Showing posts with label BRAINFOG. Show all posts
Showing posts with label BRAINFOG. Show all posts
Tuesday, February 23, 2016
Exercise physiologist Prof Keller: Brian Walitt's opinion "is intellectually embarrassing"
Exercise physiologist Prof Keller: "Given what we have learned in the past eight years about this illness, it is intellectually embarrassing to suggest that ME is a psychological illness."
# Professor Hooper: When does ignoring evidence by doctors become serious professional misconduct ?
# Prof Edward Shorter and the psychic epidemic of ignoring evidence
# Evidence that a disease is psychosomatic does NOT exist
Labels:
BRAINFOG,
CBT,
CHRONIC DISEASE,
Health,
ME,
ME/CFS,
NICE,
PACE,
Psycho blah blah,
Secondary Gains
Friday, November 6, 2015
Wednesday, September 16, 2015
Low Natural killer (NK) cells in CFS is associated with increased symptom severity
@ J Clin Cell Immunol:
Low NK Cell Activity in Chronic Fatigue Syndrome (CFS) and Relationship to Symptom Severity
David Strayer, Victoria Scott and William Carter
1617 JFK Boulevard, Suite 500, Philadelphia, PA 19103, USA
Corresponding Author :David Strayer 1617 JFK Boulevard, Suite 500 Philadelphia, PA 19103, USA Tel: + 215-988-0080 Fax: + 215-988-1739 E-mail: annmarie@hemispherx.net
Received: April 29, 2015 Accepted: July 22, 2015 Published: July 29, 2015
Citation: Strayer D, Scott V, Carter W (2015) Low NK Cell Activity in Chronic Fatigue Syndrome (CFS) and Relationship to Symptom Severity. J Clin Cell Immunol 6:348. doi:10.4172/2155-9899.1000348
Copyright: © 2015 Strayer D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background:
Natural killer (NK) cells act as an immune surveillance against invading pathogens and tumors. NK cell cytotoxicity (NKCC) has been reported to be decreased in patients with CFS.
Methods:
The objective of this review was to conduct an analysis of available publications that reported NKCC data in CFS in order to evaluate any relationships to case definitions used to define CFS and symptom severity.
Results:
Of 17 studies that evaluated NKCC in patients with CFS, defined using the CDC 1988 and/or 1994 case definition (CD), 88% (15/17) concluded that NKCC was decreased in CFS patients compared to normal controls.
The NKCC decrease was seen using two established methods, 51Cr release (11/13) and flow cytometry (4/4). The mean percent decrease in NKCC using the CDC 1988 CD (66.3%) was significantly greater than that using the CDC 1994 CD (49.7%) (p<0 data-blogger-escaped-.01="" data-blogger-escaped-br=""> This result is consistent with that of six publications showing a greater decrease in NKCC associated with increased CFS symptom severity based on the lower symptom requirement for the CDC 1994 vs. 1988 CD. In contrast, there was no significant difference in the mean percent decrease in NKCC seen comparing the CDC 1994 CD defined population using the 51Cr release (48.3%) vs. flow cytometry (50.7%) assays (p>0.5).
Finally, seven studies investigating the ability of various agents to augment NKCC in patients with CFS showed increases of NKCC with both in vitro exposure (4/5) and in vivo exposure using randomized trials (2/2).
Conclusions:
Low NKCC is commonly seen in CFS and is associated with increase symptom severity.
Low NK Cell Activity in Chronic Fatigue Syndrome (CFS) and Relationship to Symptom Severity
David Strayer, Victoria Scott and William Carter
1617 JFK Boulevard, Suite 500, Philadelphia, PA 19103, USA
Corresponding Author :David Strayer 1617 JFK Boulevard, Suite 500 Philadelphia, PA 19103, USA Tel: + 215-988-0080 Fax: + 215-988-1739 E-mail: annmarie@hemispherx.net
Received: April 29, 2015 Accepted: July 22, 2015 Published: July 29, 2015
Citation: Strayer D, Scott V, Carter W (2015) Low NK Cell Activity in Chronic Fatigue Syndrome (CFS) and Relationship to Symptom Severity. J Clin Cell Immunol 6:348. doi:10.4172/2155-9899.1000348
Copyright: © 2015 Strayer D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background:
Natural killer (NK) cells act as an immune surveillance against invading pathogens and tumors. NK cell cytotoxicity (NKCC) has been reported to be decreased in patients with CFS.
Methods:
The objective of this review was to conduct an analysis of available publications that reported NKCC data in CFS in order to evaluate any relationships to case definitions used to define CFS and symptom severity.
Results:
Of 17 studies that evaluated NKCC in patients with CFS, defined using the CDC 1988 and/or 1994 case definition (CD), 88% (15/17) concluded that NKCC was decreased in CFS patients compared to normal controls.
The NKCC decrease was seen using two established methods, 51Cr release (11/13) and flow cytometry (4/4). The mean percent decrease in NKCC using the CDC 1988 CD (66.3%) was significantly greater than that using the CDC 1994 CD (49.7%) (p<0 data-blogger-escaped-.01="" data-blogger-escaped-br=""> This result is consistent with that of six publications showing a greater decrease in NKCC associated with increased CFS symptom severity based on the lower symptom requirement for the CDC 1994 vs. 1988 CD. In contrast, there was no significant difference in the mean percent decrease in NKCC seen comparing the CDC 1994 CD defined population using the 51Cr release (48.3%) vs. flow cytometry (50.7%) assays (p>0.5).
Finally, seven studies investigating the ability of various agents to augment NKCC in patients with CFS showed increases of NKCC with both in vitro exposure (4/5) and in vivo exposure using randomized trials (2/2).
Conclusions:
Low NKCC is commonly seen in CFS and is associated with increase symptom severity.
Labels:
BRAINFOG,
CFS/ME,
CHRONIC DISEASE,
DIAGNOSING,
Health,
ME,
RESEARCH,
Science
Sunday, May 24, 2015
Once again a study demonstrating physical abnormalities in ME/CFS decides to ignore their own findings
By Ruth R Miller1 , W Darlene Reid2 , Andre Mattman3 , Cristiane Yamabayashi4 , Theodore Steiner5 , Shoshana Parker6 , Jennifer Gardy7 , Patrick Tang and David M Patrick, Published online: 20 May 2015:
Conclusions
This submaximal exercise testing protocol revealed attenuated changes in oxygenated and deoxygenated hemoglobin, which may be attributable to poor exercise tolerance and rapid fatigue seen in ME/CFS compounded by decreased fitness. Because of the variable responses among participants, it does not provide a clear distinction between cases with ME/CFS and healthy controls and is therefore not a useful diagnostic marker. However, testing did reveal a disproportionate level of perceived exertion and lower force production in cases with ME/CFS, and in two cases, adverse responses to low levels of exercise. The repetitive handgrip protocol may be useful to screen individuals for adverse responses and other conditions, including mitochondrial disease. It may also be useful for stratifying ME/CFS sufferers to determine appropriate levels of exercise prescription.
There are a number of issues with this study. I'm just going to mention a few.
Obviously the first one is "This submaximal exercise testing protocol revealed attenuated changes in oxygenated and deoxygenated hemoglobin, which may be attributable to poor exercise tolerance and rapid fatigue seen in ME/CFS compounded by decreased fitness."
So you find abnormalities which you don't want to find and and then you just come up with some nonsense to say they're not important. Typical Pinocchio doctoring.
If you look at the average BMI of the healthy controls and patients then there is a massive difference.
In patients it's on average 25.1 and in healthy controls 20.8. Simply put, I'm 175 cm. If my BMI was 25.1, my weight would be 76.9 kg and if my BMI was 20.8 it would be 63.7 kg. And that's a difference of 13.2 kilo which is 17.2 percent and that's a massive difference. And you cannot use healthy controls who are very slim and compare those with patients that are not.
If you look at the following sentence, "All cases and no healthy controls fit both the Canadian case definition and the CDC Fukuda definition of ME/CFS" it actually means that healthy controls can actually have ME/CFS as defined by Fukuda or defined by CCC but not by both. Which means that the healthy controls might not be healthy controls at all and they might actually have ME/CFS.
The researchers selected 25 ME patients and 25 healthy controls but they only analysed 16 of both. In the patient group they explained why they couldn't use 6 of the 25, which means that 3 were unaccounted and in the healthy controls 5 were accounted and 4 unaccounted. And in a small group that's a large percentage which is unaccounted. That should not happen but that is something which happens a lot in denial doctoring as Frank Twisk has shown repeatedly when he analysed studies by Nijmegen etc
There is one other interesting thing I would like to mention. "The CCD study pre-screened 102 people and excluded 52:24 with another diagnosis (e.g., sleep apnea, hypothyroidism, etc.), three who did not meet the case definitions, 11 that declined to participate, and 14 eligible patients that could not be matched to a control."
So 102 patient had a diagnosis of ME/CFS and after checking with the CCC criteria, in 24 of them, which is 23.5 %, the diagnosis was wrong. Which shows once again that doctors are not very good at diagnosing ME/CFS.
So once again a study demonstrating physical abnormalities in ME/CFS decides to ignore their own findings because it doesn't fit with their own ideas about ME/CFS for which they do not have any proof and they use psychoblahblah to do as if these physical abnormalities are not important. Whereas these abnormalities are actually "pretty diagnostic of impaired oxidative phosphorylation which is presumably where the "fear " of excercise comes from. Many patients with syndromic mitochondrial diseases fear excercise because their symtoms can worsen dramatically during or following the activity." As GJ rightly wrote on Facebook.
Their conclusion should have been something like: this clearly shows physical abnormalities related to exercise pointing towards mitochondrial problems in patients with ME/CFS which might aid doctors in diagnosing this condition
Conclusions
This submaximal exercise testing protocol revealed attenuated changes in oxygenated and deoxygenated hemoglobin, which may be attributable to poor exercise tolerance and rapid fatigue seen in ME/CFS compounded by decreased fitness. Because of the variable responses among participants, it does not provide a clear distinction between cases with ME/CFS and healthy controls and is therefore not a useful diagnostic marker. However, testing did reveal a disproportionate level of perceived exertion and lower force production in cases with ME/CFS, and in two cases, adverse responses to low levels of exercise. The repetitive handgrip protocol may be useful to screen individuals for adverse responses and other conditions, including mitochondrial disease. It may also be useful for stratifying ME/CFS sufferers to determine appropriate levels of exercise prescription.
There are a number of issues with this study. I'm just going to mention a few.
Obviously the first one is "This submaximal exercise testing protocol revealed attenuated changes in oxygenated and deoxygenated hemoglobin, which may be attributable to poor exercise tolerance and rapid fatigue seen in ME/CFS compounded by decreased fitness."
So you find abnormalities which you don't want to find and and then you just come up with some nonsense to say they're not important. Typical Pinocchio doctoring.
If you look at the average BMI of the healthy controls and patients then there is a massive difference.
In patients it's on average 25.1 and in healthy controls 20.8. Simply put, I'm 175 cm. If my BMI was 25.1, my weight would be 76.9 kg and if my BMI was 20.8 it would be 63.7 kg. And that's a difference of 13.2 kilo which is 17.2 percent and that's a massive difference. And you cannot use healthy controls who are very slim and compare those with patients that are not.
If you look at the following sentence, "All cases and no healthy controls fit both the Canadian case definition and the CDC Fukuda definition of ME/CFS" it actually means that healthy controls can actually have ME/CFS as defined by Fukuda or defined by CCC but not by both. Which means that the healthy controls might not be healthy controls at all and they might actually have ME/CFS.
The researchers selected 25 ME patients and 25 healthy controls but they only analysed 16 of both. In the patient group they explained why they couldn't use 6 of the 25, which means that 3 were unaccounted and in the healthy controls 5 were accounted and 4 unaccounted. And in a small group that's a large percentage which is unaccounted. That should not happen but that is something which happens a lot in denial doctoring as Frank Twisk has shown repeatedly when he analysed studies by Nijmegen etc
There is one other interesting thing I would like to mention. "The CCD study pre-screened 102 people and excluded 52:24 with another diagnosis (e.g., sleep apnea, hypothyroidism, etc.), three who did not meet the case definitions, 11 that declined to participate, and 14 eligible patients that could not be matched to a control."
So 102 patient had a diagnosis of ME/CFS and after checking with the CCC criteria, in 24 of them, which is 23.5 %, the diagnosis was wrong. Which shows once again that doctors are not very good at diagnosing ME/CFS.
So once again a study demonstrating physical abnormalities in ME/CFS decides to ignore their own findings because it doesn't fit with their own ideas about ME/CFS for which they do not have any proof and they use psychoblahblah to do as if these physical abnormalities are not important. Whereas these abnormalities are actually "pretty diagnostic of impaired oxidative phosphorylation which is presumably where the "fear " of excercise comes from. Many patients with syndromic mitochondrial diseases fear excercise because their symtoms can worsen dramatically during or following the activity." As GJ rightly wrote on Facebook.
Their conclusion should have been something like: this clearly shows physical abnormalities related to exercise pointing towards mitochondrial problems in patients with ME/CFS which might aid doctors in diagnosing this condition
Thursday, April 2, 2015
Simon Wessely in The Lancet: "being too stupid to know how stupid you are"
Quote from Wessely in The Lancet, 21st of march 2015 ..... (I wonder if he noticed the hysterical absurdity ...)
.... "to introduce something new to me. This is the Kruger-Dunning effect—the state of being too stupid to know how stupid you are being."
Simon Wessely in The Lancet: "being too stupid to know how stupid you are".pdf
Find by LYN.
.... "to introduce something new to me. This is the Kruger-Dunning effect—the state of being too stupid to know how stupid you are being."
Simon Wessely in The Lancet: "being too stupid to know how stupid you are".pdf
Find by LYN.
Tuesday, March 31, 2015
Markedly disturbed immune signature in CSF with a shift towards a pattern associated with autoimmunity in ME/CFS
@ nature.com; 31 march 2015:
Molecular Psychiatry , (31 March 2015) | doi:10.1038/mp.2015.29
Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome
M Hornig, G Gottschalk, D L Peterson, K K Knox, A F Schultz, M L Eddy, X Che and W I Lipkin
Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.
Molecular Psychiatry , (31 March 2015) | doi:10.1038/mp.2015.29
Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome
M Hornig, G Gottschalk, D L Peterson, K K Knox, A F Schultz, M L Eddy, X Che and W I Lipkin
Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.
Friday, January 16, 2015
Monday, September 15, 2014
Rintatolimod aka Ampligen produces objective improvement in CFS/ME
@ pubmed:
PLoS One. 2012;7(3):e31334. doi: 10.1371/journal.pone.0031334. Epub 2012 Mar 14.
A double-blind, placebo-controlled, randomized, clinical trial of the TLR-3 agonist rintatolimod in severe cases of chronic fatigue syndrome.
Strayer DR1, Carter WA, Stouch BC, Stevens SR, Bateman L, Cimoch PJ, Lapp CW, Peterson DL; Chronic Fatigue Syndrome AMP-516 Study Group, Mitchell WM.
Abstract
BACKGROUND:
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a severely debilitating disease of unknown pathogenesis consisting of a variety of symptoms including severe fatigue. The objective of the study was to examine the efficacy and safety of a TLR-3 agonist, rintatolimod (Poly I: C(12)U), in patients with debilitating CFS/ME.
METHODS AND FINDINGS:
A Phase III prospective, double-blind, randomized, placebo-controlled trial comparing twice weekly IV rintatolimod versus placebo was conducted in 234 subjects with long-standing, debilitating CFS/ME at 12 sites. The primary endpoint was the intra-patient change from baseline at Week 40 in exercise tolerance (ET). Secondary endpoints included concomitant drug usage, the Karnofsky Performance Score (KPS), Activities of Daily Living (ADL), and Vitality Score (SF 36). Subjects receiving rintatolimod for 40 weeks improved intra-patient placebo-adjusted ET 21.3% (p = 0.047) from baseline in an intention-to-treat analysis. Correction for subjects with reduced dosing compliance increased placebo-adjusted ET improvement to 28% (p = 0.022). The improvement observed represents approximately twice the minimum considered medically significant by regulatory agencies. The rintatolimod cohort vs. placebo also reduced dependence on drugs commonly used by patients in an attempt to alleviate the symptoms of CFS/ME (p = 0.048). Placebo subjects crossed-over to receive rintatolimod demonstrated an intra-patient improvement in ET performance at 24 weeks of 39% (p = 0.04). Rintatolimod at 400 mg twice weekly was generally well-tolerated.
CONCLUSIONS/SIGNIFICANCE:
Rintatolimod produced objective improvement in ET and a reduction in CFS/ME related concomitant medication usage as well as other secondary outcomes.
TRIAL REGISTRATION:
ClinicalTrials.gov NCT00215800.
Thursday, February 20, 2014
Dr Richard Schloeffel, a Sydney ME/CFS specialist GP: Occasionally patients die from ME/CFS
By Rachel Eldred:
MiNDFOOD speaks with Dr Richard Schloeffel about his work treating chronic and complex disorders, including diagnosing patients with chronic fatigue syndrome.
Occasionally patients die from CFS. They die because they get metabolic failure and heart failure. And that’s why there’s an organisation called the Alison Hunter Foundation. Alison Hunter died in the 1990s from metabolic and heart failure after they tried to treat her for CFS. I’ve had eight patients die on me in the last few years … some by suicide because they couldn’t live any longer with the illness, and definitely some, unfortunately, by the neglect of the medical professional in understanding the complexity of their medical condition.
Read more>>
Occasionally patients die from CFS. They die because they get metabolic failure and heart failure. And that’s why there’s an organisation called the Alison Hunter Foundation. Alison Hunter died in the 1990s from metabolic and heart failure after they tried to treat her for CFS. I’ve had eight patients die on me in the last few years … some by suicide because they couldn’t live any longer with the illness, and definitely some, unfortunately, by the neglect of the medical professional in understanding the complexity of their medical condition.
What do you think needs to be done to better educate the public about CFS and how debilitating it can be?
There is a lot of unfortunate mismanagement and misdiagnosis because it’s called CFS. People are devalued in the diagnostic process and the treatment process because they’ve got this label that stigmatises them, and we have got to get rid of this. CFS has nothing to do with fatigue. Fatigue is the underlying response to all of the other dysfunctions that are occurring in the body.
We need more good quality research with proper diagnostic criteria done by qualified medical people who are in the field. People like me need to publish articles, we need to publish everything we find in the patients we are seeing, and we need to have it verified.
Most of the funding for CFS goes to the people who are looking for psychological causes, and they treat it with graded exercise and Cognitive Behaviour Therapy, which is wonderful if you’re in recovery, but makes no difference to someone who is profoundly ill. Generally, people in Australia will know someone with this disorder. That’s the nature of it. Every GP has them in their practices, and every GP should know how to diagnose it.
Sunday, December 8, 2013
Immune Abnormalities in Patients Meeting New Diagnostic Criteria for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis
Immune Abnormalities in Patients Meeting New Diagnostic Criteria for
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis
Brenu EW1,2*, Johnston S1,2, Hardcastle SL1,2, Huth TK1,2, Fuller K1,2, Ramos SB1,2, Staines DR2,3 and Marshall-Gradisnik SM1,2
1School of Medical Science, Griffith University, Gold Coast, Queensland, Australia
2The National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Institute, Queensland, Australia
3Queensland Health, Gold Coast Public Health Unit, Robina, Gold Coast, Queensland, Australia
Abstract
Background: Immunological abnormalities have been identified in Chronic Fatigue Syndrome/Myalgic
Encephalomyelitis patients fulfilling the 1994 Centers for Disease Control diagnostic criteria. Significant developments have been made to diagnostic criteria, but potential immunological markers have not been assessed in patients fulfilling these latest clinical requirements. Therefore, this study evaluated immunological parameters in patients that also fulfill the latest diagnostic criteria available known as the International Consensus Criteria.
Methods: The Immunological investigations including Natural Killer cell activity and phenotyping studies for
dendritic cells, neutrophils, B cells and regulatory T cells were performed on whole blood samples collected from all participants using flow cytometric protocols. The physical functioning of all participants was also evaluated using scores from the Short Form Health Survey, and the World Health Organization Disability Adjustment Schedule.
Results were compared according 1994 Centers of Disease Control and Prevention defined patients, and
International Consensus Criteria defined patients, and healthy controls.
Results: Natural killer cell activity was consistently and significantly decreased, and regulatory T cells were
significantly increased in both patient groups compared to healthy controls. Differences were found in human
neutraphil antigens and expression of natural killer cell receptors between patient groups. Highly significant
correlations were also found between physical status and some immune parameters in International Consensus
Criteria defined patients.
Conclusion: This preliminary investigation on different diagnostic criteria suggests that the International
Consensus Criteria may be more effective a detecting salient differences in the immune system. Read more>>
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis
Brenu EW1,2*, Johnston S1,2, Hardcastle SL1,2, Huth TK1,2, Fuller K1,2, Ramos SB1,2, Staines DR2,3 and Marshall-Gradisnik SM1,2
1School of Medical Science, Griffith University, Gold Coast, Queensland, Australia
2The National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Institute, Queensland, Australia
3Queensland Health, Gold Coast Public Health Unit, Robina, Gold Coast, Queensland, Australia
Abstract
Background: Immunological abnormalities have been identified in Chronic Fatigue Syndrome/Myalgic
Encephalomyelitis patients fulfilling the 1994 Centers for Disease Control diagnostic criteria. Significant developments have been made to diagnostic criteria, but potential immunological markers have not been assessed in patients fulfilling these latest clinical requirements. Therefore, this study evaluated immunological parameters in patients that also fulfill the latest diagnostic criteria available known as the International Consensus Criteria.
Methods: The Immunological investigations including Natural Killer cell activity and phenotyping studies for
dendritic cells, neutrophils, B cells and regulatory T cells were performed on whole blood samples collected from all participants using flow cytometric protocols. The physical functioning of all participants was also evaluated using scores from the Short Form Health Survey, and the World Health Organization Disability Adjustment Schedule.
Results were compared according 1994 Centers of Disease Control and Prevention defined patients, and
International Consensus Criteria defined patients, and healthy controls.
Results: Natural killer cell activity was consistently and significantly decreased, and regulatory T cells were
significantly increased in both patient groups compared to healthy controls. Differences were found in human
neutraphil antigens and expression of natural killer cell receptors between patient groups. Highly significant
correlations were also found between physical status and some immune parameters in International Consensus
Criteria defined patients.
Conclusion: This preliminary investigation on different diagnostic criteria suggests that the International
Consensus Criteria may be more effective a detecting salient differences in the immune system. Read more>>
Sunday, July 3, 2011
Harvard Medical School: EEG spectral coherence data distinguish ME/CFS patients from healthy controls and depressed patients
Frank H. Duffy1§, Gloria B. McAnulty2, Michelle C. McCreary3, George J. Cuchural4,
Anthony L. Komaroff3:
Department of Neurology, Children’s Hospital Boston and Harvard Medical School, 300
Longwood Ave, Boston, Massachusetts 02115, USA
2 Department of Psychiatry, Children’s Hospital Boston and Harvard Medical School, 300
Longwood Ave, Boston, Massachusetts 02115, USA
3Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School,
75 Francis St, Boston, Massachusetts 02115, USA
4Department of Medicine, Tufts Medical Center, 800 Washington Street, Boston,
Massachusetts 02111, USA
§Corresponding author
Email addresses:
FHD: fhd@sover.net frank.duffy@childrens.harvard.edu
GBM: gloria.mcanulty@childrens.harvard.edu
MCM: mcmccreary@gmail.com
GJC: gcuchural@tufts-nemc.org
ALK: anthony_komaroff@hms.harvard.edu
Abstract
Background
Previous studies suggest central nervous system involvement in chronic fatigue
syndrome (CFS), yet there are no established diagnostic criteria. CFS may be difficult to
differentiate from clinical depression. The study’s objective was to determine if spectral
coherence, a computational derivative of spectral analysis of the electroencephalogram
(EEG), could distinguish patients with CFS from healthy control subjects and not
erroneously classify depressed patients as having CFS.
Methods
This is a study, conducted in an academic medical center electroencephalography
laboratory, of 632 subjects: 390 healthy normal controls, 70 patients with carefully
defined CFS, 24 with major depression, and 148 with general fatigue. Aside from fatigue,
all patients were medically healthy by history and examination. EEGs were obtained and
spectral coherences calculated after extensive artifact removal. Principal
Components
Analysis identified coherence factors and corresponding factor loading patterns.
Discriminant analysis determined whether spectral coherence factors could reliably
discriminate CFS patients from healthy control subjects without misclassifying
depression as CFS.
Results
Analysis of EEG coherence data from a large sample (n=632) of patients and
healthy controls identified 40 factors explaining 55.6% total variance. Factors showed
highly significant group differentiation (p<.0004) identifying 89.5% of unmedicated
female CFS patients and 92.4% of healthy female controls. Recursive jackknifing showed
predictions were stable. A conservative 10-factor discriminant function model was
subsequently applied, and also showed highly significant group discrimination (p<.001),
accurately classifying 88.9% unmedicated males with CFS, and 82.4% unmedicated male
healthy controls. No patient with depression was classified as having CFS. The model
was less accurate (73.9%) in identifying CFS patients taking psychoactive medications.
Factors involving the temporal lobes were of primary importance.
Conclusions
EEG spectral coherence analysis identified unmedicated patients with CFS and
healthy control subjects without misclassifying depressed patients as CFS, providing
evidence that CFS patients demonstrate brain physiology that is not observed in healthy
normals or patients with major depression. Studies of new CFS patients and comparison
groups are required to determine the possible clinical utility of this test. The results
concur with other studies finding neurological abnormalities in CFS, and implicate
temporal lobe involvement in CFS pathophysiology. Read more>>
Anthony L. Komaroff3:
Department of Neurology, Children’s Hospital Boston and Harvard Medical School, 300
Longwood Ave, Boston, Massachusetts 02115, USA
2 Department of Psychiatry, Children’s Hospital Boston and Harvard Medical School, 300
Longwood Ave, Boston, Massachusetts 02115, USA
3Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School,
75 Francis St, Boston, Massachusetts 02115, USA
4Department of Medicine, Tufts Medical Center, 800 Washington Street, Boston,
Massachusetts 02111, USA
§Corresponding author
Email addresses:
FHD: fhd@sover.net frank.duffy@childrens.harvard.edu
GBM: gloria.mcanulty@childrens.harvard.edu
MCM: mcmccreary@gmail.com
GJC: gcuchural@tufts-nemc.org
ALK: anthony_komaroff@hms.harvard.edu
Abstract
Background
Previous studies suggest central nervous system involvement in chronic fatigue
syndrome (CFS), yet there are no established diagnostic criteria. CFS may be difficult to
differentiate from clinical depression. The study’s objective was to determine if spectral
coherence, a computational derivative of spectral analysis of the electroencephalogram
(EEG), could distinguish patients with CFS from healthy control subjects and not
erroneously classify depressed patients as having CFS.
Methods
This is a study, conducted in an academic medical center electroencephalography
laboratory, of 632 subjects: 390 healthy normal controls, 70 patients with carefully
defined CFS, 24 with major depression, and 148 with general fatigue. Aside from fatigue,
all patients were medically healthy by history and examination. EEGs were obtained and
spectral coherences calculated after extensive artifact removal. Principal
Components
Analysis identified coherence factors and corresponding factor loading patterns.
Discriminant analysis determined whether spectral coherence factors could reliably
discriminate CFS patients from healthy control subjects without misclassifying
depression as CFS.
Results
Analysis of EEG coherence data from a large sample (n=632) of patients and
healthy controls identified 40 factors explaining 55.6% total variance. Factors showed
highly significant group differentiation (p<.0004) identifying 89.5% of unmedicated
female CFS patients and 92.4% of healthy female controls. Recursive jackknifing showed
predictions were stable. A conservative 10-factor discriminant function model was
subsequently applied, and also showed highly significant group discrimination (p<.001),
accurately classifying 88.9% unmedicated males with CFS, and 82.4% unmedicated male
healthy controls. No patient with depression was classified as having CFS. The model
was less accurate (73.9%) in identifying CFS patients taking psychoactive medications.
Factors involving the temporal lobes were of primary importance.
Conclusions
EEG spectral coherence analysis identified unmedicated patients with CFS and
healthy control subjects without misclassifying depressed patients as CFS, providing
evidence that CFS patients demonstrate brain physiology that is not observed in healthy
normals or patients with major depression. Studies of new CFS patients and comparison
groups are required to determine the possible clinical utility of this test. The results
concur with other studies finding neurological abnormalities in CFS, and implicate
temporal lobe involvement in CFS pathophysiology. Read more>>
Monday, January 31, 2011
Great news for Arsenal fans!
KojoTweets:
Arsenal fans! Arsene Wenger has just bought some wine gums. Just thought I'd keep you updated on TransferDeadlineDay
Arsenal fans! Arsene Wenger has just bought some wine gums. Just thought I'd keep you updated on TransferDeadlineDay
Saturday, January 22, 2011
The main core in the computers of copper oxide psychiatry
It was an absolute delight, reading some of the comments on different ME/CFS forums.
Some comments are absolutely brilliant, and even the most knowledgeable person in the universe could learn a thing or two about gagging and all sorts of other things that viruses use to make our lives miserable.
One thing I never get is that if I tell a person with a diagnosis of a broken leg, who claims that putting his two fingers in a socket has cured him of his disease, that his diagnosis was wrong, they suddenly like me very much, especially on days like yesterday, which was bear Hug Day and they squeeze me so hard that my muscles, which are already bursting because of my lingering false messi believes, explode as if operation Desert Storm has just started again.
We all know that those healthy, superfit soldiers who went to the Gulf to fill Mr. Bush his cars with petrol, and then came back as crippled persons, dying at young age from all sorts of delightful things, including Wesleyan syndrome, that they were obviously suddenly after benefits including seeing hostile doctors to brighten up their days even more.
Now we all know that the same thing happens with people with ME or with CFS even though those two things are not completely the same.
Just read Dr. Melvin Ramsey's book, yes I know I'm dispelling his name but my cognitive dysfunction, which is one of the major differences between ME and CFS is just getting in the way.
Both of them are city illnesses, but they are not the same.
A recent survey showed that in 40% of people who are diagnosed with ME the diagnosis is wrong. I would be glad, because in many cases this means that suddenly there is a chance of getting proper treatment.
Now I could continue, and then mention the lightning therapy, which apparently is based on the fact that ME patients are desperate to get well again and so they will try anything, even waiting for the god of lightning to strike, because apparently they can talk to our adrenal glands and tell them you should beheeve you little buggers and then suddenly, all is well.
Even a six-year-old understands that anybody would gets skewered by this process, either had a spontaneous cure or otherwise the diagnose was completely wrong.
Just as it is completely wrong, that these sort of people in the name of comments are putting the most ludicrous claims here there and everywhere and use all sort of foul language against people who were in the right state of ME, to the extent that ME and CFS are both shady somewhere in Bath and near the Thames but they are not the same.
But I guess people who have turned themselves into lightning quick therapists, or others who talk to the mix up in my brain so that the cells up there certainly get so scared of these silly things that they kick the XMRV or whatever viruses is causing this delightful ME chappy to ruin my life, out of my system.
By the time I'm well I will start to practice this, when a patient comes into my surgery and tells me that the antibiotic that I prescribed for his severe infection didn't do anything,
than I will first blame him,
then I will become very hostile
and then I will write to the MRC requesting £5 million so that I can write up a fantastic fairy tale that continuous bullshit telling will be the main course on the menu for doctors.
From now on.
Sorry, it has been the main core in the computers of copper oxide psychiatry for decades.
Have a good day.
Some comments are absolutely brilliant, and even the most knowledgeable person in the universe could learn a thing or two about gagging and all sorts of other things that viruses use to make our lives miserable.
One thing I never get is that if I tell a person with a diagnosis of a broken leg, who claims that putting his two fingers in a socket has cured him of his disease, that his diagnosis was wrong, they suddenly like me very much, especially on days like yesterday, which was bear Hug Day and they squeeze me so hard that my muscles, which are already bursting because of my lingering false messi believes, explode as if operation Desert Storm has just started again.
We all know that those healthy, superfit soldiers who went to the Gulf to fill Mr. Bush his cars with petrol, and then came back as crippled persons, dying at young age from all sorts of delightful things, including Wesleyan syndrome, that they were obviously suddenly after benefits including seeing hostile doctors to brighten up their days even more.
Now we all know that the same thing happens with people with ME or with CFS even though those two things are not completely the same.
Just read Dr. Melvin Ramsey's book, yes I know I'm dispelling his name but my cognitive dysfunction, which is one of the major differences between ME and CFS is just getting in the way.
Both of them are city illnesses, but they are not the same.
A recent survey showed that in 40% of people who are diagnosed with ME the diagnosis is wrong. I would be glad, because in many cases this means that suddenly there is a chance of getting proper treatment.
Now I could continue, and then mention the lightning therapy, which apparently is based on the fact that ME patients are desperate to get well again and so they will try anything, even waiting for the god of lightning to strike, because apparently they can talk to our adrenal glands and tell them you should beheeve you little buggers and then suddenly, all is well.
Even a six-year-old understands that anybody would gets skewered by this process, either had a spontaneous cure or otherwise the diagnose was completely wrong.
Just as it is completely wrong, that these sort of people in the name of comments are putting the most ludicrous claims here there and everywhere and use all sort of foul language against people who were in the right state of ME, to the extent that ME and CFS are both shady somewhere in Bath and near the Thames but they are not the same.
But I guess people who have turned themselves into lightning quick therapists, or others who talk to the mix up in my brain so that the cells up there certainly get so scared of these silly things that they kick the XMRV or whatever viruses is causing this delightful ME chappy to ruin my life, out of my system.
By the time I'm well I will start to practice this, when a patient comes into my surgery and tells me that the antibiotic that I prescribed for his severe infection didn't do anything,
than I will first blame him,
then I will become very hostile
and then I will write to the MRC requesting £5 million so that I can write up a fantastic fairy tale that continuous bullshit telling will be the main course on the menu for doctors.
From now on.
Sorry, it has been the main core in the computers of copper oxide psychiatry for decades.
Have a good day.
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Monday, January 11, 2010
Result!

Just tried to get on to the silly Daily Mail CBT Poll and it's no longer available.
http://www.dailymail.co.uk/debate/polls/poll.html?pollId=1015226
Sorry professor Wessely and all the other inappropriate illness believers ...
Labels:
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Thursday, November 26, 2009
Wednesday, November 18, 2009
ME is still not taken seriously ...
http://www.youtube.com/user/hoofbags: "In spite of the overwhelming evidence, the UK NHS still refuses to accept ME as a genuine illness and vehemently will never accept it as such. They will even go as far as torturing children to make their point and warn us no to do the same. "
Saturday, November 14, 2009
Sir Peter Spencer and the £500m Chinook “gold standard cock-up”
"Sir Peter Spencer and the £500m Chinook “gold standard cock-up”.
Sir Peter Spencer KCB was appointed Chief Executive of Action for M.E. on 30 April 2007. Prior to that he was Chief of Defence Procurement of the MOD, from May 2003.
Further details of Sir Peter’s career at the Ministry of Defence emerged yesterday. The coverage is not flattering, as newspaper headlines suggest:
“Chinook blunders cost MoD £500m”, David Hencke, Westminster correspondent, The
Guardian, Wednesday June 4 2008.
“£500m ‘wasted’ on Chinooks that have never flown”, Michael Evans, Defence Editor, The Times June 4, 2008.
“Chinook fleet sitting idle costs £422m”, By Rosa Prince, Political Correspondent, Daily Telegraph: 11:09 PM BST 03/06/2008.
--------------------------------------------------------------------------------
“MOD accused of Chinook 'cock-up'”, BBC: 2008/06/03 23:42:54 GMT."
Sir Peter Spencer KCB was appointed Chief Executive of Action for M.E. on 30 April 2007. Prior to that he was Chief of Defence Procurement of the MOD, from May 2003.
Further details of Sir Peter’s career at the Ministry of Defence emerged yesterday. The coverage is not flattering, as newspaper headlines suggest:
“Chinook blunders cost MoD £500m”, David Hencke, Westminster correspondent, The
Guardian, Wednesday June 4 2008.
“£500m ‘wasted’ on Chinooks that have never flown”, Michael Evans, Defence Editor, The Times June 4, 2008.
“Chinook fleet sitting idle costs £422m”, By Rosa Prince, Political Correspondent, Daily Telegraph: 11:09 PM BST 03/06/2008.
--------------------------------------------------------------------------------
“MOD accused of Chinook 'cock-up'”, BBC: 2008/06/03 23:42:54 GMT."
Wednesday, November 11, 2009
Two Irish hunters ...
Two Irish hunters got a pilot to fly them to Canada to hunt moose. They managed to bag 6.
As they were loading the plane to return, the pilot said the plane could take only 4 moose.
The two lads objected strongly. "Last year we shot six. The pilot let us take them all and he had the same plane as yours."
Reluctantly, the pilot gave in and all six were loaded.
However, even on full power, the little plane couldn't handle the load and went down crashing in the woods.
Somehow, surrounded by the moose bodies, Paddy and Mick survived the crash.
After climbing out of the wreckage, Paddy asked Mick, "Any idea where we are?"
Mick replied, "I think we're pretty close to where we crashed last year."
As they were loading the plane to return, the pilot said the plane could take only 4 moose.
The two lads objected strongly. "Last year we shot six. The pilot let us take them all and he had the same plane as yours."
Reluctantly, the pilot gave in and all six were loaded.
However, even on full power, the little plane couldn't handle the load and went down crashing in the woods.
Somehow, surrounded by the moose bodies, Paddy and Mick survived the crash.
After climbing out of the wreckage, Paddy asked Mick, "Any idea where we are?"
Mick replied, "I think we're pretty close to where we crashed last year."
Thursday, November 5, 2009
Saturday, October 31, 2009
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