Myalgic Encephalomyelitis [Chronic Fatigue Syndrome]: Guidelines for Doctors
April 8, 2002
Myalgic Encephalomyelitis: Guidelines for Doctors
Journal: J of Chronic Fatigue Syndrome, Vol. 10(1) 2002, pp. 65-80
Author: John Richardson, MB BS
Affiliation: John Richardson is affiliated with Newcastle Research Group,
Belle-Vue, Grange Road, Ryton, Tyne & Wear, NE403LU, England.
For those of us who are involved in the care of patients with this
condition, the recorded work of Biorn Signurdsson (1913-1953) in connection
with the Akureyn outbreak in Iceland which affected over 1000 patients,
both children and adults was repeated by Melvin Ramsay when he was involved
in the outbreak in his hospital which became known as the "Royal Free
Disease" but defined by him as Myalgic Encephalomyelitis. This was followed
by an excellent monograph in 1969 by Luis Leon-Sotomayor published by
Pageant Press International Corp., New York and entitled, "Epidemic
Diencephalomyelits; A Possible Cause of Neuropsychiatric, Cardiovascular
and Endocrine Disorders." Since then many colleagues from the U.K. and
other countries have demonstrated the pathological systemic consequences
which may occur after a viral illness and have long term effects. All this
work has been pursued by many colleagues in the U.K. and abroad since then,
amongst whom are 72 who contributed to the book of more recent origin and
published by the Nightingale Research Foundation, entitled, The Clinical
and Scientific Basis of Myalgic Encephalomyelitis.
In the U.K. for 4-5 decades, we have found that an initial illness caused
by one of the enteroviruses, was the most frequent cause of the ensuing
illness known as M.E. These enteroviruses included the three polioviruses,
the ECHO group and also the Coxsackie A and B groups. Unlike pesticides and
other inorganic substances viruses can replicate and mutate hence there can
be epidemic and endemic outbreaks. In other countries other viruses have
been involved. In the U.K. the Epstein-Barr virus has been claimed as an
initiating cause of this illness. However, in our work this has not
occurred in epidemic or endemic forms as outlined here. The acute stage may
have varying presentations which may be transient and mild, or severe and
persistent. These presentations may be respiratory infections or cardiac
infections (pericarditis, endocarditis or myocarditis) resulting in a
constrictive pericarditis or a cardiomyopathy. Not only so but Bornholm
disease may occur with severe spasmodic pain in the chest simulating angina
or abdominal pain simulating appendicitis, cholecystitis or pancreatitis.
Other viral syndromes occur such as Meniere's syndrome, or the more
sinister, viral meningitis. On the other hand, the condition may be a
general illness defined by both patient and doctor as the "flu." In any of
these conditions the prodromal infections may appear to abate but the
patient does not "get better." This is only a very brief resume of a large
number of cases, which have been seen and followed up for many years.
As with poliomyelitis, the symptoms in M.E. are somewhat diffused but do
involve the nervous system. We should consider the terms applied to the
effects of infection in the nervous system due to the poliovirus, which is
the enterovirus. The term ANTERIOR POLIOMYELITIS referred to cases where
the ANTERIOR horns of the spinal cord were chiefly affected. These neurons
subserve EFFERENT outgoing neurological impulses. Hence the effects were on
the "motor" system with some paralysis. The term POSTERIOR POLIOMYELITIS
was also used to define lesions in the POSTERIOR horns of the spinal cord.
These neurons subserve AFFERENT neurological impulses. The enteroviral
groups to which we refer in these guidelines have been shown to have a
propensity for, and cause the pathology in these AFFERENT impulse
conducting neurons. Hence, the results are more noticeable to the patient
than the doctor, which is not so with poliomyelitis. These pathological
results may not be confined to the nervous system but may result in
neurohormonal or other differing end organ effects. In CNS cases seen over
4-5 decades by one of us (Dr. John Richardson, MB BS) the computerized
records, when analysed, reveal that the male cases with M.E. numbered 224
and females 469. From these figures it can be shown, that besides the
female preponderance, the total number of varying CNS syndromes are greater
for females as can be seen in the table. The viral etiology may be doubted
by some, but if one remembers that the resulting CNS illness was
accompanied in approximately 50% of both male and female patients with some
other syndrome-ranging from cardiac, renal, pancreatic (with diabetes
ensuing in some cases) to the more obscure thyroid or adrenal effects, then
the possibility of a common etiological factor should not be ignored.
Moreover, thousands of serological viral tests (including IgM, IgG and VP1)
performed by us were positive and confirmed this relationship.
Certain CNS deformities also resulted in the offspring of mothers who had
conceived whilst the serological tests were positive for enterovirus, prior
to, or during pregnancy. In the first trimester these included agenesis of
the septum lucidum resulting in blindness, agenesis of the corpus callosum,
and also amyelination of white matter resulting in severe and diffuse lack
of development. In viral infection in the late stages of pregnancy, fully
developed organs were affected and we have shown cardiac effects such as
endocardial fibroelastosis (in two neonates), as well as brain damage in
others. These cases have been recorded on MRI, videotape and, sadly, at
autopsy. This diffuse variety of initiating and consequential illness is
briefly reported here to show that we are not dealing with a simple, single
entity, but with serious consequential illnesses. A summary of the CNS
syndromes which followed an initial, serotype positive, viral infection is
shown in the table next page.
Many other cases have come into this survey since this table was
formulated, but the relative percentages in all aspects remained the same.
The percentage of M.E. cases, compared to the total number of CNS cases is
42% for males and 46% for females showing that although the total numbers
point to female preponderance in CNS illnesses, the percentage of M.E.
cases is the same. Nowhere is a variety of systemic symptoms seen more
often than in this syndrome. Whilst M.E. is a well defined entity, other
associated organ pathology is not infrequent and can obscure the picture.
In this series about 25% developed varying autosomal antibodies of which,
for instance, antithyroid antibodies were found in 20% of cases studied.
Thus much has been claimed by some to be purely psychiatric in origin, with
labels ranging from simple depression to hysteria, and other vague hypotheses.
[Note: See table at http://www.co-cure.org/table.pdf ]
PREVALENCE AND CLINICAL DIAGNOSIS
As shown, cases may be endemic, or present in sporadic clusters. They may
follow an acute viral illness such as Bornholm disease, viral
perimyocarditis, labyrinthinitis, or viral meningitis. A vague flu-like
illness affecting the chest or bowels may be a harbinger of a more serious
consequence. The malaise not only fails to recover, but becomes more
defined, developing symptoms such as anosmia or marked concentration
difficulties in a previously highly accomplished brain which cannot now
recall a paragraph after reading it several times. Initially, muscle power
may not appear to be affected but, if examined carefully, tender "softened
spots" may be found in calf muscles and sometimes in the recti-abdomini.
One such case had to have two operations for hernias which resulted from
Muscle jitter will be found if carefully looked for in 25% of such cases.
We find over the years that the history of the illness written by the
patient is of enormous help and we have preserved these histories over four
decades and the symptoms which were commonly reported in over 400 of these
histories formed the basis of the Score chart which we in the Newcastle
Research Group use. A score of 15 on this chart is highly suggestive of M.E.
A full and careful examination, as follows, is mandatory.
This not only involves the lung fields but also careful attention should be
given to heart sounds as a pericardial friction rub in some cases can be
detected at the lower sternal border. This often signifies a pericarditis.
The blood pressure should be measured supine and then a tilt test
performed, where the patient sits up at about 45 degrees. Labile recordings
can be found in some cases and, no doubt, account for the reports of
"fainting attacks when standing erect" and a few have fainted (see Score
Chart). This labile blood pressure is usually considered to be due to
CENTRAL NERVOUS SYSTEM
Because the effects of this illness are primarily due to AFFERENT tracked
pathology, examination must be related to this. In poliomyelitis and other
syndromes primarily affecting the efferent pathways, attention to reflexes,
etc., is appropriate but in these cases a more detailed approach is
necessary to define the adverse signs resulting from the AFFERENT track
involvement. Thus the 12 cranial nerves need to be considered first as
certain abnormal sensations relating to the cranial nerves are found in
these patients. These include abnormal response to olfaction (1st), varying
abnormal optic responses (2nd, 3rd, 4th and 6th), facial/motor and sensory
responses are through the trigeminal (5th) and the facial (7th) nerves,
auditory (8th), valtal (10th). Afferent and efferent responses will be found.
[Note: See Newcastle Research Group M.E./CFS Score Chart at
A few cases suffer from anosmia, maybe due to involvement of the cortical
olfactory centers rather than peripheral receptors.
There may in some cases be paresis affecting the abducting eye muscles with
diplopia on looking sideways. There may be saccadic movements which can be
recorded and these affect the reading of small print. In some cases there
is a reversal of the Argyl-Robertson pupils, often seen in young patients,
and this is often not noticed by the examining doctor. It is described in
"Diagnosis of Nervous Diseases" by Purves Stewart and occurred in other
cases of encephalitis. The pupils are dilated and do not respond to
accommodation and also feebly to light. We have videoed these, with a
control, often a parent, sitting next to the patient. The video recordings
of these cases are retained. Occasionally the trochlear nerve is affected
as its nucleus is situated in the midbrain area and this can be assessed by
asking the patient to focus in a downward direction, when there is diplopia
aggravated by looking sideways at the same time. The effects of light are
more noticeable and many patients have to wear very dark glasses. This is
NOT due to abnormalities in the receptor areas in the calcarine nuclei, but
is due to midbrain "reading" of these visual images by forward projecting
fibers from the calcarine nuclei. Eye movements should obviously be
carefully assessed in all directions and any nystagmus, diplopia,
oscillopsia or other abnormal signs noted. In this connection the excellent
work done by Alfredo A. Sadun, MD, PhD (Doheny Eye Institute, California)
confirms these observations (Last chapter, "Clinical and Scientific Basis
of M.E./ CFS").
In a few cases such as hand-foot-and-mouth disease, the eyes can be
affected and a marked conjunctivitis seen and videoed.
Careful examination is essential. Whilst often they are relatively normal,
in some a venous "cuffing" is seen, IF CAREFULLY LOOKED FOR. In some of
these cases where MRIs have been performed unidentified objects (UBOs) have
been noted and are considered to be due to such "cuffing" in the Virchow
Robin spaces which contains CFS between the meningeal coating and cerebral
FACIAL EXAMINATION (7TH)
The three divisions of the facial nerve involve both motor and sensory
sensations. In some cases lack of sensation may be found unilaterally in
one discrete area and very occasionally some paresis. The latter has also
HEARING SENSITIVITY (8TH)
The Score Chart relates to this. Some modalities of sound, chiefly high
pitches, have very adverse, irritating effects. (This is also evident in
animals.) The audiometer test is very helpful to assess and record the
frequency and levels at which intolerance occurs.
VAGAL OUTFLOW (10TH)
This will be referred to in the section on bowel activity.
Apart from reflex and sensory activity, which should involve temperature,
touch, vibration and two point discrimination, the pronator sign should be
assessed. This involves the elevation of the arms above the head and, if
positive, the palms will face outwards due to internal rotation of the
whole limb with pronation of the forearm. This is also reported by Purves
Stewart and was seen in chorea and other cases of encephalitis. This sign
is not specific for M.E. and when it does occur it is not accompanied by
the choreaform motions of the hands. A case referred recently as M.E. had a
severe pronator sign accompanied by marked choreaform motions of the hands
and had to be diagnosed as the new variant CJD-which was sadly proven
later. Nevertheless this simple test should be performed and we have
videotaped a number of cases.
The color the palmar surfaces of the hands should be noted in the acute
stage, as the HFAM disease which occurs in some patients in the primary
stages of the illness with conjunctivitis due to enteroviral infection,
results in palmar erythematous changes.
Apart from the usual examination it is wise to do an ultrasound test. (A
simple fetal monitor can be used.) Irritable Bowel Syndrome in our series
occurs in approximately 20% of cases. We define this as the "boiling bowel
syndrome" as it sounds like this on the sonic scan. Rory McCloy, BSc, MD,
FRCS, in an excellent monograph described this and related this to the
vagal pathways, both sympathetic and parasympathetic. He postulated that
the trigger factors could be neuroneural or neuroendocrinal, resulting in
the change of myoelectric activity from the normal 6 cycles to the faster 3
cycles per minute. Skin sensitivities occur and can be shown by scratching
the abdominal skin where severe dermatographia can sometimes be seen, and
again photographed, as we have done. A stated, palpitation of the abdominal
recti for softened foci should NOT BE OVERLOOKED.
The usual check but care should be taken to note the reflex sensitivity as
it can change. Blood flow can be assessed by palpation and ultrasound. The
brainstem is "softened" in M.E. and any adverse effect, be it a RTA with
whiplash injuries or rarely a LP can have unusual adverse effects with
marked changes in the reflex activity. Thus the value of response should be
noted initially and subsequently as, mild, moderate or severe. The Babinski
response and joint position test, along with temperature, touch, and
vibration tests should ALWAYS be done. In addition muscle jitter should be
assessed. This is done by the examiner putting a hand on the patient's knee
whilst seated on the examination couch and asking the patient to elevate
the leg to the horizontal position and then slowly lower it. In some cases
rapid jitter can easily be felt, seen and again videotaped. As with the
upper limbs the temperature should be noted as in M.E. It is often much
lower than normally would be expected.
Walking ability relates to all modalities of locomotion, be it speed,
toe-to-toe, or balance, etc. Romberg's should always be performed as the
midbrain cerebellar connections are affected in a number of cases, but
balance estimation is not confined to the Romberg test (with eyes closed)
as it is impaired in the normal process of locomotion. This balance
incoordination is frequently seen to be associated with the upper limb
positive, pronator sign. Again it is not confined to M.E. but was seen and
recorded in the patient with CJD. It presents itself as a rather spastic
gait and, in M.E, the patient very often requires personal, or
walking-stick support and often a wheelchair.
It is not intended to discuss this in detail as the Score Chart and the
patients own written histories will make this evident. Suffice to say that
it can be verified by discussion. Moreover, if questioned many patients
will recall very odd verbal and motor performances, e.g., forgetting words,
or using incorrect words, or doing odd things such as, "putting the boiling
kettle into the fridge." We find that they do not often mention the latter
as they are so embarrassed, but, when sympathetically questioned, they
relate these incidents with a raw smile! As shown by the Score Chart they
find it difficult to talk or communicate with friends or relatives for long
periods, apart from their sensitivity to sound, mentioned earlier. These
various changes of activity are noted frequently by relatives as also the
periodic blanching of the face.
If there is the slightest suspicion of myocardial involvement an ECG and if
possible a 24 hour recording should be done. MRIs in some cases, if there
is venous cuffing in the optic fundus may be interesting. The "Buspirone,
Corticol/Prolactin test" is very helpful, as also the SPECT brain scans.
Papers on these have been published in the Journal of Chronic Fatigue
Thorough serological tests should be done and involve routine blood counts,
liver function tests, CPK and an autoimmune profile. Varying hormonal tests
should be done if there is suspicion of end-organ dysfunction. A full viral
screen should be mandatory and include the enteroviral groups and IgM and
IgG and, if possible the VP1 test. An ESR should be done and repeated as
necessary. In M.E. without other organ involvement it is usually normal. If
raised it would indicate a non-specific inflammatory reaction, which
requires further investigation. Tests for thyroid and adrenal function are
helpful. However, care is needed as these can be attributed, if somewhat
abnormal, to end-organ glandular failure rather than neurohormonal effects
from the HPT or HPA axis.
In one case we had a patient who, following an illness with high titers to
Coxsackie virus developed a mild proptosis, but had no goiter. This patient
was seen by a junior hospital doctor and was inadvisably given carbimozole
and, later when seen at home, was almost in a myxoedematous coma. Another
recent case has been mistakenly diagnosed as Addison's disease. As with
M.E. there are signs which are similar including weakness, fatigue and even
orthostatic hypotension. However, in true Addison's disease there is
diffuse tanning of both exposed and nonexposed areas, especially on points
such as the elbows. Freckles occur on the forehead, face and neck as well
as discoloration of the areola, lips, mouth, vagina and other mucous
membranes. THIS DISCOLORATION DOES NOT OCCUR IN ADRENAL INSUFFIENCY
SECONDARY TO PITUITARY FAILURE WHICH IS A RESULT OF THE HPA AXIS SYNDROME.
In this patient and others we have seen there is, if anything, a blanching
of the skin and a remarkable lack of pigmentation. To distinguish between
failure due to hypothalamic or pituitary stimuli, a test using
corticotrophin-releasing hormone (CRH) is useful. Patients with
hypothalamic failure DO respond, whereas those with pituitary failure do
not. This test should be done, but once again the clinical signs serve to
differentiate between true Addison's disease and HPA axis.
The Hamilton ratio score chart is useful but M.E. is not primarily a
psychiatric illness and to label it thus just adds to the patients distress
and has had devastating results. However, as with any such illness there
are obviously feelings of oppression and frustration and a desire to "try
anything that would help." Many psychiatrists recognize this and show
sympathy which is very supportive. After all TLC is the best medicine
available in many other illnesses
The profuse range of treatments which have been advocated are described in
the book, The Clinical and Scientific Basis of Myalgic Encephalomyelitis
Chronic Fatigue Syndrome. However, as with anterior poliomyelitis the
variety of treatments which have been tried, reflect the primary
difficulty, and the old aphorism remains - "Sublata Causa Tollitur
Effectus," which is "Remove the cause and the effect will cease." As can be
demonstrated in cases who have succumbed to the poliovirus, this aphorism
is not always true, for there are some effects which remain after the
infection has ceased. Thus, whilst it is desirable to remove the CAUSE, to
address the effects is a challenge in M.E. as it was in poliomyelitis. Some
of the treatments which are used are as follows:
l. IgG Infusions have been used extensively both in the U.K. and abroad and
the basis for this is considered to be the abnormal, cellular and humoral
immunity in these patients. Replacement therapy with IgG is given to
restore normal homoral immune function. Some clinicians use the I.V.
infusions but we for many years have used I.M. injections. Professor R.
Loria in personal communications has demonstrated the vortex of effects
which occur when IgG is given I.M. rather than I.V. and thus it has more
effective results. Also, instead of large amounts at extended intervals, we
find that on average about 500 mg weekly has a "smoother" and more
beneficial effect. However, before this therapy is given it is wise to do
the serological tests alluded to earlier and show these to be positive.
The protective benefits may be seen by referring to the outcome in
pregnancy. Over the years out of 249 female patients with high positive
titers to a Coxsackie virus, 66 became pregnant. Forty-five of these
(68.2%) had normal babies but the remaining 21 (31.8%) had abnormal babies.
It is significant that for varying reasons, none of the mothers who had the
abnormal babies had been protected by IgG infusions, but more than 90% of
the remainder received IgG before and during pregnancy. (The records are
2. Ampligen. Robert Suhadolnik gave a good resume of this therapy. The
immune changes he postulated might involve alterations in the 2-5A
synthetase/Rnase L pathway. These changes have to be evaluated before the
therapy is given. Ampligen is a biological response modifier which augments
natural killer (NK) cell activity. It should be available in U.K. shortly
on a named patient basis, but as shown here, it should only be used if the
RNase investigations are positive and this is usually in the early stages
of the illness.
3. Transfer Factor. Professor Hugh Fudenberg has done work on this and
bases the treatment on its effects on immune dysfunction. TF is a
dialyzable component of leukocytes and is capable of transferring delayed
type hypersensitivity and has been used where there was a defect in
4. Efamol is an essential fatty acid (EFA). In M.E. one result may be a
lowering of normal proportions of arachidonic acid and a reversal of the
normal serum ratio of linoleic and oleic acids. These EFAs are necessary
for normal cell membrane metabolism. Treatment with EFAs such as Efamol is
postulated to help correct any such abnormality in this chain reaction.
Details for these treatments are given in chapters in Byron Hyde's book.
5. Elagen. A large amount of scientific work has been done on this and it
is basically an adaptogen and is considered to stimulate the normal
activity of the immune system in response to physiological stress.
6. Thymic Hormones. Nathan Trainin's chapter in the Book summates the
effect of thymic hormones and states that "viral antibody responses in vivo
are thymus-dependent and therefore require the cooperation of viral
antigen-specific helper T-cells." Thymic humoral factor gamma 2 (THF y2)
was used. This is a very helpful chapter to read.
7. Alanthamine Hydrobromide. Galanthamine has been used by Snorrason et al.
in Iceland. This was used because of the cholinergic defects which have
been shown to occur in patients with M.E. In this connection, choline
dihydrogen citrate with vitamin C has been used by J.R. for 4 decades-see
attached notes. No adverse side-effects have been reported and very
beneficial results have been demonstrated and noted by the patients.
8. Cognitive Therapy. Varying exercise techniques and other supportive
treatments, which are too diffuse to specify have been given to help
patients. These do not address the physiological cause or consequences of
the illness. Unfortunately, in our experience over the years, both
cognitive therapy and some other aspects of psychotherapy may have adverse
effects because the patients sometimes feel that the responsibility for
succumbing to the illness is being laid upon them and that the
responsibility for recovery lies within their own remit. Maybe those of us
actively involved in seeing patients are aware that we also have the
opportunity to empathise and give support without making undue demands or
suggesting that the "patients should help themselves by taking a positive
attitude." We find that the great majority are very desirous of being able
to do this and wish to be well. However, a "listening ear" is very helpful
To return to the dictum "Sublata Causa Tollitur Effectus." It should be
apparent that the treatments which have been used with the best intentions
have limitations. In the U.K. this condition, like polio, is usually due to
enteroviral infection. However, there are many enteroviruses. To develop a
vaccine for immunization would be ideal for prevention and would be much
better than any "cure" but, the enteroviruses specific for the initiating
illness would have to be defined before a vaccine could be prepared.
Nevertheless, prevention would be more effective than cure.
CHOLINE DIHYDROGEN CITRATE
SUMMARY OF FUNCTIONS
In 1932, Best and co-workers noted that dogs which had been depancreatised
eventually developed very fatty livers, even though maintained on insulin.
Varying dietary trials demonstrated that the substance responsible for
alleviating this, was choline. However, it has other functions as we have
shown over the years, the chief of which is its action as the precursor of
acetylcholine which is the neurochemical which is active in intercellular
Other functions which interact in protecting the human body include its
role as a constituent of lecithin which is an important phospholipid. It
also has been shown to prevent the deposition of fat in the liver and
actually we have shown that it mobilizes lipids from arterial endothelium
and other adventitious sites of deposition. It is also essential as a
constituent of plasmalogens-these are essential for mitochondria, and also
for sphingomyelin, which is important in brain tissue. The ascorbic acid in
the formula sulphonizes the mobilized lipids and enables them to be water
soluble and thus able to be renally excreted.
Choline is the precursor for acetylcholine and latter is synthesized from
choline by acetyl transference and transported between brain and plasma via
the capillaries. Thus the amount available to the brain depends on the
plasma concentration of choline.
Experimental changes observed include the deposition of fat in the liver
and arterial walls. Certain renal lesions and also motor incoordination due
to nerve degeneration have been observed. These are seen in humans. Vit. B
12 and also folic acid act as cofactors also with choline.
The work by Snorrason et al. from Reykjavik, on the trial of an
acetylcholinesterase inhibitor in certain cases of M.E. showed an
improvement. They postulated that a cholinergic defect-was central to the
pathogenesis in M.E. They also showed that GHB resulted in improved sleep.
However, in this work we consider that it is more in keeping with the
natural chain to augment the acetylcholine itself, rather than inhibit the
Effects are not immediate dramatic effects. However, the effect of lipid
mobilization is seen in the demonstrable rise in serum-cholesterol as a
marker. Also, in a number of cases where there was an arcus, gradually
resolved and in some totally disappeared. In the occasional case where
there was a systolic murmur in the carotid(s) this has also resolved. Also,
viruses are generally lipotrophic and the mobilization, sulphonation and
renal elimination could be assumed to have a helpful effect in viral
TRIAL OF A SELECTIVE ACETYL CHOLINESTERASE INHIBITOR, ALANTHAMINE
HYDROBROMIDE, IN THE TREATMENT OF CHRONIC FATIGUE SYNDROME
E. Snorrason (1), A. Geirsson ( 1), K. Stafansson (2)
(I)-Dept. of Psychiatry and Internal Medicine, University of Hospital,
Landsspllallnn, Reykjavik, Iceland.
(2)-Division of Neuropathology, Dept. of Neurology, Boston Beth Israel
Hospital, Harvard Medical School, Boston, USA.
The purpose of the study was to search for means of diminishing the plight
of patients with chronic fatigue syndrome (CFS) and to test the hypothesis
that a colinergic defect is central to the pathogenesis of CFS. Forty-nine
patients who fulfilled consensus criteria for CFS were treated with the
acetylcholinesterase inhibitor, galanthamine hydrobromide.
Thirty-nine patients finished the study according to the protocol with 43%
reporting 50% improvement, in fatigue, myalgia and sleep and 70% reporting
30% improvement whereas patients in the placebo group reported only 10%
improvement in the same parameters of CFS. The improvement of patients on
galanthamine was in most cases gradual and only reached significance for
the group after four to eight weeks. The improvement was stable and no
patients who reported over 50% improvement on galanthamine relapsed to a
pretrial level of any symptom. One of the most surprising effects was the
dramatic improvement of sleep disturbances that occurred in most patients
in this medication: more than 60% of patients that finished the study
reported over 70% improvement in sleep deficit. If this is indeed true it
would be the first demonstration of a drug that can be used to correct
sleep disturbance that influences a specific stage in normal sleep.
The most common adverse effect of galanthamine, as given in this study was
mainly nausea that was dose dependent and reversible. Galanthamine
hydrobromide is relatively safe and appears to be an effective medication
against many symptoms of CFS. But the positive results of this study have
to be interpreted cautiously because of methodological limitations of this
trial. First, this study was originally organized as a double blind,
placebo controlled trial, but was changed to an optional crossover after
two weeks of treatment. Also the adverse effects of the active drug in 30%
of patients would compromise the double blind.
With these limitations in mind it is all the same tempting to conclude that
this study lends an indirect support to our hypothesis that a cholinergic
deficit may play a role in the pathogenesis of the syndrome.
© 2002 by The Haworth Press, Inc. All rights reserved.
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