ask. I will therefore leave it as is for now
and see what happens. If you have any questions please ask me.

PATIENT’S INFORMATION SHEET

THE ENIGMA AND THE PARADOX OF ME

A. WHAT IS ME/CFS?:

It is a disorder initiated by a common virus infection of
which (rather like influenza) several strains circulate annually in the general
population giving rise to sporadic cases or to local epidemics and world-wide
pandemics at 10-20 year intervals. Although clusters of infection have always
been recognised in families, schools and Health Care institutions, the
vast majority of cases (especially in the very young) are symptom free.(1, 2)

B IS IT A NEW DISEASE?: (1, 2, 3, 4)

No, it is probably as old as the human race but, in communities
living in temperate climates who enjoy high standards of housing and public
sanitation, awareness has been raised by a striking new phenomenon of the 20th
century – major epidemics of poliomyelitis (formerly a rare disease of
early childhood) followed sequentially, seasonally and geographically by a parallel
increase in ME/CFS (formerly considered to be an “atypical” or non paralytic
form of poliomyelitis).

C IS THERE ANY PROOF THAT ME/CFS IS BECOMING MORE COMMON? (3,4,5)

Undoubtedly! – between 1934 and the decline of polio following
immunisation in the early 1960’s, 38 epidemics of ME/CFS were clearly recorded
(in Northern parts of America, Canada, Europe and in southern areas of Africa,
Australia and other well developed countries with cool/temperate climates).
Since that time, outbreaks of ME/CFS have continued unabated in these areas
and have also been documented from New Zealand Japan and China. No government
has yet adequately funded a major demographic survey of the affected population
but individual studies estimate some 5 million cases between North America,
Europe and Australasia while approximately’/2 million have been reliably diagnosed
in tile UK (where a study of 360,351 members of the school population indicates
a prevalence of 70/100,000 in pupils and 500/100,000 in staff). (6.7)

D THE PARADOX AND THE ENIGMA OF ME:

Why is it that ME/CFS (like poliomyelitis) becomes more
rather than less common in communities with access to good housing, clean running
water and the high standards of sanitation which first became universally available
in the 20th century? Both disabilities are triggered by related viruses which
are finely adjusted to harmless multiplication in the juvenile respiratory and
intestinal tracts of humans.(7) This mutually beneficial adaptation between
virus and host immune system operates to ensure life-long natural immunisation
during the period between weaning from maternal antibodies in breast milk and
the onset of puberty. A major hormonal disturbance (with gradual onset from
7 years of age) begins to change the host’s immune T1/T2 orientation causing
a breakdown in host-virus adaptation. The resulting inflammatory immune response
is more severe and more chronic in pubertal females, leading to an increase
in the female to male prevalence of ME/CFS from approximate unity to 3F:1M during
the childbearing years. (8) Thus, it is the reflection of a high standard
of hygiene (blocking the natural circulation of these viruses via the respiratory
or faecal-oral routes of infection during early childhood) rather than any
genetic mutation in the viruses concerned, that leads to the paradox of “diseases
of affluence” which are artificially postponed until adult life.(1)

E. WHAT ARE THE MAIN CLINICAL AND DIAGNOSTIC FEATURES OF ME/CFS?

1. CLASSIFICATION: ME/CFS is a multisystem syndrome (group of related symptoms)
with variable involvement of cardiac and skeletal muscle, liver, lymphoid
and endocrine organs but neurological dysfunction is essential
for diagnosis. The condition is therefore classified as a neurological
disease under the World Health Organisation international classification of
diseases (ICD 10).

2. ONSET, PRODROMAL ILLNESS AND PROGRESSION TO CHRONICITY (3,4,9) In over
60% of cases the illness is triggered by a short respiratory/gastrointestinal
infection characterised by malaise, headache, dizziness, nausea and muscle
pain with or without glandular enlargement, but otherwise indistinguishable
from other ‘flu like or gastric upsets. A more dramatic onset (following viral
meningitis, myocarditis or middle ear infection, for example) is also recognised,
but a trivial illness is often forgotten. In the majority of cases the infection
terminates here. In others, after a variable interval, a systemic disease
involving many organ systems but with major brain dysfunction, develops.
This post-encephalitic process miry also resolve, but other patients go on
to acquire the classical symptoms of ME/CFS in which chronic low grade brain
dysfunction combined with viral persistence leads to loss of bodily homoeostatis
(the inability of the brain to function adequately in reception, storage and
retrieval of information, thus preventing the major organs of the body from
making a smooth programmed response).

3. DIAGNOSIS: ME/CFS has, therefore, a very distinctive and clearly recognisable
symptom pattern which is present to a varying degree in all patients and which
clearly differentiates it from other so-called ”fatigue states”, Virtually
all the cardinal symptoms of this illness can be demonstrated in a GP surgery,
if supplemented by a detailed history and a well kept daily record since the
onset of the illness, of the hours in which the patient is able to maintain
activity, (as opposed to those spent sleeping/resting), A thorough physical
examination is best carried out by a doctor familiar with the patient’s previous
health, work or school record and family circumstances and who is well informed
about ME/CFS, particularly if similar patients have been seen in the practice.
Supplementary evidence of, organic disease, whether available from simple
laboratory tests carried out locally (eg. to exclude other illness)
or from more sophisticated and expensive research procedures,(10) is not,
as yet, considered diagnostic or confirmative as it is not invariably
present in such a fluctuating illness.

 

4. SYMPTOMS: The most characteristic and disabling symptom, of ME/CFS include:

i) Episodic Post Exertional Weakness and Malaise: These episodes
are commonly provoked by physical or mental over exertion during
periods of apparent well being. After a variable interval, a sense of weakness
and impending collapse develops, when the patient needs to lie down. This
can last for 1-7 days after the triggering event – a fact constantly overlooked
in “assessment tests” or questions to ascertain the patient’s exercise capacity
without reference to subsequent debility. (4)

ii) Sleep and Temperature Disturbance: This represents a reversal
of the normal daily sleep/wake and temperature rhythm, causing difficulty
in keeping awake and attentive in conventional daytime hours, but with a
“window” of energy somewhere within the 24 hours cycle when the subject
can take advantage of recreation or study. A 24 hour temperature chart can
demonstrate inversion of normal night and daytime readings which, if taken
in conjunction with a daily activity/rest record, provides a valuable guide
to patients and doctors of energy fluctuations and the need to plan activities
within the capacity available at any particular time.

iii) Pain and Tactile Hypersensitivity: Complaints of incapacitating
pain in almost any part of the body are common. However, local abnormalities
may not be found, since the majority of these abnormal sensations reflect
central nervous system dysfunction. They may include headaches, muscle and
joint pain (without inflammation) recurrent sore or “dry” throat, tender
lymph glands, and extreme sensitivity to touch, vibration, light, noise,
taste, smell, heat and cold.

v) Cardiovascular Symptoms (11) Disturbances of the autonomic nervous
system include rapid or irregular pulse rate and a tendency for the blood
pressure to fall in the upright position, leading to inefficient
distribution of blood among vital organs. Such irregularities of the circulation
are associated with sudden faintness on standing or sitting upright and
with characteristic attacks of facial pallor or flushing as well as with
coldness of the limbs.

v) Digestive Disturbances: These include irritable bowel symptoms,
constipation/diarrhoea, persistent nausea and difficulty in swallowing which,
if added to distortions of taste and smell, may lead to serious appetite
and nutritional disturbance.

i) Endocrine Dysfunction: Owing to metabolic disturbance of the
hypothalamus (the mid-brain control centre for endocrine function) patients
with ME/CFS have a greater than normal risk of thyroid, pancreatic, adrenal,
ovarian and other endocrine gland dysfunctions. The most common endocrine
problems are associated with failure of the hypothalamic/pituitary/adrenal
response to stress (12) and a tendency to insulin resistance (causing episodes
of low blood sugar levels in previously healthy individuals and “brittle
diabetes” in diabetic patients, already stabilised on insulin) This underlines
the importance of regular meals (including breakfast!) and adequate carbohydrate
intake for all sufferers.

vii) Emotional Control(13). While this is notoriously variable in
adolescents, patients of all ages experience sudden mood swings and additional
problems often ascribed to “panic attacks” or agoraphobia when exposed to
brightly lit noisy and confusing open spaces such as supermarkets and canteens.
These sensations arise from incoordination of mid brain nerve networks (eg
the limbic system). Disbelieving family members or colleagues must be firmly
assured of the organic cause of these attacks

viii) Cognitive and Associated Neurological Disturbance: (14) This
can be profound and may include reduced attention span, verbal and mathematical
difficulties and failure of short term memory; problems with balance, fine
motor control, tactile performance, impaired perception of space and shape;
disturbance of vision, hearing and voice production. Many of these problems
also reflect subtle changes in mid brain nerve connections rather than failure
of individual sense organs.

ix) A Prolonged Relapsing Course (4 ) This is one of the main distinguishing
features of the illness in comparison with other “fatigue states” and is
characterised by a series of relapses and remissions over months or years
with variations in symptom patterns and recurrence of early features such
as inflamed throat and glandular enlargement, in some patients.

F. UNDERSTANDING THE NATURE OF BRAIN DYSFUNCTION IN ME/CFS

Some 20 years ago, studies of the electrical activity of the brain in ME/CFS
indicated abnormal slow wave patterns and unequal activity between the 2 sides
of the brain in areas associated with memory. interpretation of speech and sound,
motor control, visuospatial discrimination and other cognitive features characteristic
of the illness. However, within the past 15 years more sophisticated methods
of measuring brain activity using radioactive tracers to determine metabolism
and glucose utilisation (SPECT and PET scans)(10) have also disclosed fluctuating
metabolic activity in the mid brain and brain stem.

This is an area which encompasses the major homoeostatic nerve
centres of the body, controlling daily cycles of activity, sleep, hormone output,
fluid balance, cardiovascular regulation, motor, sensory and pain control –
all the vital nerve networks which maintain life! The fluctuating metabolic
activity in this area readily explains the many symptoms of ME/CFS from episodic
weakness to “panic attacks” – but serial SPECT scans which may indicate metabolic
improvement over time, provide an impetus for correct management to encourage
stabilisation of the illness in all grades of severity. Patients should therefore
retain their ambitions, even if in a modified form, and never give up hope of
stabilisation at some useful level of activity. To this end, they should record
all symptoms (however bizarre they may seem to those who lack understanding),
for this vital information could assist further research into the organic basis,
of brain dysfunction in ME/CFS!

G. MEDICAL MANAGEMENT

There being, as yet, no specific medical treatment for ME/CFS,
the general principles of management remain as follows:

(1) AT THE ONSET OF THE ILLNESS OR IN SEVERELY AFFECTED PATIENTS: removal
from all stress and additional exposure to infection together with a sufficient
period of rest and convalescence for the illness to stabilise, is recommended.
Early signs of stabilisation may be recognised by a slight improvement in
memory or an increase in the active versus non active energy ratio
over 24 hours.

 

(2) CONSERVATION OF ENERGY: This is the first and most important principle
of management without which further symptomatic or experimental drug
treatment cannot be expected to succeed:

a) Because most sufferers from ME/CFS are already operating at or near their
maximum energy capacity while the decrease in brain metabolism following physical
or mental over exertion leads to delayed recovery and relapse.

b) Because resting energy expenditure is high in ME/CFS patients(15)
which means that the energy available for physical activity is being
diverted to fulfil this increased requirement.

 

c) Because in some patients, there are additional metabolic defects in
skeletal muscle leading to early lactic acidosis and increased pain and
weakness, following exercise. (16)

(3) REDUCTION OF STRESS: This is best managed from the start by accepting
that the illness may be long lasting and require a change in life style commensurate
with the known reduction in hypothalamic/pituitary, adrenal response to stress
and the resulting risk of relapse. Support from friends, families, social
and financial services should be sought from an early stage but provision
for recreation, holidays, and interesting hobbies is an essential strategy
for stress reduction.

 

4) SIMPLIFICATION OF WORK. (a) For the housebound the aim must be
to retain independence as far as possible by considering financial aid for
domestic care and house conversion, and for home tuition or training to
facilitate paid work at home in the future. (b) For those whose illness
has stabilised – it is essential to organise a gradual return
to education, training or work after checking provision for mobility, modified
time table, exam concessions, and part or flexitime working. (c ) For
those fit enough to work or study full time – a choice needs
to be made of a suitable career, without undue exposure to stress, compulsary
immunisations, infection, unsocial hours, difficult travel or environmental
requirements. A graded career progression, without exam pressure and with
facilities for, refreshment breaks and adequate holidays is desirable! NB.
An initial period of voluntary work, when exercise and stress capacity can
be tested, ‘should be considered (see Dr David Bell’s “All-Work-Test”, below!)(17)

H. WHICH PEOPLE ARE MOST AT RISK OF ME/CFS

Exposure to infection is the main factor. Occupational
risks in Teaching, Health Care and paramedical professions are at least 5 times
higher than in similarly stressful jobs, where employees are not exposed to
infection. (7) The incidence of ME/CFS is also high in parents or carers of
young children, those obliged to receive multiple immunisations for travel,
as well as those engaged in sewage, refuse disposal and water industries and
participants in recreational water sports. The peak age of onset in both sexes
is between 30 and 40 years with a secondary peak at puberty (most marked in
females). As in the case of polio, schools appear to be central to amplification
and dissemination of infection to the local community. (6)

I. PROGRESS DEPENDS ON:
(a) The activity of the patient’s immune system (prior contact
and adaptation to the infection in childhood may ensure a trouble free host/virus
relationship, while youth often appears to be an advantage). (b) The tendency
of any particular strain of virus to induce serious complications (eg
cardiac). (c) The age, gender and domestic/occupational circumstances of
the patient . (d) Genetic factors, (as yet undetermined) are probably
less important than environmental factors such as common exposure
to infection. (e) Early diagnosis and appropriate advice on management
will ensure medical, domestic, educational and occupational support from
the start.

J. RELAPSES MAY BE ASSOCIATED WITH (1):

(a) Immuno suppressive events such as concurrent infection
with other microbes, immunisation, steroid or cytoxic therapy. NB smoking reduces
local mucosal immunity (b) Hormone disturbance, including puberty, menstruation,
pregnancy but following the menopause, new onset of illness in females
falls sharply. (c) Mental or physical stress arising from head injury, whiplash,
surgery, malnutrition, climatic change, domestic problems, litigation, social
security assessments etc.. (d) Exposure to drugs which are psychoactive or vasoactive
including alcohol, anti-depressants or recreational substances and to neurotoxins,
pesticides and drugs which interfere with specific neuro transmitters (eg acetylcholine).

K. CHILDREN AND ADOLESCENTS(6)

Suffer more severely than adults from sleep and learning difficulties,
weight, appetite and mood control It is essential that doctors and parents should
liaise from the onset with school and other professional staff to minimise stress
and contact with school infections by ensuring adequate sick leave. Home tuition,
modification of class work and examination concessions must also be considered
as educational deficits can be long lasting, especially in the case of young
children, where they may lead to permanent language disability.

L. PROGNOSIS

This depends not only on the factors mentioned above but also
on the knowledge and determination of the individual patient to use the energy
available wisely. Experience gained in the rehabilitation of patients suffering
from the post polio syndrome in the USA (a condition clinically similar to ME/CFS)
indicate that once the principle of energy conservation, within individual limits,
has been accepted by the patients themselves, only 10% fail to stabilise.(18.)

APPENDIX(17)

Dr David Bell’s “ALL WORK TEST” – “No young person with ME/CFS should
be considered fit to resume school, college or work, unless they can first survive
3 hours in a Shopping Mall!”

E.G. Dowsett MB ChB. Dip. Bact.
Honorary Consultant Microbiologist
47 Drewsteignton, Shoeburyness, Essex SS3 8BA
(© Revised December 1998)

References:

(1) DOWSETT. EG, Human Enteroviral Infections, Journal of Hospital Infection.
1988; 11 : 103-115

(2) ACHESON ED, The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis,
Iceland Disease and Epidemic Neuro- American Journal of Medicine. 1959; 26 : 569-595

(3) HYDE BM, GOLDSTEIN J, LEVINE P. eds. The Clinical and Scientific
Basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Ottawa, Ontario,
Canada: the Nightingale Research Foundation. 1992 (Held in Library of the Royal
Society of Medicine, 1 Wimpole Street, London W1 M 8AE)

(4) RAMSAY AM. Myalgic Encephalomyelitis and Post Viral Fatigue states – The Saga
of The Royal Free Disease. 1988 *2nd Edition). 1988 London: GOWER Press (Obtainable
from the ME Association, 4 Corringham Road, Stanford-le-Hope, Essex SS17 OAH and
from The Royal Society of Medicine Library)

(5) BEHAN PO, BEHAN WMH, Epidemic Myalgic Encephalomyelitis in Clinical Neuroepidemiology
(ROSE FC, ed) PITMAN MEDICAL 1980: 374-389.

(6) DOWSETT EG, COLBY J. Long Term Sickness Absence due to ME/CFS in UK Schools:
An epidemiological study with medical and educational Implications. Journal of
Chronic Fatigue Syndrome. 1997; 3(2) 29-42.

(7) ARZOMAND ML. Chronic Fatigue Syndrome Among School Children and Their Special
Educational Needs. Journal of Chronic Fatigue Syndrome. 1998; 4(3): 59-69

(8) HYDE BM, CAMERON B, DUNCKER A. et al. Epidemiological Aspects of Myalgic
Encephalomyelitis/Chronic Fatigue Syndrome/Post Viral Fatigue Syndrome. Ottawa,
Ontario, Canada: The Nightingale Research Foundation. 1994 : 16-20

(9) DOWSETT EG RAMSAY AM, McCARTNEY RA, BELL EJ. Myalgic Encephalomyelitis
– a persistent enteroviral infection? Post graduate Medical Journal 1990; 66
: 526-530

(10) RICHARDSON J, COSTA DC. Relationship between SPECT Scans and Buspirone
tests in patients with ME/CFS Journal Of Chronic Fatigue Syndrome, 1998; 4(3)
– 23-37

(11) STREETEN DHP, BELL DS, Circulating Blood Volume in Chronic Fatigue Syndrome.
Journal of Chronic Fatigue Syndrome. 1998; 4(1) : 3-11

(12) DEMITRACK MA, et al. Evidence for impaired activation of the Hypothalamic
Pituitary Adrenal axis in patients with Chronic Fatigue Syndrome. Journal of Clinical
Endocrinology and Metabolism. 1991; 73 : 1224-1234.

(13) LEON-SOTOMAYER I, Epidemic diencephalomyelitis – a possible cause of neuropsychiatric,
cardiovascular and endocrine disorders. 1969. New York 1003 : Pagent Press International
Corporation

(14) BASTIEN S. Patterns of neuropsychological abnormalities, and cognitive
impairment in adults and children. In Hyde, BM. Goldstein J, Levine Peds. The
clinical and scientific basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.
Ottawa. Ontario, Canada. (See reference 3 above) 1992: 453-460.

(15) CHAUDHURI A, BEHAN WMH, BEHAN PO et al. Chronic Fatigue Syndrome. Proceedings
of the Royal College of Physicians, Edinburgh, 1998; 28 : 150-163

(16) LANE RJM, BARRETT MC, WOODROW D. et al Muscle fibre characteristics and
lactate responses to exercise in CFS. J Neurology and Psychiatry 1998; 64 :
362-367

(17) BELL DS. Chronic Fatigue Syndrome in Young People with ME. Lecture given
in London on 25.8.98.

(18) BRUNO RL, Interview in “ME – The New Plague”, COLBY J, Peterborough. First
& Best in Education Ltd. 1996; 39-54