Friday, November 11, 2011

Dr. Vallings' notes on IACFS/ME Conference Presentations

Source: Rosamund Vallings
Date:   November 8, 2011

Summary of IACFS/ME conference, September 22-25,2011, Ottawa, Canada
by Rosamund Vallings MB BS

The conference opened with the keynote speaker, Christine Kozak
(Bethesda,USA), who discussed and clarified issues relating to
'Gammaretroviruses of mice and their links to Prostate cancer and
CFS/ME'. She described how MLVs cause leukaemias in mice, and
penetrate right into the cell nucleus, and can be transmitted
genomically. There are 3 categories:ectotropic, xenotropic and
polytropic. The latter two are distributed widely in house mice
species. Xenotropic viruses have a wide range of hosts, and there are
5 functional variants of receptors. XMRV can replicate in some species
of mice. Various host factors restrict XMRVs in mice, such as serum
factors, receptor block, receptor variation, Apobec 3 and Fv1 (both of
which can block viral replication at the reverse transcriptase stage)
and tetherin at the budding stage. Humans do not have Fv1, but have
TRIM5?a retrovirus restriction factor. The conclusion was that MLVs
and ERVs are found in house-mice worldwide. Receptor variants have
evolved in mice carrying XMRVs. XMRV has a distinct host range. XMRV
contributes to induced neoplastic diseases. Multiple host restriction
factors limit virus transmission. Contamination may be the reason we
see this virus in humans.

Virology research

G.Simmons (San Francisco,USA) discussed multi-laboratory evaluations
of XMRV detection assays. He presented work investigating the
prevalence of XMRV in blood donors. Published work on 22/9/11 in
Science Express showed a failure to detect XMRV in any sample. Only
one lab found clinical samples to be nucleic acid test (NAT) positive.
These positives were not reliable among replicates. Using a number of
techniques, there was very little correlation between positives from
the original WPI study and other assays. The conclusion was that
routine screening of blood donors for XMRV is not warranted. Meirleir (Brussels, Belgium) detected anti-XMRVantibodies in the
serum of patients and healthy blood donors. Of 84 Belgian CFS
patients, 21 had developed CFS after receiving a blood transfusion.
Controls were 44 healthy blood donors. 57% of CFS patients and 16% of
controls tested antibody positive. 10 of the 21 CFS patients who had
had a blood transfusion tested positive. PCR was not used. Western
blot was used to confirm the serology data. These results were
statistically significant. Samples were blinded and analysed at the WPI.

M.Hansen (NY,USA) presented work looking for MLV-like gag sequences in
blood and cell lines incubated with plasma from CFS patients and
controls. 30 were patients from D.Bell, 24 from S.Levine and 12
controls from Ithaca, NY. No XMRV was detected in the Bell group.
Cells were cultured for 30 days ? some gag sequences were found but no
other retroviral sequences could be found. There were no statistical
differences between patients and controls. Everything possible was
done to avoid contamination. The Levine samples were all negative for
gag sequences. This research is ongoing.

Post-SARS Syndrome was outlined by H.Moldofsky (Toronto, Canada). SARS
results from infection by a coronavirus A. It creeps into the brain
via the olfactory bulb in mice, and possibly via this route in humans.
250 cases occurred in Toronto, transmitted by one person who had been
in Hong Kong. There were 44 deaths and 50 cases who remained ill
post-SARS. These correlated with a diagnosis of CFS. Sleep was
disordered and this was similar to that seen in fibromyalgia syndrome
(FMS), but there was a lower rating of the alpha EEG sleep anomaly in
post-SARS as compared to FMS. The myalgia was also less severe.

J.Montoya (Stanford,USA) considered the role of the immune response in
CFS. Typical pathogens in CFS are involved, and are mostly
intracellular. There is initial tropism (e.g. respiratory or
GI)followed by involvement of target organs (eglymphatics)). Different
pathogens take similar pathways. CFS may be sustained for years, and
pathogens reactivate periodically. Reactivation tends to be at low
levels. This leads to an immune response, but this is not strong
enough to kill the organisms, so the bugs remain latent, and then
reactivate again leading to symptoms. CFS is a multi-system disease
with phases of immune response.

Peripheral blood studies are useful and convenient but imperfect.
Immune abnormalities have been inconsistent across labs, although some
are consistent. Inconsistency may be due to host variables, multiple
triggers, fluctuating nature of the disease, duration and severity.
There are also other non-CFS variables such as methodological
variables and statistical issues. There is a need to involve all
available data, apply new technology and coordinate research.

J.Mikovits (Reno,USA) and J.Coffin (Boston,USA) discussed the case for
and against human gammaretroviruses in CFS. Mikovits outlined her
earlier work involving detection of XMRV. As well as identifying the
virus in a significant number of patients, their lab have identified
an inflammatory cytokine and chemokinesignature that distinguishes
XMRV-infected patients from controls with 94% sensitivity and
specificity. Further tests are being developed for detection and
characterisation of XMRV. Coffin's lab had looked hard for XMRV in
mice, and did not find it in any mouse strain tested, but found an
XMRV ancestor in the mouse genome. A detection assay has been
developed. He pointed out that XMRV is a virus and MLV is not a virus,
but fragments.

Mice are extremely widespread, and mouse DNA can be found on
laboratory surfaces and can contaminate common reagents and materials.
Most virologists now consider XMRV to be a consequence of a collection
of artefacts originating from endogenous MLVs prevalent in the
laboratory. It is likely to be an accidental laboratory creation from
the 1990s. It is yet to be worked out how it has got into clinical
samples from CFS patients.

Treatment advances

D.Strayer (Philadelphia, USA) gave an update on the use of
Rintatolimod (previously known as Ampligen). They had studied the use
of the drug in XMRV/pMRV antibody positive patients. Of the patients
selected, 33.7% were antibody positive. The antibody negative group
had lower activity for daily living scores. Those who were
antibody-positive showed a significantly greater increase in exercise
treadmill tolerance when treated with the drug than those treated with
placebo and those who were antibody negative. The responding patients
also showed a decrease in use of other medication.

The use of Rifampicin was found to augment the effects of oxymatrine
(Equilibrant) in ME/CFS patients by J.Chia (Torrance,USA). Those with
chronic enterovirus infection had previously been shown to benefit
from oxymatrine (Equilibrant). 46 ME/CFS patients were treated with
Rifampicin 300mg bd for 7 days while taking oxymatrine and compared
with patients taking just oxymatrine, and a control group. Initially
flu-like symptoms occurred in those taking the rifampicin plus
oxymatrine, but subsequent symptomatic improvement was observed in
60%. Short courses of rifampicin may therefore be beneficial in
oxymatrine responders. Rifampicin induces nitric oxide from human
aveolar macrophages causing the initial flu-like symptoms. 2nd or
longer courses of rifampicin did not appear to help.

F.Friedberg (Stonybrook,NY) tested a brief self-management protocol
for unexplained chronic fatigue and ME/CFS in primary care. Two
self-management sessions focussing on CBT were undertaken in 3 study
conditions: 1) standard medical care alone, 2) standard medical care
plus nurse-delivered attention control condition of symptom monitoring
and 3) standard medical care plus nurse-delivered self-management CBT.
There was modest improvement in fatigue severity and patient global
impression of change (PGIC) ratings in the self-management programme.
Ratings tended to reflect different attitudes to the illness and/or
differential exposures to negative major life events. Improved
patients reported increased awareness of behaviour and affirmative
steps to pursue more healthy activities. Self-management can generate
improved outcomes.

Fibromyalgia (FM)

A lively debate followed between R.Staud (Florida,USA) and D.Clauw
(Ann Arbor,USA) entitled: 'Are tender points necessary?' Staud
outlined the American College of Rheumatology criteria for FM (1990)
which includes widespread body pain of 3 months duration and presence
of 11 out of 18 tender points. The tenderness should be with 4kg of
thumb pressure. In trials this has not been found to be reliable and a
more accurate diagnosis can be made using the 2010 provisional FM
criteria: 3/12 duration of pain with a widespread pain index in 19
areas with a severity scale of at least 9. This scoring system is
quite different, and additional symptoms include fatigue, unrefreshing
sleep, cognitive symptoms and somatic symptoms. (There is overlap with
CFS). Many different ways have been looked at for triggering pain for
measurement. Emotional 'windup' could be useful, but is not reliable.
Tonic heat and mechanical stimulation can be applied to painful and
non-painful areas. This can be used for assessment of pain or for
stimulating pain. Tenderness does correlate with pain and can be
measured by quantitative measurement of pain sensation (QST). For
clinical purposes, tender points provide little mechanistic
information about an individual's pain and associated symptoms.

Clauw feels that tender points in diagnosis are unnecessary, and
outlined 10 reasons why:
1. Convey inappropriate message about FM
2. Excludes males
3. Practitioners do not know how to do it, and often do not want to learn
4. Very few chronic pain states have a specific examination to diagnose pain
5. Tender points are an inadequate measure to assess experimental pain
6. There are better ways to assess pain threshold
7. Tender points are not normally distributed
8. Tender point count was never meant to be a 'physical exam' and
should not replace routine clinical examination
9. No evidence that they are necessary in diagnosis
10. Is the horse dead yet?!!

Case definitions

B.Carruthers (Canada) outlined the New International Criteria for ME.
The 2003 Canadian definition has been further defined. The 6 month
period is no longer required, but left to clinical judgement at 3
months. Post-Exertional Neuro-immune Exhaustion (PENE) was kept
criterial and further articulated. Modifications for paediatric cases
have been included. The illness is called ME rather than CFS. The
Canadian definition clearly separated out genuine cases, and this new
definition can be used clinically and in research and epidemiology.

L.Jason presented work contrasting case definitions. The Fukuda
definition has only 4 core symptoms, which do not include
post-exertional malaise. But this definition has been used by
researchers for over 15 years. He compared this definition with the
2003 ME/CFS Canadian criteria and the older Dowsett ME criteria. His
study suggests that the more recent criteria and the ME criteria could
be used to identify patients with more homogenous and severe
symptomatology and functional impairment.

His second paper describes Data Mining as being a useful tool in
aiding the diagnosis of ME/CFS. An objective computer-driven decision
is combined with a physician's medically influenced decision. The
Canadian criteria (compared to the Reeves 2005 criteria) were found to
have more construct validity and were more accurate, identifying 87%
of cases. Post-exertional malaise, neurocognitive symptoms and sleep
disorders were not identified as discriminating symptoms with the
Reeves criteria.

E.Unger (CDC Atlanta, USA) continued discussions about case
definitions. She explained that definitions are not specific to CFS.
They are used for epidemiological studies, clinical diagnosis and to
determine the biological basis of disease. She stressed the importance
of standardization. She asked the question 'Will refining lead to a
homogenous population?', and pointed out that heterogeneity is
challenging. Phenotypes are imperfect indicators of biology. Case
definitions may not be sufficient to discover pathways to
pathogenesis. Standardized measures will allow stratification and

Exercise challenge

B.Keller (New York,USA) studied the effects of fatigue on functional
capacity in patients with CFS. There is a need to quantify impairment.
The cardiopulmonary exercise test (CPET) measures functional
impairment and is an objective measure of energy expenditure and
physical work. It is validated and reliable in health and disease, but
she questioned whether it was useful in CFS. The purpose of the study
was to measure the effects of post-exertional malaise in CFS. She
concluded that patients' disability went from mild to moderate on
first test and from moderate to severe on second 24 hours later.
Looking at maximum exercise tests, it was shown that those with CFS
will exacerbate symptoms associated with post-exertional malaise
simply by completing normal daily activities.

C.Snell (Stockton,USA) then covered the importance of exercise
challenge, and the need for a standardised measured approach in
diagnosis and management. He described fatigue as a reduced efficiency
as a result of doing 'work'. Some measures can be indirect (e.g. heart
rate) or direct (e.g. gas exchange). Field tests are easy to
administer and require minimal equipment but are unmonitored and
therefore less likely to be accurate. Motivation and pacing both play
a big role in the results. He discussed the PACE trial and showed that
the results actually equate to 1.94 ? 2.35 mph and at 2 METS this
equates to 7ml/min/Kg oxygen. The NY Heart Association would classify
this as 'severely disabled'. Anything greater than 3mph is the
anaerobic threshold for most CFS patients. Direct assessment of
aerobic capcity should be the gold standard. CPET is uniquely able to
quantify efficiency with measures of workload and the metabolic cost
of the work. Healthy people do better on a second test, but in CFS
there is a massive drop. Post-exertional malaise (PEM) is an
exacerbation of symptoms after exertion. Most healthy people will
recover in 48 hours, but in the group studied, only one patient with
CFS recovered in 48 hours. The respiratory exchange rate (RER) is the
most reliable guage of subject effort ? it encompasses an analysis of
expired gases.


Natural killer cell (NK) function in a prospective cohort of
adolescents with CFS compared to controls following infectious
mononucleosis (IM) was discussed by B.Katz (Chicago,USA). He felt the
study was important because NK function has been much studied and
results are not always consistent. 9 with CFS and 9 matched controls
were studied. Blood was taken at 6, 12 and 24 months following IM. NK
quantification and function was measured. There was no difference in
NK cell numbers at each of the 3 points of analysis compared to
controls. However NK cell function was higher in cases than controls
at 6 months, with less differential at 12 and 24 months. The
conclusion was that there was no decrease in NK cell function in this

However, E.Brenu (Gold Coast,Australia) looked at cytotoxic function
of NK cells and CD8+T cells in CFS, and her findings showed
significant decreases in cytotoxic activity compared to controls at
baseline, at 6 and 12 months. NK CD56 bright cells remained decreased
in those with CFS. The study confirmed reduced immune function in CFS,
and she highlighted the possibility that NK cell cytotoxic function
could be a potential biomarker.

Her second study assessed proteins and receptors secreted and
expressed by CD4+T lymphocytes over time. At baseline IL-10, TNF? and
IFN? were increased in the CFS group. At 6 months, IL-2 was increased
and IL-10 and IL-!7a were significantly decreased in the CFS group,
and at 12 months only IL-2 was significantly increased in the CFS
group. The results suggest that the cytokine profile in CFS changes
over time during disease progression. Experimental findings need to be
matched with data on clinical disease progression.

The objectives of a study presented by V.Falkenberg (Atlanta, USA)
were to determine the pattern of perforin gene methylation in
conjunction with gene expression, and whether these features were
altered in CFS. Increased promoter DNA methylation correlated with
reduced perforin expression in the non-fatigued group, the
relationship was not seen in CFS. Small but significant differences in
methylation were detected over the day and there were differences
between both groups. Further studies are needed to help explain and
understand these differences.

N.Klimas (chairing this session) pointed out the importance of these
papers in helping us understand the nature of the immune response and
the variations over time.


G.Broderick (Edmonton, Canada) looked at the links between lymphocyte
metabolites and the clinical course of post-infectious fatigue in a
group of adolescents following infectious mononucleosis (IM). They
were followed over 2 years and 3 clinical courses were distinguished.
1) sustained increase in fatigue after early partial remission 2) a
monotonic decrease in fatigue and 3) slow decrease in fatigue after a
peak at 12 months. They surveyed lymphocyte gene expression. 107 genes
were differentially expressed. 40% were linked to immune metabolism
and 20% to immune signalling and cell functioning. Gene expression
supports directed functional interaction. Processes are linked to the
biochemistry of the stress response. Phenylalanine metabolic activity
supported the separation of the fatigue sub-groups. High activity was
linked to a more favourable prognosis. Results correlated with the
clinical course over 2 years.

T.Miike (Hyogo,Japan) presented a fascinating overview of the daily
life of children in Japan, with emphasis on their vulnerability for
developing CFS. These children are subject to sleep deprivation as a
result of modern daily life in Japan, and developed abnormal sleep
rhythms. He discussed the importance of reducing risk of developing
CFS by attention to children's daily life and lifestyle in Japan.

S.Tajema (Kobe,Japan) confirmed the relationship in Japan between the
abnormal biological clock system and childhood chronic fatigue. At
their newly-formed centre, they are now treating this disorder. In the
study, the treatment of children with CFS with bright light therapy,
thermal therapy (20 minutes of 60?C to the head), medication
(melatonin, clonidine and sedative psychotropics), CBT and lifestyle
training over 8 weeks was presented. Circadian rhythm and sleep
disorders were much improved, but other symptoms of CFS were not
significantly improved at this time. Recovery from the sleep
disturbances is looked on as the first stage of improvement for these

K.Rowe (Melbourne,Australia) had seen 788 paediatric patients (aged
6-18) between 1991 and 2009, and she presented follow-up to look at
the natural history of the illness. The average duration of the
illness was 5 years, with a range of 1-15 years. By 5 years, 60%
reported recovery. By 12 years 88% reported recovery, but in
approximately 1/3 of these they reported conscious monitoring of their
workload. Less than 5% were not working or studying, often due to
factors other than CFS, such as marrying or having children. 90%
completed or intended to complete post-secondary training. Treatments
used were studied and the only alternative practitioners who were
deemed helpful were those providing relief of muscle pain with massage
or who provided good dietary advice. Restrictive diets and supplements
did not reach placebo levels of response. The important issues were
balancing life to include social contact, physical activity,
educational input and a commitment to attend at least one activity
each week. Ability to engage in education was the best predictor of
functional outcome. She concluded that the outcomes for young people
in Australia with this illness are generally positive although


L.Jason (Chicago,USA) had looked at the natural history of the illness
over 10 years. His study's major finding was that rates of CFS appear
to have been relatively stable over the past decade. 67% of those with
CFS continued to have CFS over time. Some of those initially diagnosed
with Idiopathic Chronic Fatigue (ICF) had progressed to CFS,
suggesting that ICF is a group at higher risk of developing CFS. Of
those in remission, 50% went from a diagnosis of CFS to ICF,
indicating that while they no longer fitted the CFS criteria, they did
still suffer from fatigue. Post-exertional malaise is the cardinal
symptom. Of interest 29.4% of the CFS patients had had a blood

CFS knowledge and illness management among US healthcare providers was
reviewed by E.Unger (Atlanta,USA). When looking at results for health
practitioners, 94% of doctors had heard of CFS, 71% believed it was a
medical and psychological illness, 14% believed it was a psychiatric
illness, 37% had made a diagnosis. Studies of public knowledge
indicated that 57% had heard of CFS, 27% considered it a medical
condition and 2% believed it was a psychological illness. Nearly 10%
of the public knew of someone with CFS. The top 3 ways in which health
care providers manage CFS were: referral to a medical specialist
(35%), medication (29%), and referral to a psychologist/prescribing
graded exercise therapy (26%). The public sought information by
talking to family doctor (72%), searching the internet (54%) and
talking to a medical specialist (25%). Only 7% would join a support

J.Allegre (Barcelona,Spain) presented results of a study to determine
the sociodemographic, clinical and therapeutic characteristics of CFS
patients in Spain. The condition was found to affect mainly
middle-aged, educated women. Onset most often occurs following an
identifiable trigger, such as infection, delivery or stress, and was
sudden in 20%. At the time of diagnosis 62.5% were not working.
Treatments were: symptomatic medication (analgesics, antidepressants,
anxiolytics) in 78.3%, alternative treatments in 3% and physical
exercise and/or CBT in 5%.

Genomics and genetics

Expression patterns of genes relevant to immune function were
discussed by E. Brenu (Gold Coast, Australia). Her study confirmed
changes in microRNA expression in cytotoxic cells that may be related
to the poor function of these cells in CFS patients.

M.Rajeevan (Atlanta,USA) had looked at the immune and inflammatory
alterations in CFS to determine if genetic variants in inflammation
and immune pathways could be linked to CFS, as well as to quantitative
measures of functional impairment, fatigue and symptom inventory.
Compared to controls, CFS was associated with 34 functionally relevant
single nucleotide polymorphisms (SNPs). 12 of these are in pathways
related to complement cascade, chemokines and cytokines/cytokine
signalling and Toll-like receptor signalling. Differences in these
associations found for subjects with exclusionary conditions otherwise
meeting criteria for CFS, suggests important differences between these

L.Bateman (Salt lake City,USA) presented work to determine whether
baseline and/or post-exercise expression of genes involved in
signalling and modulating sensory fatigue and muscle pain are
potential biomarkers for distinguishing those with CFS and FM from
healthy controls. At least 2 sub-groups of patients were identified by
gene expression following exercise. The larger subgroup showed
increases in mRNA for sensory ion channels and adrenergic receptors
and a cytokine. Symptom severity was associated with greater
post-exercise increases in these genes. The smaller subgroup were
mainly patients with orthostatic intolerance and there was no
post-exercise increase in any gene, and was defined by decreases in
mRNA for ?2A adrenergic receptor. The FM only patients were identified
by baseline increases in 3 genes. Post-exercise increase in 4 genes
distinguished CFS from controls, and could be an objective biomarker
for CFS. Diagnosis based on gene expression may eventually be possible.

Following work with Gulf War veterans, L.Steele (Waco,USA)
investigated, with a small sample whether exposure to neurotoxicants
are risk factors for developing Gulf War Illness (GWI). Some troops
who were exposed however did not develop illness, so genetic
differences may have been implicated. Findings are supportive that GWI
may be associated with the PON1 genotype. PON1 is a detoxifying
enzyme. GW veterans whose PON1 genotype is known to provide slower
hydrolysis of some organophosphate pesticides are at greater risk of
GWI in relation to reported use of pesticides and prolonged use of
pyridostigmine. And GW veterans who carry the R allele PON1192, which
is known to provide inefficient hydrolysis of sarin were at increased
risk of GWI if they had heard chemical alarms, which indicated
potential exposure.

L.Garcia (Miami,USA) compared gene expression patterns in CFS and GWI.
Study was based on Jonathan Kerr's work which had identified 79 genes
associated with CFS with defined subgroups. Her group used gene
activation patterns in CFS and GWI during and after exercise challenge
to better understand the mediators of persistence and relapse. Kerr's
earlier findings were confirmed in the CFS group. There were
significant differences when compared to controls. There were
important overlaps with GWI. EB12 (an EBV induced gene) was 6-fold
higher in CFS than in controls, and 2-fold higher in GWI. ETS1 was
upregulated in both groups. Transcription factor 3 was markedly
elevated in GWI and less so in CFS, though was significant. Apoptosis
genes were markedly elevated in both groups though 400 fold higher in
GWI. The overall trend however was that most of the gene regulation
activities associated with CFS were not significantly different
between GWI and controls. Additional genes specific to GWI have
however been identified by the group. With exercise challenge, there
were changes in genes at peak of exercise which were unique to CFS.
This was accompanied by altered immune signalling pathways.

Brain and neuro-endocrine functioning

I.Treasaden (London,UK) looked at volumetric changes in regional grey
and white matter in CFS using Voxel 3D MRI techniques. He compared 26
CFS patients with controls. In the CFS patients there was reduced grey
matter in the occipital lobes (associated with visual processing), in
the right angular gyrus (involved in perceptual sequence learning,
conscious awareness of actions) and in the posterior division of the
left parahippocampalgyrus (associated with memory function and
retrieval). There was also reduction of white matter in the left
occipital lobe. This data helps to confirm a neurological diagnosis,
and needs to be correlated with biochemical changes.

That there is evidence for reduced aldosterone in those with CFS was
presented by R.Boneva (Atlanta,USA). Many of the symptoms in some CFS
patients do overlap with those of Addison's disease. These include
orthostatic intolerance, orthostatic tachycardia and heat/cold
intolerance. Maintenance of blood volume may be poor and this is
dependent on regulation by aldosterone and mineralocorticoid receptors
in the brain. In this study of 70 CFS patients and 212 controls, those
with CFS had comparatively lower aldosterone levels. A previous study
(Wichita) had reported higher plasma renin levels. Further studies
should measure aldosterone response to salt restriction and postural

A.Miller (Atlanta,USA) presented 2 papers. The first was on behalf of
J.Jones (Atlanta,USA) using functional MRI (fMRI). It has been
suggested that CFS symptoms may be linked to altered cognitive or
pre-cognitive processing in the CNS. This study investigated the sense
of 'self' and 'illness-related semantic information'. The focus was on
the right anterior insula, an area associated with awareness and
self-related processing. Conclusions were that there is a real
alteration of body physiology in CFS. The interoceptive landscape is
acquired cognitively and precognitively in an altered way, enhancing
the prominence of symptoms related to fatigue.

The second paper demonstrated decreased basal ganglia activity in CFS
associated with fatigue by fMRI. Results compared to controls, showed
decreased activation in the right caudate and right globuspallidus.
The decreased activation in the right globuspallidus was significantly
correlated with increased mental fatigue, general fatigue and reduced
activity. Dopamine has a central role in basal ganglia regulation, so
alterations in dopamine metabolism may be involved. Dopamine
transmission and metabolism in these areas may be due to activated
immune pathways. Pharmacologic strategies targeting dopamine and the
basal ganglia may be therapeutic possibilities.

J.Dyke (New York,USA) discussed a new brain imaging technique known as
arterial spin labelling MRI was used to compare regional cerebral
blood flow (rCBF) in CFS, patients with major depression (MDD) and
healthy controls. The 2 patient groups were psychotropic-medication
free for 1 week prior to scanning. rCBF was significantly decreased in
CFS in the left anterior cingulate cortex and the right lingual region
compared to controls, while those with MDD had a trend towards
significantly lower rCBF in the left anterior cingulate cortex. rCBF
for CFS and MDD did not differ significantly. It is unclear whether
the hypoperfusion in rCBF in CFS would account for previous
observation of increased ventricular lactate. This increase could be
due to oxidative stress, mitochondrial dysfunction or decreased rCBF.

Conference summary

The conference ended with an excellent over view by Anthony Komaroff
(Boston,USA). He mentioned an informal meeting which had taken place
to discuss multicentre research initiatives. He stressed the
importance of a variety of initiatives pulling clinicians and
researchers together. Forms, laboratory tests etc. need to be
standardised. He pointed out that 'Research Needs Money'.

(c) 2011 Rosamund Vallings

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