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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Infection as one possible cause of fibromyalgia - Part V
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    Infection as one possible cause of fibromyalgia

    Part V

    1. Detection of Mycoplasma pneumoniae in the airways of adults with chronic asthma
      Monica Kraft, Gail H. Cassell, Jan E. Henson, Harold Watson, Jan Williamson, B.P. Marmion, Charlotte A. Gaydos and Richard J. Martin, Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, Colorado; Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama; Royal Hobart Hospital, University of Tasmania, Hobart, Tasmania; Institute of Medical and Veterinary Science, University of Adelaide, Australia; and Department of Medicine, The Johns Hopkins University, Baltimore, Maryland - Am. J. Respir. Crit. Care Med., Volume 158, Number 3, September 1998, 998-1001
      Infection with Mycoplasma pneumoniae has been shown to exacerbate asthma in humans.
      However, the role of M. pneumoniae in the pathogenesis of chronic asthma has not been defined.
      Eighteen asthmatics with chronic, stable asthma and 11 nonasthmatic control subjects underwent evaluation of the upper and lower airways and serologic analysis to determine the presence of M. pneumoniae, Chlamydia pneumoniae and seven respiratory viruses through culture, enzyme-linked immunoassay (EIA) and polymerase chain reaction (PCR).
      M. pneumoniae was detected by PCR in 10 of 18 asthmatics and one of 11 control subjects (p = 0.02).
      In nine of the 10 patients, the organism was detected in bronchoalveolar lavage or bronchial biopsies.
      Seven of 18 asthmatics and one of 11 control subjects were also positive for M. fermentans and M. genitalium by PCR.
      All patients' cultures, EIAs and serology were negative for M. pneumoniae.
      All PCR and cultures were negative for C. pneumoniae and all EIAs for respiratory viruses were negative in all subjects.
      Nine asthmatics and one control subject exhibited positive serology for C. pneumoniae (p = 0.05).
      M. pneumoniae was present in the lower airways of chronic, stable asthmatics with greater frequency than control subjects and may play a role in the pathogenesis of chronic asthma.
      Cfr. :

    2. Detection of mycoplasmal infections in blood of 565 chronic illness patients detected by polymerase chain reaction
      Nasralla M, Haier J, Nicolson GL - Intern J Med Biol Environ 2000; 28(1):15-23
      Garth L. Nicolson, PhDb, a, f1, Marwan Y. Nasralla, PhDc, a, Joerg Haier, MD, PhDd, a and John Pomfret, PhDb - a Molecular Biology Laboratory, Department of General Surgery, University Hospital Muenster, Muenster, Germany - b Gulf War ALS Research Project, Parsons Walk, Wigan, UK - c International Molecular Diagnostics, Inc. Huntington Beach, California, USA - d Department of Surgery, Wilhelm University, Muenster, Germany - f1 Correspondence to : Prof. Garth L. Nicolson, Molecular Biology Laboratory, Department of General Surgery, University Hospital Muenster, Waldeyerstrasse 1, 48149 Muenster, Germany – Tel. : +1-714-903-2900; Fax : +1-714-379-2082 - Website : – E-mail : - Journal of Clinical Neuroscience, Volume 9, Issue 5, September 2002, Pages 525-529 - © 2002 Elsevier Science Ltd.

      The presence of systemic mycoplasmal infections in the blood of Gulf War veterans (n=8) and civilians (n=28) with Amyotrophic Lateral Sclerosis (ALS) and age matched controls (n=70) was investigated by detecting mycoplasma gene sequences with forensic
      Polymerase Chain Reaction (PCR) and back hybridization with a radiolabeled internal oligonucleotide probe.
      Almost all ALS patients (30/36 or not, vert, similar83%) showed evidence of Mycoplasma species in blood samples, whereas <9% of controls had blood mycoplasmal infections (P<0.001).
      Using PCR ALS patients with a positive test for any mycoplasmal infection were investigated for the presence of M. fermentans, M. pneumoniae, M. hominis and M. penetrans in their blood.
      All Gulf War veterans with ALS were positive for M. fermentans, except one that was positive for M. genitalium.
      In contrast, the 22/28 civilians with detectable mycoplasmal infections had M. fermentans (13/22, 59%) as well as otherMycoplasama species in their blood and two of the civilian ALS patients had multiple mycoplasma species (M. fermentans plus M. hominis).
      Of the few control patients that were positive, only two patients (2/70, 2.8%) were positive for M. fermentans (P<0.001).
      The results support the suggestion that infectious agents may play a role in the pathogenesis and/or progression of ALS or alternatively ALS patients are extremely susceptible to systemic mycoplasmal infections.
      Cfr. :

    3. Detection of Mycoplasmal infections in blood of patients with rheumatoid arthritis
      Haier J. (1), Nasralla M. (1), Franco A. R. (2), Nicolson G. L. (1) - (1) Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041, Etats-Unis - Arthritis Center of Riverside, Riverside, CA 92501,Etats-Unis - Rheumatol 1999; 38:504-509
      Objective - Mycoplasmal infections are associated with several acute and chronic illnesses.
      Some mycoplasmas can enter a variety of tissues and cells and cause system-wide or systemic signs and symptoms.
      Methods - Patients (14 female, 14 male) diagnosed with rheumatoid arthritis (RA) were investigated for mycoplasmal infections in their blood leucocytes using a forensic polymerase chain reaction (PCR) procedure.
      Amplification was performed with genus- and species-specific primers and a specific radiolabelled internal probe was used for Southern hybridization with the PCR product.
      Patients were investigated for the presence of Mycoplasma spp. and positive cases were further tested for infections with the following species : M. fermentans, M. hominis, M. pneumoniae and M. penetrans.
      Results - The Mycoplasma spp. sequence, which is not entirely specific for mycoplasmas, was amplified from the peripheral blood of 15/28 patients (53.6%) and specific PCR products could not be detected in 13 patients (46.4%).
      Significant differences (P < 0.001) were found between patients and positive healthy controls in the genus test (3/32) and in the specific tests (0/32).
      Moreover, the incidence of mycoplasmal infections was similar in female and male patients.
      Using species-specific primers, we were able to detect infections with M. fermentans (8/28), M. pneumoniae (5/28), M. hominis (6/28) and M. penetrans (1/28) in RA patients.
      In 36% of the patients, we observed more than one Mycoplasma species in the blood leucocytes.
      All multiple infections occurred as combinations of M. fermentans with other species.
      Conclusions - The results suggest that a high percentage of RA patients have systemic mycoplasmal infections.
      Systemic mycoplasmal infections may be an important cofactor in the pathogenesis of RA and their role needs to be explored further.Cfr. :

    4. Detection of RNA sequences in cultures of a stealth virus isolated from the cerebrospinal fluid of a health care worker with Chronic Fatigue Syndrome - Case report
      Martin JW, Center for Complex Infectious Diseases, Rosemead, Calif., USA - Pathobiol ogy1997; 65: 57-60 - © 1997 S. Karger AG, Basel
      A cytopathic stealth virus was cultured from the cerebrospinal fluid of a nurse with chronic fatigue syndrome.
      Reverse transcriptase-polymerase chain reaction (RT-PCR) performed on the patient's culture yielded positive results with primer sets based on sequences of a previously isolated African green monkey simian-cytomegalovirus-derived stealth virus.
      The same primer sets did not yield PCR products when tested directly on DNA extracted from the cultures.
      The findings lend support to the possibility of replicative RNA forms of certain stealth viruses and have important implications concerning the choice of therapy in this type of patient.
      Cfr. :

    5. Development of an amplification and hybridization assay for the specific and sensitive detection of Mycoplasma fermentans DNA
      Berg S, Lüneberg E, Frosch M, Institut für Medizinische Mikrobiologie, Medizinische Hochschule, Hannover, Germany - Mol Cell Probes. 1996 Feb;10(1):7-14 - PMID: 8684379
      A polymerase-chain-reaction-based detection system for Mycoplasma fermentans was established.
      The highly conserved tuf gene, which encodes elongation factor Tu of prokaryotes, served as target sequence for the PCR.
      With two PCR oligodeoxynucleotides, which were selected from M. fermentans specific sequences of the tuf gene, we amplified a 850 base pair DNA fragment.
      Via the biotin-moiety of one primer the PCR fragments were immobilized on streptavidin-coated microtitre plates.
      After alkaline denaturation a digoxigenin-labelled M. fermentans specific DNA probe was hybridized to the single stranded immobilized PCR fragment.
      Detection was performed by addition of an alkaline phosphatase conjugated anti-digoxigenin antibody. 4-methyl-umbelliferyl-phosphate was used as a fluorogenic substrate.
      Amplification of 10 fg chromosomal target DNA was detected by this 'DNA enzyme immuno assay (DEIA)' technique, corresponding to seven genome copies.
      Our study supports the presumption that the tuf gene proves to be a suitable target sequence for the PCR based detection of any bacterial species.
      Furthermore, hybridization of PCR fragments with radio-labelled DNA probes should no longer be necessary, because a very sensitive non-radioactive test system can easily be established with the 'DEIA' technique.
      Cfr. :

    6. Diagnosis and integrative treatment of intracellular bacterial infections in Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness, Rheumatoid Arthritis and other chronic illnesses
      Nicolson GL, Nasralla M, Franco AR, Nicolson NL, Erwin R, Ngwenya R, Berns PA - Clin. I'racl. Ail.Med, 2000; 1:92-102
      Cfr. :

    7. Diagnosis and treatment of chronic infections in chronic fatigue syndrome, fibromyalgia syndrome and Gulf War illness
      G.L. Nicolson and N.L. Nicolson - International Journal of Occupational Medicine, Immunology and Toxicology 1996 ; 5 : 69-78
      Cfr. :

    8. Diagnosis and treatment of chronic mycoplasmal infections in Fibromyalgia and Chronic Fatigue Syndromes - Relationship to Gulf War Illness
      Nicolson GL. Nasralla M. Haier and Nicolson NL - Biomed. Ther, 1998;16:266-71
      Cfr. :

    9. Diagnosis and treatment of mycoplamsmal infections in Persian Gulf War Illness – CFIDS patients
      Nicolson GL, Nicolson NL - International Journal of Occupational Medicine, Immunology and Toxicology 1996; 5: 67-78
      Veterans of Operation Desert Storm returned from the Persian Gulf Theater of Operations and developed multiple signs and symptoms characterized by disabling fatigue, arthralgia, intermittent fever, myalgia, impairments in short-term memory, headaches, skin rashes, diarrhea and additional symptoms that have defied a disease case definition but has been called Gulf War Illness (GWI).
      In a sampling of GWI patients and symptomatic family members (n=30) we have used the technique of Gene Tracking and have found evidence of mycoplasmal infections in the blood leukocytes of approximately one-half of these cases.
      Mycoplasma-positive patients can be successfully treated with several 6 week courses of doxycycline (200 mg/d) or other antibiotics.
      Of the 14/30 patients that were mycoplasma-positive, 11/14 completely recovered after multiple cycles of antibiotics and 3/14 are still undergoing antibiotic therapy and relapsing.
      Cfr. :

    10. Dietary supplement Healthy Curb for reducing weight, girth, body mass, appetite and fatigue while improving blood lipid values with NTFactor Lipid Replacement Therapy
      Garth L Nicolson, PhD, Rita Ellithorpe, MD, Robert Settineri, MS - J. IiME 2009; 3(1): 39-48 – Source : Journal of IiME, May 28, 2009 (note : the full text of this article with charts is available free online in the Spring 2009 issue of the Journal of IiME - -; dr. Nicolson presented the results at the recent International IiME Conference]
      Often Chronic Fatigue Syndrome (CFS) patients have weight issues and weight reduction regimens can increase fatigue.
      Therefore, we initiated a weight loss clinical trial using an all natural oral supplement mixture containing an FDA-approved amylase inhibitor plus NTFactor®, which is known to safely reduce fatigue in aged subjects, chronic fatigue and CFS.
      The objective was to see if subjects could safely lose weight without increasing appetite and fatigue and without changing eating or exercise patterns or using drugs, herbs or caffeine.
      A 2-month open label clinical trial was initiated with 30 patients who used an oral mixture (Healthy Curb™) of amylase inhibitor (500 mg white kidney bean extract) plus 500 mg of NTFactor 30 min before each meal.
      Weight and measurements were taken weekly, appetite was assessed and fatigue was determined using the Piper Fatigue Scale.
      - Sixty-three percent of the participants lost an average of 3 pounds, with average reductions of 1.5 and 1 inch waist and hip circumference, respectively.
      - Participants experienced gradual and consistent weight loss along with waist and hip, body mass index (BMI) and basal metabolic rate (BMR) reductions during the entire trial.
      - There was a 44% reduction in overall hunger with reduced cravings for sweets; therefore, notable appetite suppression occurred.
      - Using the Piper Fatigue Scale the entire test group showed an average of 23% decrease in overall fatigue.
      - Blood lipid profiles generally improved, suggesting improved cardiovascular health and
      - no adverse effects were noted clinically or found in blood chemistries.
      Conclusions - The vast majority of the subjects in this trial lost weight, showed decreased waist and hip measurements and overall body mass.
      Their overall fatigue was reduced and they experienced marked appetite suppression.
      The product was completely safe and void of any side effects and was extremely well tolerated.
      Healthy Curb appears to be a safe and effective means for CFS patients to manage weight without changes in eating or exercise patterns.
      Cfr. :

    11. Do infections trigger fibromyalgia ?
      DL Goldenberg - Arth & Rhu, 1993; 36: 1489-92
      Cfr. :

    12. Doxycycline treatment and Desert Storm
      Garth L. Nicolson, PhD, The University of Texas M. D. Anderson Cancer Center Houston - Nancy L. Rosenberg-Nicolson, PhD, Rhodon Foundation for Biomedical Research Kingwood, Tex – JAMA 1995;273(8):618-619
      Cfr. :

    13. Effective treatment of chronic fatigue syndrome and fibromyalgia—A randomized, double-blind, placebo-controlled, intent-to-treat study
      Jacob E. Teitelbaum a; Barbara Bird a; Robert M. Greenfield b; Alan Weiss b; Larry Muenz c; Laurie Gould d - a Annapolis Research Center for Effective FMS/CFIDS Therapies and the Anne Arundel Medical Center, Annapolis, MD, USA - b Anne Arundel Medical Center, Annapolis, MD, USA - c Larry Muenz resides in Gaithersburg, MD, USA - d Annapolis Research Center for Effective FMS/ CFIDS Therapies, Annapolis MD, and also the USDA, Beltsville, MD, USA - Journal Of Chronic Fatigue Syndrome, Volume 8, Issue 2 May 2000 , pages 3 – 15
      Cfr. :

    14. Emerging concepts in the neurobiology of chronic pain - Evidence of abnormal sensory processing in fibromyalgia
      Bennett RM, Division of Arthritis and Rheumatic Diseases, Oregon Health Sciences University, Portland 97201, USA - Mayo Clin Proc. 1999 Apr;74(4):385-98 - PMID: 10221469
      Chronic pain often differs from acute pain.
      The correlation between tissue pathology and the perceived severity of the chronic pain experience is poor or even absent.
      Furthermore, the sharp spatial localization of acute pain is not a feature of chronic pain; chronic pain is more diffuse and often spreads to areas beyond the original site.
      Of importance, chronic pain seldom responds to the therapeutic measures that are successful in treating acute pain.
      Physicians who are unaware of these differences may label the patient with chronic pain as being neurotic or even a malingerer.
      During the past decade, an exponential growth has occurred in the scientific underpinnings of chronic pain states.
      In particular, the concept of nonnociceptive pain has been refined at a physiologic, structural and molecular level.
      This review focuses on this new body of knowledge, with particular reference to the chronic pain state termed "fibromyalgia".
      Cfr. :
      Aslo read the comment on this article :
      Fibromyalgia and pain management
      Sartin JS - Mayo Clin Proc. 2000 Mar;75(3):316-7 - PMID: 10725965
      Cfr. :

    15. Empiric parenteral antibiotic treatment of patients with fibromyalgia and fatigue and a positive serologic result for Lyme disease - A cost-effectiveness analysis
      Lightfoot RW Jr, Luft BJ, Rahn DW, Steere AC, Sigal LH, Zoschke DC, Gardner P, Britton MC, Kaufman RL, Division of Rheumatology, Kentucky Clinic J515, University of Kentucky Medical Center, Lexington 40536-0284 - Ann Intern Med. 1993 Sep 15;119(6):503-9 - PMID: 8357117
      Purpose -
      To examine the cost-effectiveness of empirical, parenteral antibiotic treatment of patients with chronic fatigue and myalgia and a positive serologic result for Lyme disease who lack classic manifestations.
      Data sources - Peer-reviewed journals, opinion of experts in the field and published epidemiologic reports.
      Study selection - Consensus by authors on articles that indicated methods for patient selection; on criteria used for diagnosis; on immunologic methods used for classifying patients; on the dose and duration of therapy; and on criteria by which responses to therapy were ascertained.
      Data extraction - In a cost-effectiveness model, the costs and benefits of empirical parenteral therapy for patients seropositive for Lyme disease were compared with a strategy in which only patients having classical symptoms of Lyme disease were treated.
      Data synthesis - In areas endemic for Lyme disease, the incidence of false-positive serologic results in patients with nonspecific myalgia or fatigue exceeds by four to one the incidence of true-positive results in patients with nonclassical infections.
      Treatment of the former group of patients costs $86,221 for each true-positive patient treated.
      The empirical strategy causes 29 cases of drug toxicity for every case in the more conservative strategy.
      If patients were willing to pay $3485 to eliminate anxiety about not treating possible true Lyme disease, the empirical strategy would break even.
      Conclusion - For most patients with a positive Lyme antibody titer whose only symptoms are nonspecific myalgia or fatigue the risks and costs of empirical parenteral antibiotic therapy exceed the benefits.
      Only when the value of patient anxiety about leaving a positive test untreated exceeds the cost of such therapy is the empirical treatment cost-effective.
      Cfr. :
      Also read the comments on this article :
      - Appropriateness of parenteral antibiotic treatment for patients with presumed Lyme disease - A joint statement of the American College of Rheumatology and the Council of the Infectious Diseases Society of America
      Ann Intern Med. 1993 Sep 15;119(6):518 - PMID: 8357119
      Cfr. :
      - Simplifying the diagnosis of obstructive sleep apnea
      Pack AI - Ann Intern Med. 1993 Sep 15;119(6):528-9 - PMID: 8204127
      Cfr. :

    16. Established fibromyalgia syndrome and parvovirus B19 infection
      Berg AM, Naides SJ, Simms RW, Arthritis Section, Boston University, MA - J Rheumatol. 1993 Nov;20(11):1941-3 - PMID: 8308782
      Objective - To determine the seroprevalence of prior and persistent parvovirus B19 (B19) infection in a group of patients with fibromyalgia (FS) compared with controls.
      Methods - Fifteen female patients with FS who recalled a viral prodrome (+VP) preceding the onset of FS symptoms and eleven patients with FS who did not recall any such illness (-VP) were selected from a referral practice.
      We excluded patients with FS who described a history of trauma prior to the onset of FS symptoms.
      Twenty-six female medical workers served as controls.
      Serum IgM and IgG anti-B19 antibodies were measured by ELISA.
      Polymerase chain reaction (PCR) products from serum were analyzed by dot blot hybridization for B19 DNA.
      Fisher's 2-tailed exact test was used to compare the proportion of positive serologies in each group.
      Results - No patient or control had positive IgM levels.
      For all patients with FS, the prevalence of prior B19 infection was comparable to that of healthy controls (11/26 vs 12/26, p = 1.00) and that of the general population.
      No significant difference was found in the prevalence of prior B19 infection in FS + VP and FS-VP patients (8/15 vs 3/11, p = 0.25).
      None of the patients or controls showed evidence for persistent B19 viremia, as determined by PCR analysis.
      Conclusion - Our data do not suggest that B19 plays a pathogenic role in this population of patients with FS.
      Testing for IgM against B19 within 2-3 months of symptom onset may prove more helpful in further defining the role of B19 in FS.
      Cfr. :

    17. Evidence for bacterial (mycoplasma, Chlamydia) and viral (HHV-6) co-infections in chronic fatigue syndrome patients
      Garth L. Nicolson a; Marwan Y. Nasralla b; Kenny De Meirleir c; Robert Gan b; Joerg Haier - a Institute for Molecular Medicine, Hunting-ton Beach, CA, USA - b International Molecular Diagnostics, Inc., Huntington Beach, CA, USA - c Department of Internal Medicine, Free University of Brussels, Brussels, Belgium - Journal Of Chronic Fatigue Syndrome, Volume 11, Issue 2 March 2003 , pages 7 - 19
      Cfr. :

    18. Evidence for Brucella spp. and Mycoplasma spp. co-infections in blood of chronic fatigue syndrome patients
      Nicolson GL, Gan R, Haier J - J Chronic Fatigue Syndr 2005; 12(2):5-17
      Cfr. :

    19. Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders
      Nicolson GL, Gan R, Nicolson NL, Haier J, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA : - J Neurosci Res. 2007 Apr;85(5):1143-8 - PMID: 17265454 - © 2007 Wiley-Liss, Inc.
      We examined the blood of 48 patients from central and southern California diagnosed with autistic spectrum disorders (ASD) by using forensic polymerase chain reaction and found that a large subset (28/48 or 58.3%) of patients showed evidence of Mycoplasma spp. infections compared with two of 45 (4.7%) age-matched control subjects (odds ratio = 13.8, P < 0.001).
      Because ASD patients have a high prevalence of one or more Mycoplasma spp. and sometimes show evidence of infections with Chlamydia pneumoniae, we examined ASD patients for other infections.
      Also, the presence of one or more systemic infections may predispose ASD patients to other infections, so we examined the prevalence of C. pneumoniae (4/48 or 8.3% positive, odds ratio = 5.6, P < 0.01) and human herpes virus-6 (HHV-6, 14/48 or 29.2%, odds ratio = 4.5, P < 0.01) coinfections in ASD patients.
      We found that Mycoplasma-positive and -negative ASD patients had similar percentages of C. pneumoniae and HHV-6 infections, suggesting that such infections occur independently in ASD patients.
      Control subjects also had low rates of C. pneumoniae (1/48 or 2.1%) and HHV-6 (4/48 or 8.3%) infections, and there were no coinfections in control subjects.
      The results indicate that a large subset of ASD patients shows evidence of bacterial and/or viral infections (odds ratio = 16.5, P < 0.001).
      The significance of these infections in ASD is discussed in terms of appropriate treatment.
      Cfr. :

    20. Examination of Mycoplasmas in blood of 565 chronic illness patients by polymerase chain reaction
      Marwan Y. Nasralla, Jörg Haier, Nancy L. Nicolson and Garth L. Nicolson.*, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041 USA, Tel. : 1-714-903-2900 – Fax : 714-379-2082 - *Correspondence to: Prof. Garth L. Nicolson, The Institute for Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649-1041 USA, Tel: 1-714-903-2900, Fax: 1-714-379-2082 – Website : – E-mail : - International Journal Medicine Biology Environment 2000; 28(1):15-23
      Mycoplasmal infections are associated with several acute and chronic illnesses.
      Patients with Chronic Fatigue Syndrome (CFS), myalpic encepthalomyelitis (ME) and/or Fibromyalgia Syndrome (FMS) were examined for systemic mycoplasmal infections by analysis of blood specimens.
      Using an optimized protocol for forensic polymerase chain reaction (PCR) blood samples from 565 CFS or FMS patients (401 female, 164 male) and 71 healthy controls were investigated for presence of Mycoplasma spp. and M. fermentans infections.
      The Mycoplasma spp. sequence was amplified from the peripheral blood of 300/565 patients (53.1 %).
      Specific PCR products could not be detected in 265 patients (46.9 %).
      A significant difference (p<0.001) was found between mycoplasma-positive patients and healthy controls (7/71; 9.9%).
      The prevalence of M. fermentans infections (24.6%) was also significantly (p<0.001) higher in CFS/FMS patients than in controls (2/71; 2.8%).
      Moreover, the prevalence of mycoplasmal infections was similar in female and male CFS patients.
      The data indicate that mycoplasmas can be detected in blood specimens from a high proportion of CSF/FMS patients.
      M. fermentans can be an opportunistic infection, cofactor or causative agent resulting in morbidity in these patients.

    21. Fibromyalgia - Is there an infectious connection ?
      The Road Back Foundation
      Fibromyalgia (FM) is a commonly misunderstood, sometimes misdiagnosed rheumatic disease.
      The main symptoms are achiness, pain (more in the muscles than in the joints), stiffness, fatigue, accompanied by headaches, depression, sleep disorders, Raynaud's and irritable bowel syndrome.
      The sites of pain are located in specific areas call-ed tender or trigger points.
      The painful tender points are located where the ligament attaches the muscle to the bone.
      There are 18 tender point locations. Sensitivity at 11 points defines a diagnosis of fibromyalgia.
      FM is not life threatening nor does it cause physical deformities.
      Many lab tests are within normal range.
      In fact, most patients look extremely well and fit, making it difficult to account for the degree of clinical suffering they are experiencing, yet 10-30% of fibromyalgia patients are disabled to some degree because of their disease symptoms.
      It is 9 times more common among women than men, usually between the ages of 40 and 60, is more common in Caucasians than other races and is the second or third most common disorder treated by rheumatologists.
      Potential Pathogens As is the case of most forms of "arthritis", no known cause has been established, but a number of possibilities are mentioned in the medical literature.
      Like many forms of arthritis, the cause of FM is probably not limited to one single factor.
      55% of patients identify a "flu-like" or viral type illness, 33% physical trauma/injury and 14% emotional stress as a precursor to the onset of symptoms.
      The connection of FM to infections is well documented in the literature, especially in relation to Lyme disease, mycoplasma, Chlamydia pneumoniae., Hepatitis C, Parvovirus B19, HIV and Epstein-Barr.
      It is believed as many as 25-40% of long-term Lyme patients develop fibromyalgia-like symptoms, particularly pain and fatigue; as many as 25% of HIV patients, 57% of RA patients and 24% of Psoriatic Arthritis patients also have FM symptoms.
      A 1993 Annals of Internal Medicine article (Lightfoot et al) found 10% of patients with Lyme Disease would have arth-ritis develop as a result of the spirochete infection.
      Because this organism (like mycoplasma) is difficult to culture, the diagnoses is based on the occurrence of (1) one or more of the classical features and (2) serum antibodies to the etiologic spirochete after the first 4 to 6 weeks of illness.
      Some Lyme/FM patients do not respond to courses of antibiotics, causing researchers to dismiss the possibility of an organism as a trigger for the disease and antibiotics as a therapy.
      This might be a misleading assumption as explained by Garth Nicholson, PhD, in a recent article (Environmental Phys, 1997).
      "Are chronic, systemic mycoplasmal infections the answer to CFS, FMS, GWI* and other disorders ? Of course not ! This is likely to be an appropriate explanation for a rather large subset of CFS, FMS, GWI* and some arthritis patients, but certainly not every patient will have the same chronic infections. Some patients may have chemical exposures or other environmental problems as the underlying reason for their chronic signs and symptoms. In these patients, antibiotics should have no effect whatsoever".
      Nicholson has found mycoplasma infections in approximately one half of patients with FM as well as arthritis.
      "The identification of mycoplasma infections in the leukocyte blood fractions of a rather large subset of CFS, FMS and arthritis patients suggests that mycoplasmas and probably other chronic infections as well, may be an important source of morbidity in these patients. If such infections are important in these disorders, then appropriate treatment with antibiotics should result in improvement and even recovery. This is exactly what has been found" (Nicholson JAMA 1995).
      "Only antibiotics that are effective against the pathogenic mycoplasmas result in recovery, and some antibiotics, such as penicillins, can worsen the condition" (Nicholson, 1996, & 1997).
      Goldenberg suggests two possibilities for an infectious cause :
      1) the infectious agent would either directly invade tissues such as the joints or central nervous system or
      2) "trigger" factors that would cause the chronic myalgias, fatigue, headaches, sleep disturbances and mood disturbances...
      Infectious agents are capable of activating cytokines which may in turn cause severe myalgias, fatigue and neurocognitive disturbances...
      The potential role of a microbial agent as a trigger to fibromyalgia remains tenable.
      Antibodies to Chlamydia pneumoniae have been found in 78.3% of FM patients tested or 67.4% for unselected rheumatic patients.
      These high numbers point to a possible connection between Chlamydia pneumoniae and fibromyalgia.
      In a Spanish study, Rivera et al found 15% of 112 FM patients had Hepatitis C viral Infection (HCV) and among HCV patients, 10% had FM.
      The incidence of FM in the control group was less than 2%; the prevalence of FM in the general population was 2%.
      "The presence of active infection by HCV is more likely to trigger FM than the stress and anxiety produced by the disease" (Rivera et al, 1997).
      Other researchers have described HCV infection as a trigger for autoimmune disorders (Pawlotsky 1994 & Agnello 1992).
      "In the remaining 85%, other known and unknown viruses that can produce chronic infections, could be responsible for FM symptoms. We think the presence of such viruses should be sought in patients with FM symptoms" (Rivera et al, 1997).
      Parvovirus B19 infection as a trigger for autoimmune disorders (Pawlotsky 1994 & Agnello 1992).
      "In the remaining 85%, other known and unknown viruses that can produce chronic infections, could be responsible for FM symptoms. We think the presence of such viruses should be sought in patients with FM symptoms" (Rivera et al, 1997).
      Parvovirus B19 has been implicated as a cause in cases of chronic arthritis and may mimic rheumatoid arthritis.
      Berg et al identified patients with established FM who had symptoms consistent with recent or distant B19 infection.
      In fact, 30-60% of the general population test positive for Parvovirus B19 and the incidence increases with age.
      The timing of testing for PV B19 appears to be critical.
      Testing too early or too late will yield negative results.
      25% of HIV patients experience fibromyalgia symptoms, adding additional discomfort and anxiety.
      Epstein Barr Virus (EBV) has been considered a possible cause of FM or CFS because of similarity of symptoms, but so far, a connection has not been proven.
      Most observers currently believe that no single infectious agent is likely to be the cause of CFS (or FM).
      Yet it has been shown that chronic persistent viruses may often be reactivated during this illness.
      Is this merely an epiphenomenon ?
      Or, once reactivated, do these viruses go on to produce many of the symptoms of the disease ?
      And what reactivates these viruses ?
      If it is some defect in immunologic containment, what causes the defect ?
      Could it be stress ? Genetics ? infection with other viruses ?
      In the view of Komaroff et al, it is reasonable to speculate that all these factors are capable triggers, with different factors playing different roles in different individuals.
      Common FM symptoms
      - Chronic, widespread pain - most fatigue : 70-90%
      - morning stiffness : 80%
      - migraine headaches : 50%
      - depression : 25-50%
      - sleep disturbances : 70%
      - anxiety : 25%
      - Raynaud's-like syndrome : 33%
      - numbness, tingling : 75%
      - irritable bowel syndrome : 50%
      - positive ANA : 10%.
      Organisms that might be connected to FM
      Borellia borgdorferi (Lyme)
      - Hepatitis C
      - Epstein-Barr Virus
      - Mycoplasma
      - Chlamydia pneumoniae
      - Parvovirus B19
      - HIV
      Cfr. :

    22. Fibromyalgia - Up close and personal
      Mark J. Pellegrino, MD - Anadem Publishing; 2 edition (January 2005) - ISBN-10: 1890018503 - ISBN-13: 978-1890018504
      'Fibromyalgia - Up close & personal' is packed with 43 chapters of "inside" medical information and "hands-on" practical advice for everyday living.
      Dr. Mark J. Pellegrino brings readers up-to-date with the newest drug and physical treatments for fibromyalgia.
      He also presents the latest thinking on diet and exercise to help people with this condition lead a full life.
      Recognized by fibromyalgia sufferers for understanding what they are going through, Dr. Pellegrino is a welcoming and encouraging presence for everyone with this condition and this quality comes through very clearly in his writing.
      It’s as if each person reading his book is having a private consultation about their shared disease.
      In 'Up close & personal' Dr. Pellegrino has enlisted two leading attorneys to bring readers much needed insight into disability and personal injury issues.
      Also, he asked a knowledgeable physician to contribute a chapter on common pain problems.
      Cfr. :

    23. Fibromyalgia – Ultimately a disease of amplified pain
      Mark J. Pellegrino, MD, May 26, 2008 - © 2009 ProHealth, Inc.
      Excerpted with permission from Chapter 9 of Dr. Mark Pellegrino’s very popular book 'Fibromyalgia - Up close and personal' and reproduced with permission (this book may now be purchased from the store – cfr. : -).
      Dr. Pellegrino has seen more than 20,000 FM patients in his practice at the Ohio Rehab Center and has been a Fibromyalgia patient himself since childhood ---
      Many conditions can lead to permanent changes in the pain transmission mechanism and result in chronic pain that overwhelms the body’s pain defense mechanisms.
      One such condition is Fibromyalgia.
      Fibromyalgia may not cause destruction along the pain pathways as other conditions I have mentioned can [rheumatoid arthritis, carpal tunnel syndrome, shingles, multiple sclerosis, for example].
      However, Fibromyalgia does cause chronic abnormal changes along all the pathway components and this results in chronic pain via both peripheral (from skin, muscles and nerves) and central (from spinal cord and brain) neurological mechanisms.
      The end result of Fibromyalgia’s abnormal changes appears to be a state of pain amplification that cause severe generalized pain.
      Fibromyalgia is ultimately a disease of amplified pain.
      Dr. Robert Bennett has written and presented excellent information that explains why we hurt with Fibromyalgia (e.g. “Emerging Concepts in the Neurobiology of Chronic Pain - Evidence of Abnormal Sensory Processing in Fibromyalgia” - Mayo Clinic Proceedings at : -).
      If we trace the pain signals through the various parts of the pain pathway (from the nociceptors - or specialized pain nerve endings – to the nerves to the spinal cord to the brain) in people with Fibromyalgia, we find various abnormalities along the way.
      Many studies have shed light on different points along the complete pain pathway.
      I want to briefly summarize some of these different abnormalities and possible problems encountered by Fibromyalgia pain signals on the path to the brain.
      Nociceptors - Pain originates from the nociceptors
      Trauma is a common trigger of Fibromyalgia.
      Tissue injury - damage to the muscles and soft tissues – activates the nociceptors.
      Some studies have suggested that microscopic injury occurs in specific parts of the muscles (for those who want the medical names: muscle spindles, intrafusal fibers and calcium pumps).
      Localized tissue injury probably activates arachidonic acid (a biological protein), which turns into “bad” prostaglandans (called Cox-II prostaglandins) and cause inflammation and pain.
      In addition to trauma, autoimmune factors may be another pain nerve activator.
      Perhaps autoimmune processes create compounds which act as irritants and activate the nociceptors chronically to the point where they become “permanently” sensitized and irritated.
      As a result, biochemical, hormonal, and red blood cell changes occur that interfere with the cells’ ability to receive adequate supplies of oxygen, glucose and other nutrients.
      Blood flow, energy formation and the cells’ electrical and neurological harmonies are all disrupted.
      Since the nociceptors remain “faulty” the electrical and neurological balance remains abnormal and nociceptors continue to be activated.
      Pain-producing neurotransmitters are released and accumulate as long as the nociceptors stay activated at the peripheral level (skin and muscles, especially).
      These persistent pain signals we experience may be interpreted as an itching, burning, swelling, or tingling at one end of the spectrum or – at the other end – knife-stabbing, burning or throbbing.
      One nociceptor can signal different pain signals and sensations depending on its level of irritation – the more irritated it is, the more severe the pain.
      These changes can become permanent and cause the nerves to become sensitized to the point where they are easily activated to send pain, even in the absence of any noxious stimulus.
      In other words, persistent pain signals can spontaneously arise from peripheral nerve endings and bombard the rest of the pain pathway.
      So, instead of waiting for outside stimulation such as trauma, pressure, temperature or touch to signal the nociceptors, these nociceptors send pain signals on their own, without any outside help.
      This “spontaneous” pain is what we complain about the most !
      The nerves, especially the sensory nerves and the autonomic nerves, “wonder what is happening” because they are getting bombarded by all of these signals from the nociceptors.
      At first, they try to diminish these painful signals by using accommodation and gate mechanisms.
      However, the signals persist and they, too, undergo a sensitization process.
      They become hypersensitized and react with an exaggerated response instead of a normal or diminishing response (accommodation).
      Now we get even more pain, numbness, swelling, burning and other sensations.
      Some of the hypersensitization may be mediated by nerve growth factor, which has been found in higher levels in Fibromyalgia.
      A high nerve growth factor may indicate the nerves are trying to regenerate or repair themselves.
      But instead of repairing the nerves so they act normal again, the opposite seems to happen.
      Nerve growth factor is probably enhancing the nerves’ abilities to transmit pain to the spinal cord.
      More pain results, not less.
      Spinal cord - Amplification, wind-up, allodynia, Substance P, generalization
      At the spinal cord level, the Fibromyalgia begins to take control.
      It is here that additional changes occur to perpetuate the pain and spread it to different levels.
      When pain generators first start firing, the spinal cord pain processing centers may act at first like a dry sponge and easily soak up all the signals.
      Our bodies may have many pain generators at any given time, but if they are slowly and intermittently firing, drug sponges can soak up the signals and not cause any bothersome symptoms.

    Go to Part VI

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    Infection as one possible cause of fibromyalgia

    Part VI

    From time to time there may be an acute exacerbation of a problem leading to a lot of pain signals being generated and if a lot of pain signals are dumped at once into the spinal cord sponge, only a little bit gets absorbed and a lot gets passed through and perceived as acute pain.
    In Fibromyalgia, however, the different pain generators continue to send signals and eventually the dry sponges becomes a wet sponge and it can’t soak up any more.
    The additional oncoming continuous signals will spill over the wet sponge and this leads to persistent pain.
    The two main changes that occur at the spinal cord include :
    - pain amplification (by specialized nerves called NMDA receptors) and
    - loss of pain filtering (by the diffuse noxious inhibitory control system).
    Spinal cord nerves are bombarded by continuous stimulation from the peripheral nerves, causing a progressive increase in electrical signals to be sent up to the brain.
    This phenomenon is called “wind-up” and is the neurological mechanism for the amplification of pain.
    Once this wind-up phenomenon occurs, a central sensitization results in which various types of sensory signals - not just pain - will arrive in the spinal cord, become amplified and be sent to the brain as pain.
    The spinal cord becomes more sensitized to sending pain, lots of it.
    Once this happens, the spinal cord is not able to properly sort out and filter various sensory signals.
    As a result, different sensory signals such as touch, pressure, temperature and joint movement all become amplified and sent up the pain pathways, resulting in pain signals instead of the appropriate touch, pressure, temperature or joint motion signals.
    This defect in pain transmission where there is increased sensitivity to all stimuli – even those which normally do not evoke pain – is called allodynia.
    Unfortunately for the person with Fibromyalgia, the spinal cord is now “wired” to interpret nearly all sensory signals as pain – severe pain !
    We can still appreciate touch, pressure, temperature, joint movement and other non-pain signals, but pain contaminates these signals and we feel the pain.
    Another key change at the spinal cord level is an increased formation of Substance P and other neurotransmitters.
    Substance P’s primary role at the spinal cord level is to transmit pain signals and to sensitize the spinal cord so it is readily available to transmit pain.
    When Substance P reaches high concentrations (as it does in Fibromyalgia), it can migrate up and down the spinal cord, away from the initial location of the pain signal.
    As a result, multiple levels of the spinal cord undergo sensitization and send increased pain signals, leading to a “generalization” of the Fibromyalgia.
    This spreading of pain explains how one can develop generalized Fibromyalgia from an initial regional area of pain.
    A common example of this occurs following a motor vehicle accident where a particular body part, such as the neck, was injured.
    Over time, the pain begins to involve the mid-back, low back and ultimately the whole body, even though these areas were never injured.
    The Substance P-induced spinal cord changes can explain this migration of pain from the neck to the entire body.
    Our poor brains have no chance, do they ?
    Any pain memory stored in the past will be re-awakened by this process.
    Fibromyalgia is notorious for causing previously injured areas to hurt more once it develops.
    This previously injured area may have settled down and become essentially pain-free, but the pain memories remained, although inactive.
    Thanks to the Fibromyalgia pain amplification process, the inactive memories are reactivated.
    The pain centers of our brain, the limbic system and the cerebral cortex, are continuously fed these amplified signals from the spinal cord.
    Changes occur :
    - serotonin levels decrease,
    - brain waves change,
    - sleep stages are affected,
    - blood flow and glucose [blood sugar] metabolism are affected.
    The brain gets overwhelmed with these pain signals and spends a lot of attention and energy monitoring the pain.
    Fibrofog occurs.
    Emotional components are “attached” to pain, including fear, depression, anxiety, anger, hopelessness and helplessness, which can further amplify the pain.
    In patients with Fibromyalgia, functional reorganization (brain plasticity) in both sensory and motor portions of the brain has been observed and appears directly related to the chronicity of the pain (Dr. H. Flor, 2003).
    These brain changes may be viewed as pain memories that influence how painful and non-painful signals affect the body’s sensory and motor responses.
    The brain makes these changes to enhance its ability to perceive pain – brain amplified pain.
    This type of abnormal brain plasticity can be measured. Doctors Richard H. Gracely, Richard A. Harris, Daniel J. Clauw et al. at the University of Michigan Chronic Pain and Fatigue Research Center have published studies which demonstrated abnormal “hyperactive” areas of the brains and abnormal “quiet” areas of the brains in Fibromyalgia test subjects who underwent functional MRIs.
    This provides objective evidence to support brain plasticity with both hypersensitive amplified pain, and turning off the ability to inhibit pain.
    Fibromyalgia pain summary
    To summarize, Fibromyalgia changes our pain pathways.
    It may start off as a peripheral irritant, but eventually it becomes a self-perpetuating process that affects the entire pathway from the nociceptors to the brain.
    The main problem, in a nutshell, is amplified pain.
    The amplified pain is the result of our nervous system gaining the ability to magnify pain and losing the ability to inhibit pain.
    What comes in at a signal of a “1” does not end up in the brain as a signal of a “1” as it would in people without Fibromyalgia.
    Our pain signal of a “1” gets amplified and magnified and by the time it reaches our brain, it is a “10” !
    Other non-painful signals get thrown into this pain amplification pathway and arrive at our brain as pain signals.
    Even tiny subconscious pain signals can get amplified or the nerve pathways can automatically “fire away” without any obvious noxious stimulus to cause spontaneous pain.
    These are not your everyday aches and pains, these are severe pains that cannot be ignored.
    This severe, chronic pain can completely disrupt one’s life.
    And by the way, while all of this is happening, we continue to look completely normal on the outside.
    Cfr. :

    1. Fibromyalgia among central sensitivity syndromes
      Adrienne Dellwo, Guide to Fibromyalgia & CFS, Wednesday June 27, 2007
      Fibromyalgia syndrome (cfr. :
      -) is a chronic condition characterized by widespread pain, sleep problems, fatigue and depression, among other symptoms.
      Tender points (cfr. : -) have been used to diagnose the condition.
      Muhammad B. Yunus, M.D. and colleagues published the first controlled study of the clinical characteristics of fibromyalgia 25 years ago in Seminars in Arthritis and Rheumatism.
      That article is credited for leading to formal recognition of fibromyalgia by the medical community.
      In the June 2007 issue of Seminars in Arthritis and Rheumatism (cfr. : -), Dr. Yunus again is being credited for contributing to the understanding of chronic pain and fatigue syndromes.
      Dr. Yunus, through a review of 225 publications and his own experience studying fibromyalgia and related diseases, describes 13 separate conditions that are related to "central sensitization".
      The 13 conditions related to central sensitization, which occurs when the central nervous system (brain and spinal cord) becomes hypersensitive to stimuli which normally would not cause pain, include :
      - Chronic fatigue syndrome – cfr. :
      - Depression – cfr. :
      - Fibromyalgia syndrome – cfr. :
      -&- -&- -&- -&-
      - Interstitial cystitis – cfr. :
      - Irritable bowel syndrome – cfr. :
      - Migraines – cfr. :
      - Multiple chemical sensitivity – cfr. :
      - Myofascial pain syndrome / Regional soft-tissue pain syndrome – cfr. :
      - Post-traumatic stress disorder – cfr. :
      - Primary dysmenorrhea – cfr. :
      - Restless legs syndrome – cfr. :

      - Temporomandibular disorders – cfr. :
      - Tension-type headaches – cfr. :
      Dr. Yunus concludes that central sensitivity syndromes involve a "biopsychosocial" model of disease.
      Read the full article "Fibromyalgia and Overlapping Disorders - The Unifying Concept of Central Sensitivity Syndromes" from Dr. Yunus at : -(you'll find an abstract at : -).
      Cfr. :

    2. Fibromyalgia and its relation to chronic fatigue syndrome, viral illness and immune abnormalities
      Goldenberg DL, Newton-Wellesley Hospital, Department of Medicine, Tufts University School of Medicine, MA 02162 - J Rheumatol Suppl. 1989 Nov;19:91-3 - PMID: 2607516
      Fibromyalgia and chronic fatigue syndrome have similar clinical and demographic features.
      We found that most patients with chronic fatigue syndrome have a tender point examination similar to patients with fibromyalgia.
      Similar pathophysiologic mechanisms are also being explored in each syndrome, including a potential role for viral induced immune dysfunction.
      Cfr. :

    3. Fibromyalgia and other chronic fatigue syndromes - Is there evidence for chronic viral disease ?
      Goldenberg DL, Department of Medicine, Boston University School of Medicine, MA 02118 - Semin Arthritis Rheum. 1988 Nov;18(2):111-20 - PMID: 3064302
      Cfr. :

    4. Fibromyalgia and overlapping disorders - The unifying concept of central sensitivity syndromes
      Yunus MB, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, One Illini Drive, Peoria, IL 61605, USA - Semin Arthritis Rheum. 2007 Jun;36(6):339-56. Epub 2007 Mar 13 - PMID: 17350675
      Objectives - To discuss fibromyalgia syndrome (FMS) and overlapping conditions eg, irritable bowel syndrome, headaches and chronic fatigue syndrome, within the concept of central sensitivity syndromes (CSS).
      Methods - A critical overview of the literature and incorporation of the author's own views.
      Results - The concept of CSS seems viable. It is based on mutual associations among the CSS conditions as well as the evidence for central sensitization (CS) among several CSS members.
      However, such evidence is weak or not available in other members at this time, requiring further studies.
      The biology of CSS is based on neuroendocrine aberrations, including CS, that interact with psychosocial factors to cause a number of symptoms.
      Conclusions - CSS is an important new concept that embraces the biopsychosocial model of disease.
      Further critical studies are warranted to fully test this concept.
      However, it seems to have important significance for new directions for research and patient care involving physician and patient education.
      Each patient, irrespective of diagnosis, should be treated as an individual considering both the biological and psychosocial contributions to his or her symptoms and suffering.
      Cfr. :

    5. Fibromyalgia and parvovirus infections
      Lawrence J. Leventhal, MD *, Stanley J. Naides, MD, Bruce Freundlich, MD, From the Section of Rheumatology, Department of Medicine, University of Pennsylvania School of Medicine and the Presbyterian Medical Center, Philadelphia, Pennsylvania and the Division of Rheumatology, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City - * Correspondence to : Lawrence J. Leventhal, Address reprint requests to Lawrence J. Leventhal, MD, 570 Maloney Building, Hospital of the University of Pennsylvania, 3600 Spruce Street, Philadelphia, PA 19104
      An infectious cause of fibromyalgia (FM) has been hypothesized based upon the observed similarity of this entity and chronic fatigue syndrome.
      Three patients developed symptoms of FM after documented episodes of acute parvovirus B19 infections.
      B19 antibody determinations were obtained approximately 1 month after the symptoms began; both IgM and IgG titers were positive at that time.
      All 3 patients met criteria for FM. Polysomnography performed on 2 of the patients revealed profound alpha-wave intrusion throughout non-rapid eye movement sleep.
      A more careful search for viral infections in FM patients whose symptoms appear following a flu-like illness appears warranted.
      Cfr. :

    6. Fibromyalgia and related central sensitivity syndromes - Twenty-five years of progress
      John B. Winfield, MD, University of North Carolina School of Medicine - Seminars in Arthritis and Rheumatism, Volume 36, Issue 6, Pages 335-338
      Cfr. :

    7. Fibromyalgia and the therapeutic domain - A philosophical study on the origins of fibromyalgia in a specific social setting
      I. Hazemeijer and J. J. Rasker1, Department of Military Forensic and Social Psychiatry, PO Box 3003, 3800 DA Amersfoort and 1 Department of Rheumatology, Hospital Medisch Spectrum Twente and Department of Communication Studies, Faculty of Philosophy and Social Sciences, University of Twente, Enschede, The Netherlands - Rheumatology 2003; 42: 507-515 - © 2003 British Society for Rheumatology
      Objectives - Fibromyalgia has always attracted controversy. Wolfe states that fibromyalgia will always exist regardless of the name given to the syndrome. Hadler describes fibromyalgia as a form of illness behaviour escalated by labelling. However, we believe that fibromyalgia, as other functional somatic syndromes, is not waiting below the surface until it becomes manifest by labelling.
      Methods - We developed our hypothesis on the relationship between a specific social setting (called the therapeutic domain) and fibromyalgia using empirical philosophical arguments based on Foucault and Hacking.
      A therapeutic domain is a real and heterogeneous medical domain in which people, their thoughts and practices and medical technology in any form coexist and communicate.
      In this domain blood is aspirated, radiographs are taken and classification criteria are made and applied.
      It is a domain where patient and therapist have initiated a relationship, which is influenced by the media and political pressure.
      This results in a looping effect where classification criteria and images give structure to perceptions and form the description for human behaviour; the person thus diagnosed (!) constantly has to grow into the conformity of these classification criteria, which also have to be constantly revised.
      The fibromyalgia concept becomes manifest in an individual as non-specific aches and pains along with other features.
      Results - In other times and settings this resulted in analogue syndromes like railway spine, telegraph wrists, neurocirculatory asthenia or perhaps repetitive strain injury.
      In the application of American College of Rheumatology fibromyalgia classification criteria, labels and medical technology it is possible that invisible experiences manifest themselves in a therapeutic domain.
      It is not only a phenotype induced by the physician, but in this domain a certain power creates reality making the ‘disease’ become manifest.
      Conclusion - The only certainty in fibromyalgia is that it is still being diagnosed.
      For prevention and treatment of fibromyalgia, doctors as well as politicians and media have to start by fundamentally changing the therapeutic domain.
      In such a renewed setting, fibromyalgia cannot become manifest in an individual and thus fibromyalgia syndrome can no longer exist.
      A firm public message that symptoms can be psychological in origin to prevent their spread, as Wessely recently stated in the comparable case of mass psychogenic illness, is only a part of the answer.
      Cfr. :

    8. Fibromyalgia as a complication of injuries
      Dr. Mark J. Pellegrino, MD, October 7, 2009 - © ProHelath
      --- Dr. Pellegrino is a specialist in Physical Medicine & Rehabilitation who sees many people with chronic pain including Fibromyalgia. This information is excerpted with permission from Dr. Pellegrino’s book 'Fibromyalgia - Up close & personal' which includes chapters on trauma, the whiplash injury and specific types of whiplash, the evaluation and treatment of injuries and the legal aspects of post-traumatic fibromyalgia ---
      The pain started after the car accident, and it has never gone away. Before the accident I was perfectly healthy, and now I hurt all over and nothing has helped”.
      This is a typical story I hear from patients who have chronic pain after a whiplash injury.
      Some of the treatments may have helped reduce the pain, but it didn’t disappear.
      Many times, the pain is localized at first to the neck, shoulders and upper back areas, but over time, other areas of the body begin to hurt just as bad.
      Eventually, the person may say the classic four-word sentence that practically epitomizes Fibromyalgia : “I hurt all over”.
      Fibromyalgia caused by trauma is called post-traumatic Fibromyalgia (PTF)
      Trauma to the body causes tissue damage.
      Whereas healing is the expected outcome for trauma, it doesn’t always happen and PTF can develop.
      PTF does not occur immediately after an injury; it takes time to evolve and fully develop the characteristic tender points in distinct locations.
      Just as trauma other than motor vehicle accidents can cause whiplash-type injuries, trauma other than whiplash-related ones can lead to PTF.
      Lifting injuries, falls, work injuries, sports injuries and repetitive-type injuries are examples of other kinds of non-whiplash trauma.
      The medical literature has numerous examples of persistent pain following trauma.
      Since fibromyalgia criteria were established by the American College of Rheumatology study published in 1990, various articles have appeared in the medical literature about PTF.
      • Dr. T.J. Romano wrote in 1990 about patients with PTF who continued to require treatment for their condition years after settlement of litigation (cfr. “Clinical experiences with post-traumatic Fibromyalgia syndrome” - Romano TJ, Department of Medicine, West Virginia University School of Medicine - W V Med J 1990;86(5):198-202 at : -).
      - In 1992 Dr. S. Greenfield published a paper describing reactive Fibromyalgia syndrome in patients who report trauma as a precipitating event (cfr. “Reactive Fibromyalgia Syndrome” zt : -).
      - Dr. G.W. Waylonis published a paper entitled “Post-traumatic Fibromyalgia, a long term follow-up” (cfr. : -) in 1994 that described a follow-up of 176 patients with PTF.
      - Dr. F. Wolfe wrote a paper “Post-traumatic Fibromyalgia - A case report narrated by the patient” in 1994 (cfr. : -).
      - Dr. D. Buskila’s 1997 study showed a higher rate (about 22%) of fibromyalgia following trauma to the cervical spine (neck) (cfr. “Increased rates of fibromyalgia following cervical spine injury - A controlled study of 161 cases of traumatic injury” at : -).
      A study by Dr. H.R. Walen (cfr. “Traumatic events, health outcomes and health care use in patients with fibromyalgia” - Journal of Musculoskeletal Pain, 2001 at : -) showed a remarkably high prevalence of over 90% of patients reporting at least one traumatic event prior to the onset of fibromyalgia symptoms.
      More and more researchers seem to be reporting on the importance of physical trauma as a factor in the development of fibromyalgia.
      Among doctors in private practice, many (including me) have reported over half of fibromyalgia patients attribute the onset of their symptoms to a traumatic event.
      In my own private practice, about 65% of patients report a traumatic injury as the cause of their fibromyalgia...
      Diagnosing PTF
      Trauma-related fibromyalgia, or PTF, is a specific medical condition that exists regardless of individual physician’s beliefs or opinions.
      This diagnosis is never assumed before a patient is seen or from the patient’s history alone.
      In order for a physician to diagnose PTF, information from the overall clinical evaluation needs to be analyzed.
      This evaluation includes the patient’s history and physical exam, supplemented by any diagnostic testing and review of any previous medical records.
      The final diagnosis of PTF is made if the total clinical picture “fits”.
      PTF can be diagnosed if these features are present :
      1/ No previous pain complaints before the trauma similar to those experienced since the trauma. That is, the person didn’t already have a pre-existing fibromyalgia diagnosis or fibromyalgia-like symptoms before the trauma.
      2/ History of a trauma that led to the pain.
      3/ Pain resulting from the trauma that has persisted ever since the trauma. I call this the “unbroken chain of pain”.
      4/ Widespread pain persisting for at least 6 months after the injury, well beyond the usual soft tissue healing time.
      5/ The presence of characteristic painful tender points as defined by the American College of Rheumatology criteria; i.e., at least 11 of 18 positive tender points. If consistent reproducible tender points are present only in an injured region and not widespread, a subset of fibromyalgia – post-traumatic regional fibromyalgia – may be considered.
      A person can be diagnosed with PTF after one evaluation with an experienced physician.
      The physician does not have to order specific tests first, or reevaluate the patient over time, to conclude PTF is present.
      The tender points are the key findings on exam, but muscle spasms and trigger points may be helpful to the physician to clarify the diagnosis.
      The physician’s exam will provide clues if something other than fibromyalgia (e.g., inflammation or neurological disorder) or in addition to fibromyalgia is present.
      Conditions in addition to PTF are often present
      They can include, but are not limited to, post-concussive syndrome, disc disease, facet dysfunction and reflex sympathetic dystrophy.
      After the initial diagnosis of PTF, the patient may visit the physician for subsequent evaluations to review the condition and effects of any treatment.
      Re-demonstrating the initial tender points upon follow-up examination is a reliable and supportive physical finding of PTF.
      The exam abnormalities are expected to persist over time in PTF and the physician can confirm this expectation upon re-evaluation at a later date.
      The ability to diagnose PTF is not dependent upon the person being seen immediately after the trauma.
      PTF takes time to develop, and once it does, it leaves telltale puzzle clues.
      If the pieces of the puzzle fit and form the “big picture”, a diagnosis of PTF can be made...
      Mechanisms of PTF
      There is a difference between cause and mechanism.
      The cause is WHY something developed.
      Trauma is the cause of PTF.
      The mechanism is HOW something developed or the pathological events that led to the problem.
      If you fall on the ground and break your hip, trauma is the cause of the broken hip (WHY you have a hip fracture).
      The pathological mechanism of injury (the HOW) is that high amounts of compressive forces (momentum) impacted the hip and resulted in a fracture.
      Many times it is difficult to determine if an abnormal research finding is part of the cause or the mechanism of fibromyalgia.
      Changes occur after fibromyalgia has developed, so an abnormality can be one of the consequences of fibromyalgia.
      It’s like asking the famous question : “What came first, the chicken or the egg ?”.
      Onjury pain mechanisms
      Damage to body tissues from an injury can occur from muscle strains, ligament sprains, disc tear or herniation, joint impaction, direct nerve trauma, swelling and inflammation.
      A combination of injuries activates the normal pain cascades from multiple locations, bombarding the spinal cord and brain with pain signals.
      Dr. Rajesh Munglani recently published a good review article on the neurobiologic mechanisms that can occur with whiplash injuries (cfr. “Neurobiological mechanisms underlying chronic whiplash associated pain” - Journal of Musculoskeletal Pain, 2000 at : -).
      His descriptions help explain how some people develop chronic pain and others do not.
      The road to PTF travels first through acute pain and then chronic pain.
      As noted, PTF does not happen immediately after the accident.
      It takes time to fully evolve.
      Presently, we have no way to determine which injured people will get PTF and which ones will heal and not develop chronic pain.
      Complete healing without residual pain is attempted in all with injuries and expected in most.
      If chronic pain persists several months after an injury, complete healing is not likely to occur and the risk for getting PTF increases.
      Let’s review the neurobiological mechanisms that lead to fibromyalgia after an injury.
      • Nerve injuries, tissue inflammation, soft tissue damage and scarring activate the nociceptors (specialized nerve endings where pain originates) and signal pain. Localized injuries to the muscle components (spindles, intrafusal fibers, calcium pumps) can create biochemical, hormonal and red blood cell changes that interfere with cells’ ability to receive oxygen, glucose and other nutrients.
      • Blood flow, energy formation and bioelectrical harmony are all disrupted. In those who ultimately develop PTF, the nociceptors probably remain “faulty” and continue to signal pain. Like faulty electrical short-circuits, the nociceptors continue to release pain-producing neurotransmitters.
      • Hypersensitization of the nociceptors also occurs, so they respond more dramatically to any stimulation (called allodynia). The nerves cannot “turn off” these continuous painful signals and undergo profound functional changes. Pain arises spontaneously from the nerves, causing the person to hurt “for no obvious reason”. Instead of waiting to be signaled from outside sources such as trauma, pressure, touch or temperature changes, the nerves signal spontaneous pain without any outside help.
      • Furthermore, permanent nerve changes cause outside sensory signals to be misinterpreted as pain. Instead of feeling ordinary touch, movement or pressure, one feels painful touch, throbbing movement and stabbing pressure. This exaggerated painful interpretation of ordinarily non-painful sensations is known as allodynia.
      --- For a detailed plain-language explanation of the mechanisms by which trauma and tissue injury may trigger persistent activation step-by-step throughout the pain pathway from nociceptors to brain cfr. Dr. Pellegrino’s article “Fibromyalgia – Ultimately a Disease of Amplified Pain” at : ---
      Persistent triggers
      Ongoing peripheral input that feeds into the centrally sensitized “fibromyalgia pain cascade” comes from different injured tissues.
      These areas are known as “triggers” or “pain generators” and can occur wherever there is residual damager or instability from injury.
      A number of pain generators exist and include :
      1/ Muscle triggers
      Ongoing muscle spasms and restrictive muscle scars are examples of persistent triggers that can exist in muscles.
      Muscle bundles may go into protective spasms whenever there is inflammation or potential irritation in the region.
      For example, someone with a low back disc herniation may have spasms in the low back muscles as an involuntary attempt to protect or guard from movements of the back.
      Any back movement could cause further damage or inflammation from the already damaged disc.
      In PTF, muscles have a double whammy effect on the pain-generating cascade.
      The injury itself caused muscle damage and persistent localized spasms, causing ongoing pain signals.
      But the muscles may be forced to work harder because tother tissues (e.g., discs, facets, ligaments) were permanently damaged and cannot do their jobs of stabilizing the spine.
      Hence, the muscles tighten and spasm up to assist in the stabilization and more persistent pain signals are sent… the double whammy effect.
      2/ Facet joint dysfunctions
      Australian researcher Nikolai Bogduk and his colleagues have demonstrated how the cervical facet joints (joints in the vertebra of the neck) especially are a major trigger of chronic pain ( cfr. “Chronic whiplash and whiplash-associated disorders: an evidence-based approach” at : -).
      The facet joints may be unstable because the capsular ligaments were damaged or overstretched from the whiplash.
      Loose ligaments cannot hold the joints together as tightly as needed to stabilize them and any “extra” movement in the facet joints triggers pain.
      The facet joints may be too restricted or tight, leading to instability.
      Muscle spasms can tighten or restrict the facet joints, causing pain from immobility.
      3/ Intervertebral discs
      These areas can become chronic pain generators if the whiplash trauma caused tears or defects in the disc’s annular ligament.
      Dr. Bogduk’s work noted up to 50% of chronic whiplash patients have problems with these discs.
      4/ Nerve injuries
      Direct injuries to nerves can result in chronic pain generation, as opposed to indirectly signaling chronic pain through normal uninjured nerves.
      Nerve roots, brachial plexus and sympathetic nerves can all be bruised, stretched or damaged from the whiplash trauma and never heal properly, causing chronic pain signals.
      All of the above sources can feed into the sensitized central nervous system (spinal cord and brain) and maintain, aggravate, and permanently worsen the PTF’s chronic pain state.
      Treatment of post-traumatic fibromyalgia (PTF)
      Just as in nontraumatic fibromyalgia, no one single treatment eliminates the symptoms of PTF.
      Currently there is no cure for this disorder.
      However, various treatments can help those with PTF even if the condition is not cured.
      Each person’s treatment program needs to be individualized and what works for some may not work for others.
      Hopefully each patient will find some treatment that helps to deal with the chronic pain.
      --- Other chapters on medications, therapeutic injections and physical medicine treatments review in detail the various treatments for fibromyalgia. The treatments for PTF are really the same, since fibromyalgia is fibromyalgia regardless of the cause ! ---
      Treatment goals
      Overall, six main treatment goals can be identified for each person with PTF :
      1/ Decrease pain
      The ideal goal is to eliminate pain altogether, but this rarely happens because PTF has no known cure at this time.
      Many treatments can reduce the pain, however, even if it is still present.
      Sometimes a remission occurs where the pain is hardly noticed although painful tender points are still palpable on exam.
      2/ Improve function
      The ability to perform everyday activities such as dressing oneself, driving, moving about and eating is the basis for “quality of life” issues.
      If pain interferes with basic daily activities, the patient with PTF usually reports a poorer quality of life.
      Pain can interfere with work abilities, especially if the job requires a lot of reaching, bending or lifting.
      Optimizing job functions is an important treatment goal.
      3/ Promote healing of any residual injuries
      If residual damage to tissues is still present and contributing to pain, instability, ongoing irritation or inflammation, then treatments to promote healing of this damage should help.
      4/ Prevent worsening or complications
      If residual damage to tissues is present and cannot be healed, then the goal becomes avoiding further damage or complications.
      5/ Decrease the risk of re-injury or flare-up
      If PTF is chronic and permanent, than a goal is to keep it at a stable baseline or a level where the pain can be successfully managed.
      A stable baseline free from annoying flare-ups may sound boring, but is exactly what is hoped for.
      6/ Find a successful home program to control symptoms
      This goal is the ultimate prize. One hopes the therapy program works and learns to do the program on his/her own to maintain a stable baseline.
      In PTF, various types of treatments are prescribed in order to achieve as many individual treatment goals as possible.
      Some treatments may work better than others, and usually the combination of all the different treatments can lead to overall improvement.
      Cfr. :

    9. Fibromyalgia in human immunodeficiency virus infection
      Buskila D, Gladman DD, Langevitz P, Urowitz S, Smythe HA, University of Toronto Rheumatic Disease Unit, Wellesley Hospital, ON, Canada - J Rheumatol. 1990 Sep;17(9):1202-6 - PMID: 2290162
      Tenderness was assessed by point count and by scored palpation in 51 patients with human immunodeficiency virus (HIV) infection as well as 51 patients with rheumatoid arthritis (RA) and 50 patients with psoriatic arthritis (PsA).
      Fifteen of 51 (29%) patients with HIV infection met criteria for fibromyalgia, based on the presence of 10 tender (of 14) "fibrositic" points.
      Similar results were observed among patients with PsA (24%).
      The prevalence of fibromyalgia was higher among patients with RA (57%).
      Patients with HIV and PsA were less tender than patients with RA. Fibromyalgia in patients with HIV was significantly associated with myalgia and arthralgia, but not with age, duration of HIV infection, stage of HIV disease or zidovudine therapy.
      Cfr. :

    10. Fibromyalgia-associated hepatitis C virus infection
      Rivera J, de Diego A, Trinchet M, García Monforte A, Rheumatology Unit, Hospital General Universitario Gregorio Marañón, Madrid, Spain - Br J Rheumatol. 1997 Sep;36(9):981-5 - PMID: 9376995
      The objective was to determine whether there might be an association between hepatitis C virus (HCV) chronic infection and fibromyalgia (FM).
      We determined the prevalence of HCV infection in 112 FM patients, in comparison with matched rheumatoid arthritis (RA) patients from the out-patient clinic of a teaching tertiary care general hospital.
      Furthermore, we looked for evidence of FM in 58 patients diagnosed with chronic hepatitis due to HCV, compared with matched surgery clinic patients, HCV antibodies were determined by enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA).
      Serum RNA of HCV (HCV-RNA) was determined by polymerase chain reaction.
      In the group of FM patients, HCV antibodies were found by ELISA in 17 (15.2%) patients and in six (5.3%) of the RA controls (P < 0.05).
      RIBA was positive in 16 and indeterminate in one of the FM patients.
      Serum HCV-RNA was found in 13 of these FM patients.
      In eight (47%) FM patients, alanine aminotransferase (ALT) was normal, although HCV-RNA was detected in four (50%) of them.
      In the group of patients with chronic hepatitis due to HCV, all patients had HCV antibodies and the presence of HCV-RNA in serum.
      Within these patients, 31 (53%) had diffuse musculoskeletal pain, while six (10%) fulfilled FM diagnostic criteria.
      In the control group, 13/58 (22%) had diffuse musculoskeletal pain (P < 0.001), whereas only one female patient (1.7%) fulfilled FM criteria (P < 0.05).
      Serum ALT was 51.7 +/- 38.4 in FM patients, whereas it was 122 +/- 76.3 in patients with HCV chronic hepatitis but without FM (P < 0.001).
      There were no statistical differences in autoimmune markers between patients with and without FM.
      These data suggest that there exists an association between FM and active HCV infection in some of our patients.
      FM is not associated with liver damage or autoimmune markers in these patients.
      HCV infection should be considered in FM patients even though ALT elevations were absent.
      Cfr. :

    11. Fibromyalgia, chronic fatigue syndrome and myofascial pain syndrome
      Goldenberg DL, Newton-Wellesley and Tufts University School of Medicine, Massachusetts, USA - Curr Opin Rheumatol. 1995 Mar; 7(2):127-35 - PMID: 7766493

      Two important studies in which nuclear magnetic resonance spectroscopy was used convincingly demonstrated that muscle is not the primary pathologic factor in fibromyalgia.
      There were further studies reporting that fibromyalgia-chronic fatigue syndrome may follow well treated Lyme disease or mimic Lyme disease.
      The longest therapeutic trial to date in fibromyalgia demonstrated an initial modest effect of tricyclic medications, but at 6 months that efficacy was no longer evident.
      Investigation in both fibromyalgia and chronic fatigue syndrome now focuses on the central nervous system.
      The use of new technology, eg, neurohormonal assays and imaging such as single-photon emission computed tomography scan, may be important in understanding these elusive conditions.
      Cfr. :

    12. Fibromyalgia, infection and vaccination - Two more parts in the etiological puzzle
      Jacob N. Ablina, Yehuda Shoenfeldb and Dan Buskilac - aDepartment of Rheumatology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv University, 6 Weizman St., 64239 Tel-Aviv, Israel - bDepartment of Medicine ‘B’ and Center for Autoimmune Diseases, Sheba Medical Center Tel-Hashomer and Sackler Faculty of Medicine, Tel-Aviv University, Israel - cRheumatic Disease Unit, Department of Medicine, Soroka Medical Center, Beer Sheba, Israel
      As the pathogenesis of fibromyalgia continues to raise debate, multiple putative triggers have been implicated.
      The current review summarizes the available data linking fibromyalgia to either infection or vaccination.
      Multiple infectious agents have been associated with the development of either full-blown fibromyalgia (e.g. hepatits C) or with symptom complexes extensively overlapping with that syndrome (e.g. chronic Lyme disease).
      The cases of Lyme disease, mycoplasma, hepatits C and HIV are detailed.
      Despite the described associations, no evidence is available demonstrating the utility of antibiotic or anti-viral treatment in the management of fibromyalgia.
      Possible mechanistic links between fibromyalgia and HIV are reviewed.
      Associations have been described between various vaccinations and symptom complexes including fibromyalgia and chronic fatigue syndrome.
      The case of Gulf War syndrome, a functional multisystem entity sharing many clinical characteristics with fibromyalgia is discussed, with emphasis on the possibility of association with administration of multiple vaccinations during deployment in the Persian Gulf and the interaction with stress and trauma.
      Based on this example a model is proposed, wherein vaccinations function as co-triggers for the development of functional disorders including fibromyalgia, in conjunction with additional contributing factors.
      Cfr. :

    13. Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients
      DV Ablashi, HB Eastman et al. Journal of Clinical Virology 2000:16:179 -191
      Cfr. :

    14. Gulf War Illnesses - Causes and treatments
      Nicolson GL - Armed Forces Med Dev 2001; 2:41-44
      Cfr. :

    15. Gulf War Illnesses - Chemical, radiological and biological exposures resulting in chronic fatiguing illnesses can be identified and treated
      Nicolson GL, Berns P, Nasralla M, Haier J, Nicolson NL, Nass M - J Chronic Fatigue Syndr 2003; 11(1):135-154
      Cfr. :

    16. Gulf War Illnesses - Chemical, radiological and hiological exposures resulting in chronic l'aliQuing illnesses can be idemificd and treated
      Nicolson GL, Berns P, Nasralla M, Haicr J, Nicolson NL, Nass M - Chronic tigne Syndr. 2003; ll(l):21-36

    17. Gulf War Illnesses - Role of chemical, radiological and biological exposures
      Nicolson GL, Nasralla M, Haier J, Nicolson NL – In : 'War or Health' - H. Tapanainen, Ed., 431-446, Zed Press, Helinsiki, 2001
      Cfr. :

    Go to Part VII

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    Infection as one possible cause of fibromyalgia

    Part VII

    1. Gulf War Syndrome finally declared real - Illness caused by exposure to pesticides and other neurotoxic chemicals
      Boston University School of Public Health
      Cfr. :

    2. Gulf War veterans - Evidence for chromosomal alterations and their significance
      Nigs J, Nicolson GL - J Chronic Fatigue Syndr 2004; 12(1):79-83
      Cfr. :

    3. Health and exposures oT United Kingdom Gull war veterans - Part II - The relation of health to exposure
      Cherry N. Creed 1'. Sii man A, Dunn G. Baxter G, S medley J. et al. - J. Occup. Environ. Med, 2001;58:299-306

    4. Health of UK servicemen who served in the Persian Gulf War
      Unwin C, Blatchley N, Coker W, Ferry S, Hotopf M, Hull L et al. Lancet, 1999;353:169-178
      Cfr. :

    5. Hepatitis C virus infection in Italian patients with fibromyalgia
      C. Palazzi1, E. D’Amico2, S. D’Angelo3, 5, A. Nucera4, A.Petricca1 and I.Olivieri3 – 1 Division of Rheumatology, Villa Pini Clinic, Chieti, Italy – 2 Liver Unit, Spirito Santo Hospital, Pescara, Italy – 3 Rheumatology Department of Lucania, S. Carlo Hospital of Potenza and Madonna delle Grazie Hospital of Matera, Potenza, Italy – 4 Section of Medical Statistics & Epidemiology, Department of Health Sciences, University of Pavia, Pavia, Italy – 5 Rheumatology Department of Lucania, San Carlo Hospital, Contrada Macchia Romana, Via Potito Petrone—Padiglione E, 85100 Potenza, Italy - Clin Rheumatol. 2008 Jan; 27(1):101-3. Epub 2007 Oct 18
      We evaluated the prevalence of hepatitis C virus (HCV) infection in Italian patients suffering from fibromyalgia (FM), in comparison with patients affected by non-HCV related rheumatic degenerative disorders.
      Consecutive patients with FM and a statistically comparable group of patients suffering from peripheral osteoarthritis (OA) or sciatica due to L4-L5 or L5-S1 herniated disc were tested for HCV infection with a third-generation microparticle enzyme immunoassay (MEIA).
      In the positive cases, a third-generation recombinant immunoblot assay (RIBA) confirmatory test and serum HCV-RNA test were performed.
      Fisher’s exact test was performed to compare the prevalence of HCV infection (MEIA- and RIBA-positive results) obtained in the two enrolled groups.
      Enrolled were 152 subjects suffering from FM and 152 patients with peripheral OA or sciatica.
      Anti-HCV antibodies were found in 7/152 (4.6%) patients suffering from FM and in 5/152 (3.3%) of control subjects.
      No statistically significant differences in HCV prevalence were detected between cases and controls.
      Our present report does not confirm previous data indicating an increased prevalence of HCV in FM patients and does not seem to support a significant pathogenetic role of HCV under this condition.
      Cfr. :

    6. High frequency of systemic mycoplasmal infections in Gulf War veterans and civilians with Amyotrophic Lateral Sclerosis (ALS)
      Nicolson GL, Berns P, Nasralla M, Haier J, Pomfret J - J Clin Neurosci 2002; 9:525-529
      Cfr. :

    7. High prevalence of mycoplasmal infections among European Chronic Fatigue Syndrome patients - Examination of four Mycoplasma species in Chronic Fatigue Syndrome patients
      Nijs J, Nicolson GL, De Becker P, Coomans D, De Meirleir K - FEMS Immunol Med Microbiol 2002; 34:209-214
      Cfr. :

    8. High prevalence of mycoplasmal infections in symptomatic (Chronic Fatigue Syndrome) family members of mycoplasma-positive Gulf War Illness patients
      Nicolson GL, Nasralla M, Nicolson NL, Haier J - J Chronic Fatigue Syndr 2003; 11(2):21-36
      Cfr. :

    9. Higher prevalence of fibromyalgia in patients infected with human T cell lymphotropic virus type I
      Cruz BA; Catalan-Soares B; Proietti F, Rheumatology Department, Biocor Instituto, Nova Lima, Minas Gerais, Brazil : - J Rheumatol. 2006 Nov;33(11):2300-3 - PMID : 17086610
      Objective - Inflammatory rheumatic conditions including rheumatoid arthritis and Sjogren's syndrome have been reported in individuals infected with human T cell lymphotropic virus type I (HTLV-I).
      Other chronic lymphotropic virus infections such as hepatitis C and human immunodeficiency virus are associated with fibromyalgia (FM).
      There are no reports about the association between HTLV-I infection and FM.
      We evaluated the association between FM and HTLV-I infection.
      Methods - We conducted a case-control study with prevalent cases.
      Ex-blood donation candidates with HTLV-I infection from a blood bank cohort and healthy blood donors as a control group, were submitted to rheumatologic evaluation to compare the prevalence of FM.
      The following covariables were also evaluated: other rheumatic diseases, age, sex, personal income, level of education and depression.
      Results - One hundred individuals with HTLV-I infection and 62 non-infected blood donors were studied.
      Thirty-eight (38%) HTLV-I infected individuals and 3 (4.8%) individuals from the control group presented the diagnosis of FM (OR 12.05, 95% CI 3.53-41.17).
      Other rheumatic diseases were also more prevalent in the infected group (37% vs 12.9%; OR 3.80, 95% CI 1.63-8.86).
      In multivariate analysis adjusted by the covariables, the association between HTLV-I and FM was statistically significant (OR 9.14, 95% CI 2.42-34.52).
      Conclusion - Our study shows a greater prevalence of FM in HTLV-I infected individuals, suggesting that FM may be associated with this viral infection.
      Cfr. :;jsessionid=21CED400A6252607545D

    10. How chlamydia pneumoniae causes such a plethora of diseases, 2006-2-24
      Cfr. :

    11. Identification and treatment of chronic infections in CFIDS, fibromyalgia sydrome and rheumatoid arthritis patients that cause morbidity and illness progression
      Prof. Garth Nicolson - Doctor's Educational Booklet, CFIDS Assoc. of America, 1998
      Cfr. :

    12. Identification and treatment of chronic infections in CFIDS, fibromyalgia syndrome and rheumatoid arthritis
      G.L. Nicolson, CFIDS Chronicle 1999; 12(3): 19-21
      Cfr. :

    13. Identification of mycoplasma fermentans in synovial fluid samples from arthritis patients with inflammatory disease
      Johnson S, Sidebottom D, Bruckner F, Collins D - Journal of Clinical Microbiology 2000; 38: 90-3
      Cfr. :

    14. Illness, cytokines and depression
      Yirmiya R, Pollak Y, Morag M, Reichenberg A, Barak O, Avitsur R, Shavit Y, Ovadia H, Weidenfeld J, Morag A, Newman ME, Pollmächer T, Department of Psychology, Hebrew University, Hadassah Hospital, Jerusalem, Israel : - Ann N Y Acad Sci. 2000;917:478-87 - PMID: 11268375
      Various medical conditions that involve activation of the immune system are associated with psychological and neuroendocrine changes that resemble the characteristics of depression.
      In this review we present our recent studies, designed to investigate the relationship between the behavioral effects of immune activation and depressive symptomatology.
      In the first set of experiments, we used a double-blind prospective design to investigate the psychological consequences of illness in two models : (1) vaccination of teenage girls with live attenuated rubella virus and (2) lipopolysaccharide (LPS) administration in healthy male volunteers.
      In the rubella study, we demonstrated that, compared to control group subjects and to their own baseline, a subgroup of vulnerable individuals (girls from low socioeconomic status) showed a significant virus-induced increase in depressed mood up to 10 weeks after vaccination.
      In an ongoing study on the effects of LPS, we demonstrated significant LPS-induced elevation in the levels of depression and anxiety as well as memory deficits.
      These psychological effects were highly correlated with the levels of LPS-induced cytokine secretion.
      In parallel experiments, we demonstrated in rodents that immune activation with various acute and chronic immune challenges induces a depressive-like syndrome, characterized by anhedonia, anorexia, body weight loss and reduced locomotor, exploratory and social behavior.
      Chronic treatment with antidepressants (imipramine or fluoxetine) attenuated many of the behavioral effects of LPS, as well as LPS-induced changes in body temperature, adrenocortical activation, hypothalamic serotonin release and the expression of splenic
      TNF-alpha mRNA. Taken together, these findings suggest that cytokines are involved in the etiology and symptomatology of illness-associated depression.
      Cfr. :

    15. Immune cell apoptosis and chronic fatigue syndrome
      Frémont M, D’Haese A, Roelens S, De Smet K, Herst CV, Englebienne P – In : 'Chronic Fatigue Syndrome - A biological approach' - Englebienne P, De Meirleir K, editors - Boca Raton: CRC Press 2002, p. 131-74
      Cfr. :

    16. Immunology of chronic fatigue syndrome – Review
      R. Patarca et al. - J. Chronic Fatigue Syndr. 2000; 6(3/4): 69-107
      Cfr. :

    17. Immunophenotyping predictive of mycoplasma infection in patients with chronic fatigue syndrome
      Nijs J, Coomans D, Nicolson GL, De Becker P, Demanet C, De Meirleir K - J Chronic Fatigue Syndr 2003; 11(2):51-70
      Cfr. :

    18. In fibromyalgia antibiotic therapy is not indicated
      Dtsch Med Wochenschr. 2002 Jun 7; 127(23):1273-4
      Cfr. :

    19. Increased rates of fibromyalgia following cervical spine injury - A controlled study of 161 cases of traumatic injury
      Dr. D. Buskila (1997)
      Cfr. :

    20. Interferon-alpha-induced changes in tryptophan metabolism - Relationship to depression and paroxetine treatment
      Capuron L, Neurauter G, Musselman DL, Lawson DH, Nemeroff CB, Fuchs D, Miller AH, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia 30322, USA - Biol Psychiatry. 2003 Nov 1;54(9):906-14 - PMID: 14573318
      Background - Tryptophan (TRP) degradation into kynurenine (KYN) by the enzyme, indoleamine-2,3-dioxygenase, during immune activation may contribute to development of depressive symptoms during interferon (IFN)-alpha therapy.
      Methods - Twenty-six patients with malignant melanoma were randomly assigned in double-blind fashion to receive either placebo or paroxetine, beginning 2 weeks before IFN-alpha treatment and continuing for the first 12 weeks of IFN-alpha therapy.
      At treatment initiation and at 2, 4, and 12 weeks of IFN-alpha treatment, measurements of TRP, KYN and neopterin (a marker of immune activation), were obtained, along with structured assessments of depression, anxiety and neurotoxicity.
      Results - Regardless of antidepressant treatment status, all patients exhibited significant increases in KYN, neopterin and the KYN/TRP ratio during IFN-alpha therapy.
      Among antidepressant-free patients, patients who developed major depression exhibited significantly greater increases in KYN and neopterin concentrations and more prolonged decreases in TRP concentrations than did nondepressed, antidepressant-free patients.
      Moreover, in antidepressant-free patients, decreases in TRP correlated with depressive, anxious and cognitive symptoms, but not neurovegetative or somatic symptoms.
      No correlations were found between clinical and biological variables in antidepressant-treated patients.
      Conclusions - The results suggest that reduced TRP availability plays a role in IFN-alpha-induced depressive symptoms, and paroxetine, although not altering the KYN or neopterin response to IFN-alpha, attenuates the behavioral consequences of IFN-alpha-mediated TRP depletion.
      Cfr. :

    21. Interrelations between fibromyalgia, thyroid autoantibodies and depression
      Ribeiro LS; Proietti FA, Department of Rheumatology, Governador Israel Pinheiro Hospital, Belo Horizonte, Brazil : - J Rheumatol. 2004 Oct;31(10):2036-40 - PMID :15468372
      Objective - To detect and quantify the association between fibromyalgia (FM) and thyroid autoimmunity.
      Methods - This cross-sectional study comprised 146 women with FM and 74 case-controls, all 18 years of age or older.
      FM was diagnosed according to the American College of Rheumatology 1990 classification criteria.
      The Mini-International Neuropsychiatric Interview (MINI) was applied for the diagnosis of depression, previously considered as an important confounding factor.
      Thyroid autoimmunity was defined as the occurrence of detectable antithyroid peroxidase antibodies and/or antithyroglobulin antibodies by the immunometric assay.
      Cases of diffuse connective tissue diseases and thyroid dysfunctions (hypo or hyperthyroidism) were excluded in both groups.
      Results - Univariate analysis detected an association between FM and thyroid autoimmunity (odds ratio, OR = 3.87, 95% confidence interval, CI = 1.54-10.13), depression (OR = 3.94, 95% CI = 1.97-7.93) and age (OR = 1.04, 95% CI = 1.01-1.07).
      In the final logistic regression model, after adjustment for depression and age, the association between FM and thyroid autoimmunity was strengthened (OR = 4.52, 95% CI = 1.86-11.0).
      Conclusion - Our results suggest an association between FM and thyroid autoimmunity.
      Cfr. :;jsessionid=21CED400A6252607545D

    22. Interviewing Prof. Garth Nicolson - CFS National Radio Program
      Dr. Roger G. Mazlen interviewing Prof. Garth Nicolson, 11/21/00
      Cfr. :

    23. Is RA27/3 rubella immunization a cause of chronic fatigue ?
      Allen AD, Biomedical Sciences Division, Algorithms, Incorporated, Northridge, California 91325 - Med Hypotheses. 1988 Nov;27(3):217-20 - PMID: 3211019
      Patients with chronic fatigue syndromes (primary fibrositis syndrome, major affective disorder etc) have elevated IgG serum antibodies to multiple common viruses.
      Only IgG rubella antibodies are positively correlated with the intensity of symptoms and have a height that is clearly significant compared to healthy controls.
      The lymphotropic properties of the rubella virus could account for the multiple elevated antibodies.
      Adult women are over-represented in the population of patients with chronic fatigue and are especially susceptible to developing such symptoms following exposure to attenuated rubella virus.
      A new more potent strain of live rubella vaccine (strain RA27/3) was introduced in 1979.
      Within three years reports of patients with chronic fatigue began surfacing in the literature.
      Considering all this, the possible role of rubella immunization in the etiology of chronic fatigue syndromes deserves further study.
      Cfr. :

    24. Is there a biologic connection between inflammatory disease and depression ?
      Colby Stong - NeuroPsychiatry Reviews, September 2004, Vol. 5, No.7
      Nearly a third of patients with an inflammatory disease may develop depression, which until recently has been attributed to their inability to cope with the disease.
      However, research on patients who are aided via immunotherapy has challenged this theory.
      Robert Dantzer, DVM, PhD, and Keith Kelley, PhD, believe that they have found strong evidence of a relationship between a molecular pathway in the brain and development of psychopathology.
      Depression is a risk factor for a bad outcome,” said Dr. Dantzer in an interview with Neuropsychiatry Reviews : “What our research is showing is that you have to put everything in a different perspective. The idea is that the depression is linked biologically to the disease. It is not just the way that the molecules are involved in the disease process but [that] the physiology of the disease acts on the brain and is responsible for depression. Actually, the severity of the disease will result in a higher risk for depression. So it’s a mirror image of the usual interpretation that people give of the association between depression and disease”.
      Dr. Dantzer is an Adjunct Professor of Psychoneuroimmunology in the Department of Animal Sciences, University of Illinois at Urbana–Champaign and Director of the Laboratory of Integrative Neurobiology at the University of Bordeaux, France.
      The prevalence of depression in the general population is about 3% to 5%.
      In patients with chronic inflammation—such as occurs with coronary heart disease or type 2 diabetes mellitus—the prevalence of depression increases to between 12% and 30%.
      Immunotherapy, which involves the injection of cytokines, also causes depression in about a third of patients, noted Dr. Dantzer. Symptoms of depression begin within days to weeks of treatment and disappear when the treatment ends.
      Thus, Dr. Dantzer wanted to help patients avoid depression while they still benefited from the immune-boosting effects of cytokine treatments.
      Tryptophan, cytokines and depression
      Drs. Dantzer and Kelley conducted a series of experiments on mice to show how cytokine treatment causes serotonin depletion.
      They hypothesized that cytokines suppress serotonin by activating the enzyme indoleamine-2,3-dioxygenase (IDO) that catabolizes tryptophan.
      Dr. Dantzer explained that in the brain, IDO prevents tryptophan from being turned into serotonin, which causes decreased levels of serotonin and leads to the symptoms of depression.
      From clinical studies, we have learned that depressed patients either suffering from chronic inflammatory disorders or who are treated with cytokines have decreased plasma levels of tryptophan,” he said : “Second, we have observed that the enzyme responsible for that is induced not only at the periphery but in the brain”.
      Dr. Dantzer pointed out that his current research is built on a concept that he had ignored a few years ago, which is the fact that the brain is representing what is going on in the body—“what we already knew for quite a long time, but in terms of inflammation and it is doing that with the same molecules as the ones that are promoting inflammation at the periphery. If you have an inflammatory response in your body, it will be represented in the brain with exactly the same molecules that in your body are responsible for inflammation. This normally is responsible for what we call sickness behavior—why you feel sick and behave in a sick way when you are ill”.
      On target for new treatments
      Dr. Dantzer said that if his hunches are correct, then logical targets for decreasing the risk of depression in patients with inflammatory disorders are the cytokine system or the IDO enzyme to avoid both the decrease in serotonin and the generation of neuroactive compounds derived from tryptophan.
      For example, he said, antioxidants may be used in an effort to decrease free radicals, which may enhance the IDO activation.
      By suppressing the IDO activity, more tryptophan should be available to be converted to serotonin, he theorized.
      If antioxidant treatment proves effective in the mice, then humans eventually may benefit from the approach.
      The main potential of clinical application is the discovery of new targets for drugs aiming at decreasing the risk of developing mood disorders when you are sick,” he said.
      Treating all patients who will undergo interferon therapy with an antidepressant is not necessarily the right preventive solution, stressed Dr. Dantzer.
      It is not yet known whether antidepressant treatment will affect interferon treatment for the disease, he said—“in this case, the immune cells of the body and their ability to kill tumor cells. You are preventing the occurrence of depression with an antidepressant treatment, but at the same time this antidepressant treatment could also act on immune cells so that they are less able to do what they are supposed to do. My own advice would be to tell the clinician to try to identify those patients who are at risk for developing depression. We know that patients who are at risk for developing depression are already high in terms of depressed moods”.
      Suggested reading
      - Interferon-alpha-induced changes in tryptophan metabolism - Relationship to depression and paroxetine treatment - Capuron L, Neurauter G, Musselman DL et al. - Biol Psychiatry. 2003;54:906-914 at :
      - Baseline mood and psychosocial characteristics of patients developing depressive symptoms during interleukin-2 and/or interferon-alpha cancer therapy - Capuron L, Ravaud A, Miller AH, Dantzer R - Brain Behav Immun. 2004;18:205-213 at : -.
      Cfr. :

    25. Lack of association of fibromyalgia with hepatitis C virus infection
      Narváez J, Nolla JM, Valverde-García J, Department of Rheumatology, Hospital Universitario de Bellvitge-IDIBELL, Barcelona, Spain : - J Rheumatol. 2005 Jun;32(6):1118-21 - PMID: 15940777
      Objective - An association between chronic hepatitis C virus (HCV) infection and fibromyalgia (FM) remains controversial, mainly because previous studies were based on prevalent case series or comparisons with less than optimal control groups.
      We investigated whether there might be an association between chronic HCV infection and FM.
      Methods - We prospectively investigated the prevalence of HCV infection in a series of 115 patients with FM and compared it with the prevalence in the general population of our community reported in the same period.
      Anti-HCV antibodies were determined by ELISA.
      In positive cases, infection was confirmed by recombinant immunoblot assay and HCV-RNA was detected by PCR using sera samples.
      Differences between prevalence rates were assessed by chi-square test.
      Results - : HCV infection was confirmed in 3 of 115 patients with FM (2.6%).
      Two of these patients (1.74%) had active HCV infection shown by the presence of viral RNA in serum, whereas HCV RNA was undetectable in the third patient.
      In these cases, liver disease had previously been undiagnosed and HCV infection manifested itself by extrahepatic symptoms.
      Although the prevalence of HCV infection was slightly higher in patients with FM than in the general population in the age groups 25-44 and 45-64 years, when we compared prevalence rates in the total group and the different age groups, no statistically significant differences were found.
      Conclusion - From our results, it seems unlikely that HCV infection plays a pathogenic role in FM.
      Cfr. :

    26. Lipid replacement and antioxidant nutritional therapy for restoring mitochondrial function and reducing fatigue in chronic fatigue syndrome and other fatiguing illnesses
      Nicolson and Ellithorpe - Journal of Chronic Fatigue Syndrome 2006; 13(1): 57-68
      Cfr. :

    27. Lipid replacement as an adjunct therapy in chronic fatigue, anti-aging and restoration of mitochondrial function
      Nicolson GL - JANA 2003; 6(3):22-28
      Cfr. :

    28. Management of post-viral fatigue syndrome
      Wessely S, David A, Butler S, Chalder T - Br J Gen Pract. 1990 Feb;40(331):82-3 - PMID: 2107860

      Cfr. :

      This article is a comment on:
      Patient management of post-viral fatigue syndrome
      Ho-Yen DO, Raigmore Hospital, Inverness - Br J Gen Pract. 1990 Jan;40(330):37-9 - PMID: 2107839
      A case definition for post-viral fatigue syndrome is proposed within which various subgroups of patients exist.
      Any one treatment may not apply to all the subgroups.
      In particular, patients' experiences do not show that avoidance of exercise is maladaptive.
      It is proposed that the recently ill often try to exercise to fitness whereas the chronically ill have learnt to avoid exercise.
      Recovery is more likely to be achieved if patients learn about their illness and do not exhaust their available energy.
      Cfr. :

    29. Melatonin as antioxidant under pathological processes
      Cristina Tomás-Zapico, Ana Coto-Montes, Departamento de Morfología y Biología Celular, Facultad de Medicina, Universidad de Oviedo, 33006 Oviedo, Spain - Recent Patents on Endocrine, Metabolic & Immune Drug Discovery 2007, 1, 63-82 63 - © 2007 Bentham Science Publishers Ltd.
      Many are the diseases which course with free radical formation.
      These disorders cover a great range of fields such as neurodegenerative, immune, inflammatory and mitochondrial-related diseases.
      Melatonin is the main pineal gland product and it functions as “time-giver” in the regulation of circadian rhythms, among others.
      But the actions of melatonin are not only restricted to the neuroendocrine physiology.
      In fact, it has been known as a radical scavenger, a role that has been deeply studied in all those conditions where free radicals are generated.
      Furthermore, melatonin has been shown to act as an indirect antioxidant, since it is able to increase the activity and expression of the main antioxidant enzymes, the machinery for the glutathione synthesis and many others direct or indirectly implicated in the free radical removal.
      Melatonin can also diminish the activity or expression of enzymes or factors that are considered as prooxidants.
      Thus, researchers have paid attention to the possible actions of melatonin in the attenuation of those processes where free radical overproduction is implicated.
      This review summarizes some of the proposed melatonin mechanisms for different free radical-dependent pathological situations, as well as some patents on melatonin significance recently reported for the treatment of attention deficit, hyperactivity disorders, stress-related diseases, chronic fatigue syndrome, diabetes, Parkinson’s disease.
      Alzheimer’s disease, age associated cognitive dysfunction and cancer.
      Full text at :

    30. Melatonin inhibits expression of the inducible NO synthase II in liver and lung and prevents endotoxemia in lipopolysaccharide-induced multiple organ dysfunction syndrome in rats
      Elena Crespo,* Manuel Maci´as,* David Pozo,† Germaine Escames,* Miguel Marti'n,* Francisco Vives,* Juan M. Guerrero,† and Dari'o Acun˜ A-Castroviejo*,1 - *Departamento de Fisiologı´a, Instituto de Biotecnologı´a, Universidad de Granada, Spain - †Departamento de Bioquı´mica Me´dica y Biologı´a Molecular, Facultad de Medicina, Universidad de Sevilla, Spain - FASEB J. 13, 1537–1546 (1999)
      We evaluated the role of melatonin in endotoxemia caused by lipopolysaccharide (LPS) in unanesthetized rats.
      The expression of inducible isoform of nitric oxide synthase (iNOS) and the increase in the oxidative stress seem to be responsible for the failure of lungs, liver and kidneys in endotoxemia.
      Bacterial LPS (10 mg/kg b.w) was i.v. injected 6 h before rats were killed and melatonin (10–60 mg/kg b.w.) was i.p. injected before and/or after LPS.
      Endotoxemia was associated with a significant rise in the serum levels of aspartate and alanine aminotransferases, g-glutamyl-transferase, alkaline phosphatase, creatinine, urea, and uric acid and hence liver and renal dysfunction.
      LPS also increased serum levels of cholesterol and triglycerides and reduced glucose levels.
      Melatonin administration counteracted these organ and metabolic alterations at doses ranging between 20 and 60 mg/kg b.w.
      Melatonin significantly decreased lung lipid peroxidation and counteracted the LPSinduced NO levels in lungs and liver.
      Our results also show an inhibition of iNOS activity in rat lungs by melatonin in a dose-dependent manner.
      Expression of iNOS mRNA in lungs and liver was significantly decreased by melatonin (60 mg/kg b.w., 58–65%).
      We conclude that melatonin inhibits NO production mainly by inhibition of iNOS expression.
      The inhibition of NO levels may account for the protection of the indoleamine against LPS-induced endotoxemia in rats.
      Fullt text at :

    31. Migraine - A chronic sympathetic nervous system disorder
      Perouta SJ - Headache. 2004 Jan;44(1):53-64 - © 2004 Blackwell Publishing
      Objective - To determine the degree of diagnostic and clinical similarity between chronic sympathetic nervous system disorders and migraine.
      Background - Migraine is an episodic syndrome consisting of a variety of clinical features that result from dysfunction of the sympathetic nervous system.
      During headache-free periods, migraineurs have a reduction in sympathetic function compared to nonmigraineurs.
      Sympathetic nervous system dysfunction is also the major feature of rare neurological disorders such as pure autonomic failure and multiple system atrophy.
      There are no known reports in the medical literature, however, comparing sympathetic nervous system function in individuals with migraine, pure autonomic failure and multiple system atrophy.
      Methods - A detailed review of the literature was performed to compare the results of a wide variety of diagnostic tests and clinical signs that have been described in these 3 heretofore unrelated disorders.
      Results - The data indicate that migraine shares significant diagnostic and clinical features with both pure autonomic failure and multiple system atrophy, yet represents a distinct subtype of chronic sympathetic dysfunction.
      Migraine is most similar to pure autonomic failure in terms of reduced supine plasma norepinephrine levels, peripheral adrenergic receptor supersensitivity and clinical symptomatology directly related to sympathetic nervous system dysfunction.
      The peripheral sympathetic nervous system dysfunction is much more severe in pure autonomic failure than in migraine.
      Migraine differs from both pure autonomic failure and multiple system atrophy in that migraineurs retain the ability, although suboptimal, to increase plasma norepinephrine levels following physiological stressors.
      Conclusions - The major finding of the present study is that migraine is a disorder of chronic sympathetic dysfunction, sharing many diagnostic and clinical characteristics with pure autonomic failure and multiple system atrophy.
      However, the sympathetic nervous system dysfunction in migraine differs from pure autonomic failure and multiple system atrophy in that occurs in an anatomically intact system.
      It is proposed that the sympathetic dysfunction in migraine relates to an imbalance of sympathetic co-transmitters.
      Specifically, it is suggested that a migraine attack is characterized by a relative depletion of sympathetic norepinephrine stores in conjunction with an increase in the release of other sympathetic cotransmitters such as dopamine, prostaglandins, adenosine triphosphate and adenosine.
      An enhanced understanding of the sympathetic dysfunction in migraine may help to more effectively diagnose, prevent and/or treat migraine and other types of headache.
      Cfr. :

    32. Multiple co-infections (mycoplasma, chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients - Association with signs and symptoms
      Nicolson GL, Gan R, Haier J, The Institute for Molecular Medicine, Huntington Beach, California 92649, USA : - APMIS. 2003 May;111(5):557-66 - PMID: 12887507
      Previously we and others found that a majority of chronic fatigue syndrome (CFS) patients showed evidence of systemic mycoplasmal infections and their blood tested positive using a polymerase chain reaction assay for at least one of the four following Mycoplasma species : M. fermentans, M. hominis, M. pneumoniae or M. penetrans.
      Consistent with previous results, patients in the current study (n=200) showed a high prevalence (overall 52%) of mycoplasmal infections.
      Using forensic polymerase chain reaction we also examined whether these same patients showed evidence of infections with Chlamydia pneumoniae (overall 7.5% positive) and/or active human herpes virus-6 (HHV-6, overall 30.5% positive).
      Since the presence of one or more infections may predispose patients to other infections, we examined the prevalence of C. pneumoniae and HHV-6 active infections in mycoplasma-positive and -negative patients.
      Unexpectedly, we found that the incidence of C. pneumoniae or HHV-6 was similar in Mycoplasma-positive and -negative patients, and the converse was also found in active HHV-6-positive and -negative patients.
      Control subjects (n=100) had low rates of mycoplasmal (6%), active HHV-6 (9%) or chlamydial (1%) infections and there were no co-infections in control subjects.
      Differences in bacterial and/or viral infections in CFS patients compared to control subjects were significant.
      Severity and incidence of patients' signs and symptoms were compared within the above groups.
      Although there was a tendency for patients with multiple infections to have more severe signs and symptoms (p<0.01), the only significant differences found were in the incidence and severity of certain signs and symptoms in patients with multiple co-infections of any type compared to the other groups (p<0.01).
      There was no correlation between the type of co-infection and severity of signs and symptoms.
      The results indicate that a large subset of CFS patients show evidence of bacterial and/or viral infection(s), and these infections may contribute to the severity of signs and symptoms found in these patients.
      Cfr. :

    33. Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients
      Nasralla M, Haier J, Nicsolosn GL - European Journal of Clinical Microbiology and Infectious Diseases 1999; 18: 859-65
      Cfr. :

    34. Multiplex PCR for the detection of Mycoplasma fermentans, M hominis and M penetrans in patients with Chronic Fatigue Syndrome, Fibromyalgia, Rheumatoid Arthritis and Gulf War Syndrome
      Vojdani A, Franco AB - Journal of Chronic Fatigue Syndrome Chronic Fatigue Syndr 1999; ¾ : 187-97
      Cfr. :

    35. Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis and M. penetrans in cell cultures and blood samples of patients with Chronic Fatigue Syndrome
      Choppa PC, Vojdani A, Tagle C et al. - Mol Cell Probes 1998; 12: 301-308
      Cfr. :

    36. Mycoplasma infection and rheumatoid arthritis - Analysis of their relationship using immunoblotting and an ultrasensitive PCR
      Hoffman RW, O’Sullivan FX, Schafermeyer KR, Moore TL, Roussell D, Watson-McKown R et al. - Arthritis and Rheumatism 1997; 40: 1219-28
      Cfr. :

    37. Mycoplasmal Infections and Chronic /Fatigue Illness (Gulf War Illness) Associated with Deployment to Operation Desert Storm
      GL Nicholson, NL Nicholson, M Nasralla - Int J Med, 1997
      Cfr. :

    38. Mycoplasmal Infections in Blood from Patients with Chronic Fatigue Syndrome, Fibromyalgia Syndrome or Gulf War Illness
      G.L. Nicolson et al. - International CFS Congress, Sydney, Australia, 1998
      Cfr. :

    39. Mycoplasmal infections in chronic illnesses - Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis
      Nicolson GL, Nasralla M, Haier J, Erwin R, Nicolson NL, Ngwenya R - Med Sentinel 1999; 4:172-176
      Cfr. :

    40. Mycoplasmal infections in fatigue illnesses - Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness and Rheumatoid Arthritis
      Nicolson GL, Nasralla M, Franco AR, De Meirlier K, Nicolson NL, Ngwenya R, Haicr J - J. Chronic Fatigue Syndr, 2000;6(3):23-39
      Cfr. :

    41. Mycoplasmal infections--Diagnosis and treatment of Gulf War Syndrome/CFIDS
      Nicolson GL, Nicolson NL - CFIDS Chronicle  1966; 9(3):66-69
      Cfr. :

    42. Mycoplasmas - The Missing Link in Fatiguing Illnesses
      Michael Guthrie - Alternative Medicine; 2001; Sept: 60-70
      Cfr. :

    43. Myofascial trigger points in intercostal muscles secondary to herpes zoster infection of the intercostal nerve
      Shu-Min Chen MD, Jo-Tong Chen MD, Ta-Shen Kuan MD and Chang-Zern Hong MD, Department of Physical Medicine and Rehabilitation, National Cheng-Kung University Hospital, Tainan, Taiwan - Archives of Physical Medicine and Rehabilitation, Volume 79, Issue 3, March 1998, Pages 336-338 - © 1998 Published by Elsevier Science (USA)
      Cfr. :

    44. Neuroendocrine mechanisms in fibromyalgia–chronic fatigue
      Best Practice & Research Clinical Rheumatology, Volume 15, Issue 5, Pages 747-758 - © 2009 Elsevier B.V.
      Fibromyalgia and chronic fatigue syndrome are poorly understood disorders that share similar demographic and clinical characteristics.
      Because of the clinical similarities between both disorders it was suggested that they share a common pathophysiological mechanism, namely, central nervous system dysfunction.
      This chapter presents data demonstrating neurohormonal abnormalities, abnormal pain processing and autonomic nervous system dysfunction in fibromyalgia and chronic fatigue syndrome.
      The possible contribution of the central nervous system dysfunction to the development and symptomatology of these conditions is discussed.
      The chapter concludes by reviewing the effect of current treatments and emerging therapeutic modalities in fibromyalgia and chronic fatigue syndrome.
      Cfr. :

    45. New Treatments for Chronic Infections Found in CFS, Fibromyalgia Syndrome and Gulf War Illnesses
      Prof. Garth Nicolson - American Academy of Environmental Medicine Newsletter (Winter 1997)
      Cfr. :

    46. No serological evidence that fibromyalgia is linked with exposure to human parvovirus B19
      Narváez J, Nolla JM, Valverde J - Joint Bone Spine. 2005 Dec;72(6):592-4. Epub 2005 Mar 22 - PMID: 16376806
      Cfr. :

    47. Olanzapine for the treatment of fibromyalgia symptoms
      Kiser RS, Cohen HM, Freedenfeld RN, Jewell C, Fuchs PN, Texas Pain Medicine Clinic, 5327 N. Central Expressway, Dallas, TX 75205, USA - J Pain Symptom Manage. 2001 Aug;22(2):704-8
      Cfr. :

    48. Patients with rheumatoid arthritis are more tender than those with psoriatic arthritis
      Buskila D, Langevitz P, Gladman DD, Urowitz S, Smythe HA, University of Toronto Rheumatic Disease Unit, Wellesley Hospital, ON, Canada - J Rheumatol. 1992 Jul;19(7):1115-9 - PMID: 1512768
      Articular and nonarticular tenderness was examined in 51 patients with rheumatoid arthritis (RA) and 50 patients with psoriatic arthritis (PsA) by scored palpation and dolorimeter readings.
      Fifty-seven percent of patients with RA had 10 or more tender fibrositic points vs 24% of patients with PsA (p = 0.0008).
      Thresholds of tenderness measured by dolorimetry of 6 fibrositic point sites were 3.97 (1.99) [mean (SD)] for RA vs 5.95 (2.28) for PsA (p less than 0.0001).
      Thresholds over actively inflamed joints were 4.19 (1.53) for RA vs 6.78 (2.55) for PsA (p less than 0.0001).
      In both RA and PsA, fibrositic sites were more tender than actively inflamed joints (p less than 0.0001).
      Nonarticular control sites were also more tender in subjects with RA with dolorimeter thresholds at 5.99 (1.96) in RA vs 7.58 (1.60) in PsA (p less than 0.0001).
      These data demonstrate that actively inflamed joints, fibrositic and control nonarticular sites were all more tender in patients with RA than PsA.
      Both groups were similar in their disease duration and clinical assessments of joint inflammation and damage.
      We suggest that there may be a disease specific diffuse increase in tenderness in patients with RA, which is not related to joint inflammation.
      Similarly, the severity of articular inflammation may be underestimated in subjects with PsA.
      Cfr. :

    Go to Part VIII

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    Infection as one possible cause of fibromyalgia

    Part VIII

    1. Persistent active human herpesvirus six (HHV-6) infections in patients with chronic fatigue syndrome
      Knox KK, Brewer JH and Carrigan DR - J Chron Fatigue Syndr 1999;5:245-246
      Cfr. :

    2. Persons with chronic conditions - Their prevalence and costs
      Hoffman C, Rice D, Sung H-Y - JAMA 1996; 276:1473-1479
      Cfr. :
      Also read the comment on this article :
      The high cost of lost opportunities for prevention
      Havas S - JAMA. 1997 Feb 5;277(5):375-6 - PMID: 9010165
      Cfr. :

    3. Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature
      Gieffers J, van Zandbergen G, Rupp J, Sayk F, Krüger S, Ehlers S, Solbach W, Maass M, Institute for Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany : - Eur Respir J. 2004 Apr;23(4):506-10 - PMID: 15083745

      Chlamydia pneumoniae, a major cause of community-acquired pneumonia, primarily infects the respiratory tract.
      Chronic infection of nonrespiratory sites, such as the vascular wall, the brain or blood monocytes, requires evasion from the lungs and spreading via the bloodstream.
      The cell types involved in dissemination are insufficiently characterised.
      In this study, New Zealand White rabbits were infected intratracheally with C. pneumoniae, and lung manifestation and systemic dissemination were monitored by polymerase chain reaction and immunohistochemistry.
      Infection of the lungs was characterised by an early phase dominated by granulocytes and a late phase dominated by alveolar macrophages (AM). Granulocytes, AM and alveolar epithelial cells acted as host cells for chlamydiae, which remained detectable for up to 8 weeks.
      AM transported the pathogen to the peribronchiolar lymphatic tissue and subsequently C. pneumoniae entered the spleen and the aorta via dissemination by peripheral blood monocytes.
      In conclusion, Chlamydia pneumoniae-infected alveolar macrophages transmigrate through the mucosal barrier and give the pathogen access to the lymphatic system and the systemic circulation.
      Infected peripheral blood monocytes are the vector system within the bloodstream and transmit the infection to the vascular wall.
      This is the first description of granulocytes acting as a reservoir for Chlamydia pneumoniae early in infection.
      Cfr. :
      Also read the comment on this article :
      Chlamydia pneumoniae - Crossing the barriers ?
      Blasi F, Centanni S, Allegra L - Eur Respir J. 2004 Apr;23(4):499-500 - PMID: 15083742
      Cfr. :

    4. Pioneering fibromyalgia doctor continues to advance understanding
      The MiFio Network
      Fibromyalgia, a chronic, widespread pain in muscles and soft tissues accompanied by fatigue, is a fairly common condition that does not manifest any structural damage in an organ.
      Twenty-five years ago, Muhammad B. Yunus, MD and colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome.
      That seminal article, published in Seminars in Arthritis and Rheumatism, led directly to formal recognition of this disease by the medical community.
      In the June 2007 issue of Seminars in Arthritis and Rheumatism, Dr. Yunus once again makes an important contribution to the field of chronic pain and fatigue by meticulously synthesizing and interpreting the extensive body of scientific literature on fibromyalgia and his own insights into the concept of central sensitivity syndromes (CSS).
      Fibromyalgia, affecting approximately 2% of the US population, is an example of a class of maladies called CSS.
      These diseases are based on neurochemical abnormalities and include irritable bowel syndrome, migraine and restless legs syndrome.
      Incorporating a critical review of over 225 publications and the author's broad experience in fibromyalgia and related diseases, Dr. Yunus describes 13 separate conditions that are related to central sensitization (CS), where the central nervous system (spinal cord and brain) becomes extremely sensitized on certain parts of the body, so that even mild pressure or touch would cause much pain.
      Such hypersensitivity may also be associated with other symptoms such as poor sleep and fatigue.
      According to Dr. Yunus : "CSS are the most common diseases that are based on real neurochemical pathology and cause real pain and suffering. In some patients stress and depression may contribute to the symptoms but they are all based on objective changes in the central nervous system".
      Dr. Norman L. Gottlieb, Editor of Seminars in Arthritis and Rheumatism, believes that this article "advances our understanding of fibromyalgia, unifies and advances concepts and suggests that this and several other common disorders have much in common in terms of their biopsychosocial development. This, hopefully, will expand both clinical and research interest in this group of diseases and lead to advances in therapy for many of them".
      In an accompanying editorial John B. Winfield, MD, comments : "Without question, Muhammad Yunus is the father of our modern view of fibromyalgia.... Yunus, who took a rather more biological approach to fibromyalgia in the past, now emphasizes a biopsychosocial perspective. In my view, this is tremendously important because it is the only way to synthesize the disparate contributions of such variables as genes and adverse childhood experiences, life stress and distress, posttraumatic stress disorder, mood disorders, self-efficacy for pain control, catastrophizing, coping style and social support into the evolving picture of central nervous system dysfunction vis-a-vis chronic pain and fatigue ....Science and medicine now have a rational scaffolding for understanding and treating chronic pain syndromes previously considered to be 'functional' or 'unexplained.' ...Neuroscience research will continue to reveal the mechanisms of CS, but only if informed through a biopsychosocial perspective and with the interdisciplinary collaboration of basic scientists, psychologists, sociologists, epidemiologists and clinicians".
      Dr. Yunus concludes that CSS is an important new concept that embraces the biopsychosocial model of disease.
      He advocates further critical studies to fully test this concept which seems to have important significance for new directions for research and patient care involving physician and patient education.
      "Each patient, irrespective of diagnosis," says Dr. Yunus, "should be treated as an individual, considering both the biological and psychosocial contributions to his or her symptoms and suffering".
      The article is "Fibromyalgia and overlapping disorders - The unifying concept of central sensitivity syndromes" by Muhammad B. Yunus, MD, Professor of Medicine, Section of Rheumatology, The University of Illinois College of Medicine at Peoria, Peoria, Illinois (cfr. : -).
      The accompanying editorial is "Fibromyalgia and related central sensitivity syndromes - Twenty-five years of progress" by John B. Winfield, MD, University of North Carolina School of Medicine. Both appear in the June issue of Seminars in Arthritis and Rheumatism, Vol. 36:6, published by Elsevier (cfr. : -).
      Cfr. :

    5. Population study of tender point counts and pain as evidence of fibromyalgia
      Croft P, Schollum J, Silman A, Arthritis and Rheumatism Council Epidemiology Research Unit, University of Manchester - BMJ. 1994 Sep 17;309(6956):696-9 - PMID: 7950521
      - To determine the relation between tender points, complaints of pain and symptoms of depression, fatigue and sleep quality in the general population.
      - Two stage cross sectional study with an initial questionnaire about pain to classify those eligible for an examination of tender points.
      - Two general practices in north west England.
      - Stratified random sample of adults from age-sex registers.
      Of the responders, 250 were selected for examination of tender points on the basis of their reported pain complaints; 177 subsequently participated.
      Main outcome measures
      - Tender point count (0 to 18) grouped into four categories with the highest (> or = 11) corresponding to the criteria of the American College of Rheumatology for fibromyalgia.
      Assessment of pain (chronic widespread, regional, none).
      Measures of depression, fatigue and difficulty with sleeping.
      - Women had a higher median tender point count (six) than did men (three).
      Counts were higher in those with pain than in those who had no pain and in those with widespread compared with regional pain.
      Most subjects with chronic widespread pain, however, had fewer than 11 tender points (27/45; 60%).
      Two people with counts of 11 or more were in the group reporting no pain.
      Mean symptom scores for depression, fatigue and sleep problems increased as the tender point count rose (P value for trend < 0.001).
      These trends were independent of pain complaints.
      - Tender points are a measure of general distress.
      They are related to pain complaints but are separately associated with fatigue and depression.
      Sleep problems are associated with tender points, although prospective studies are needed to determine whether they cause tenderness to develop.
      Fibromyalgia does not seem to be a distinct disease entity.
      Cfr. :

      Also read the comment ons this article :
      Chronic fatigue syndrome and fibromyalgia
      Ho-Yen DO - BMJ. 1994 Dec 3;309(6967):1515 - PMID: 7804073
      Cfr. :

    6. Positron emission tomography in patients with fibromyalgia syndrome and healthy controls
      Muhammad B. Yunus 1 *, Carter S. Young 2, S. Atezaz Saeed 1, James M. Mountz 3, Jean C. Aldag 1 - 1University of Illinois College of Medicine at Peoria - 2Methodist Medical Center of Illinois, Peoria, Illinois - 3School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania - E-mail : Muhammad B. Yunus : - *Correspondence to : Muhammad B. Yunus, Department of Medicine, University of Illinois College of Medicine at Peoria, PO Box 1649, Peoria, IL 61656
      Objective - Abnormal brain findings have previously been described in fibromyalgia syndrome (FMS) by single-photon-emission computed tomography.
      Our goal was to investigate change in regional cerebral glucose metabolism in people with FMS by positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG).
      Methods - Twelve patients with FMS and no comorbid psychiatric diagnosis and 7 healthy pain-free controls were studied with FDG-PET in a blinded manner.
      Those with a psychiatric diagnosis were excluded.
      Brain scans were obtained using a PET scanner.
      Semiquantitative analysis of regional 18F-FDG uptake was performed in both cortical and subcortical brain structures.
      Results - In the resting state, there were no significant differences in 18F-FDG uptake between patients and controls for all brain structures measured.
      Conclusion - FDG-PET scan findings in FMS were not significantly different from healthy controls.
      Normal results in our study may be explained by discordance between regional cerebral blood flow and regional cerebral glucose metabolism.
      Cfr. :

    7. Reactive Fibromyalgia Syndrome”
      Dr. S. Greenfield (1992)
      Cfr. :

    8. Research Overview - Professor Garth Nicolson's Studies and Treatments Explained
      Deborah Cooper - Treatment & Research Library, November 14, 2000
      Cfr. :

    9. Review of juvenile primary fibromyalgia and chronic fatigue syndrome
      Breau LM, McGrath PJ, Ju LH, Department of Psychology, Dalhousie University, Halifax, Canada - J Dev Behav Pediatr. 1999 Aug; 20(4):278-88 - PMID: 10475602
      This article reviews the current literature on childhood fibromyalgia and chronic fatigue syndrome.
      In doing so, it questions assumptions about the presumed nature of the disorders-that they are distinct from each other and are duplicates of their adult counterparts.
      It also attempts to synthesize the available data to reach some preliminary judgments about these disorders : that fibromyalgia and chronic fatigue syndrome may be related in children and may not be duplicates of the adult disorders; that psychological and psychosocial factors are unlikely contributors to the etiology of these disorders; and that the evidence is increasingly pointing to a role for genetic factors in their etiology.
      A discussion of the research into treatments for childhood fibromyalgia and chronic fatigue syndrome highlights the lack of well-designed, controlled studies.
      Finally, directions for future research are offered where results of the current literature are unclear.
      Cfr. :

    10. Role of Mycoplasmal infections in Fatigue Illnesses - Chronic Fatigue and Fibromylagia Syndromes, Gulf War Illness and Rheumatoid Arthritis
      Nicolson GL, Nasralla MY, Franco AR, De Meirleir K, Nicolson NL, Ngwenya R, Haier J - Journal of Chronic Fatigue Syndrome 2000; 6: 23-39
      Cfr. :

    11. Studying Tenderness - A Clue to Understanding Fibromyalgia
      P Langevitz, D Buskila - Isr J Med Sci, 1992; 28:" 41-42
      Cfr. :

    12. The "Chronic Active Epstein-Barr Virus Infection" Symdrome and Primary Fibromyalgia
      D Buchwald, DL Goldenberg, JL Sullivan, AL Komaroff - Arth & Rhu, 1987; 30:10, 1132-1136
      Cfr. :

    13. The chlamydia pneumoniae handbook
      This "Handbook" is an attempt to organize and pull together information on Chlamydia pneumoniae, it's impact on human diseasesi and it's treatment via combined antibiotic protocolsi into a more easily accessible, organized and up to date format.
      Some of the material has already been posted on - website and is simply linked here in a more organized way.
      Some of the material in this handbook is new and represents the most current, state of the art information on Cpn, CAPi, and the various supplementsi which have been found helpful in clinical experience.
      We will endeavor to update and expand the Cpn Handbook as new information becomes available.
      Cfr. :

    14. The chronic fatigue syndrome - A return to common sense
      Denman AM, Division of Immunological Medicine, Northwick Park Hospital, Harrow, Middlesex, UK - Denman AM. Postgrad Med J. 1990 Jul; 66(777):499-501 - Postgrad Med J. 1990 Jul;66(777):499-501 - PMID: 2217006
      Cfr. :

    15. The chronic fatigue syndrome - Definition, current studies and lessons for fibromyalgia research
      Komaroff AL, Goldenberg D, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115 - J Rheumatol Suppl. 1989 Nov;19:23-7 - PMID: 2691680
      Chronic fatigue syndrome (CFS) is characterized by chronic, debilitating fatigue lasting greater than 6 months.
      Frequent chronic and recurrent findings include fever, pharyngitis, myalgias, adenopathy, arthralgias, difficulties in cognition and disorders of mood.
      In the majority of patients, the illness starts suddenly with an acute, "flu-like" illness.
      The following laboratory abnormalities are seen with some frequency, although none are seen in all patients: lymphocytosis, atypical lymphocytosis, monocytosis, elevation of hepatocellular enzymes, low levels of antinuclear antibodies, varying levels of antithyroid antibodies, partial hypergammaglobulinemia, elevated CD4:CD8 ratio, decreased cytolytic activity of natural killer cells and low levels of immune complexes.
      Clinical and serologic studies suggest an association of CFS with all of the human herpesviruses, particularly Epstein-Barr virus (EBV) and the recently discovered human B lymphotropic virus (HBLV) or human herpesvirus 6; neither EBV nor HBLV has yet been shown to play a causal role in the illness.
      Preliminary evidence suggests that many of these features of CFS also are seen in patients with fibromyalgia.
      Cfr. :

    16. The fibromyalgia spectrum - Part of the big picture in understanding fibromyalgia
      Excerpted from 'Fibromyalgia - Up close and personal' by Mark J. Pellegrino, MD - July 29, 2009 - © 2009 ProHealth, Inc.
      As a senior resident at The Ohio State University in 1988, I gave a lecture on fibromyalgia at the Physical Medicine Grand Rounds.
      One of my lecture slides was entitled “Fibromyalgia - A spectrum of conditions ?”.
      I discussed how Fibromyalgia appears to be a “broader” condition with specific subsets.
      Fibromyalgia was in that area between normal and disease – the “gray” area.
      Some of the subsets were closer to normal, involving regional pain only or milder symptoms without numerous associated conditions.
      Some subsets were closer to abnormal, with some features of connective tissue or rheumatic diseases, but were not quite “there.”
      Today I’m convinced fibromyalgia is indeed a “broader” condition with various subsets.
      I believe this information is helpful in explaining why everyone’s symptoms are different even though they all have fibromyalgia.
      This chapter addresses how the fibromyalgia spectrum is part of the big picture in understanding fibromyalgia.
      Fibromyalgia is a distinct medical entity and appropriately so
      We have long recognized, however, that many conditions overlap it and various conditions exist that can lead to secondary fibromyalgia.
      Dr. Muhammad Yunus, MD, [a professor and FM specialist at the University of Illinois College of Medicine] has developed the concept of Dysregulation Spectrum Syndrome (DSS) to describe how conditions overlap.
      --- Mohammad B. Yunus, a professor at the University of Illinois College of Medicine, was the first to publish a study describing FM’s clinical characteristics 25 years ago.
      In 2000 he published the article “
      Central Sensitivity Syndromes: A unified concept for Fibromyalgia and other similar maladies” (cfr. : -). And recently in June 2007, Yunus et al. published a report in the journal Seminars in Arthritis and Rheumatism suggesting that fibromyalgia and overlapping disorders be categorized as “Central Sensitivity Syndromes” (CSS), based on “mutual associations” and evidence for central sensitization (hypersensitization of the central nervous system) among several of the disorders (cfr. “Fibromyalgia and Overlapping Disorders - The Unifying Concept of Central Sensitivity Syndromes” at : -) ---
      Dr. Yunus describes DSS as representing various associated conditions that share similar clinical characteristics and pathologic mechanisms with fibromyalgia.
      Ten conditions are in the DSS umbrella : fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, tension headaches, migraine headaches, primary dysmenorrhea, periodic limb movement disorder, restless leg syndrome, temporomandibular pain syndrome and myofascial pain syndrome.
      He predicts other entities will be added to this list in the future.
      According to Dr. Yunus, conditions in DSS share a number of characteristics
      - Patients with different conditions sharing similar profiles;
      - Common shared symptoms, such as pain, poor sleep, fatigue and female predominance.
      - Hypersensitivity to pain;
      - No “diagnostic” pathology that can be measured;
      - Shared psychological complaints such as depression and anxiety;
      - Shared common genetic factor likely;
      - Common neurohormonal dysfunctions;
      - Treatments directed at the central nervous system leading to improvement;
      - TMJ [temporomandibular joint] dysfunction.
      I have discussed the fibromyalgia spectrum with my patients to help them understand the various subsets possible.
      I do not see fibromyalgia as a member of a bigger family, but as the main condition.
      It is the “founding father” and keeps its name.
      If fibromyalgia is the founding father, then the various overlapping conditions and subsets become the children.
      The name 'fibromyalgia' remains, but different subsets have unique characteristics and together they become the fibromyalgia spectrum.
      This diagram shows the concept of the Fibromyalgia spectrum.
      The fibromyalgia entity partially overlaps with the normal entity on one side and the disease entity on the other side.
      Within the fibromyalgia entity are 8 subsets.
      The first subset is in the most “normal” portion of fibromyalgia and the 8th subset is in the most “diseased” portion of fibromyalgia.
      Each number represents a distinct subset with distinct characteristics.
      --- Cfr. : ---
      The eight subsets of the fibromyalgia spectrum
      - Predisposed state;
      - Prodromal [preceding] state;
      - Undiagnosed fibromyalgia;
      - Regional fibromyalgia;
      - Generalized fibromyalgia.
      - Fibromyalgia with particular associated conditions;
      - Fibromyalgia with coexisting mild disease;
      - Secondary fibromyalgia reactive to disease.
      An individual can move up this spectrum – from a lower numbered subset to a higher numbered subset, but once in a particular subset, she/he does not return to a lower numbered subset.
      One can achieve a remission, but stays in that subset.
      In other words, there is no going back.
      Let’s review the features of each subset.

      Subset 1: Predisposed state
      The individual is asymptomatic.
      Clinical fibromyalgia is not present in this state.
      The individual is at risk for developing fibromyalgia due to hereditary factors, which may include one or both parents with fibromyalgia or a rheumatic/connective tissue disease or a sibling or first-degree relative with fibromyalgia.
      Subset 2 - Prodromal state
      Prodromal means preceding or the state leading to the condition.
      Clinical fibromyalgia is still not present.
      There is no widespread pain or painful tender points.
      The individual is not asymptomatic, however.
      Associated conditions common with fibromyalgia may be present in this stage, such as headaches, restless leg syndrome, fatigue or irritable bowel syndrome.
      Pain may be present at times, but intermittently (not chronic, persistent pains).
      Even though the individual may have one or more associated condition(s), widespread persistent pain is not present, so therefore Fibromyalgia is not yet present.
      Typical fibromyalgia pain must be present before we can diagnose clinical fibromyalgia, no matter how many associated conditions may be present, but those who have numerous associated conditions are at risk.
      Subset 3 - Undiagnosed fibromyalgia
      Chronic pain is now present, either regional or generalized in nature.
      This is the point of no return.
      The person has painful tender points which may or may not meet the American College of Rheumatology-defined 11 of 18 criteria.
      The person in this stage usually has milder symptoms and has not yet seen a doctor or been officially diagnosed with fibromyalgia.
      If this individual were to see a knowledgeable physician, that diagnosis would be made.
      Subset 4 - Regional fibromyalgia
      Individuals in this stage have been diagnosed with fibromyalgia, but not generalized.
      Chronic pain is limited to one or a few areas such as the upper body or the low back.
      The symptoms may wax and wane.
      Usually, this subset is triggered by a trauma.
      I believe myofascial pain syndrome is part of this regional fibromyalgia and both terms are essentially synonymous.
      Myofascial pain syndrome has become familiar through the work of the late Dr. Janet Travell, MD and Dr. David Simons, MD.
      --- Drs. Travell and Simons are authors of the two-volume set 'Travell & Simons' Myofascial Pain and Dysfunction - The Trigger Point Manual
      ' – cfr. : ---
      Myofascial pain syndrome is defined by painful muscles and the presence of triggerpoints and taut bands of muscle fibers which are ropey and painful when palpated.
      An involuntary shortening of the fibrous muscle band can create a local twitch response.
      Some of those who work with myofascial pain syndrome will argue that it is a separate distinct entity from fibromyalgia.
      I disagree.
      The similarities between myofascial pain syndrome and fibromyalgia are far greater than their differences.
      They both have trigger points, tender points, ropey muscles, sympathetic nerve dysfunction, ATP abnormalities, peripheral and central mechanisms, regional and generalized versions and associated conditions.
      Sound familiar ?
      The treatments are essentially the same.
      As our clinical experience has evolved and our knowledge and research have become more refined, I think it is clear that myofascial pain syndrome is a part of the overall fibromyalgia spectrum.
      Individuals with regional fibromyalgia, over time, often develop generalized fibromyalgia.
      Or they can remain in this stage indefinitely.
      Identifying the regional stage early and treating it can definitely help to prevent progression.
      Subset 5 - Generalized fibromyalgia
      Individuals in this stage have widespread pain and tender points.
      They will usually meet the American College of Rheumatology-defined 11 of 18 criteria, but as previously explained, one can still have generalized fibromyalgia with fewer tender points.
      Various associated conditions seen with fibromyalgia can be present – sleep disorder, irritable bowel syndrome, depression, fatigue and so on.
      These associated conditions are not taking on a life of their own, so to speak, but are part of the whole and managed with the overall fibromyalgia treatment.
      Regional fibromyalgia can progress to this subset.
      Various causes of generalized fibromyalgia include genetic factors, trauma, infections and more, but secondary fibromyalgia from a primary disease is not included in this subset.
      Subset 6 - Fibromyalgia with particular associated conditions
      People in this group have developed associated conditions that are giving them particular problems which appear as “separate” entities requiring separate attention.
      Some of these particular associated conditions include irritable bowel syndrome, chronic fatigue syndrome [ME/CFS], fatigue, tension/migraine headaches and depression.
      None of these conditions in themselves have “classic” disease laboratory markers or cause tissue destruction, yet they may require treatments in addition to the overall fibromyalgia treatment.
      Another associated condition is dysautonomia (dysfunction of the small nerves), which can cause abnormalities such as hypoglycemia [low blood sugar], hypotension [low blood pressure], cardiac arrhythmia, irritable bowel syndrome and vascular headaches.
      Subset 7 - Fibromyalgia with coexisting disease
      Individuals in this category have a specific disease and also have fibromyalgia.
      The disease doesn’t necessarily cause fibromyalgia, but can aggravate it if it’s already present.
      Examples of diseases that can be present and worsen the fibromyalgia symptoms include :
      - hormonal problems (hypothyroidism, low estrogen, low growth hormone and low cortisol);
      - infectious problems (yeast, parasite or viral infections);
      - low grade rheumatic or connective tissue disease (lupus, autoimmune disorders, dry eyes syndrome described by Dr. Don Goldenberg, MD, [Chief of Rheumatology at Newton-Wellesley Hospital and Professor of Medicine at Tufts University School of Medicine] may be part of a low grade Sjogren’s syndrome);
      - arthritic conditions (cervical spinal stenosis, osteoarthritis, osteoporosis, scoliosis);
      - neurological conditions (multiple sclerosis, polio sequelae, neuropathy, head injury residuals), for example, people who have both diabetes and fibromyalgia will often have more painful fibromyalgia because the diabetes caused the nerves to be more sensitive (diabetes is a common cause of neuropathy or damage to the small nerves, which is painful in itself and even more so with fibromyalgia; one needs to keep the diabetes under good control to help the pain);
      - lung conditions (I see a number of people who have fibromyalgia along with a lung problem such as emphysema, asthma, chronic bronchitis, or heavy tobacco use; cigarette smoking can increase fibromyalgia pain; the nicotine in the smoke causes constriction of the blood vessels, decreasing blood flow, oxygen and nutrients to the muscles, thereby increasing pain and spasms; also, carbon monoxide in smoke enters the bloodstream and binds to the hemoglobin molecules in the blood. this blocks oxygen from binding to the hemoglobin, further decreasing oxygen availability to the muscles (and increasing pain); stop smoking and your muscles will feel better !
      These diseases exist concurrently with fibromyalgia but probably do not cause it.
      Any of these diseases can progress from a mild to a more severe state and fibromyalgia worsens as the disease worsens.
      The physician determines if the disease is coexisting with and aggravating fibromyalgia (subset 7) or if a disease caused the fibromyalgia (subset 8).
      Subset 8 - Secondary fibromyalgia reactive to disease
      Individuals in this category have secondary fibromyalgia.
      They have a primary disease (for example lupus, rheumatoid arthritis) - and fibromyalgia developed as a result of this disease.
      People in this subset probably wouldn’t have fibromyalgia if they never had the primary disease.
      The primary disease requires treatment and Fibromyalgia may improve with this treatment.
      However, the fibromyalgia often requires its own treatment and can continue to be a major problem even when the primary disease is treated or is in remission.
      Overall - A useful explanatory model
      I find that the fibromyalgia spectrum provides a useful clinical model for me when evaluating and treating my patients.
      It helps me to “organize” them better !
      When I diagnose fibromyalgia, I try to be as specific as possible about what the cause is and what subset it fits.
      This helps me to better explain fibromyalgia to the patients and to individualize their treatment programs.
      Of course, if I’ve diagnosed fibromyalgia it would be subset 4 or greater.
      The patient wouldn’t be seeking a medical consultation for subsets 3, 2 or 1.
      If possible, I note the cause.
      Each subset can have flare-ups or remissions within it and I note that as well, if appropriate.
      Subsets 1, 2 and 3 [predisposed state, prodromal state, undiagnosed fibromyalgia] are useful in appreciating the progression of fibromyalgia through the spectrum and can be helpful when advising patients and family members who have specific concerns and questions.
      Let’s review some patient profiles to determine the subset they fit into in the fibromyalgia spectrum
      Patient #1
      Mary is a 25-year-old receptionist with severe neck and shoulder pain.
      She had always been very active with aerobics and bicycling and had never had any pain requiring treatment until after a motor vehicle accident… when she was rear-ended and suffered a whiplash injury.
      The pain never went away and when I saw her I found numerous painful tender points and trigger points with localized spasms in the neck and shoulder muscles.
      Mary has regional fibromyalgia (subset 4).
      She was most likely predisposed to fibromyalgia and a traumatic event triggered the development of her regional fibromyalgia.
      She “leaped” from predisposed state (subset 1) to regional fibromyalgia (subset 4).
      Patient #2
      Martha is a 30-year-old housewife.
      She was diagnosed with Fibromyalgia 5 years ago and she was at a stable baseline with her home program of stretches, exercises and using a hot tub.
      In the past year, she has been having increasing pain and fatigue and difficulty managing her fibromyalgia.
      She reports that in the past year she has been getting frequent yeast infections.
      She is on birth control pills and has had a couple of bladder infections requiring antibiotics in the past year.
      Her more recent history is otherwise unremarkable.
      Martha has fibromyalgia with a coexisting disease - chronic yeast infection (subset 7).
      Her birth control pills, antibiotic treatment and perhaps fibromyalgia have contributed to the chronic yeast infection.
      In turn, the yeast infection has aggravated her fibromyalgia (cfr. also Dr. Pellegrino’s explanation of “Candidiasis – Yeast infection and nutritional repair” at : -].
      Patient #3
      Jamie is a 38-year-old school teacher.
      She has lupus, diagnosed when she was 13 years old and has been on various medications since then.
      She has been in remission for a number of years, but has developed widespread pain.
      Her sedimentation rate is not elevated to suggest active inflammation.
      Her clinical exam does not reveal any joint inflammation or active lupus findings, but she does have 16 of 18 painful tender points.
      Jamie has secondary fibromyalgia from a disease (subset 8).
      In her case, the lupus is in remission, but her fibromyalgia is causing her problems and needs to be treated.
      Patient #4
      Jamie’s 12-year-old son has been complaining of leg pains.
      The pains occur at nighttime and Jamie has to rub the legs and use warm compresses.
      The pediatrician told her his pains were growing pains.
      Jamie’s son gets occasional headaches and sometimes he feels exhausted.
      He plays many sports and if he works out a lot his muscles are very sore for several days.
      On exam, there are no areas of pain or painful tender points.
      Jamie’s son is probably in a prodromal state (subset 2).
      He is at risk because his mother has fibromyalgia and a connective tissue disease and he has some associated conditions with intermittent pains, but has not developed the persistent widespread pain or painful tender points yet.
      Patient #5
      Bob is 42 years old and has an awful lot of pain for his age.
      His pains are more severe than everyday pain and sometimes he has had to miss work.
      He is an assembly line worker.
      He mentions this to his primary care doctor when he is there for his yearly physical.
      He is examined and found to have 12 of 18 positive painful tender points.
      Bob had undiagnosed Fibromyalgia (subset 3) until he became official, “entering the books” with generalized fibromyalgia (subset 5) after he saw his primary care doctor.
      In conclusion
      There is much disagreement and controversy among medical professionals and patients about categories and subsets of fibromyalgia or similar conditions.
      I'm not attempting to stir the waters with my version of the fibromyalgia spectrum - rather I'm trying to help you understand the fairly complicated nature of the condition and the different types I see.
      I find this model useful and practical in my everyday clinical practice.
      Remember one of my mottos : keep things as simple as possible and make sure they make sense !
      --- This chapter of 'Fibromyalgia - Up close and personal' also offers a "Fibromyalgia spectrum test" that outlines several cases, posing questions about them and provides the answers ---
      Cfr. :

    17. The Fibromyalgia Syndrome, Primer on the Rheumatic Diseases
      B Freundlich, L Leventhal - Arthritis Found, 1993; 247-249

    18. The immune system, atherosclerosis and persisting infection
      Pigarevskii P V; Mal'tseva S V; Seliverstova V G, Vestnik Rossiiskoi akademii meditsinskikh nauk - Rossiiskaia akademiia meditsinskikh nauk 2005;(2):17-22
      The paper demonstrates that lymph nodes situated in the vicinity of magistral blood vessels are the source of immune and inflammatory response to LDL as the main pathogenetic factor in atherosclerosis.
      The activation of T-cell-mediated immunity takes place in them at the very early stages of the disease, resulting in forming of CD4+T-lymphocytes, activated mononuclear cells and immunostabilizing B-lymphocytes.
      The cell changes in lymph nodes correlate with the severity of atherosclerotic lesions in the vessel intima and closely reflect the peculiarities of immune inflammation development in fatty streaks and atherosclerotic plaques in human atherogenesis.
      A paradoxical reaction was observed in cases with Chlamydia pneumoniae found in the wall of aorta and paraaortal lymph nodes.
      No evident immune response on the part of immunocompetent cells took place, but, on the contrary, the function of mononuclear cells, including T-lymphocytes, was suppressed.
      This phenomenon may be explained by the fact that intracellulari localization of Chlamydia pneumoniae hides it from immune system control or by the possible microorganism capability of direct immunosuppressive influence on lymphoid cells both in the blood vessel wall and in regional lymph nodes.
      Cfr. :

    19. The importance of B-cells and ecto-5'nucleotidase in Mycoplasma fermentans infection and the relevance to rheumatoid arthritis
      Johnson SM, Department of Basic Medical Sciences, St. George's University of London, London, UK : - Immunology. 2008 Feb;123(2):187-96. Epub 2007 Aug 4 - PMID: 17680797
      The aim of this work was to discover if Mycoplasma fermentans, which is known to infect B cells, could be the cause of the raised ecto-5'-nucleotidase observed in the synovial fluid of rheumatoid arthritis patients.
      The ecto-5'-nucleotidase activity in the patients' serum has been shown to correlate with the erythrocyte sedimentation rate and DNA from the mycoplasma has been found in the synovial fluid.
      B lymphoblastoid cell lines were exposed to 16 strains of Mycoplasma fermentans and their ecto-5'-nucleotidase, CD73, was measured both biochemically and by mouse antibodies to human ecto 5'-nucleotidase using the fluorescence activated cell sorter.
      The type strain, PG 18, did not grow with the B cells.
      Some of the mycoplasma strains (9/15) increased the cellular ecto-5'-nucleotidase activity from twice to 17 fold, and usually showed 5'-nucleotidase activity themselves.
      At least one strain, M106, induced human 5'-nucleotidase on the normally 5'-nucleotidase negative Daudi and Raji Burkitt's lymphoma cell lines, and increased sevenfold the 5'-nucleotidase on the monocyte/macrophage cell line THP-1.
      Growing the cells in aged medium increased the level of mycoplasma infection.
      This mycoplasma-induced enzyme showed a conformational change and an increase in activity with a glycosylation change involving mannose groups.
      The other group of strains, mostly of respiratory or cell culture origin, usually did not have any 5'-nucleotidase of their own and decreased the B-cell enzyme activity by about half.
      Electron microscopy and flow cytometry showed that the strain M106 was filamentous and could be found inside the B-cells.
      The 5'-nucleotidase-inducing strains of M. fermentans may be important in the aetiology of rheumatoid arthritis.
      Cfr. :

    20. The pathogenesis and treatment of mycoplasmal infections
      Nicolson GL, Nasralla M, Nicolson NL - Antimicrob Infect Dis Newsl 1999; 17(11):81-88
      Cfr. :

    21. The prevalence of Mycoplasma incognitus in the peripheral blood mononuclear cells of normal controls or patients with AIDS or Chronic Fatigue Syndrome
      Huang W, See D, Tiles J - J Clin Microbiol 1998; 231:457-467
      Cfr. :

    22. The Role of Chronic Infections in the Maintenance and Progression of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, Rheumatoid Arthritis, Immune Deficiency Syndromes and Gulf War Illness
      G.L. Nicolson et al. - ME/CFS Congress, Sydney, Australia, 1999
      Cfr. :

    Go to Part IX

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Infection as one possible cause of fibromyalgia - Part IX
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    Infection as one possible cause of fibromyalgia

    Part IX

    1. The role of gender in fibromyalgia syndrome
      Muhammad B. Yunus, College of Medicine at Peoria, University of Illinois, One Illini Drive, PO Box 1649, 61656 Peoria, IL, USA : - Current Rheumatology Reports, Volume 3, Number 2 / March, 2001
      Fibromyalgia syndrome (FMS), characterized by widespread pain and tenderness on palpation (tender points), is much more common in women than in men in a proportion of 9:1.
      Two recent studies have shown important gender differences in various clinical characteristics of FMS.
      In a community and a clinic sample, women experienced significantly more common fatigue, morning fatigue, hurt all over, total number of symptoms and irritable bowel syndrome.
      Women had significantly more tender points.
      Pain severity, global severity and physical functioning were not significantly different between the sexes, nor were psychologic factors eg, anxiety, stress and depression.
      Gender differences have also been observed in other related syndromes eg, chronic fatigue syndrome, irritable bowel syndrome and headaches.
      The mechanisms of gender differences in these illnesses are not fully understood, but are likely to involve an interaction between biology, psychology and sociocultural factors.
      Cfr. :

    2. The role of microorganism infections in chronic illnesses - Support for antibiotic regimens
      Nicolson GL - CFIDS Chronicle 1999; 12(3):19-21
      Cfr. :

    3. Traumatic events, health outcomes and health care use in patients with fibromyalgia
      Dr. H.R. Walen - Journal of Musculoskeletal Pain, 2001
      Cfr. :

    4. Travell & Simons' Myofascial Pain and Dysfunction - The Trigger Point Manual (2-Volume Set)
      Drs. Travell and Simons - Lippincott Williams & Wilkins - ISBN-10: 0683307711 - ISBN-13: 978-0683307719

      Cfr. :

    5. Treatment with staphylococcus toxoid in fibromyalgia/chronic fatigue syndrome – A randomised controlled trial
      Zachrisson O, Regland B, Jahreskog M, Jonsson M, Kron M, Gottfries CG, Psychiatry Section, Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden : - Eur J Pain. 2002;6(6):455-66 - PMID: 12413434
      We have previously conducted a small treatment study on staphylococcus toxoid in fibromyalgia (FM) and chronic fatigue syndrome (CFS).
      The aim of the present study was to further assess the efficacy of the staphylococcus toxoid preparation Staphypan Berna (SB) during 6 months in FM/CFS patients.
      One hundred consecutively referred patients fulfilling the ACR criteria for FM and the 1994 CDC criteria for CFS were randomised to receive active drug or placebo.
      Treatment included weekly injections containing 0.1 ml, 0.2 ml, 0.3 ml, 0.4 ml, 0.6 ml, 0.8 ml, 0.9 ml and 1.0 ml SB or coloured sterile water, followed by booster doses given 4-weekly until endpoint.
      Main outcome measures were the proportion of responders according to global ratings and the proportion of patients with a symptom reduction of > or =50% on a 15-item subscale derived from the comprehensive psychopathological rating scale (CPRS).
      The treatment was well tolerated. Intention-to-treat analysis showed 32/49 (65%) responders in the SB group compared to 9/49 (18%) in the placebo group (P<0.001).
      Sixteen patients (33%) in the SB group reduced their CPRS scores by at least 50% compared to five patients (10%) in the placebo group (P< 0.01).
      Mean change score on the CPRS (95% confidence interval) was 10.0 (6.7-13.3) in the SB group and 3.9 (1.1-6.6) in the placebo group (P<0.01).
      An increase in CPRS symptoms at withdrawal was noted in the SB group.
      In conclusion, treatment with staphylococcus toxoid injections over 6 months led to significant improvement in patients with FM and CFS. Maintenance treatment is required to prevent relapse.Cfr. :

    6. Update on Gulf War Illnesses - Relationship to Fibromyalgia Syndrome, Chronic Fatigue Syndrome/M.E. and the Possible Role of Vaccines
      Prof. Garth Nicolson - The Fibromyalgia Survivor, 2001
      Cfr. :

    7. Upregulation of the 2-5A synthetase/Rnase L antiviral pathway associated with chronic fatigue syndrome
      Suhadolnik RJ, Reichenbach NL, Hitzges P, Sobol RW, Peterson DL, Henry H et al. - Clinical Infectious Diseases 1994; 18 Suppl 1: 96-104
      Cfr. :

    8. Why weight gain is a problem with fibro and what to do about it
      Mark J. Pellegrino, MD – ProHealth, July 13, 2009
      Cfr. :

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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Challenges to conventional thinking about mind and body
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    ‘‘When an ordinary person is contacted by a painful feeling,           
    he feels two feelings — a bodily one and a mental one


    Challenges to conventional thinking about mind and body

    Paul Grossman, Freiburg Institute for Mindfulness Research, Konradstrasse 32, 79100, Freiburg, Germany - E-mail address : - Journal of Psychosomatic Research 55 (2003) 491–492 - D 2003 Elsevier Inc.

    The notion that physical symptoms of sane individuals may sometimes bear little or no relationship to measurable physiological functioning is counterintuitive to most us, whether we are lay people, psychologists, physicians or even psychosomatic experts.
    Such an idea profoundly violates nearly everyone’s ordinary view of reality and challenges our sense of safety in the world : if we cannot trust those filtered cortical transmissions telling us that something is happening to our body, what can we believe ?

    If our bodily perceptions are so error-prone, how do we know when we ought to be truly alarmed by somatic symptoms ?
    If we possess a nervous or fearful disposition, does this mean we are doomed to ‘invent’ or ‘amplify’ physical symptoms and are even more unable than less anxious types to distinguish between genuine physiological alterations and misperceptions ?

    Precisely, these kinds of issues are raised by the research in this issue by Houtveen et al.

    The authors report that the extent of self-rated somatic symptoms during mental stress and CO2 rebreathing was generally unrelated to a variety of cardiovascular, autonomic and ventilatory measures, but it was, on the other hand, strongly and positively associated with trait anxiety and a history of physical complaints.

    These findings correspond to a number of studies that have found no exaggerated physiological reactivity to relevant laboratory stressors among individuals marked by a heightened proclivity to physical complaints and/or chronic anxiety.
    However, it remains unclear why still other investigations of anxiety accompanied by extreme physical symptoms, as in panic disorder, sometimes do find concurrent evidence of atypical physiological levels or reactivity.

    Do these other findings represent real distinctions between normal individuals and patients with distinct types of anxiety disorder, as suggested by differences in laboratory studies of cardiovascular autonomic control between panic patients and normal controls (e.g., Ref. [1]) or by Klein’s suffocation alarm theory of panic disorder [2] in which impaired central regulation of respiration is proposed as a primary cause of the disorder ?
    Or could it merely be that most studies have taken place not in the real world, but in a laboratory environment, often without sufficient time for subjects to adapt themselves to the unfamiliar setting and physiological measurement devices.

    One might reasonably assume that particularly under nonadapted conditions, chronically anxious patients may display greater laboratory physiological responses than nonanxious controls, but that these variations may not necessarily reflect real-life, neurophysiological differences between the groups, as so often suggested in the literature.

    Regarding panic disorder, such laboratory specificity of response is supported by several studies : for example, Stein and Asmundson [3,4] found no autonomic or cardiovascular differences during rest or challenge between panic patients and controls after they employed an extended acclimatization phase.
    An ambulatory study of panic disorder patients and healthy controls also found no differences in cardiac activity between groups under reallife conditions [5].
    Still other research reviewed by Houtveen et al. indicates that even under typical laboratory conditions, highly relevant stressors, such as public speaking, often produce no exaggerated physiological reactions among social phobics, although somatic symptom reporting and anxiety are greatly elevated.
    Furthermore, even when we consider those publications where differences between patient and control groups are reported, there are always large proportions of the patient groups who produce no atypical physiological baseline levels or reactions to stressors, although subjective reports of physical symptoms and anxiety are consistently elevated among these patients.
    When such diverse evidence is considered, incongruence between physiology and experience of anxiety and somatic complaints seems very credible.

    But how can we understand this lack of concordance between physiology and symptomatology ?

    In general, the literature has primarily focused upon the cognitive–behavioral explanation that chronically anxious individuals manifest a tendency toward increased attention to and amplification of bodily symptoms related to consequences of negative, often catastrophic appraisal of somatic sensations.
    However, equally plausible is the possibility that states of anxiety actually alter the central nervous system circuitry so that visceral perceptions are, indeed, more unpleasant or painful.
    Subsequent negative appraisal and aversive responses to bodily sensation may be epiphenomenal to this altered central processing of somatic sensation.
    Increasing support for this second hypothesis has been gathered by imaging and pharmacological studies in recent years, especially by investigations examining relations between pain and anxiety.

    Interactions between serotonergic and endorphinic systems and chemical–perceptual mapping of cortical regions, provide evidence of central links between anxiety and interoceptive experience [6,7].
    Also, emotion-related limbic functioning has been tied to central sensory up-regulation [8] and specific hippocampal networks that exacerbate pain under anxiety-provoking conditions have been identified [9].

    These are just a few examples of the growing body of evidence that indicate that the experience of unpleasant or painful bodily sensations does, in fact, reflect accurate perception during anxious times, despite the lack of heightened peripheral physiological activity.

    Should such an intimate connectedness of emotion and somatic experience continue to be supported by future investigation, we may need to rethink current ideas about mind–body relations.
    At least in terms of interpreting subjective experience of psyche and soma, it may be useful to reexamine pre-Cartesian, even ancient Buddhist views of an inseparable mind/body, in which emotional state (among other things) centrally conditions our every perception.
    For example, the simple wisdom : ‘‘When an ordinary person is contacted by a painful feeling, he feels two feelings — a bodily one and a mental one’’ [10].
    In this light, one may gain courage to attempt to answer the questions posed at the beginning of this commentary : unpleasant somatic symptoms may always tell us something is awry, but only sometimes is peripheral physiological functioning the problem.

    Paying close and impartial attention to our bodies during emotional states may also teach us that we store much of our emotional dysphoria in our bodily sensations, even if these sensations are mainly located at the top of our heads : we ought not to forget that physical symptoms constitute major diagnostic criteria for almost all clinical psychiatric disorders and these symptoms are rarely accompanied by convincing evidence of actual physiological dysfunction.
    Studies like that of Houtveen et al. force us to step out of our perhaps dated scientific paradigms and consider other ways of understanding the embodied mind.

    References :

    1. Psychophysiological response patterns in panic disorder
      Hoehn-Saric R, McLeod DR, Zimmerli WD, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 - Acta Psychiatr Scand. 1991 Jan;83(1):4-11 - PMID: 2011954
      To determine whether panic disorder patients exhibit physiological hyperarousal during rest or during mild, non-panic-inducing stress, 18 patients who experienced frequent panic attacks were compared with nonanxious controls on a battery of physiological assessments.
      During baseline, patients with panic disorder exhibited higher forehead electromyographic activity, higher systolic blood pressure and higher heart rates than non-anxious volunteers.
      During psychological stress, heart rate and systolic blood pressure rose more in patients with panic disorder than in nonanxious controls.
      The skin conductance response, however, was greater and more variable in the nonanxious controls.
      The results suggest that panic disorder patients with frequent panic attacks exhibit heightened cardiovascular arousal and decreased electrodermal flexibility than nonanxious people, even in nonthreatening situations.
      Cfr. :

    2. False suffocation alarms, spontaneous panics, and related conditions - An integrative hypothesis
      Klein DF, Department of Psychiatry, Columbia University, New York - Arch Gen Psychiatry. 1993 Apr;50(4):306-17 - PMID: 8466392
      A carbon dioxide hypersensitivity theory of panic has been posited.
      We hypothesize more broadly that a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system.
      This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic and the urge to flee.
      Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor.
      If other indicators of potential suffocation provoke panic this theoretical extension is supported.
      We broadly pursue this theory by examining Ondine's curse as the physiologic and pharmacologic converse of panic disorder, splitting panic in terms of symptomatology and challenge studies, reevaluating the role of hyperventilation and reinterpreting the contagiousness of sighing and yawning, as well as mass hysteria.
      Further, the phenomena of panic during relaxation and sleep, late luteal phase dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety and treatment are used to test and illuminate the suffocation false alarm theory.
      Cfr. :
      Also read the comments on this article :
      - Klein's suffocation theory of panic
      Taylor S, Rachman S - Arch Gen Psychiatry. 1994 Jun;51(6):505-6 - PMID: 8192555
      Cfr. :
      - Panic attacks - Klein's false suffocation alarm, Taylor and Rachman's data and Ley's dyspneic-fear theory
      Ley R - Arch Gen Psychiatry. 1996 Jan;53(1):83-5 - PMID: 8540781
      Cfr. :
      - Nonresponse of adrenocorticotropic hormone in first-ever lactate-induced panic attacks in healthy volunteers
      Kellner M, Wiedemann K - Arch Gen Psychiatry. 1998 Jan;55(1):85-6 - PMID: 9435765
      Cfr. :
      - Response differences of spontaneous panic and fear
      Klein DF - Arch Gen Psychiatry. 2002 Jun;59(6):567-9 - PMID: 12044206
      Cfr. :
      - D-lactate and the false suffocation alarm
      Davies DR, Davies DD - Arch Gen Psychiatry. 2002 Mar;59(3):287-8 - PMID: 11879169
      Cfr. :

    3. Autonomic function in panic disorder - Cardiorespiratory and plasma catecholamine responsivity to multiple challenges of the autonomic nervous system
      Presented in part at the 1992 Annual Meeting of the American College of Neuropsychopharmacology, San Juan, Puerto Rico, December 16, 1992 and at the 48th Annual Meeting of the Society for Biological Psychiatry, San Francisco, CA, May 20, 1993
      Murray B. Steinab, Gordon J.C. Asmundsonab – a From the Anxiety Disorders Research Program, Department of Psychiatry, University of Manitoba, Winnipeg, Manitoba, Canada – b Department of Pharmacology, University of Manitoba, Winnipeg, Manitoba, Canada - Address reprint requests to : Murray B. Stein, MD, FRCPC, Anxiety & Traumatic Stress Disorders Research Program, Department of Psychiatry, University of California, San Diego Veterans Administration Medical Center, 3350 La Jolla Village Drive, San Diego, California 92161, USA - Biol Psychiatry 1994;Volume 36, Issue 8, Pages 548-558 (15 October 1994)
      We are grateful to Mariette J. Chartier, RN, BSc, for help in conducting the autonomic function studies, to Thomas W. Millar BSc(Eng) for his development of the data acquisition and reduction software, to Ken Dhalla and Dr. Naranjan S. Dhalla for providing the catecholamine assays, to Doug Tataryn, PhD for his assistance with data analysis and to Anjala Bharadwaj for her help in setting up and piloting the autonomic testing procedures. We are also indebted to Meir H. Kryger, MD for the use of his clinical laboratory facilities.
      This investigation was supported in part by grant MA-11344 (to MBS) and a Scholarship Award (to MBS) both from the Medical Research Council of Canada and a Postdoctoral Fellowship Award (to GJGA) from the Manitoba Health Research Council.

      Panic disorder has been widely hypothesized to be associated with dysfunction of the autonomic nervous system.
      In this study, 24 patients with panic disorder and 26 healthy control subjects took part in a broad battery of autonomic function tests, each designed to stress the autonomic nervous system in a particular fashion.
      Testing consisted of postural challenge, isometric exercise, cold pressor and Valsalva maneuver.
      Dependent measures included heart rate, vagal tone, blood pressure, respiratory frequency, end-tidal CO2 levels and plasma norepinephrine and epinephrine levels.
      The testing procedures reliably produced changes in autonomic output in the expected directions, but patients with panic disorder were not found to differ from healthy controls in their cardiorespiratory or plasma catecholaminergic responses.
      This pattern of normal autonomic responsivity in the patients with panic disorder was evident across multiple test conditions with varying autonomic demand characteristics, thereby supporting the integrity of autonomic regulatory systems in this illness.
      These data run counter to a simple notion of autonomic dysfunction in panic disorder.
      Cfr. :

    4. Vagal attenuation in panic disorder - An assessment of parasympathetic nervous system function and subjective reactivity to respiratory manipulations
      Asmundson GJ, Stein MB, Department of Psychiatry, University of Manitoba, Winnipeg, Canada - Psychosom Med. 1994 May-Jun;56(3):187-93 - PMID: 8084962
      We examined the effects of hyperventilation and other manipulations of respiratory pace on parasympathetic nervous system function and subjective reactivity in 15 patients with panic disorder, 15 patients with social phobia and 15 healthy control subjects.
      After a 30-minute rest period subjects completed a 2.5-minute trial of each of hypoventilation, normoventilation and hyperventilation.
      Trials were separated by a 3 minute inter-trial interval. Incidence of panic attacks, symptom severity, vagal tone, heart rate, end-tidal carbon dioxide level and respiratory frequency were measured throughout.
      Resting physiological measures did not differ between groups.
      Each respiratory manipulation resulted in the expected physiological changes (e.g., hyperventilation attenuated vagal tone), however, groups did not exhibit differential physiological reactivity to the manipulations.
      There were no panic attacks reported during either the hypoventilation or normoventilation phases; however, two social phobic subjects (13.3%) and two panic disorder patients (13.3%) reported panic attacks during hyperventilation.
      Although both groups of anxiety patients reported greater severity of hyperventilation-induced symptoms than did control subjects, symptom severity did not correlate significantly with vagal tone or heart rate.
      These results suggest that parasympathetic function is unlikely to be aberrant in PD patients and that diminished parasympathetic activity is not sufficient for the experience of panic attacks.
      Cfr. : -&-
      Also read the comment on this article :
      Inferring vagal tone from heart rate variability
      Jennings JR, McKnight JD - Psychosom Med. 1994 May-Jun;56(3):194-6 - PMID: 8084963
      Cfr. :

    5. Motor activity and tonic heart rate in panic disorder
      Clark DB, Taylor CB, Hayward C, King R, Margraf J, Ehlers A, Roth WT, Agras WS, Western Psychiatric Institute and Clinic, University of Pittsburgh, PA 15213 - Psychiatry Res. 1990 Apr;32(1):45-53 - PMID: 2349312
      Motor activity and tonic heart rate were monitored in 62 drug-free panic disorder patients and 40 normal control subjects.
      Mean daily activity, mean waking heart rate controlled for activity and mean sleeping heart rate were determined.
      Panic disorder patients without phobic avoidance showed higher activity than control subjects or patients with limited or extensive avoidance.
      Similarly, an "inverted U", relationship between trait anxiety and activity was observed.
      On the other hand, neither mean waking nor sleeping heart rate showed significant differences between patients and controls, suggesting that the differences previously reported in laboratory studies result from anticipatory anxiety.
      Cfr. :

    6. Brain chemistry reflects dual states of pain and anxiety in chronic low back pain
      Grachev ID, Fredrickson BE, Apkarian AV, Department of Anesthesiology, SUNY Upstate Medical University, Syracuse, NY, USA : - J Neural Transm. 2002 Oct;109(10):1309-34 - PMID: 12373563
      The neurobiology of the interaction between pain and anxiety is unknown.
      The present study examined interrelationships between : regional brain chemistry (as identified by in vivo proton magnetic resonance spectroscopy [(1)H-MRS] in dorsolateral prefrontal cortex [DLPFC], orbitofrontal cortex [OFC], cingulate and thalamus), pain (as measured by short form of the McGill Pain Questionnaire [SF-MPQ]) and anxiety (measured by the State-Trait Anxiety Inventory) in chronic low back pain (CLBP) patients and contrasted to the relationship between brain chemistry and anxiety in sex and age-matched normal subjects.
      The results show that brain chemistry depends on a 3-way interaction of brain regions examined, subject groups (normal vs. CLBP) and anxiety levels (high vs. low).
      The concentration of N-Acetyl aspartate (the largest peak in (1)H-MRS) in OFC could distinguish between anxiety levels and between subject groups.
      Chemical-perceptual relationships were analyzed by calculating correlations between regional chemicals and perceptual measures of pain and anxiety.
      To isolate pain from anxiety, these maps were subdivided based on anxiety and, in the CLBP patients along anxiety-more-related vs. anxiety-less-related pain descriptors and along sensory vs. affective pain descriptors.
      There was a precise relationship between perception and brain chemistry.
      The chemical-perceptual network best related to pain in CLBP patients was comprised of the DLPFC and OFC; the chemical-anxiety network was best related to the OFC chemistry in normals and to all four regions studied in CLBP patients; and the cingulate was best related to the affective component of pain.
      We conclude that the chemical-perceptual mapping differentiates between closely related perceptual states of pain and anxiety in chronic pain and provides a brain regional-chemical-perceptual description of the long-term reorganization that occurs with chronic pain.
      Cfr. :

    7. Serotonin-mediated increases in the extracellular levels of beta-endorphin in the arcuate nucleus and nucleus accumbens - A microdialysis study
      Zangen A, Nakash R, Yadid G, Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel - J Neurochem. 1999 Dec;73(6):2569-74 - PMID: 10582620
      Although the involvement of both endogenous opioid and serotonergic systems in modulation of pain and emotion was suggested, the neurochemical interaction between these systems in the brain has not previously been studied directly.
      Herein, the effects of the local application of serotonin (5-HT) and fluoxetine (a 5-HT reuptake inhibitor) on extracellular levels of beta-endorphin in the arcuate nucleus and nucleus accumbens were assessed in freely moving rats using in vivo microdialysis.
      The mean basal concentrations of beta-endorphin in dialysates obtained from the arcuate nucleus and nucleus accumbens were 259.9 and 143.3 pM, respectively.
      Specific lesion of the serotonergic system by 5,7-dihydroxytryptamine (5,7-DHT) caused a significant decrease in these dialysate beta-endorphin levels.
      When 5-HT (0.25-5 microM) was added to the perfusion solution, the levels of beta-endorphin in the dialysate from the arcuate nucleus increased (186-296% of baseline), in a concentration-dependent manner.
      In the nucleus accumbens, 0.5 and 2 microM 5-HT in the perfusion fluid did not affect the levels of beta-endorphin in the dialysate, whereas 5 and 10 microM 5-HT caused an increase of approximately 190% of baseline.
      When fluoxetine (250 microM) was present in the perfusing solution, the levels of beta-endorphin in the dialysates from the arcuate nucleus and nucleus accumbens increased two- to threefold.
      This effect was not obtained in the 5,7-DHT-lesioned rats.
      Thus, 5-HT, either endogenously or exogenously delivered, appears to facilitate the release of beta-endorphin in the arcuate nucleus and nucleus accumbens.
      This indication of an interaction between serotonergic and endorphinic systems may be relevant for assessing pain and mood disorder circuits and the mode of action of antidepressant drugs.
      Cfr. :

    8. Role of the brain and sensory pathways in gastrointestinal sensory disorders in humans
      Mertz H, Vanderbilt University Medical Center, Nashville 37232-5340, USA : - Gut. 2002 Jul;51 Suppl 1:i29-33 - PMID: 12077061
      Several features of the irritable bowel syndrome (IBS) suggest involvement of the emotional limbic system in the brain.
      Abnormalities which upregulate afferent (sensory) signal intensity anywhere in this system, from the gastrointestinal tract to the brain, could induce hypersensitivity, leading to the pain and discomfort that characterise IBS and other functional disorders.
      Functional gastrointestinal disorders are likely to be heterogeneous given the complexity of the afferent system and a number of different perturbations are possible.
      Intestinal hypersensitivity to pain and discomfort and associated reflex alterations in motility might explain the symptoms of functional bowel diseases.
      Cfr. :

    9. Role of the brain and sensory pathways in gastrointestinal sensory disorders in humans
      Mertz H, Vanderbilt University Medical Center, Nashville 37232-5340, USA : - Gut. 2002 Jul;51 Suppl 1:i29-33 - PMID: 12077061
      Several features of the irritable bowel syndrome (IBS) suggest involvement of the emotional limbic system in the brain.
      Abnormalities which upregulate afferent (sensory) signal intensity
      anywhere in this system, from the gastrointestinal tract to the brain, could induce hypersensitivity, leading to the pain and discomfort that characterise IBS and other functional disorders.
      Functional gastrointestinal disorders are likely to be heterogeneous given the complexity of the afferent system and a number of different perturbations are possible.
      Intestinal hypersensitivity to pain and discomfort and associated reflex alterations in motility might explain the symptoms of functional bowel diseases.
      Cfr. :

    10. The Connected Discourses of the Buddha – A Translation of the Samyutta Nikay
      Bikkhu Bodhi - Wisdom Publications (2nd edition), September 25, 2002 - ISBN-10: 0861713311 - ISBN-13: 978-0861713318
      This is a complete translation of the Samyutta Nikaya, containing all of the important suttas ('Discourses of the Buddha') on such key Buddhist concepts as the Four Noble Truths, dependent origination, the seven factors of enlightenment and the Noble Eightfold Path.
      'The Connected Discourses of the Buddha' ranks as one of the most inspiring compilations in the Buddhist canon.
      Bhikkhu Bodhi's distinguished and precise translation, his insightful introductory materials and his extensive notes guide the reader through this vast collection of the Buddha's ancient teachings.
      This is the third title in Wisdom Publications' award-winning Teachings of the Buddha Series, following 'The Long Discourses of the Buddha' and 'The Middle Length Discourses of the Buddha'.
      Like its two predecessors and 2005's anthology of 'Discourses of the Buddha', this volume belongs in the library of every student of Buddhism
      Cfr. :

    16-11-2009 om 19:37 geschreven door Jules

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    Tags:5,7-DHT, irritable bowel syndrome, anxiety, autonomic nervous system, central nervous system, hypersensitivity, hyperventilation, IBS, mind and body, pain, panic disorder, physical symptoms, physiology, psychosomatic, serotonin, sleep, somatic symptoms
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.What is CFS and what is ME ?
    Klik op de afbeelding om de link te volgen


    What is CFS and what is ME ?

    Peter White, October 20th 2009

        Abnormal appetite; anorexia; anxiety; ataxia; back pain; benign myalgic encephalomyelitis; bladder dysfunction; brain stem; cardiac arrhythmias; categorizing retrieval; CDC symptoms; central nervous system; CFS; chronic fatigue syndrome NOS; chronic fatigue syndrome; chronic physical disorders; cognitive overload; concentration; confusion; COPD; cranial nerves; Da Costa syndrome; delayed postural hypotension; depression; disabling fatigue; disorientation; dizziness; emotional overload; exertional dyspnoea; extreme pallor; fasciculations; fatigue; fibromyalgia; flu-like symptoms; functional disorders; functional somatic syndromes; general malaise; hypersensitivity to noise; hypnoeic; IBS; ICD-10; inability to focus vision; infections; information processing; insomnia; intolerance of extremes of heat and cold; irritable bowel syndrome; light-headedness; loss of adaptability; loss of thermostatic stability; major depressive illness; marked diurnal fluctuation; marked weight change; ME; migraine; mood disorders; muscle weakness; Myalgic Encephalomyelitis; nausea; nausea; neurally mediated hypotension (NMH); neurasthenia; neurocirculatory asthenia; sensitivity to chemicals; sensitivity to food; sensitivity to medications; obese; orthostatic intolerance; overload phenomena; palpitations; peptic ulcers; perceptual disturbances; photophobia; post-exertional fatigue; post-exertional malaise; postural orthostatic tachycardia syndrome (POTS); postviral fatigue syndrome; recurrent feelings of cold extremities; recurrent feelings of feverishness; recurrent flulike symptoms; recurrent sore throat; regional pain disorders; senile asthenia; sensory disturbances; sensory overload; short-term memory; sleep; somatoform autonomic dysfunction; somatoform disorder; spatial instability; spine; stress; subnormal body temperature; substantial reduction in activity; sweating episodes; tender lymph nodes; undifferentiated somatoform disorder; urinary frequency; word retrieval; XMRV

    Cfr. :

    16-11-2009 om 01:38 geschreven door Jules

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    Tags: CFS, chronic fatigue syndrome, disabling fatigue, emotional overload, fibromyalgia, flu-like symptoms, infections, ME, migraine, mood disorders, muscle weakness, Myalgic Encephalomyelitis, post-exertional fatigue, short-term memory, sleep, stress, XMRV
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.CVS-Referentiecentra - Opheffing en sluiting
    Klik op de afbeelding om de link te volgen

    Michael Maes, M.D., Ph.D.

           - Opheffing en sluiting -

            Jan van Roijen - Help ME Circle, 13-11-2009

    Ook in Nederland is de trukendoos-wetenschap van de nutteloze, geld verslindende CVS-Referentiecentra een doorn in het oog van de 60 a 70 duizend wanhopige patienten.

    En ook in ons land is de hier onder vermelde dr. Van Houdenhove een beruchte persoon.

    Hij was lid van de 'Commissie CVS' van de Gezondheidsraad.
    Aldus was hij mede-auteur van het frauduleuze rapport dat deze commissie in elkaar flansde.
    Alle duizenden wetenschapelijke studies waarin wordt aangetoond dat ME/CVS een zeer ernstige, multi-systemische ziekte is bleven onvermeld.

    In strijd met de richtlijnen van de WHO, werd ME/CVS als een psychiatrische aandoening bestempeld.

    De voorzitter van deze commissie, Mevr. Borst, maakte het zelfs zo bont dat ze tijdens een bijeenkomst een groep ernstig zieke, op brancards liggende patienten toesnauwde : "... ME-patienten kunnen genezen door Graded Exercise... !".

    Open brief

    Aan :

    Dr. Mark Waer, Rector
    Katholieke Universiteit Leuven
    Oude Markt 13
    3000 Leuven

    Dr. Guy Mannaerts, Voorzitter Bestuurscomité
    Dr. Johan Kips, Gedelegeerd Bestuurder,
    UZ Leuven, Netwerkziekenhuizen
    Herestraat 49
    3000 Leuven

    Antwerpen, 11 november 2009

    Re : Eis tot opheffing en sluiting van uw CVS-referentiecentra

    Mijnheer de Rector, Mijnheer de Directeur, Mijnheer de Bestuurder,

    Uit de evaluaties van het KCE en het Rijksinstituut voor ziekte- en invaliditeitsverzekering blijkt zonneklaar dat de Belgische CVS-referentiecentra hebben gefaald : de CGT/GET-aanpak is niet effectief gebleken.
    Ook de vorige Minister van Volksgezondheid Demotte diende toe te geven dat CBT/GET geen
    curatieve therapie is (Twisk en Maes, 2009).

    Meer nog, de objectieve beoordelingscriteria onderbouwen de stelling dat veel patienten er in uw
    CVS-referentiecentra op achteruit gaan : de gemiddelde arbeidsparticipatie van patienten neemt zelfs af na de “rehabilitatiebehandeling” gebaseerd op CGT/GET.

    We hebben aangetoond dat patienten die in de CVS-referentiecentra - en derhalve ook die in Leuven - “behandeld” worden met CGT/GET eigenlijk lijden aan een zwaar, invaliderende, organische ziekte, gekenmerkt door talrijke biologische stoornissen vastgesteld in bloed en urine (Maes en Twisk, 2009a).

    Uw referentiecentrum slaagt er kennelijk niet in en/of weigert om deze organische afwijkingen op te sporen.

    Uit overzichtsartikelen (Twisk en Maes, 2009; Maes en Twisk, 2009a) blijkt dat de aan uw universiteit toegepaste CGT/GET-aanpak elke wetenschappelijke onderbouwing ontbeert en zelfs contraproductief is.

    De toestand van veel ME/CVS-patienten verslechtert omdat inspanning en dus zeker uw “revalidatieprogramma's” de pathofysiologische afwijkingen nog verder doen toenemen (Twisk en Maes, 2009).

    Niettegenstaande de vaststelling dat U op de hoogte bent of zou moeten zijn van het feit dat de door uw referentiecentrum gepropageerde en toegepaste aanpak van ME/CVS-patienten nutteloos is en vaak zelfs de patient verdere schade toebrengt wordt de CGT/GET-koers gewoon verder voortgezet.

    Dit is in flagrante strijd met de deontologie van de geneeskundige codeleer en is zelfs zeer onethisch.

    Ondanks dat ww medewerkers, zoals dr. Van Houdenhove, op de hoogte zijn van het gegeven dat
    de door hen vurig uitgedragen en toegepaste aanpak nutteloos is en de gezondheidstoestand van veel patienten verder doet verslechteren publiceren ze dat CGT/GET "veelbelovende resultaten" toont en dat CGT/GET de “enige afdoende behandeling” is voor ME/CVS (van Houdenhove and Luyten, 2009).

    Dr. Van Houdenhove, de Belgische beleidsmaker, is van mening dat toekomstig onderzoek over ME/CVS zich nog meer moet toespitsen op CGT/GET (Van Houdenhove en Luyten, 2009).

    Blijkbaar vindt hij dat er nog niet voldoende overheidsgeld is verspild aan een aanpak die niet
    alleen ineffectief is, maar zelfs potentieel schadelijk voor veel patienten.

    De zwabberkoers van dr. Van Houdenhove uit zich onder meer in het feit dat hij in hetzelfde jaar als waarin hij CGT/GET voorstelt als de enige ware aanpak voor ME/CVS (Van Houdenhove en Luyten, 2009), hij in een ander tijdschrift aanbeveelt dat onderzoek zich in de toekomst zou moeten
    toespitsen op stoornissen in het afweersysteem (Van Houdenhove en Heijnen, 2009).

    Hierbij haalt hij zijn inspiratie uit... onderzoek naar ontstekingen bij depressies.
    Dr. Van Houdenhove interpreteert de bestaande inzichten verkeerd en misbruikt hierbij de ontstekingstheorie van depressies, zoals ik kan weten, aangezien ik de grondlegger ben van die theorie (Maes et al., 2009; Maes en Twisk, 2009b).

    Erger nog, dr. Van Houdenhove “vergeet” te verwijzen naar de meer dan 4.000 studies, waaronder
    genexpressie-studies die aantonen dat ontstekingen, immuundysfunctie, infecties, oxidatieve stress, auto-immuniteit, mitochondriale disfunctie etc. de hoofdrol vertolken in de organische verklaring voor ME/CVS (Maes, 2009).

    Dr. Van Houdenhove “vergeet” te refereren aan de diermodel-experimenten van ME/CVS die eveneens bewijzen dat ontstekingen en oxidatieve stress veel typische ME/CVS-klachten veroorzaken (Maes, 2009).

    Dr. Van Houdenhove “vergeet” te wijzen naar succesvolle medische behandelingen van subgroepen van ME/CVS-patienten (Maes, 2009; Maes en Twisk, 2009b).

    Dit soort “citatieamnesie” is niet alleen onwetenschappelijk, maar vormt tevens een vrijgeleide om ME/CVS patienten een biomedische diagnose en behandeling aan uw CVS-referentiecentrum te onthouden (Maes en Twisk, 2009b).

    Daarom eis ik dat U :

    a) dit CVS-referentiecentrum opheft en voorgoed sluit, dan wel minstens er bij de bevoegde minister op aandringt om het referentiecentrum te sluiten en

    b) dr. Van Houdenhove onder curatele plaatst, dan wel hem minstens belet onzin en onwaarheden te
    publiceren en mij hierover in te lichten bij gebreke waarvan we U na een maand zullen dagvaarden wegens de medisch-onethische behandelingen van patienten in uw CVS referentiecentrum.

    Michael Maes, M.D., Ph.D.


    • Maes, M. (2009)
      Inflammatory and oxidative & nitrosative stress (IO&NS) pathways underpinning chronic fatigue, somatization and psychosomatic symptoms
      Maes M, Clinical Research Centre of Mental Health (CRC-MH), Antwerp, Belgium : - Curr Opin Psychiatry. 2009 Jan;22(1):75-83 - PMID: 19127706
      Purpose of review - The aim of this paper is to review recent findings on inflammatory and oxidative and nitrosative stress (IO&NS) pathways in chronic fatigue and somatization disorder.
      Recent findings - Activation of IO&NS pathways is the key phenomenon underpinning chronic fatigue syndrome (CFS) : intracellular inflammation, with an increased production of nuclear factor kappa beta (NFkappabeta), cyclo-oxygenase-2 (COX-2) and inducible NO synthase (iNOS); and damage caused by O&NS to membrane fatty acids and functional proteins.
      These IO&NS pathways are induced by a number of trigger factors, for example psychological stress, strenuous exercise, viral infections and an increased translocation of LPS from gram-bacteria (leaky gut).
      The 'psychosomatic' symptoms experienced by CFS patients are caused by intracellular inflammation (aches and pain, muscular tension, fatigue, irritability, sadness and the subjective feeling of infection); damage caused by O&NS (aches and pain, muscular tension and fatigue); and gut-derived inflammation (complaints of irritable bowel).
      Inflammatory pathways (monocytic activation) are also detected in somatizing disorder.
      Summary - 'Functional' symptoms, as occurring in CFS and somatization, have a genuine organic cause, that is activation of peripheral and central IO&NS pathways and gut-derived inflammation.
      The development of new drugs, aimed at treating those disorders, should target these IO&NS pathways.
      Cfr. :

    • Maes, M., Twisk, F.N.M. (2009a)
      Chronic Fatigue Syndrome - La bête noire of the Belgian Health Care System
      Maes M, Twisk FN, Maes Clinics, Antwerp, Belgium : - Neuro Endocrinol Lett. 2009 Aug 26;30(3):300-311 [Epub ahead of print] - PMID: 19855351
      The World Health Organization acknowledges Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) to be a medical illness.
      ME/CFS is characterized by disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways.
      In 2002, the Belgian government started with the development of CFS "Reference Centers", which implement a "psychosocial" model.
      The medical practices of these CFS Centers are defined by the Superior Health Council, e.g. treatment should be based upon Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET); and biological assessments and treatments of ME/CFS should not be employed.
      Recently, the Belgian government has evaluated the outcome of the treatments at the CFS Centers.
      They concluded that a "rehabilitation therapy" with CBT/GET yielded no significant efficacy in the treatment of ME/CFS and that CBT/GET cannot be considered to be curative therapies.
      In case reports, we have shown that patients who were "treated" at those CFS centers with CBT/GET in fact suffered from IO&NS disorders, including intracellular inflammation, an increased translocation of gram-negative enterobacteria (leaky gut), autoimmune reactions and damage by O&NS.
      Considering the fact that these findings are exemplary for ME/CFS patients and that GET may even be harmful, it means that many patients are maltreated by the Belgian CFS Centers.
      Notwithstanding the above, the government and the CFS Centers not only continue this unethical and immoral policy, but also reinforce their use of CBT/GET in patients with ME/CFS treated at those Centers.
      Cfr. :

    • Maes, M., Twisk, F.N.M. (2009b)
      Reaction on 'Chronic fatigue syndrome - A psychoneuroimmunological perspective' (1)
      Maes M, Twisk FN - Tijdschr Psychiatr. 2009;51(10):783-4; author reply 784-6 - PMID: 19821247
      Cfr. :
      This article is a comment on :
      Chronic fatigue syndrome - A psychoneuroimmunological perspective
      Van Houdenhove B, Heijnen CJ - Tijdschr Psychiatr. 2009;51(8):603-10 - PMID: 19658073
      Cfr. :

    • Maes, M., Yirmyia, R., Noraberg, J., Brene, S., Hibbeln, J., Perini, G., Kubera, M., Bob, P., Lerer, B., Maj, M. (2009)
      The inflammatory & neurodegenerative (I&ND) hypothesis of depression - Leads for future research and new drug developments in depression
      Maes M, Yirmyia R, Noraberg J, Brene S, Hibbeln J, Perini G, Kubera M, Bob P, Lerer B, Maj M, Clinical Research Center for Mental Health, Olmenlaan 9, Antwerp Wilrijk 2610, Belgium : - Metab Brain Dis. 2009 Mar;24(1):27-53. Epub 2008 Dec 16 - PMID: 19085093
      Despite extensive research, the current theories on serotonergic dysfunctions and cortisol hypersecretion do not provide sufficient explanations for the nature of depression.
      Rational treatments aimed at causal factors of depression are not available yet.
      With the currently available antidepressant drugs, which mainly target serotonin, less than two thirds of depressed patients achieve remission.
      There is now evidence that inflammatory and neurodegenerative (I&ND) processes play an important role in depression and that enhanced neurodegeneration in depression may-at least partly-be caused by inflammatory processes.
      Multiple inflammatory-cytokines, oxygen radical damage, tryptophan catabolites-and neurodegenerative biomarkers have been established in patients with depression and these findings are corroborated by animal models of depression.
      A number of vulnerability factors may predispose towards depression by enhancing inflammatory reactions, e.g. lower peptidase activities (dipeptidyl-peptidase IV, DPP IV), lower omega-3 polyunsaturated levels and an increased gut permeability (leaky gut).
      The cytokine hypothesis considers that external, e.g. psychosocial stressors and internal stressors, e.g. organic inflammatory disorders or conditions, such as the postpartum period, may trigger depression via inflammatory processes.
      Most if not all antidepressants have specific anti-inflammatory effects, while restoration of decreased neurogenesis, which may be induced by inflammatory processes, may be related to the therapeutic efficacy of antidepressant treatments.
      Future research to disentangle the complex etiology of depression calls for a powerful paradigm shift, i.e. by means of a high throughput-high quality screening, including functional genetics and genotyping microarrays; established and novel animal and ex vivo-in vitro models for depression, such as new transgenic mouse models and endophenotype-based animal models, specific cell lines, in vivo and ex vivo electroporation and organotypic brain slice culture models.
      This screening will allow to :
      1) discover new I&ND biomarkers, both at the level of gene expression and the phenotype; and elucidate the underlying molecular I&ND pathways causing depression; and
      2) identify new therapeutic targets in the I&ND pathways; develop new anti-I&ND drugs for these targets; select existing anti-I&ND drugs or substances that could augment the efficacy of antidepressants; and predict therapeutic response by genetic I&ND profiles.
      Cfr. :

    • Twisk, F.N.M., Maes, M. (2009)
      A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS) - CBT/GET is not only ineffective and not evidence-based, but also potentially harm
      Frank NM Twisk 1, Michael Maes 2 - 1) ME-de-patiënten Foundation, Limmen, the Netherlands, the Netherlands - 2) Clinical Research Center for Mental Health (CRC-MH), Antwerp, Belgium - Neuroendocrinol Lett Vol 30 issue 3, 2009. pp. 275-420
      Benign Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) is a debilitating disease which, despite numerous biological abnormalities has remained highly controversial.
      Notwithstanding the medical pathogenesis of ME/CFS, the (bio)psychosocial model is adopted by many governmental organizations and medical professionals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS.
      Justified by this model CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively.
      In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust.
      CBT/GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration.
      Moreover, this review shows that exertion and thus GET most likely have a negative impact on many ME/CFS patients.
      Exertion induces post-exertional malaise with a decreased physical performance/aerobic capacity, increased muscoskeletal pain, neurocognitive impairment, “fatigue”and weakness and a long lasting “recovery” time.
      This can be explained by findings that exertion may amplify pre-existing pathophysiological abnormalities underpinning ME/CFS, such as inflammation, immune dysfunction, oxidative and nitrosative stress, channelopathy, defective stress response mechanisms and a hypoactive hypothalamic-pituitary-adrenal axis.
      We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful “rehabilitation therapies”, such as CBT/GET.
      Cfr. :

    • Van Houdenhove B, Heijnen CJ (2009)
      Chronic fatigue syndrome - A psychoneuroimmunological perspective
      Van Houdenhove B, Heijnen CJ, Universitaire Ziekenhuizen Leuven en als buitengewoon hoogleraar Medische ene Gezondheidspsychologie aan de Faculteit Geneeskunde, KU Leuven : - Tijdschr Psychiatr. 2009;51(8):603-10 - PMID: 19658073
      This article casts light on the contribution that psychoneuroimmunology can make in the search for the cause of chronic fatigue syndrome (cfs).
      Several studies suggest that psychosocial and physical stress may play an important predisposing, precipitating and perpetuating role in cfs.
      Moving on from these studies we now discuss recent research into the stress-related pathophysiological mechanisms of the illness.
      Although there is evidence for a hypofunctional stress response, a hyperactive immune response and disturbances in the interaction between both, the findings are not consistent.
      Longitudinal studies are needed to unravel the pathophysiology of cfs still further.
      In such studies the concept of 'sickness response' and 'sickness behaviour' may perform an important heuristic function.
      Cfr. :
      Also read the comments on this article :
      - Reaction on 'Chronic fatigue syndrome - A psychoneuroimmunological perspective' (1)
      Maes M, Twisk FN - Tijdschr Psychiatr. 2009;51(10):783-4; author reply 784-6 - PMID: 19821247
      Cfr. :
      - Reaction on 'Chronic fatigue syndrome – A psychoneuroimmunological perspective' (2)
      Den Broeder G, Arnoldus R - Tijdschr Psychiatr. 2009;51(10):786-7; author reply 787-8 - PMID: 19821248
      Cfr. :

    • Van Houdenhove, B., Luyten, P. (2009)
      Treatment of chronic fatigue syndrome - How to find a 'new equilibrium' ?
      Van Houdenhove B, Luyten P, Department of Psychiatry, University of Leuven, Leuven, Belgium : - Patient Educ Couns. 2009 Nov;77(2):153-4. Epub 2009 Sep 20 - PMID: 19773143
      Cfr. :
      Dit artikel is een reactie op :
      - Learning to cope with chronic illness - Efficacy of a multi-component treatment for people with chronic fatigue syndrome
      Goudsmit EM, Ho-Yen DO, Dancey CP, School of Psychology, University of East London, London, UK : - Patient Educ Couns. 2009 Nov;77(2):231-6. Epub 2009 Jul 2 - PMID: 19576714
      Objective - The aim of this study was to determine the efficacy of an out-patient, multi-component programme developed for patients with chronic fatigue syndrome (CFS).
      Methods - Twenty-two patients were assessed before and after six months of treatment.
      Findings were compared with 22 individuals on the waiting list.
      The programme offered medical care as well as information and counselling to help patients to understand, accept and cope with their illness.
      Results - At six months, there were significant differences between the groups for fatigue, self-efficacy and anxiety.
      Overall, 82% of the treated patients reported feeling better and 23% had improved to such a degree that they were discharged from the clinic.
      The gains were maintained at twelve months.
      Conclusion - This programme was found to be both helpful and acceptable and may provide a useful first-line intervention for many patients with CFS.
      Practice implications - Short, pragmatic programmes may be as effective as cognitive-behaviour therapy.
      Cfr. :
      - The impact of energy modulation on physical functioning and fatigue severity among patients with ME/CFS
      Jason L, Benton M, Torres-Harding S, Muldowney K, DePaul University, Center for Community Research, Chicago, IL 60614, USA : - Patient Educ Couns. 2009 Nov;77(2):237-41. Epub 2009 Apr 8 - PMID: 19356884
      Objective - The energy envelope postulates that patients with Myalgic Encephalomyelitis / chronic fatigue syndrome (ME/CFS) will improve functioning when maintaining expended energy levels at the same level as available energy level.
      Methods - Estimated weekly Energy Quotients were established by dividing expended energy level by perceived energy level and multiplying by 100.
      Two groups of patients were identified following participation in a non-pharmacologic intervention trial.
      Some were able to keep expended energy close to available energy and others were not successful at this task.
      Results - Those who were able to stay within their energy envelope had significant improvements in physical functioning and fatigue severity.
      Conclusion - Findings suggest that helping patients with ME/CFS maintain appropriate energy expenditures in coordination with available energy reserves can help improve functioning over time.
      Practice implications - Health care professionals that treat patients with ME/CFS might incorporate strategies that help patients self-monitor and self-regulate energy expenditures.
      Cfr. :

    Een beetje geschiedenis :

    1. Chronisch vermoeidheid - Een acuut probleem
      Marleent Teugels – Bron : Knack, nr. 31, jaargang nr. 8, 21-02-2001
      Cf. :

    2. Chronisch Vermoeidheidssyndroom - Diagnose, behandeling en zorgorganisatie
      KCE reports 88A - Federaal Kenniscentrum voor de Gezondheidszorg (KCE), 30-09-2008
      Cfr. :

    3. Chronisch Vermoeidheidssyndroom - Zorgverleners moeten meer samenwerken
      Persbericht Federaal Kenniscentrum voor de Gezondheidszorg (KCE), 30-09-2008
      Cfr. :

    4. Evaluatierapport - CVS-referentiecentra België : CGT/GET is niet effektief maar toch... met deze "behandeling" doorgaan !
      Cfr. :

    5. Evaluatierapport over de referentiecentra voor het Chronisch vermoeidheidssyndroom (CVS)
      RIZIV, 2007
      Cfr. :

    6. Geen enkele patiënt genezen
      ME/CVSNet, 01-10-2008
      Cfr. :
      Cfr. ook :

    7. Minister van Volksgezondheid van België Rudy Demotte - De behandeling van de referentiecentra - Gedragstherapie (CGT) en graduele oefentherapie(GET) is niet effektief gebleken maar de soap gaat door : een andere verpakking gaat wellicht wel succes opleveren...
      Cfr. :

    8. Open brief dr. Michael Maes aan Minister Onkelinx
      Cfr. :
      Cfr. ook :
      Open brief aan Minister Onkelinx - dd. 02-11-2008

    9. Referentiecentra - Deel 253 : Minister Onkelinx wil doorgaan op de heilloze weg - Maggie de Block dringt aan op verandering
      Cfr. :

    10. MEAB on tour (protestaktie tegen werkwijze referentiecentra)
      Cfr. :

    11. Referentiecentra schieten tekort - Reden voor het mislukken van CGT/GET onduidelijk !
      De Standaard
      Cfr. :

    12. Referentiecentra voor chronisch vermoeidheidssyndroom
      Maggie de Block, 08-10-2008
      Cfr. :
      Cfr. ook :

    13. Referentiecentra voor het chronisch vermoeidheidssyndroom - Vraag van mevrouw Maggie De Block aan de vice-eersteminister en minister van Sociale Zaken en Volksgezondheid over "de referentiecentra voor het chronisch vermoeidheidssyndroom" - Staatssecretaris Jean-Marc Delizée antwoordt
      Cfr. :
      Cfr. ook :

    14. Vlaanderen investeert in een CVS-therapie die volgens dokters en patiënten niet werkt
      De Morgen, 25-10-2008
      Cfr. :

    15. Vraag nr. 748 van mevrouw Annemie Turtelboom van 10 mei 2006 (N.) aan de minister van Sociale Zaken en Volksgezondheid : 16-10- 2006
      Belgische Kamer van Volksvertegenwoordigers, 2007, 5e zitting van de 51e zittingsperiode
      Cfr. :

    14-11-2009 om 23:41 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 3/5 - (1 Stemmen)
    Tags:CGT/GET, CFS, COX-2, CVS, iNOS, intracellular inflammation, IO&NS, ME, ME/CFS, ME/CVS, mitochondriale disfunctie, Nfkappabeta, O&NS, oxidatieve stress, pain, psychological stress, rehabilitation therapy, sadness, somatization, strenuous exercise
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Heb ik voldoende ontspanning ?
    Klik op de afbeelding om de link te volgen

     - Test -

    Heb ik voldoende ontspanning ?

    Met behulp van deze test kunt u erachter komen of u voldoende ontspanning heeft in relatie tot uw werk.

    De test is anoniem.
    Er wordt niet gevraagd naar uw naam en adresgegevens.

    Cfr. :

    13-11-2009 om 18:57 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 3/5 - (2 Stemmen)
    Tags:ontspanning, stress, werk
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.7 tips tegen een overactieve blaas
    Klik op de afbeelding om de link te volgen


    'Als ik ergens naar toe ga, zoek ik eerst de toiletten’                     
    'Ik moet er elke nacht een paar keer uit
    Mijn moeder had het ook, ik dacht dat het erbij hoorde’                     

    7 tips tegen een overactieve blaas

    Jan Willem Wensink -, 12-11-2009 – Bronnen : NHG, urolog, Elsevier

    Ongeveer 8% van de Nederlanders vanaf 20 jaar kampt met plasklachten door een overactieve blaas.
    7 tips om je blaas onder controle te houden.

    Een blaas is ‘overactief’ als zij vaak een signaal van aandrang geeft (cfr. 'Incontinentie voor urine' op : -).
    Als je vaker dan 8 keer per dag moet plassen en soms last hebt van ongewild urineverlies, dan kun je stellen dat je blaas overactief is.
    Een overactieve blaas is een aandoening die ook wel 'aandrangsincontinentie' wordt genoemd.
    Het kan zijn dat de spieren in de wand van de blaas snel samentrekken en een ongewilde lediging van de blaas in gang zetten.
    Maar het kan ook voorkomen dat ondanks een voortdurend gevoel van aandrang het plassen niet of nauwelijks lukt.


    Het gevoel van verlies over controle van de blaas geeft veel onzekerheid.
    Het kan zelfs leiden tot een sociaal isolement, omdat mensen die er veel last van hebben uit angst voor urineverlies bijeenkomsten, feestjes en dagjes uit gaan mijden.
    Een ander veelvoorkomend gevolg is dat mensen minder gaan drinken, zodat ze minder vaak naar de wc hoeven.
    Op termijn ligt echter uitdroging op de loer, bovendien nemen de klachten er niet door af.
    Een overactieve blaas kan zowel bij mannen als vrouwen voorkomen.
    Wie er last van heeft, kan het best met de huisarts overleggen.
    Die zorgt voor een behandelplan en kan eventueel medicijnen (cfr. 'Vesicare 10 mg tablet' op: -) voorschrijven.
    Oorzaken van een overactieve blaas

    De blaas kan door verschillende oorzaken overactief worden.
    Het kan komen door een blaasontsteking (cfr. : -) of een verdikking in de blaaswand waardoor spieren en receptoren niet meer goed samenwerken.
    Soms zijn er afwijkingen aan de zenuwbanen van de blaas of stoornissen in de hersenen, waardoor controle over de blaas wordt bemoeilijkt.
    Bij mannen kan een opgezette prostaat (cfr. 'De gevolgen van een vergrote prostaat' op : -) de aanleiding zijn voor overactiviteit, bij vrouwen komt het nogal eens voor dat de bekkenbodemspieren (cfr. 'Inspanningsincontinentie' op : -) een rol spelen.
    Als die onbewust worden aangespand, kan in de blaas aandrang ontstaan.
    Maar bekkenbodemspieren kunnen ook verslapt zijn, bijvoorbeeld door een bevalling.
    Dan zorgen ze voor een minder goed werkende afsluiting van de blaas.
    Een overactieve blaas kan soms ook het gevolg zijn van bijwerkingen van bepaalde medicijnen.

    7 Tips om je blaas onder controle te houden

    Tip1 - Hou een dagboekje bij
    Zorg eerst dat je overzicht krijgt over je blaasproblemen.
    Hou een dagboekje bij en zet daarin wat je drinkt, wanneer en hoeveel je drinkt, wanneer je naar de wc gaat en hoeveel je plast, wanneer je plotselinge aandrang hebt en wanneer je eventueel te maken hebt met ongewild urineverlies.
    Het dagboekje geeft je inzicht in de ernst van je problemen en is handig als je de huisarts van wat gegevens wil voorzien.

    Tip 2 - Blijf voldoende drinken
    Mensen die last hebben van plasklachten zijn geneigd minder te gaan drinken (cfr. 'Voedingsstoffen die goed zijn voor je lichaam' op : ).
    Dat is niet alleen voor het hele lichaam ongezond, maar de conditie van de blaas wordt er ook nog slechter van en het kan juist meer plasklachten opleveren.
    Uit onderzoek van de Universiteit van Maastricht blijkt dat iets meer water drinken, verspreid over de dag, goed is voor een overactieve blaas.
    Het vergroot de capaciteit van de blaas, verbetert de reacties van de blaaswand en de plasklachten nemen op termijn iets af.

    Tip 3 - Train je blaas
    Door je blaas te trainen leer je de spieren van je blaas om niet meteen gevolg te geven aan de aandrang om te plassen.
    Bij een blaastraining leer je om je plas steeds iets verder uit te stellen.
    De blaas raakt daardoor gewend om meer urine te kunnen bevatten zonder dat dit meteen tot controleproblemen leidt.
    Een plasdagboekje helpt hierbij, omdat je zo kunt bijhouden of je in staat bent om het plassen steeds iets meer uit te stellen.
    Uw arts kan u informatie geven over een blaastraining en kan eventueel medicijnen geven.

    Tip 4 - Train je bekkenbodemspieren
    Over de spieren in je blaas heb je niet veel te zeggen, maar je kunt wel controle hebben over de bekkenbodemspieren waarop je blaas rust.
    Leer jezelf hoe je de bekkenbodemspieren kan aanspannen en ontspannen.
    Ga op een stoel zitten en span de spieren aan waarmee je een denkbeeldige plas moet ophouden.
    Dit zijn je bekkenbodemspieren.
    Laat de spieren weer los en span ze weer aan.
    Probeer voor voor jezelf duidelijk te krijgen om welke spieren het gaat.
    Probeer verspreid over de dag 100 keer de spieren aan te spannen.

    Tip 5 - Plas in 'streepjes'
    Je kunt de oefening met de bekkenbodemspieren ook op de wc doen, tijdens het plassen.
    Het wordt wel ‘streepjesplassen’ genoemd; probeer het plassen steeds even te stoppen door de bekkenbodemspieren aan te spannen.
    Na verloop van tijd worden de spieren sterker en krijg je meer controle.

    Tip 6 - Let op koffie en alcohol
    Zonder dat je dat misschien beseft kunnen prikkelende stoffen je blaas dwingen tot overactiviteit. Cafeïne (cfr. 'Wat je nog niet wist over koffie' op : -) en alcohol (cfr. 'Lekker gesport – Biertje ?' op : -) kunnen de blaaswand irriteren en aanzetten tot overactiviteit.

    Tip 7 - Verlies gewicht
    Overgewicht kan een overactieve blaas veroorzaken of de bestaande blaasproblemen verergeren.
    Een dikke buik kan op de blaas drukken.
    Volgens een wetenschappelijk onderzoek kan gewicht verliezen een behoorlijk gunstige uitwerking hebben op problemen met incontinentie.
    Hoewel in het onderzoek niet duidelijk werd wat precies de oorzaak was, werkte een combinatie van gezond eten en meer bewegen het beste.

    Cfr. :

    Blaas is zelfdenkende holle spier

    Jan Willem Wensink -, 12-11-2009 - Bronnen : NHG, Urolog, Elsevier

    De blaas lijkt slechts een simpel reservoir dat urine opvangt uit de nieren.
    Maar het is een van de meest wonderlijke spieren in je lichaam.

    Leeg is je blaas niet veel groter dan een peer.
    Vol kan ze wel tot een ruime halve liter urine bevatten.
    Een gevoel van aandrang zal je krijgen vanaf het moment dat de blaas voor ongeveer eenderde gevuld is.
    De blaas is een holle spier die voorzien is van een soort neurologische tankmeter, waardoor de hersenstam vrij nauwkeurig weet hoe veel urine er in zit.
    Dankzij dat in twee richtingen communicerende zenuwnetwerk zijn je hersenen ook in staat om de blaas op commando te legen.

    Besturing in de blaaswand

    Het laten leeglopen van de blaas is nog niet zo’n eenvoudige taak.
    Als je plast zal de blaas zichzelf samenknijpen, terwijl de sluitspier van de blaas, die om de plasbuis heen ligt, zich dan juist moet ontspannen.
    Om dat allemaal goed te laten verlopen wordt een deel van de ‘besturing’ ook in de blaaswand zelf geregeld.
    Wetenschappers denken dat bepaalde cellen in de blaaswand zelf processen kunnen aansturen.

    Automatisch noodsysteem

    De blaas is voorzien van een automatisch noodsysteem dat ingrijpt als je zelf vergeet of weigert te plassen.
    Stel dat je in korte tijd veel bier drinkt of in een diepe slaap verkeert, terwijl de blaas overvol raakt.
    Dan zorgt het noodsysteem zelf voor aanspanning van spieren en ontspanning van de sluitspier.
    Zo werkt het nog niet volledig ontwikkelde besturingssysteem bij babies ook.
    Die plassen vanzelf als hun blaas vindt dat dat nodig is.
    Het systeem voorkomt zo dat er schade optreedt aan de blaaswand en dat er urine terugvloeit naar de nieren.

    Buiten de buikholte

    Hoewel je zou denken dat de blaas zich in je buikholte bevindt, is dat niet zo.
    Ze ligt onderaan de buik, buiten de buikholte en dus ook niet tussen de darmen.
    Bij mannen loopt de endeldarm (laatste deel van de dikke darm) net achter de blaas langs, bij vrouwen zit de baarmoeder daar nog tussen.
    De blaas steunt voor een groot deel op de bekkenbodemspieren, die ook een rol spelen bij de afsluiting rond de plasbuis.
    Als je je spieren aanspant om sneller te kunnen plassen, dan zet je niet je blaasspieren onder spanning, maar die van je buik.
    Deze spieren kunnen juist een deel van de plasbuis dichtknijpen.
    Ontspannen plassen is het beste voor blaas en plasbuis.


    Als gevolg van zijn bijzondere functie en werking is de blaas een gevoelig orgaan.
    Veel mensen, ongeveer 900.000 Nederlanders, ondervinden in de een of andere vorm hinder van hun blaas.
    Blaasontstekingen (cfr. : -) komen vrij vaak voor, vooral bij vrouwen.
    Maar de meest voorkomende blaasproblemen zijn ongewild urineverlies (incontinentie) en een ‘overactieve blaas’.
    Bij een overactieve blaas lijkt het systeem dat het gevoel van aandrang regelt, in de war te zijn.
    Mensen die er last van hebben, moeten per dag minstens 8 keer plassen.
    Bovendien hebben ze vaak weinig controle over hun blaas.
    Een overactieve blaas wordt ook wel ‘aandrangincontinentie’ genoemd.


    Er is nog een andere vorm van incontinentie.
    Die wordt 'inspanningsincontinentie' of 'stress-incontinentie' genoemd.
    Het komt vooral voor bij vrouwen.
    Meestal zijn verslapte bekkenbodemspieren de oorzaak, als gevolg van zwangerschap.
    Bij stressincontintentie is het moeilijk of onmogelijk om urine op te houden bij lichamelijke inspanning, zoals bij tillen of hoesten.

    Cfr. :

    Cfr. ook :

    1. Urine-incontinentie algemeen (NGH-patiëntebrief, versie oktober 2006)
      Nederlands Huisartsengenootschap (NHG)
      Deze patiëntenbrief is bedoeld als ondersteuning van het consult door de huisarts.
      De huisarts geeft de brief mee aan patiënten met de betreffende ziekte of aandoening.
      De tekst gaat ervan uit dat de patiënt al door de huisarts is gezien en dat de informatie uit de brief is besproken.
      De adviezen in de brief gelden alleen voor mensen bij wie de diagnose is gesteld.
      De informatie dient niet als vervanging van een consult door de huisarts.
      Bedenk bij het lezen dat uw gezondheidssituatie anders kan zijn dan in de teksten wordt beschreven.
      Wat is incontinentie voor urine ?
      Incontinentie voor urine wil zeggen dat u uw plas niet goed kunt ophouden.
      Het kan zijn dat u de urine niet goed kunt ophouden bij inspanning, zoals hoesten, niezen, lachen, tillen, traplopen, rennen of springen.
      Dit wordt 'inspanningsincontinentie' of 'stressincontinentie' genoemd.
      Het kan ook zijn dat u plotseling aandrang voelt om te plassen en het niet kunt tegenhouden tot u bij het toilet bent.
      Dit wordt 'aandrangsincontinentie' of 'urge-incontinentie' genoemd.
      Sommige mensen hebben last van beide vormen van incontinentie.
      Hoe werken de urinewegen ?
      Urine wordt in de nieren geproduceerd en gaat via de urineleiders naar de blaas.
      De urine wordt in de blaas opgeslagen tot deze gevuld raakt en komt dan via de plasbuis naar buiten.
      De plas wordt opgehouden door een sluitspier rond de uitgang van de blaas.
      Bovendien vormen de bekkenbodemspieren een afsluiting rond de plasbuis.
      De bekkenbodemspieren vormen een soort strakke hangmat waar uw blaas op steunt.
      Bij het opslaan van de urine wordt uw blaas opgerekt.
      Bij 150 tot 200 milliliter vulling van de blaas krijgt u aandrang om te plassen.
      Door het aanspannen van de spieren in de blaaswand en het ontspannen van de spieren rond de uitgang van de blaas en rond de plasbuis, kunt u plassen.
      Hoe ontstaat urine-incontinentie ?
      Stressincontinentie ontstaat als de afsluiting van de blaas niet goed werkt.
      Dit komt vooral voor bij vrouwen bij wie de bekkenbodemspieren verslapt zijn.
      De bekkenbodemspieren kunnen verzwakken of oprekken door een zwangerschap of bevalling.
      U kunt er ook aanleg voor hebben.
      Als de bekkenbodemspieren zijn verslapt en de blaas vol loopt, is de sluitspier soms niet sterk genoeg om de urine tegen te houden.
      Door hoesten, niezen, lachen, tillen, traplopen, rennen, dansen of springen neemt de druk in de buik toe.
      Dat geeft ook druk op uw blaas, waardoor u ongewild urine kunt verliezen.
      Ook bij overgewicht neemt de druk op de blaas toe.
      Aandrangsincontinentie ontstaat als de blaas extra prikkelbaar of ‘overactief’ is.
      Dit komt bij mannen én vrouwen voor.
      Doordat de spieren in de blaaswand plotseling samentrekken wordt de urine uit de blaas geperst.
      Dit kan zowel ’s nachts als overdag gebeuren.
      Het kan ontstaan door een aandoening van de blaas of van het zenuwstelsel of door een bijwerking van bepaalde medicijnen.
      Ook koffie en cafeïne houdende dranken hebben er invloed op.
      Het lijkt erop dat soms de angst voor urineverlies zoveel spanning geeft dat ook dat de blaasspieren plotseling doet samentrekken.
      Door een incontinentiedagboek bij te houden, kunt u ontdekken of u last heeft van inspannings- of aandrangsincontinentie (of beide).
      Zo wordt duidelijk welke oefeningen u het best kunt doen om de klachten te verbeteren.
      Bijvoorbeeld oefeningen voor de bekkenbodemspieren of voor de blaasspieren.
      Door het dagboek bij te houden, kunt u zien of de klachten verbeteren.
      Schrijf telkens op bij welke activiteit en op welk tijdstip u aandrang voelt om te plassen.
      Noteer ook wanneer u ongewild urine heeft verloren en op welke tijden u op het toilet heeft geplast.
      Hoe gaat het verder ?
      Wanneer u het dagboek voor een of twee weken heeft ingevuld, bekijken we het op de praktijk.
      We bespreken wat nu de volgende stappen zijn en welke oefeningen u eventueel kunt doen.
      Heeft u nog vragen ?
      Als u na het lezen van deze brief nog vragen heeft, dan kunt u daar bij een volgend contact op terugkomen.
      Cfr. :

    2. Blaas, (last update) 09-08-2008
      De urineblaas is min of meer bolvormig en bevindt zich, aan het eind van de twee urineleiders, onderaan de buik, achter het schaambeen.
      Vol kan de blaas gemiddeld zo'n 400 ml. urine bevatten; leeg is-ie niet veel groter dan een biljartbal.
      De beide urineleiders komen van de zijkant de blaas binnen.
      Ze lopen eigenlijk schuin door de blaaswand heen, zodat ze, als de blaas voller wordt een beetje plat gedrukt worden; op die manier wordt een soort ventiel gevormd dat verhinderd dat urine kan terugstromen naar de nier.
      De inmonding van de urineleiders ligt vrij laag in de blaas, vlakbij de uitgang.
      Er ontstaat zo een soort driehoekje (Latijn : 'trigonum') met op de punten respectievelijk de beide openingen van de urineleiders en de blaasuitgang oftewel het begin van de plasbuis (Latijn : 'urethra').
      Hoewel de blaas onderaan de buik ligt, ligt hij er eigenlijk niet in : met de darmen heeft de blaas niets te maken en het is mogelijk om operatief de blaas open te maken zonder de buikholte zelf te hoeven openen.
      Bij de man loopt de endeldarm direct achter de blaas langs, terwijl de prostaat vlak eronder is gemonteerd, om de plasbuis heen.
      Bij de vrouw ligt uiteraard de baarmoeder (Latijn : 'uterus') en schede (Latijn : 'vagina') tussen blaas en endeldarm in.
      Overigens is de plasbuis bij de vrouw (die heeft immers geen penis) tamelijk kort : slechts enkele centimeters.
      Van beide kanten komen diverse bloedvaten om de blaas van bloed te voorzien, zodat het orgaan, in noodgevallen - bijvoorbeeld na een ongeval - , best een paar bloedvaten kan missen voordat er problemen ontstaan.
      Ook de zenuwvoorziening is ruim; er loopt een heel netwerk van kleine zenuwtjes naar de blaas toe èn er vanaf.
      Zelfs is er voorzien in een aantal zenuwcellen ter plaatse, zodat een gedeelte van de besturing van de blaas ter plekke wordt geregeld.
      De urineblaas is een relatief simpel orgaan.
      De urine, die door de nieren wordt geproduceerd, wordt via de urineleiders naar de blaas getransporteerd om daar tijdelijk te worden opgeslagen.
      De blaas fungeert dus als een tijdelijke opslagruimte voor urine, zodat wij mensen niet de gehele dag urine verliezen.
      Blijkbaar was het in de evolutie belangrijk dat wij op deze wijze de urine konden bewaren; waarschijnlijk zouden we in de natuur door voortdurend verlies van urine een te gemakkelijk op te sporen prooi zijn geweest voor roofdieren.
      Een tweede belangrijke functie van de blaas is het uitdrijven van de opgeslagen urine, zodra daar een gelegenheid (bijvoorbeeld een toilet) voor is.
      Om dit vlot te laten gebeuren is de blaaswand voorzien van een spierlaag, die in staat is zichzelf, de blaas dus, tot een klein balletje samen te knijpen.
      Het legen van de blaas lijkt een eenvoudig gebeuren, maar dat is het niet.
      In tegenstelling tot wat veel mensen denken, gebeurt e.e.a. niet door de buikspieren.
      Persen (dus : de buikspieren aanspannen) is eigenlijk vrij ineffeciënt vanuit het oogpunt van blaaslediging.
      Door persen wordt weliswaar de druk op de blaas verhoogd en dus de urinestraal krachtiger gemaakt, maar tevens wordt ook de plasbuis erdoor wat samengeknepen, waardoor de urine moeilijker de blaas uit komt.
      Daarom heeft de natuur de blaas zelf een spierlaag gegeven om zo de urine efficiënt uit de blaas te verwijderen.
      Tegelijkertijd moet echter ook de sluitspier van de blaas, die zich om de plasbuis bevindt, worden ontspannen : als je de kraan niet open zet, dan komt er niets uit.
      Gelukkig hoeven we daar bij het plassen niet bij na te denken; alles gebeurt automatisch en wordt vanuit het ruggemerg geregeld.
      Hèt gevoelige plekje in de blaas is het driehoekje tussen de plasbuis en de beide urineleiders, het trigonum.
      Op een gegeven moment wordt de blaas zo vol dat ook dit gebiedje iets wordt uitgerekt; U krijgt dan, via de gevoelszenuwen in dit driehoekje, een seintje dat de blaas vol begint te worden.
      Naarmate de blaas voller wordt zullen de signalen steeds heftiger worden om U ertoe te bewegen de blaas te legen; als U zich echter blijft verzetten (of, bijvoorbeeld na een alcoholrijk feestje, niet wakker wordt) zal het regelcentrum in het ruggemerg op een gegeven moment de zaak van U overnemen en het plasmechanisme zelf aanzetten : het plassen gaat dan volautomatisch door tot de blaas leeg is.
      Babies plassen altijd volautomatisch; pas op latere leeftijd leren we de signalen van de blaas te begrijpen en worden we zindelijk.
      Ziekten en klachten
      Ziekten van de blaas kunnen worden verdeeld in een aantal categoriën :
      1/ Ziekten van de blaas zelf
      * Blaaskanker - Bij kwaadaardige tumoren van de blaas is er sprake van kanker van de binnenbekleding van de blaas.
      Deze zogenaamde 'poliepen' zien er meestal uit als paddestoelen (met een steeltje).
      Ook goedaardige poliepen komen wel in de blaas voor, maar eigenlijk alleen bij jonge mensen (onder de twintig).
      Blaaskanker verraadt zich meestal doordat het fragiele kankerweefsel gemakkelijk bloedt, resulterend in een rode verkleuring van de urine.
      Hoewel zoiets toch een alarmerend teken is, gaan veel mensen die bloed in de urine zien hiermee niet direct naar de dokter; de bloeding houdt vaak vanzelf weer op en het kan weken tot maanden 'rustig' blijven - de tumor groeit echter in de tussentijd wel door.
      Zolang de kanker beperkt blijft tot de binnenbekleding kan e.e.a. meestal relatief gemakkelijk worden verwijderd.
      Het komt echter geregeld weer terug, zodat regelmatige controles gedurende jaren noodzakelijk zijn.
      Indien de blaaskanker niet behandeld wordt, dan kan het dieper in de blaaswand doorgroeien en ook uitzaaien, bijvoorbeeld naar de lymfeklieren.
      Als het zover komt, dan wordt een behandeling uiteraard moeilijker.
      De binnenbekleding van de blaas is van het zelfde type als dat van de urineleiders en het nierbekken.
      Bij controles wegens een blaastumor zullen dan ook vaak foto's van nieren en urinewegen worden gemaakt om zeker te zijn dat ook daar geen tumoren zijn ontstaan.
      * Blaasontsteking - Een infectie van de blaas behoort tot de meest voorkomende infecties bij de mens.
      Bacteriën komen gemakkelijk via de plasbuis in de blaas, vooral bij de vrouw (die van nature een korte plasbuis heeft).
      Normaliter worden de bacteriën met de urine weer gemakkelijk uit de blaas gespoeld, maar in sommige gevallen (weinig drinken/plassen, veel bacteriën, agressieve bacteriën, verminderde weerstand tijdens griep) kan toch een infectie ontstaan.
      Het zijn meestal 'eigen' bacteriën (bijvoorbeeld uit het darmkanaal) maar er kunnen natuurlijk ook 'vreemde' bacteriën (geslachtsziekten) in het spel zijn.
      Bij de man komt een blaasontsteking minder vaak voor (want hij heeft een langere plasbuis en dus een wat minder 'bereikbare' blaas).
      Als een man een blaasontsteking krijgt, dan is er vaak meer aan de hand : (blaas-)stenen, prostaatvergroting etc.
      Ook leidt een blaasontsteking bij de man vaak tot een prostaatontsteking of een bijbalontsteking.
      * Blaasstenen - Blaasstenen ontstaan meestal niet in de blaas zelf.
      Het zijn vaak nierstenen, die via de urineleider in de blaas terecht gekomen zijn.
      Hoewel die relatief kleine stenen, in verhouding tot de breedte van de plasbuis, normaliter gemakkelijk worden uitgeplast, kan het vóórkomen dat ze, bijvoorbeeld door een vergrote, in de weg zittende prostaat, de blaas niet uit kunnen en groter worden (aangroeien).
      Blaasstenen komen vooral bij mannen voor.
      Een blaassteen kan als het ware geïmpregneerd zijn met bacteriën, zodat een blaasontsteking slechts kan genezen als de blaassteen is verwijderd.
      * Interstitiële cystitis - Interstitiële cystitis, ook wel 'blaaspijnsyndroom' of kortweg 'IC' genoemd, is een nog grotendeels onbegrepen ziekte van de blaas die gepaard gaat met verschijnselen van een blaasontsteking, vaak plassen, pijn in de onderbuik en soms bloed in de urine, terwijl geen sprake is van een bacteriële infectie.
      2/ Ziekten betreffende de functie van de blaas
      Enerzijds kan het voorkomen dat de blaasspier verslapt is, waardoor de blaas tijdens het plassen niet leeg komt.
      Anderzijds kan het zijn dat de blaas als het ware té actief is of té gevoelig, waardoor sommige mensen heel vaak moeten plassen of zelfs urine verliezen.
      Of de sluitspier van de blaas is te slap, waardoor eveneens urineverlies (incontinentie) kan optreden.
      Er zijn diverse mogelijkheden om de blaas te onderzoeken.
      Niet alle onderzoeken zijn uiteraard altijd nodig.
      Over het algemeen zal de uroloog op basis van te verwachten afwijkingen een keuze maken.
      Ook is het niet zo dat de meest moderne onderzoeken altijd beter zijn dan de al langer bestaande.
      In sommige gevallen kunnen de nieuwere onderzoeken aanvullende informatie bieden, maar dit gaat niet altijd op; zo is een CT-scan bijvoorbeeld zeer geschikt om nierkanker goed in kaart te brengen, maar kan het soms lastig zijn op die manier een blaastumor of een blaassteen te vinden die bij een cystoscopie of op een 'gewone' Röntgenfoto gemakkelijk te zien is.
      Hieronder volgen een aantal vaak verrichte onderzoeken.
      Er zijn er nog meer, maar dat zou de lijst te lang maken.
      * Is er een infectie in het lichaam (bijvoorbeeld in de nieren, blaas of prostaat) ?
      Hiervoor zijn bijvoorbeeld de meting van de bloedbezinking en het aantal witte bloedlichaampjes (leucocyten) belangrijk.
      * Hoe staat het met stoffen waarvan we weten dat ze in verhoogde hoeveelheden soms aanleiding kunnen geven tot nier- en/of blaassteenvorming ?
      Bijvoorbeeld urinezuur en calcium (kalk).
      * Is er een infectie van de blaas ?
      Vaak is aan de urine niet te zien waar in de urinewegen (nieren, blaas, prostaat) de infectie precies zit, maar soms verraadt een nierinfectie zich door grote hoeveelheden witte bloedcellen, dat zijn afweercellen tegen infecties, in de urine.
      Doorgaans is een blaasontsteking minder heftig en zijn de aantallen witte bloedcellen ook kleiner.
      * Zit er bloed in de urine ?
      Dit kan bijvoorbeeld voorkomen bij infecties, maar ook bij nier- en/of blaaskanker.
      * Zit er veel calcium of urinezuur (of andere steenvormende stoffen) in de urine, zodat de kans op blaasstenen groter is ?
      * Hoe zit het met de zuurgraad van de urine ?
      De urine behoort, als bescherming tegen infecties iets zuur te zijn.
      Op een 'gewone' Röntgenfoto kun je vaak zien of iemand een blaassteen heeft.
      De blaas zelf is echter op zo'n foto niet te zien.
      Bij een cystogram ('cyst' = 'blaas', 'grafie' = 'afbeelding') wordt via een catheter (een slangetje dat via de plasbuis in de blaas wordt gelegd) de blaas met een vloeistof gevuld die op een Röntgenfoto zichtbaar is.
      Hiermee kunnen grotere tumoren zichtbaar worden, terwijl, na legen van de blaas, tevens beoordeeld kan worden in hoeverre de blaas leeg komt.
      Bij een IVP (intraveneus pyelogram) krijg je het cystogram er 'gratis' bij.
      Middels een echografie kan de blaas met ultrageluidsgolven (dus onhoorbaar en niet voelbaar) worden afgetast.
      Door de buikwand heen is de (gevulde) blaas heel goed te zien en kunnen vaak ook andere organen, zoals de baarmoeder en eileiders bij de vrouw, worden bekeken.
      De grootte van de blaas kunnen worden beoordeeld, er kan gemakkelijk worden gezien of de blaas na het plassen goed leeg is gekomen en stenen en grote tumoren vallen goed op.
      Bij een cystoscopie wordt via de plasbuis met een rechte (starre) of slappe (flexibele) kijker in de blaas gekeken.
      Dit is wellicht het belangrijkste onderzoek van de blaas, omdat daarmee zowel de aanwezigheid van stenen of blaastumoren kan worden vastgesteld, terwijl - en passant - meteen de plasbuis zelf en de prostaat kunnen worden beoordeeld.
      Ook is het mogelijk om tijdens dit onderzoek een indruk te krijgen omtrent de conditie (de sterkte) van de blaas.
      Urodynamisch onderzoek
      Door middel van een urodynamisch onderzoek kan de functie van de blaas worden getest.
      Bij dit onderzoek wordt, nadat de blaas is geleegd, een dun slangetje via de plasbuis in de blaas gebracht, waardoor, in een langzaam tempo (druppelsgewijs), de blaas weer wordt gevuld terwijl tegelijkertijd de mate van vulling en de blaasdruk worden gemeten.
      Zo is het mogelijk om te weten te komen hoe groot de blaas is, wanneer men aandrang krijgt om te plassen (gevoeligheid van de blaas) en wat er gebeurt tijdens het plassen.
      Het onderzoek is vooral belangrijk om de conditie van de blaas te beoordelen en om de oorzaak van incontinentie, urineverlies, op te sporen.
      Het is geen pijnlijk onderzoek, wel oncomfortabel (en nat).
      Het is onmogelijk om hier alle mogelijke behandelingsvormen voor verschillende ziekten van de blaas te vermelden.
      Daarom zal worden volstaan met enkele veel voorkomende ziektebeelden.
      De behandeling is afhankelijk van de oorzaak.
      Is er alleen maar sprake van een blaasontsteking, dan is een behandeling met antibiotica (penicilline of andere antibiotica) noodzakelijk.
      Soms is er echter meer aan de hand.
      Zo kan er sprake zijn van een blaassteen die met bacteriën is 'geïmpregneerd'.
      In dat geval moet ook de steen worden behandeld.
      Of er is sprake van een afvloedbelemmering door een vernauwing van de plasbuis of een prostaatvergroting.
      Er blijft dan regelmatig na het plassen urine in de blaas achter, waardoor de kans groot is dat de infectie weer terugkomt.
      Ook als bijvoorbeeld de prostaat mee ontstoken is zal de blaas telkens weer geïnfecteerd raken.
      Ook kan er sprake zijn van een verminderde weerstand tegen blaasontstekingen, bijvoorbeeld doordat de urine niet zuur genoeg is.
      De meest voorkomende oorzaak van een blaasontsteking is onvoldoende plassen.
      Als dit schoonmaak-mechanisme van de blaas wordt verstoord, bijvoorbeeld door overmatig transpireren tijdens warme zomerdagen, dan zal de blaas onvoldoende worden schoongespoeld, waardoor bacteriën de kans krijgen zich te vermenigvuldigen.
      Als de steen niet te groot is (niet groter dan enkele centimeters), dan kan deze over het algemeen met behulp van een kijkbuisje via de plasbuis worden kapot gemaakt en verwijderd.
      Op deze wijze kan de steen in de blaas met een trilsonde worden vergruisd en het gruis vervolgens uitgespoeld.
      Grotere stenen dienen echter soms nog via een operatie verwijderd te worden.
      Ook moet er aan gedacht worden een eventuele oorzaak van de steen (nierstenen, een vergrote prostaat) te behandelen, anders komt de steen weer snel terug.
      De behandeling van blaastumoren is sterk afhankelijk van de grootte en de mate waarin ze in de blaaswand zijn doorgegroeid.
      Tevens is het belangrijk te weten of er uitzaaiingen zijn.
      Een oppervlakkige, niet uitgezaaide tumor kan vrij gemakkelijk via de plasbuis worden verwijderd (TURT : 'TransUrethrale Resectie Tumor'); in de blaas rest daarna slechts een klein littekentje.
      Frequente controle middels cystoscopie is noodzakelijk om eventuele nieuwe tumoren tijdig te kunnen verwijderen.
      In het geval van een diep in de blaaswand doorgegroeide tumor is het niet meer mogelijk om deze via de plasbuis geheel te verwijderen.
      In dat geval zal een operatie noodzakelijk zijn, waarbij een deel van de blaas, met daarin de tumor, moet worden verwijderd.
      Vaak zal in dat soort gevallen de gehele blaas moeten worden verwijderd, waarna de urineleiders via een stukje darm op de buikhuid uitkomen (stoma).
      Dit is een grote operatie, die bij sommige mensen wegens hun lichamelijke conditie niet geschikt is.
      In die gevallen kan besloten worden tot bestraling.
      In voorkomende gevallen kan ook besloten worden tot een aanvullende behandeling met medicijnen of kan een operatie gecombineerd worden met bestraling.
      Indien de (oppervlakkige) blaastumoren vaak terugkomen, kan soms met blaasspoelingen met een tumordodend middel getracht worden om deze frequentie terug te brengen; het is met deze middelen helaas niet mogelijk om de blaastumoren te genezen - wel lukt het vaak om te bereiken dat ze aanzienlijk minder vaak de kop opsteken.
      De behandeling van incontinentie is ook sterk afhankelijk van de oorzaak.
      Als het veroorzaakt wordt door een zeer gevoelige blaas (de patiënt moet dan ook meestal erg vaak plassen en kan de urine dan soms niet meer ophouden), dan is een behandeling met medicijnen, die de blaas wat rustiger maken, vaak de beste oplossing.
      Als het probleem schuilt in een slappe sluitspier, dan is er een keuze.
      Ofwel oefentherapie, al of niet onder begeleiding van de fysiotherapeut, die tot doel heeft om de sluitspier sterker te maken.
      Deze behandeling is langdurig en vraagt veel inzet van de patiënt; bij volhouden blijft het effect echter vaak levenslang bestaan.
      Bij de andere oplossing, een operatie, is dat helaas vaak niet het geval.
      Door een operatie kunnen de weefsels rondom de sluitspier strak getrokken worden, waardoor direct na de ingreep resultaat is bereikt; na verloop van tijd verslapt het weefsel echter toch weer, zodat na enkele jaren vaak een nieuwe ingreep noodzakelijk is.
      Veel patiënten kiezen echter toch voor de operatie, waarschijnlijk omdat dat makkelijker is en eigen inzet niet nodig is...
      Tegenwoordig zijn er simpelere operatieve oplossingen.
      Zo is het mogelijk om een kunststof bandje als een soort hangmatje onder de plasbuis te plaatsen om op die manier het te slappe weefsel te ondersteunen.
      Het bandje (TVT : 'Tensionfree Vaginal Tape') kan middels een kleine snede in de vagina en een tweetal kleine sneetjes juist boven het schaambeen of in de liezen worden geplaatst.
      Meestal onder verdoving met een prik in de rug of zelfs plaatselijk.
      De meeste patiënten gaan dezelfde of de volgende dag weer naar huis.
      Een andere oplossing is het inspuiten van een gel-achtige substantie juist onder het slijmvlies in de plasbuis.
      Daardoor wordt de plasbuis als het ware een beetje dichtgedrukt, waardoor het urineverlies vermindert.
      De anatomie en de precieze aard van het urineverlies bepaalt welke oplossing bij een bepaalde patiënt het beste is.
      Cfr. :

    3. Plastuit - Whiz Freedom
      HotFrog, 27-07-2009
      De Whiz Freedom is een revolutionaire nieuwe plastuit voor vrouwen.
      Doelgroep : vrouwen, van jong tot oud.
      : reizen, kampeerders, wandelaars, sport, evenementen, zieken/bedliggende vrouwen etc.
      : overal waar smerige toiletbrillen zijn of waar vrouwen niet in staat zijn zittend te plassen.
      Vrouwen kunnen met de Whiz nu comfortabel staand plassen.
      De Whiz Freedom is gemaakt van een flexibel, waterafstotend, hygiënisch en uitwasbaar materiaal en ontworpen om perfect aan te sluiten op de vormen van het vrouwlijk lichaam.
      De ergonomische vorm van de trechter voorkomt lekken of morsen en de waterafstotende eigenschappen van het materiaal zorgen ervoor dat deze plastuit met één keer uitschudden droog is.
      Het materiaal voorkomt tevens dat de urine en de daarbij behorende bacteriëen zich kunnen hechten aan het oppervlak.
      Met de Medical Design Excellence Award 2009 en een reeks patenten en goedkeuringen vanuit de medische wereld op zak is deze plastuit een nieuwkomer waar nog veel van te verwachten valt.
      Meer informatie over de Whiz Freedom is te vinden op : –.
      De voordelen van de Whiz Freedom op een rijtje :
      – niet langer plas ophouden voor vrouwen
      – eindelijk plassen als een man
      – lekt niet, door de ergonomische vorm en de kwaliteit van het materiaal
      – voorkomt zitten op een smerige toiletbril (veelal aanwezig op reis, o.a. in het vliegtuig)
      – discreet op te bergen in een speciaal tasje
      – hygiënisch door antibacteriele stoffen en waterafstotend (urine hecht zich niet aan de oppervlakte)
      – herbruikbaar tijdens de reis
      – 1 x uitschudden en de Whiz is volledig droog en schoon
      – doordat staand plassen mogelijk is wordt de blaas volledig geleegd en blijft er geen urine achter wat blaasontsteking kan veroorzaken en zelfs ergere gezondheidsproblemen op latere leeftijd waardoor plassen via een catherer nodig is.

      Cfr. :

    4. Short-term effects of increased urine output on male bladder function and lower urinary tract symptoms
      M.Spigt, J.Knottnerus, C.van de Beek, P.van Kerrebroeck, L.van Amelsvoort, C.van Schayck- Urology, Volume 64, Issue 3, Pages 499-503
      Objectives - To determine whether the human bladder can also adapt to an increased physiologic load, because bladder dysfunction is considered to be an important factor in the development of lower urinary tract symptoms.
      Animal studies have shown that bladder function can be improved by increasing the urine output.
      Methods - A total of 44 men between 55 and 75 years of age were asked to increase their daily fluid intake by 2 L for a 2-month period.
      The objective outcome measures were maximal urinary flow rate (Da Capo home uroflowmeter), maximal voided volume (frequency-volume chart) and average voided volume (frequency-volume chart).
      The International Prostate Symptom Score and global perceived benefit of the intervention were recorded to assess the subjective effects of the intervention.
      Results - The maximal flow rate increased by 13% (2.3 mL/s), the maximal voided volume increased by 23% (93.8 mL) and average voided volume increased by 25% (60.1 mL).
      Of the 44 participants, 56% reported an improvement in their lower urinary tract function, but the International Prostate Symptom Score increase was statistically significant at 1.2 point.
      Conclusions - The human bladder seems able to adapt to an increased load.
      Future randomized effectiveness studies with longer follow-up should be done to determine the upper limit of objective bladder adaptation.
      In addition, future studies should address the long-term efficacy in the prevention of symptoms.
      Cfr. :

    13-11-2009 om 11:01 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 2/5 - (1 Stemmen)
    Tags:aandrangsincontinentie, blaastraining, incontinentiedagboek, inspanningsincontinentie, plasbuis, plasdagboekje, plastuit voor vrouwen, prostaat, streepjesplassen, stress-incontinentie, trigonum, urge-incontinentie, urine-incontinentie, urineverlies
    >> Reageer (0)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Wallen en kringen onder de ogen
    Klik op de afbeelding om de link te volgen


    Wallen en kringen
    onder de ogen

    Rhijja Jansen –, 12-11-2009 - Bron : Dr Velthuis - Velthuis Kliniek : 

    Stress, vermoeidheid, roken, luchtvervuiling, slecht werkende organen...

    Wallen onder de ogen zijn voor veel mensen een bron van irritatie.
    Er bestaan ook veel misverstanden over.
    Zo worden wallen vaak verward met donkere kringen.
    Gelukkig kun je er iets aan doen.

    Wallen en kringen onder de ogen klinken hetzelfde, maar zijn twee verschillende dingen.
    Dit beaamt ook dermatoloog dr Peter Velthuis, medisch directeur van de Velthuis Kliniek : 'Een wal is een uitbochting onder het oog naar buiten en ontstaat door een te veel aan huid of vet. Het vet onder het oog dient als stootkussentje en zorgt ervoor dat het oog kan draaien ten opzichte van de kas. Bij sommige mensen is de oogkas anatomisch gezien te klein voor het stootkussentje oftewel het vet. Dit is genetisch bepaald. Als je ouders wallen hebben, dan is de kans dus groter dan jij ze hebt of ook zult krijgen.'


    Ouderdom speelt hierbij ook een grote rol. Velthuis : 'Het vet onder je oog wordt door een bindweefselschotje op zijn plaats gehouden. Dit schotje wordt slapper als je ouder wordt. Tel de zwaartekracht daarbij op en het vet zakt naar voren, wat een wal creëert.'


    Als mensen klagen over hun wallen, dan hebben ze het meestal eigenlijk over kringen : de donkere kleur onder hun ogen.
    Velthuis : 'Bij een kring hebben we het over de groef onder de wal, het greppeltje. Deze is donker van kleur. Deze kleur kan genetisch bepaald zijn, maar ontstaat ook door een gebrek aan vocht onder het oog. Bijvoorbeeld als je een tekort aan vocht in je lichaam hebt. Of doordat je vochthuishouding door een of andere reden in de war is door ziekte of slecht slapen. Hierdoor wordt de huid onder je ogen dunner en kijk je als het ware door de huid heen. Dan zie je de kleur van het grijze botvlies van je schedel, en de blauwige bloedvaten : dat is de kring.'


    Gelukkig kun je hier iets aan doen: goed slapen, voldoende water drinken en weinig of geen alcohol of cafeïne drinken, zodat je voldoende vocht vasthoudt.
    Daarnaast helpt het om niet te roken en gevarieerd en niet te zout te eten.


    Er zijn op internet veel 'remedies' te vinden die kringen onder de ogen tegen zouden gaan.
    Bijvoorbeeld door koude compressen of ijs op je ogen te leggen.
    Velthuis : 'Dit zorgt er misschien wel voor dat je kringen door de kou krimpen en dus kleiner lijken. Maar na een kwartier is dat effect weer weg, want dan houd je de kou er niet meer op.'


    Ook natte natte theezakjes en komkommers op je ogen zou helpen om vocht in te brengen.
    Velthuis zet hier zijn vraagtekens bij : 'Die komkommers zouden misschien kunnen helpen. Maar zover ik weet is hier geen wetenschappelijk bewijs voor. De theezakjes kunnen volgens mij alleen voor irritaties zorgen.'


    Koning van de 'wondermiddeltjes' is een opvallende vondst van Hollywood, dat veelvuldig door sterren en topmodellen gebruikt wordt: aambeienzalf.
    Volgens Velthuis is dit zeker een manier om je kringen (tijdelijk) tegen te gaan.
    Alleen kan dit op de langere termijn de boel alleen maar erger maken.
    'Want', zegt Velthuis : 'Aambeienzalf irriteert de huid een beetje. Dat zorgt voor een zwelling onder je ogen, waardoor je huid minder dun is, en de donkere kleur voor een paar uur wegtrekt. Maar als je dit elke dag gebruikt, krijg je geheid eczeem en gaat de huid schilferen en beschadigen.'


    Ten slotte worden we doodgegooid met serums, crèmes en vochtinbrengende sticks van de grote cosmeticamerken die donkere kringen te lijf zouden gaan.
    Dit kan helpen, maar ook hier zitten volgens Velthuis haken en ogen aan : 'Doordat in deze middelen een hoge concentratie aan fruitzuren zit, wordt er weefsel aangemaakt waardoor het moeilijker is om door de huid heen te kijken. Maar ik raad af om dit dagelijks te gebruiken, zoals veel mensen doen. Je kunt het eerst een paar keer per maand gebruiken om te zien of je huid ertegen kan. Daarna kun je het vaker gaan gebruiken. Sowieso moet je geen verschillende crèmes door elkaar gaan gebruiken, omdat je hiervan eczeem of een hypergevoelige huid krijgt.'

    Wallen bestrijden

    Het bestrijden van wallen is een ander verhaal.
    In tegenstelling tot wat veel mensen denken, bestaan wallen voor maar 10% uit vocht.
    De rest van de wal is gevuld met vet.
    Dr. Velthuis : 'Je kunt dit vocht deels weg masseren. Je duwt dan met je vingers van je neus naar je jukbeenderen, in de wal. Op deze manier duw je het vocht in de lymfebanen, die het vervolgens afvoeren.'

    Plastische chirurgie

    Maar daarmee krijg je de wal dus niet volledig weg.
    Er rest dan niet zoveel dan je wallen te accepteren en te weten dat ongelofelijk veel mensen ze hebben.
    Kun je ze desondanks niet aanzien, dan zou plastische chirurgie een laatste redmiddel kunnen zijn.
    Velthuis : 'Hierbij wordt een klein sneetje net onder de wimpers gemaakt. Dat geeft toegang tot de vetpocket, waaruit het vet verwijderd kan worden. Als de wal uit overtollig huid bestaat, wordt dit verwijderd.'


    Een kring krijgt een tegenovergestelde behandeling : ‘Omdat er hier juist iets ontbreekt, waardoor de huid doorschijnend is, spuiten we op deze plekken Restylane in. Deze behandelingen worden geen van allen vergoed. Chirurgisch verwijderen van het vet geeft een permanente verbetering. Overtollige huid neemt geleidelijk met het ouder worden weer toe. Een middel als Restylane blijft ongeveer 1- 1½ jaar zitten.

    Cfr. :

    12-11-2009 om 19:16 geschreven door Jules

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    Tags:aambeienzalf, compressen, cosmetica, donkere kringen, huid, huid, kringen, luchtvervuiling, lymfebanen: masseren, ogen, oog, oogkas, plastische chirurgie, Restylane, roken, slecht werkende organen, stress, vermoeidheid, vet, wallen
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Recovered CFS/ME Patient Goes to Washington, D.C.
    Klik op de afbeelding om de link te volgen

    Recovered CFS/ME Patient Goes to Washington, D.C.
    - MIke Dessin testifies for the CFSAC about his remarkable recovery -

    Planet Thrive, November 7, 2009

    Last year around this time, Mike Dessin almost died from severe myalgic encephalomyelitis.
    He credits his recovery to a physician in Ohio who treated him with an experimental twist on a time-tested treatment from Germany : neural therapy (cfr. : -).
    Neural therapy usually entails injecting Procaine (Novocain), a common local anesthetic, into certain areas of the body.
    This doctor uses homeopathics rather than anesthesia.
    The treatment is based on the theory that trauma can produce long-standing disturbances in the electrochemical function of tissues.

    MIke’s story is well documented on Cort Johnson’s excellent new forum “Phoenix Rising” here at New Day Treatment – cfr. : -.

    Since recovering much of his health, one of Mike’s goals has been to help educate physicians about CFS/ME through his own experience with this poorly understood disease.
    Below is his recent testimony for the Chronic Fatigue Syndrome Advisory Committee (CFSAC) in Washington, D.C.

    Here is the transcript of this speech, including the part that he was unable to read at the end due to time limitations :

    Cfr. : 
    Hi, my name is Mike Dessin,
    I’ve had Myalgic Encephalomyelits for 14 years, a disease
    that is unjustly named 'Chronic Fatigue Syndrome' in the U.S.
    I had one of the most severe cases of ME/CFS ever recorded, with subsequent remission.

    At the worst stage of my illness, which was about a year ago, I suffered beyond what most humans can comprehend.

    I was completely bedridden and unable to lean up more than a few inches.
    I was unable to read, write, understand words when spoken too or complete a thought process.
    Even a bit of thinking would hyper stimulate my nervous system too much.
    I had severe dementia.
    I couldn’t see the walls around me.
    Neurological dysfunction too obscure to put into words.
    In the last month before my recovery I was unconscious an estimated 90% of the time, not sleeping but literally unconscious.
    I was basically comatose.

    I’m nearly 6’3 and last December I weighed 102 pounds.
    I had heart failure, severe pancreatitis and my lungs collapsed.
    My body was producing just enough energy to sustain a heartbeat.

    To make things even worse, I was confined to a pitch black room isolated from the world.
    Unable to tolerate the slightest bit of light or noise much of the time.
    I had sensory overload so bad, I couldn’t be touched, as it was too stimulating.
    The consequences of being over stimulated resulted in further exhaustion and seizures.

    In addition, I had EXTREME chemical and Electromagnetic Frequency sensitivities. Needless to say, I had to be in a very special environment to stay alive.
    It is painstakingly difficult to care for someone in the condition I was in.

    I was as sick as an end stage AIDS and MS patient put TOGETHER.
    Immune deficiency similar to what an AIDS patient presents and more nervous system abnormalities than most MS patients.
    But I don’t have MS or AIDS.
    I have a disease called 'Chronic Fatigue Syndrome', which merely describes a symptom these diseases share.
    I was left for dead; I was left withering away in my dark room.
    I was left to die due to the extreme lack of knowledge, compassion or regard by our medical community.

    I had spent 10 years searching for help from doctors.
    I would hear, oh it’s JUST allergies, it’s JUST chronic Epstein Barr, it’s JUST depression, oh it’s JUST chronic fatigue syndrome and there is nothing we can do.
    In the fall of 06’ I fell down in a hotel lobby in New York, I was suffering from CFS related exhaustion.
    My dad called 911 and the ambulance came to pick me up.
    On the way to the hospital, I told the tech “I had severe exhaustion and I had Chronic Fatigue Syndrome,” some know the disease as 'Myalgic Encephalomyelitis'.
    The tech said there was no such thing as Myalgic Encephalomyelitis.

    When I arrived at the hospital they said my vitals were normal and they put me in the psychiatric unit.
    I spent 24 hours there, where I was strip searched, repeatedly questioned about my personal life and given a cocktail of psychiatric drugs.
    Shortly after, I went into my last relapse that would nearly end my life.

    Now who’s to blame for all of this ?
    Clearly this disease and its millions of sufferers have been shortchanged in an EPIC way over the last 20 years by the government, medical community and the public at large.
    There has been a false stigma attached to the disease created by lack of research and inaccurate information disseminated by the CDC.

    One major cause in this disease not getting the proper recognition stems from the naming and definition.
    The CDC wrongly changed the name of Myalgic Encephalomyelitis to 'CFS', in an attempt to undermine the serious nature of this disease, in favor of politics and economics.
    In saying that, I am just one of thousands upon thousands of ME/CFS patients who are currently suffering near the extent I was.
    The only difference, they most likely won’t live to share their experience, unless things change.
    Many ME/CFS patients succumb to cancer, heart failure, pancreatitis and other co-morbid conditions that come along with having this disease.
    Many will die from suicide, committing suicide at a rate, double that of MS patients.

    They are not committing suicide because of depression or stress.
    They are committing suicide for multiple reasons which include.

    Suicide from decrease in quality of life, created by this disease.
    Their committing suicide because, the medical community, family and friends, don’t understand what is happening to them and there is little hope for a cure.

    They are committing suicide because they can’t bare the extreme physical and neurological dysfunction.
    They are committing suicide because many of them are inundated with toxic poisoning.
    They are committing suicide because they have dozens upon dozens of infections that human beings are not supposed to get.
    They are committing suicide because they have no safe place to go, no special facilities that have staff trained to care for ME/CFS patients.
    No special facilities that are free of chemicals or sensory stimulus.
    These patients have NO WHERE TO TURN.

    So while these patients are being suffocated by toxins and destroyed by viruses, suffering greatly, the CDC’s answer, let’s spend money to research the effectiveness of cognitive behavioral therapy and graded exercise therapy.

    I’m alive and speaking to you today because I got proper treatment.
    A treatment that focuses on the true biomedical basis of this disease rather than the MYTHS created surrounding this disease.

    Myths, such as treating this disease with cognitive behavioral therapy (CBT) and psychological intervention should be primary treatments and coping mechanisms.
    As well as using Graded Exercise Therapy for increased exercise threshold.
    These therapies do not even come close to a real cure and can be extremely dangerous UNLESS they are integrated into a therapy that addresses underlying issues.

    I realize that this is the easy way out for Reeves and his side kick Simon Wessley in the U.K.
    If we think this is an effective treatment, why do I speak with thousands of ME/CFS patients who feel differently ?
    Why is there no person in this room with true CFS …..who has been helped by these therapies ?

    Why have ME/CFS patients died from extreme relapses brought on by these therapies ?
    They die, because if done at times where they have difficulty processing information, cognitive input can put them into extreme relapse.
    Yes, it actually progresses the disease.
    They die because they think graded exercise is beneficial.
    In reality, exercise in many cases can lead to further damages to their body and a downward progression of the disease.
    Yes, pacing is a good thing and that is what ME/CFS patients should do….on their own terms.

    Blaming stress and depression instead of looking for a legit biomedical explanation of this disease seems to be another easy way out for the CDC.
    It’s highly unlikely ENTIRE outbreaks have been caused by stress and depression.
    Entire towns just suddenly get ME/CFS because there stressed and depressed.
    Truth is, due to abnormalities in the nervous system brought on by this disease, stress or depression can cause disease progression, just as with most other diseases.

    You’ve been listening to patient testimony for years.
    If you really thought this is a serious issue, why do most doctors still have no idea what CFS is and many have never heard of ME ?

    Why have government funds for the study of this disease dwindled over recent years ?

    Why is this disease not taken serious by our researchers ?

    Why do our peers not take this disease seriously ?

    Why hasn’t the name chronic fatigue syndrome been changed, to accurately reflect the nature of this disease ?

    Why does the U.S have the most watered down definition of Chronic Fatigue Syndrome ?

    Why are there no facilities equipped to take care of severely ill ME/CFS patients ?

    Why are patients not covered by insurance when they seek the help of alternative minded doctors, when these doctors are the ones saving the lives of ME/CFS patients ?

    These issues still remain, because they solely reflect what you are NOT doing for our community.

    I nearly lost my life, and many others are suffering and will die prematurely, if we all don’t step up and do the right thing.

    It’s time for a New Day to begin.”

    Bravo Mike, keep up the great work speaking out for those who are unable !

    Mike Dessin testimony

    Watch the video
    at :

    12-11-2009 om 00:00 geschreven door Jules

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    Tags:CFS/ME, chronic fatigue syndrome, cognitive behavioral therapy, depression, electromagnetic frequency sensitivities, exhaustion, graded exercise therapy, homeopathics, immune deficiency, ME/CFS, myalgic encephalomyelitis, neural therapy, stress, testimony
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Chronische vermoeidheid zit niet tussen de oren
    Klik op de afbeelding om de link te volgen

    Chronische vermoeidheid zit niet tussen de oren

    Amber van Pinxteren - Gezondheid.Blog, 07-11-2009 – Bron : ME/CVS-Stichting

    Het chronisch vermoeidheidssyndroom zit niet – zoals vaak wordt gedacht – tussen de oren.
    De kans is groot dat een virus de boosdoener is.
    Dat meldt de ME/CVS-Stichting Nederland (cfr. : -).

    Amerikaanse wetenschappers ontdekten onlangs dat tweederde van de patiënten met het chronisch vermoeidheidsyndroom is besmet met het XMRV-virus.
    Hiermee denken de onderzoekers te kunnen bewijzen dat ME/CVS een lichamelijke oorzaak heeft.

    De onderzoekers bekeken het bloed van 101 deelnemers met ME/CVS en ruim 200 gezonde proefpersonen.
    Bij tweederde van de ME/CVS-patiënten was het XMRV-virus actief, terwijl slechts 4% procent van de gezonde mensen geïnfecteerd was.

    Het XMRV-virus blijkt bij mensen met het chronisch vermoeidheidsyndroom eiwitten aan te maken, waardoor het zich kan delen en verspreiden.
    Het lichaam schakelt hierop een afweermechanisme in, waarbij heftige reacties optreden.

    Bij gezonde mensen produceert het virus geen eiwitten en is er daarom ook geen reactie van het lichaam.

    De ontdekking roept echter ook vragen op, want het is niet bekend of virus de aanstichter van het vermoeidheidssyndroom is of een gevolg ervan.
    Om daar antwoord op te krijgen is verder onderzoek nodig.

    Lees ook :

    Verband tussen chronische vermoeidheid en virus
    Amber van Pinxteren - Gezondheid.Blog, 08-10-2007
    Er is een veelbelovende stap gezet in de zoektocht naar de oorzaken van het chronische vermoeidheidssyndroom (CVS).
    De aandoening houdt mogelijk verband met een virus in de maag.
    In een Belgisch onderzoek werd bij 80% van 154 onderzochte patiënten sporen van virussen aangetroffen die tot darmontstekingen leiden.
    Van de gezonde mensen beschikte slechts 7% over de virussen.
    Professor Kenny De Meirleir van het Universitair Ziekenhuis Brussel waarschuwt wel dat de ontdekking slechts het topje van de ijsberg is.
    Er is nog veel aanvullend onderzoek nodig.
    Cfr. :

    Cfr. :

    Chronisch vermoeidheidsyndroom niet tussen de oren
    - Virus in bloed mogelijk bewijs lichamelijke oorzaak -

    Persbericht - Hilversum, 5 november 2009

    Een doorbraak in het onderzoek naar het Chronisch Vermoeidheidsyndroom (ME/CVS) : Amerikaanse wetenschappers ontdekten onlangs dat tweederde van de patiënten met het chronisch vermoeidheidsyndroom is besmet met het XMRV-virus.
    Hiermee denken de onderzoekers te kunnen bewijzen dat ME/CVS, in tegenstelling tot wat vaak wordt gedacht, niet tussen de oren zit maar een lichamelijke oorzaak heeft.

    Onderzoekers Vincent Lombardi van het Whittemore Peterson Institute (Verenigde Staten) en zijn collega’s zijn verantwoordelijk voor deze interessante ontdekking.
    Zij bekeken het bloed van 101 deelnemers met ME/CVS en ruim 200 gezonde proefpersonen.
    Bij tweederde van de ME/CVS-patiënten was het XMRV-virus actief, terwijl slechts vier procent van de gezonde mensen geïnfecteerd was.

    Virus actief in lichaam patiënten

    De onderzoekers zagen dat het XMRV-virus bij gezonde mensen geen eiwitten produceert.
    Daarom reageert het afweersysteem van deze personen ook niet op de indringer.
    Bij mensen met het chronisch vermoeidheidsyndroom ligt dat anders.
    Bij hen maakt het virus actief eiwitten aan en deelt en verspreidt het zich.
    Het lichaam reageert hierop door een specifieke afweer tegen XMRV in te schakelen.
    Met heftige lichamelijke afweerreacties en besmetting tot gevolg.

    Het XMRV-virus is dus aanwezig en actief in het lichaam van ME/CVS-patiënten, dat is wat dit onderzoek uitwijst.
    Maar het roept ook nieuwe vragen op.
    Want is dit virus misschien niet de aanstichter en profiteert het alleen maar van het verzwakte afweersysteem van patiënten ?
    Om daar antwoord op te krijgen is verder onderzoek nodig.
    Dit onderzoek geeft echter wel een duidelijke lichamelijke afwijking aan bij ME/CVS-patiënten en het bevestigt ook andere onderzoeken die lichamelijke afwijkingen laten zien bij mensen met ME/CVS.
    Steeds meer onderzoek wijst er bijvoorbeeld op dat ook ontregelde mechanismen in het centrale zenuwstelsel een grote rol spelen bij het veroorzaken van geestelijke en lichamelijk uitputting bij ME/CVS.

    CDA Kamerlid Ans Willemse-Van der Ploeg

    De ME/CVS-Stichting Nederland heeft alle onderzoeken die er de afgelopen jaren zijn gedaan gebundeld in een patiëntengids.
    Ook het laatste onderzoek van de Amerikaanse wetenschappers staat hierin vermeld.
    De informatiegids wordt op woensdag 11 november aanstaande overhandigd aan CDA kamerlid Ans Willemse-Van der Ploeg tijdens een symposium van de Stichting in het kader van de “Week Chronisch Zieken”.
    U ben van harte welkom om het symposium bij te wonen.
    Het middagsymposium is van 13.30 tot 16.30 uur in het Beatrixgebouw van de Jaarbeurs, Jaarbeursplein 6 te Utrecht (naast het NS-station van Utrecht).
    Parkeermogelijkheid : Parkeergarage Jaarbeursplein.

    Naar schatting één procent van de wereldbevolking lijdt aan het chronisch vermoeidheidsyndroom.
    De ziekte kenmerkt zich door een slopende vermoeidheid die vele jaren kan aanhouden.
    De ziekte is lastig te behandelen zolang de oorzaak onduidelijk blijft.
    De ME/CVS-Stichting Nederland is de patiëntenorganisatie voor mensen met het chronisch vermoeidheidsyndroom (ME/CVS).

    Cfr. :

    11-11-2009 om 13:32 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 1/5 - (3 Stemmen)
    Tags:chronisch vermoeidheidssyndroom, chronische vermoeidheid, CVS, ME/CVS, virus, XMRV-virus, XMRV
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Dr. Bauer heeft mijn leven gered
    Klik op de afbeelding om de link te volgen

    Dr. Bauer heeft mijn leven gered

    Joke Mot – Gastenboek,.10-11-2009


    Ik heb waarschijnlijk sinds mijn derde jaar FMS.
    Ik had altijd pijn in mijn benen en later ging dat over naar mijn nek, handen en rug.

    Op een gegeven moment ben ik gewoon van school gestuurd omdat de opleiding door deze ziekte voor mij te zwaar werd.

    In 2004 ontmoette ik bij toeval een thuishulp die me erop wees dat ik waarschijnlijk fibromyalgie had .
    Ik heb mij er toen op laten onderzoeken en het bleek inderdaad FMS te zijn.

    Wat later leerde ik iemand kennen die toevallig ook FMS had.
    Ze had toen al van Dr. Bauer had gehoord.

    Eerst dacht ik : 'Ja hoor, 't zal wel weer de zoveelste zijn die denkt dat hij mensen kan genezen...' : ik had al zoveel onderzoeken, behandelingen en therapieen ondergaan dat ik er gewoon niet meer in geloofde.

    Totdat ze zich liet opereren en ik zag hoe goed ze vooruitging.
    Ik begon er zowaar in te geloven !

    In Januari 2009 ben ik naar Dr Bauer gegaan.
    Nadat hij mij onderzocht had bevestigde ook hij dat ik FMS had, in alle vier de quadranten.
    Ik kreeg van hem een lijst met alle mogelijke klachten die je zo kan hebben als FMS patient... en dat waren er best veel !

    Ik schrok : er was maar één klacht waarvan ik niet zeker was dat ik ze ook had.
    Ik was flink van slag omdat ik nu met de neus op de feiten werd gedrukt van hoe ziek ik eigenlijk wel was.
    Ik wist dat ik ziek was, maar zó ziek, dat besefte ikzelf niet : in december, de maand vóór de operatie, had ik zelfs een afscheidsbrief klaar omdat ik gewoon niet meer wist hoe het verder moest.
    Het was gewoon niet meer te dragen : ik kon niet meer liggen, zitten en staan, alles deed pijn en slapen kon ik daardoor ook niet meer.
    Het was écht héééél erg !

    Tegen mijn huisarts had ik gezegd dat als ik niet wist dat ik in januari geopereerd zou worden ik niet meer zou willen verder leven.
    Zij sprak me evenwel moed in : 'Dan moet je tóch een weg zien te vinden om door te gaan'.

    Mensen begrijpen niet hoeveel pijn FMS patienten eigenlijk allemaal moeten doorstaan.

    Doordat ik zo een vertrouwen gekregen had in Dr Bauer heb ik die afscheidsbrief verscheurd : in je binnenste wil je immers helemaal niet dood, maar op het einde zie je gewoon geen uitweg meer !

    Gelukkig vond ik Dr. Bauer...

    Ik ben dan ook blij dat ik op 13 januari 2009 geopereerd ben, aan mijn rechterarm.
    Ik voelde al meteen verbeteringen !

    Ik sliep meteen na de operatie goed en dat na jaren niet goed kunnen slapen.

    Als ik s'morgens wakker werd rende ik naar de kraan om mijn handen onder warm water te houden want die voelden zeer verdoofd aan, alsof ze heel erg sliepen en dat deed pijn en door de warme water ging die weg.

    Ik had ook altijd al last van mijn stuitje.
    Ook die pijn is weg en dat was natuurlijk ook een hele verbetering !

    Op 20 oktober 2009 ben ik voor de 2e operatie bij Dr Bauer geweest.
    Nu was mijn rechterenkel aan de beurt.

    Ik ben zo blij dat ik geopereerd ben.

    Ik had sinds Pinksteren heel veel last van spierkrampen/ spasmes.
    Ik ben daarvoor een aantal keer naar het ziekenhuis gebracht omdat ik gewoon dreigde te stikken.
    Maar in het ziekenhuis namen ze me niet serieus.
    Ze hebben me zelfs op een gegeven moment het ziekenhuis uitgezet !

    Tot mijn vriendin me weer haar een CVT-apparaat (cfr. : -) te leen gaf (ik had het namelijk al eerder geprobeerd) : toen ze eens bij me was en ik weer last kreeg van spierkrampen/ spasmes stelde ze voor het CVT-apparaat opnieuw te gaan gebruiken en – ja hoor – door de trillingen verdwenen ze.
    We stonden beiden versteld : ook hier was er beterschap !

    Ondanks alles wilde Dr Bauer toch dat ik neurologisch onderzocht zou worden.
    In afwachting annuleerde hij een eerder gemaakte afspraak (die in juni gepland was), want mochten de klachten inderdaad een neurologische oorzaak hebben dan bestond de kans dat ik tijdens de operatie zo een aanval zou krijgen en dat kon natuurlijk niet !

    Ik was wel erg teleurgesteld...

    Maar ik heb zijn raad opgevolgd en onderzoek wees uit dat het allemaal helemaal niet neurologisch was en dus kon ik (op 20 oktober) geopereerd worden.
    Al ging die operatie bijna toch niet door : er was een administratieve fout !
    Gelukkig hebben we dat recht kunnen zetten, mede dankzij de bereidwillige inzet van George en mijn vriendin.

    Ik kreeg een injectie in mijn been, maar ik viel niet meteen in slaap zoals bij de eerste operatie.
    Ik ben zelfs de ganse tijd bij bewustzijn gebleven !

    Ik weet nog dat de vrouw van Dr Bauer zei dat als ik pijn voelde ik dat maar moest aangeven.
    Dat deed ik ook en dan kreeg ik meteen weer een kleine prik en voelde ik meteen niets meer.
    Ze zei ook nog : 'Ja, wie beter wil worden moet pijn lijden'.
    Ik antwoordde dat het niks was in vergelijking met wat wij FMS-patienten dágelijks voelen.
    We moesten er alle drie om lachen en ze bevestigde het : 'Ja, dat is waar, dus kunnen we rustig doorgaan...'

    Na de operatie ben ik - na een afspraak gemaakt te hebben voor controle de volgende dag - richting hotel gegaan en daar heb ik heerlijk geslapen.

    Vóór de operatie had ik nog altijd een heel strak gevoel rond mijn vingers, maar dat was na deze operatie meteen weg.

    Ook kon ik weer met mijn handen onder mijn hoofd liggen.
    Dat kon ook al jaren niet meer, want dan begonnen ze pijn te doen.
    Nu kon dat meteen al, zonder er last van te krijgen !

    Er waren dus weer verbeteringen voelbaar...

    De volgende dag, toen ik voor controle moest komen, kreeg ik net weer last van die spierspasmes/ krampen.
    Mijn vriendin zei : 'Laat ze nu maar komen : dan kan Dr. Bauer ze ook zien !'.
    Toen konden beiden, Dr. Bauer en zijn echtgenote, vaststellen dat die spierspasmes/ krampen helemaal niet neurologisch waren, maar Dr. Bauer dacht wel aan een medicatievergiftiging.
    Hij zei me meteen te stoppen met o.a Tramadol (ook met alle andere medicatie trouwens !).
    Mocht blijken dat de spierspasmes/ krampen daarna nog blijven bestaan, dan moet één en ander verder onderzocht worden, maar – zo zei hij - Tramadol kán inderdaad spierkrampen/ spasmes opwekken, net als Tramagetic (ik vermeld dit als waarschuwing voor anderen met dezelfde problemen).
    Voor mij is het nu dus afwachten...

    Ik heb – sinds mijn thuiskomst in Nederland - geen spierkrampen/ spasmes meer gehad.
    Toevallig vandaag heb ik echter weer een aanval gekregen, maar door de medicatie is die gelukkig weer onder controle (sinds de operatie gebruik ik eigenlijk alleen maar zonodig Paracetamol, wat op zich al een hele grote verbetering is als je weet wat ik vroeger aan medicatie gebruikte !).

    Nu dus afwachten wat het resultaat van de operatie in de loop der maanden zal zijn voor mijn lichaam...

    Maar ik ben zo blij !

    Dr Bauer heeft écht mijn leven gered en ik ben hem zeer dankbaar.

    Ook George wil ik heel hartelijk bedanken !
    Dank je, Georges, voor de tijd en de energie die jij besteed hebt opdat de operatie kon doorgaan.

    Ik hoop dat er meer mensen de weg naar Dr Bauer zullen gaan maken, want écht het werkt.

    Succes !

    Groeten, Joke.

    11-11-2009 om 05:06 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 4/5 - (4 Stemmen)
    Tags:Bauer Dr., CVT-apparaat, cycloïde vibratie therapie (CVT), FMS, medicatie, medicatievergiftiging, operatie, pijn, quadranten, slapen, spierkrampen, spierspasmes
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Has your marriage been damaged by fibromyalgia or chronic fatigue syndrome ?
    Klik op de afbeelding om de link te volgen


    Has your marriage been damaged
    by fibromyalgia or chronic fatigue syndrome ?

    Adrienne Dellwo, Guide to Fibromyalgia & CFS –, November 7, 2009

    I recently came across a poll on the impact fibromyalgia (FMS – cfr. : -) has on marriage and I asked if I could share the results here (thanks, Ray !).
    It's not a scientific poll, but it shows some interesting trends, so I wanted to ask some of the same questions here and also broaden it to include chronic fatigue syndrome (CFS or ME/CFS – cfr. : -& - -).

    Of the participants, 96% were women, and the vast majority were under 40 both at the time of diagnosis and when the poll was taken.
    Just over 60% said they were either married or in a long-term committed relationship when their symptoms appeared.
    When asked if the symptoms and limitations changed their relationship, here's what they said :

    • for the better : 16.7%

    • not much change : 16.7%

    • caused a strain : 38.9%

    • caused the relationship to end : 27.8%.

    It's certainly not surprising that a major, life-changing illness can damage a relationship, but it's especially disturbing to me that more than a quarter of respondents said it ended their relationship.
    Also, it caused a strain in more than double the relationships it changed for the better.
    It's sad that 65% of these people have had to deal with relationship problems and/or divorce on top of being sick.
    I have to wonder if a more widely accepted diagnosis makes a difference in how well our spouses, as a whole, would be able to accept the changes forced upon them.

    What has your illness done to your relationship(s) ?
    Did the length of time you'd been together make a difference ?

    Share your stories and take the polls at :

    Living with someone who has fibromyalgia or chronic fatigue syndrome
     - Bridging the gap between your old life and your new one -

    Adrienne Dellwo –, (updated) February 20, 2009 (reviewed by the Medical Review Board)

    Living with someone who has fibromyalgia1 (FMS) or chronic fatigue syndrome2 (CFS or ME/CFS3) is a tough job, whether that person is completely disabled, 50% functional or goes through occasional flares.
    In all likelihood, having a chronically ill person in your household will impact your life.

    You can, however, take steps to make things easier for yourself.
    Do you feel guilty for even wanting that ?
    You're not alone -- a lot of people in your situation feel like they should be worried about the sick person and not themselves.
    My husband has struggled with that, and we've both had to learn that it's OK for him to be frustrated with the situation.
    Your first step is to accept that living with someone who has fibromyalgia or chronic fatigue syndrome doesn't mean you forfeit your right to feelings of your own.

    But let's be completely honest here : those of us with FMS or ME/CFS can be difficult people to deal with at times.
    When you're feeling especially burdened by housework, financial matters and caretaking, a sharp tongue or blank stare doesn't help matters at all.
    You may not be able to discuss your feelings with the sick person in your life as she might not be in a place to accept that your feelings are directed at the situation and not at her.
    It's a good idea to find support from other places to get you through this.

    Feeling the loss of "how things were"

    Both you and your loved one will have to come to terms with changes in your life.
    FMS and ME/CFS are chronic conditions, which means your life is not likely to ever be what it was before.
    That's a tough thing to accept and you'll each need to reach acceptance in your own way and in your own time.

    Essentially, you need to grieve for what you've lost.
    The stages of grief are :

    • denial : a refusal to accept what is happening.

    • anger : feeling like it's not fair or being angry in general.

    • bargaining : promising something such as being a better person if the situation goes away.

    • depression : giving up, not caring what happens.

    • acceptance : coming to terms with the situation and being ready to move forward.

    Where are you in the grief process ?
    Identify it now, and look at what the next stages are likely to bring.
    If you feel like you've been stuck in one stage, find someone to talk to about it.
    If you feel like you need a professional counselor to help you, don't be ashamed of that and talk to your doctor.
    If you become clinically depressed or simply cannot accept your new situation, you won't be doing any good for yourself or for the sick person in your life.

    Managing your expectations - Three steps

    Part of accepting the situation is managing your expectations.
    For example, my husband and I used to go for bike rides, do some hiking, maybe take a canoe out on the river.
    He's had to change his expectations about how we will spend our time together.
    I also left my career and my income behind and hoped that I'd be able to find something I could do from home.
    That meant he had to change expectations about our financial future as well.

    Step #1

    The first step toward managing your expectations is to take an honest look at your situation and ask yourself : "What do I know about the circumstances ?".
    Taking a little time to learn about and understand the condition will help you deal with the reality it creates.

    What do you know about your loved ones illness ?
    Do you really understand it ?
    Here are resources that can help :

    Step #2

    Second, take a long-term look at things.
    Think : "If things stay just as they are now for a year or longer, how will that impact me, my family, and the person who is sick ?".
    This can be an overwhelming question, when you consider financial, emotional, social and emotional issues.
    Approach them one at a time and try to stay logical.

    Once you've identified what is likely to change, allow yourself to grieve for the things that have to fall by the wayside (at least for now) and let them go.
    Then focus on the areas where you foresee big problems and work toward realistic solutions.

    Step #3

    Don't feel like you're alone in finding solutions.
    Involve your sick loved one as much as possible, call on friends, family, doctors, clergy, social services, your insurance company and anyone else who may be able to help you find ways to get through this.

    Moving on with your life

    Once you've gone through the stages of grief and the steps outlined above for changing your expectations, you'll likely be better equipped to move forward with your life and to be supportive of the sick person in your life.
    On behalf of that person, I thank you for taking the time to care.


    Cfr. :

    11-11-2009 om 00:00 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags:chronically ill, acceptance, anger, caretaking, CFS, chronic conditions, chronic fatigue syndrome, denial, depression, divorce, fibromyalgia, financial matters, FMS, grief, housework, ME, ME/CFS, moving on with you live, relationship, sick, support
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    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Vijf grootste bedreigingen gezondheid
    Klik op de afbeelding om de link te volgen




    Vijf grootste bedreigingen gezondheid

    ConsuMed., 10-11-2009

    Vijf factoren spelen een rol bij ongeveer een kwart van de sterfgevallen wereldwijd.

    Het gaat om :

    1. onveilige seks,

    2. overmatig alcoholgebruik,

    3. ondervoeding bij kinderen,

    4. slechte hygiëne en

    5. hoge bloeddruk.

    Door die aan te pakken kan de gemiddelde levensverwachting met vijf jaar worden verhoogd.
    Dat zegt de Wereld Gezondheidsorganisatie (WHO) na onderzoek naar 24 belangrijke gezondheidsrisico`s.

    Ondervoeding bij kinderen in ontwikkelingslanden is een probleem, maar overgewicht in rijkere landen evenzeer.

    In de nabije toekomst zou de situatie kunnen ontstaan dat vroegtijdig overlijden als gevolg van te veel eten meer voor komt dan overlijden door ondervoeding, zeggen de onderzoekers.

    Cfr. :

    10-11-2009 om 20:04 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 4/5 - (2 Stemmen)
    Tags:gemiddelde levensverwachting, gezondheidsrisico`s, hoge bloeddruk, ondervoeding bij kinderen, ondervoeding, ontwikkelingslanden, onveilige seks, overgewicht, overlijden, overmatig alcoholgebruik, slechte hygiëne, te veel eten, vroegtijdig overlijden
    >> Reageer (1)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Onbegrepen lage rugpijn beter te behandelen
    Klik op de afbeelding om de link te volgen


    Onbegrepen lage rugpijn beter te behandelen, 09-11-2009 – Bron : Erasmus MC (cfr. : -)

        ROTTERDAM - Op dit moment richt de behandeling van onbegrepen lichamelijke klachten zich met name op de psychosociale kant van het probleem.
    Volgens promotie-onderzoek van Jan-Paul van Wingerden aan het Erasmus MC zou een combinatie van behandelingen beter zijn.

    Van Wingerden vindt het belangrijk dat de fysieke aspecten weer worden bekeken bij het begrijpen en behandelen van chronische rugklachten (cfr. : -).

    Tegenwoordig is bekend dat spieren zich bij klachten anders en niet optimaal gaan gedragen.
    Gewone dagelijkse activiteiten, zoals lopen, staan, bukken of tillen, leveren hierdoor sneller overbelasting op.

    Met zijn combinatietherapie bekeek Van Wingerden ook hoe mensen in het dagelijks leven zich bewegen en hielp ze aan een gezondere houding.
    Zo kunnen zij hun dagelijkse activiteiten uitbreiden zonder terugval.

    Van de 245 uitbehandelde patiënten met chronische lage rugklachten heeft 53 procent met deze therapie minder last van pijn en kan 62 procent zich vrijer bewegen.

    Lage rugpijn

    Bijna een derde van de Nederlandse bevolking van 25 jaar en ouder heeft langer dan drie maanden last van rug of nek.
    Meer dan 3 miljoen mensen hebben chronische lage rugklachten (cfr. :

    Van Wingerden promoveert woensdag op zijn onderzoek.

    Cfr. :

    10-11-2009 om 19:04 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 2/5 - (3 Stemmen)
    Tags:bewegen, bukken, chronische rugklachten, lage rugpijn. Lopen, nek, onbegrepen lichamelijke klachten, overbelasting, pijn, rug, spieren, staan, tillen
    >> Reageer (1)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Je beste antistresstip
    Klik op de afbeelding om de link te volgen


    Mijn moeder is een stresskip

    Kinderen Voor Kinderen

    Het is weer eens zo'n dag
    Dat ik niks van mijn moeder mag
    Ik weet het is weer mis,
    als ze zo chagarijnig is.
    Hoe dat komt dat weet ik wel
    ze doet alles veel te snel
    relexe toch eens
    denk ik dan
    daar wordt je minder gestressd van

    Refrein :

    M'n moeder is een stresskip (ojeh)
    M'n moeder is een stresskip (ojeh)
    M'n moeder is een stresskip (ooohjehh)

    Zit ik op mn kamer
    Lekker niks te doeoen
    Dan hoor ik haar weer.
    Ik erger me geel en groen
    Naar beneden komen ruim je rommel op
    of ik het doe of niet
    ik krijg toch op mn kop
    Ze is wel lief maar soms zit ze erdoorheen
    Komt ze ver uit de hoek
    en doet ze best gemeen

    Refrein :

    M'n moeder is een stresskip (ojeh)
    M'n moeder is een stresskip (ojeh)
    M'n moeder is een stresskip (ojehhhh ooojehjehjehjeh)
    M'n moeder is een stresskip ( is ene stresskip)
    M'n moeder is een stresskip ( zo'n stresskip)
    M'n moeder is een stresskip (oooojehh)

    Ik hou me rustig en gedijst
    tot ze zoveel van me ijst
    dat ik uit m'n vel spring
    uit m'n vel spring

    Refrein :

    M'n moeder is een stresskip (is een stresskip)
    M'm moeder is een stresskip (zo'n stresskip)
    M'n moder is een stresskip (ooojehhh oohhhjehjehjehjeh)
    M'n moeder is een stresskip (is een stresskip)
    M'n moeder is een stresskip (zo'n stresskip)
    M'n moeder is een stresskip (ooojehhh oooohhjehjehjehjeh)
    (M'n moeder, m'n moeder ) ongeloffelijke stresskip
    (M'n moeder, m'n moeder) een super duper stresskip
    (m'n moeder m'n moeder)wat een stresskip

    M'n moeder !

    Cfr. :

    Geef een gouden tip, 10-11-2009 - Artikelnummer 6923

    Ben jij een echte stresskip of kun je net heel gemakkelijk de knop omdraaien ?

    Wat doe jij om te ontstressen ?

    Post je beste antistresstip

    via :

    of lees er de
    tips van anderen

    Stem op de beste tip en bepaal wie kans maakt op een mooie prijs.

    Elke week is er een Bongobon ter waarde van 50 euro te winnen en op het einde van de rit wordt de beste tip beloond met een vakantiecheque van 1 500 euro.

    Doe je mee ?

    Deze stresstip van Pascale Roskam uit Sint-Gillis-Waas haalde vorige week de meeste stemmen bij de actie ' van CM' :

    'Luister eens naar de stilte'.

    Cfr. :


    Doe de stresstest

    - -


    10-11-2009 om 11:00 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 3/5 - (1 Stemmen)
    Tags:ontstressen. stress, stresskip, stresstest
    >> Reageer (1)
    Klik hier om een link te hebben waarmee u dit artikel later terug kunt lezen.Sufferers of chronic fatigue see life as a balancing act
    Klik op de afbeelding om de link te volgen


    Janet Krause (Lebanon Township) suffers from chronic fatigue syndrome and
    fibromyalgia, which force her to spend a lot of her time resting on the couch
    - John C. Whitehead, The Patriot-News -

    Sufferers of chronic fatigue see life as
    a balancing act

    Body and Mind staff -, November 08, 2009

    Janet Krause keeps a set of golf clubs in her Lebanon Township home even though it’s been 10 years since she has swung one.

    They represent hope to her — hope that one day she will have the stamina to play golf and not be limited by the effects of the chronic fatigue and immune dysfunction syndrome that marks her daily life.

    Commonly called 'chronic fatigue syndrome' (cfr. : -), it is a debilitating and complex disorder characterized by profound fatigue that is not improved by bed rest and that may be worsened by physical or mental activity, according to the Centers for Disease Control (cfr. : -).

    People with CFS suffer from fatigue often accompanied by insomnia, weakness, muscle pain, impaired memory and/or mental concentration, a chronic sore throat and irritable bowel syndrome, among other symptoms.

    Life for us is different. We have to constantly balance what we can do and people don’t understand that. That’s why a lot of relationships and friendships break up,” said Krause, 58, who suffered from the disorder for at least 15 years before receiving a diagnosis.

    Not only is CFS hard to diagnose — labeled as such only after tests come back negative for other things such as lupus, Lyme disease, multiple sclerosis or various cancers — it also carries a stigma of being more mental than physical, a challenge for sufferers to overcome.

    The ‘It’s all in your head’ comments ? I get those from everybody, even my family,” said Krause, who leads the Chronic Fatigue and Immune Dysfunction Syndrome Support Group of Lebanon County : “When I say I’m tired, I hear : ‘Well I’m tired, too. All you need is a little extra sleep.’ That’s a slap in my face. Tired is one thing, but body systems breaking down is another.”

    Chronic fatigue syndrome is a viable medical condition. It’s not ‘all in your head,’” said Dr. Robert Matsko Sr., a physician at Broad Street Family Health Center in Marysville, part of the Holy Spirit Health System : “The problem is that there’s no specific test for CFS, and symptoms can be transitory.”

    Studies have shown that between 1 million and 4 million Americans suffer from CFS, but less than 20 percent have been diagnosed and about half of the sufferers haven’t even consulted a doctor.

    The symptoms are nonspecific and so people don’t come in because of this,” Matsko said : “They think they’ll just live with it, but it only gets worse. There are many different levels of it, from people still being able to work to people who can’t get out of bed.”

    There’s no known cause for CFS, however, a recent study published in the journal Science, pinpointed a newly discovered virus, called xenotropic murine leukemia virus-related virus or XMRV, as a possible cause of CFS.

    Researchers from the National Cancer Institute and the Cleveland Clinic said XMRV affects the immune system, might cause a variety of illnesses and could join with other viruses to initiate CFS.

    Krause, who began having symptoms in her 20s, has suffered from skin rashes, breathing trouble, sinus problems, chemical sensitivity, migraines (cfr. : -), sore throats, eye focus problems, arthritic pain and crushing fatigue.
    She also has fibromyalgia, a similar condition that some experts think is another variant of CFS.
    Generally, CFS patients experience severe fatigue, while fibromyalgia patients experience more pain.

    Realizing that she might have to quit her job in hospital food service, Krause began going to night school to learn medical transcription.
    It was then that she began learning about a condition she recognized in herself — chronic fatigue.

    I put all this together before I got an accurate diagnosis,” she said. “It was a great relief to have a diagnosis, but it was also somewhat devastating because as you read about all the things it can affect, you begin to live under this fear of : What might it do to me ?

    In 2005, when she began dropping boxes at work, couldn’t hold a pencil and was ready to sleep at 3 p.m., Krause knew she had to quit her job.
    Now on disability, she has good days — which she defines as feeling almost like a normal person — and bad days where she has to take a rest after any small excursion.

    Twenty years ago, no one had heard of CFS, but today doctors are better at recognizing it and treating it,” Matsko said.
    There’s no catch-all remedy, so doctors might prescribe a combination of medications to treat inflammation, pain, sleep problems and depression as well as recommend lifestyle changes such as not overexerting oneself, reducing stress (cfr. : -), eating a diet rich in fresh rather than processed foods, weight control and light exercise,” he said.

    The sooner a person is diagnosed and begins treatment, the more favorable his or her long-term outcome.
    However, probably only 5 percent to 10 percent of people fully recover from CFS, studies state.

    A positive attitude is crucial,” Krause said.
    I try to help our support group people be as independent as possible, to trust themselves to go out there and do as much as they can without overdoing,” she said : “Having a can-do attitude and having things to look forward to helps offset the sadness of all you’ve lost.”

    To learn more

    • Join the Chronic Fatigue and Immune Dysfunction Syndrome Support Group of Lebanon County by calling Janet Krause at 273-9036.
      The group meets the second Thursday of every month from 3 p.m. to 5 p.m. at Philhaven, 283 S.
      Butler Road in Mount Gretna.
      The group welcomes anyone in the south-central Pennsylvania area.

    • Visit the CFIDS Association of America Web site at : -.

    Cfr. :

    10-11-2009 om 09:54 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 0/5 - (0 Stemmen)
    Tags:chronic fatigue syndrome, depression, fibromyalgia, immune system, inflammation, insomnia, pain, positive attitude, sadness, sinus problems, skin rashes, sleep problems, sore throats, stress, virus, weakness, weight control, XMRV
    >> Reageer (1)
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    Klik op de afbeelding om de link te volgen

    08-11-2009 om 23:39 geschreven door Jules

    0 1 2 3 4 5 - Gemiddelde waardering: 1/5 - (3 Stemmen)
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